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Ministry of Health Care of Uzbekistan
CENTRE FOR MEDICAL EDUCATION
TASHKENT MEDICAL ACADEMY
"APPROVED"
Vice President for Academic Affairs, TMA
Professor Teshaev OR
"_________" ___________________ 2012
Educational-methodological development for the practical sessions on common technical
SYSTEM IN THE SUBJECT "Endocrinology"
.
For students year 6
therapeutic and "military-medical" faculty
Tashkent - 2012
1
Compiled by:
Azizova Pokiza Khusanovna - dotsent
The educational technology is approved:
At the meeting of chair
Minute № from «_____» ____________ 2012 city.
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Ministry of Health Care of Uzbekistan
CENTRE FOR MEDICAL EDUCATION
TASHKENT MEDICAL ACADEMY
Department of Internal Medicine TRAINING GP endocrinologist
The subject of "Endocrinology"
Topic: "The syndrome of polyuria and polydipsia"
concept. The influence of hormones on diuresis. Diseases of the endocrine system, leading to
polyuria and polydipsia: diabetes insipidus, Conn's syndrome, hyperparathyroidism. Diabetes.
Classification, diagnosis. Differential diagnosis of type 1 and 2 diabetes. Tactics GPs.
Educational and methodical development
(For teachers and students)
Tashkent - 2012
3
Process chart one
Syndrome of polyuria and polydipsia.Term.The influence of hormones on diuresis.Diseases of
the endocrine system, leading to polyuria and polydipsia: diabetes insipidus, Conn's syndrome,
hyperparathyroidism.Diabetes.Classification, diagnosis.Differential diagnosis of type 1 and 2
diabetes.Tactics GPs.
№
e tapas practice session
f rma classes
m of esto
Th e
literature
classes
225 min.
1 Centuries odnaya part (study subject)
2 Judgment about topics practice session with new teaching op grew discussion
technologies ("Snezhkov," "The Weakest Link"), as well as training room
demonstration material (boards, sets of medical records, tables,
poster, X-rays, blood glucose meter, test strips, case studies) to
determine the original level .
3 You discuss water
4 The definition of reference for the practical part - n
of judgment
rofessionalny questioning. Explanation of the provisions and
training room
recommendations for the job to fill medical records.
10
40
5 Military wasps practical training under the guidance of a Prospect ofes sional
teacher.
questions, talk with
patients filling medical
records, case studies.
Department of
Endocrinology Clinic 1TTA
6 John interpretation of the survey data of patients - complaints, tory studies of the disease,
inspection, palpation, percussion and auscultation of patients laboratory data situational
as well as laboratory and instrumental studies
problems
Department of
Endocrinology Clinic 1TTA
7 Judgment on the theoritical and practical knowledge of the mustache tny survey,
students, fixing material, the level of learning assessment.
tests, discussion,
identification of practical
skills
Department of
Endocrinology Clinic 1TTA
8 The definition of output on practical training, evaluation of infor mation, questions for
100-point system, and ad evaluations. Homework the next homework.
practice session (a collection of questions).
training room
20
Lesson number one
4
10
20
25
75
25
1.Syndrome of polyuria and polydipsia.Term.The influence of hormones on diuresis.Diseases of
the endocrine system, leading to polyuria and polydipsia: diabetes insipidus, Conn's syndrome,
hyperparathyroidism.Diabetes.Classification, diagnosis.Differential diagnosis of type 1 and 2
diabetes.Tactics GPs.
educational time: 6:00
Art structure training session 1. cafedra to internal medicine training
GPs with an endocrinologist, endokrinologichessome branch 1 TTA clinic, clinical
1-clinic laboratory TTA;
2. Sets of tables, methodological recommendations
tion, laboratory and instrumental data, video;
3. TCO: computer, video
The training session:
- The acquisition of knowledge and skills in students GPs to diagnose
and differential diagnosis of endocrine diseases, accompanied by
polyuria and polydipsia.
- N know how to use modern classifications of these diseases;
- N find out early detection and prevention of diseases on the basis of individual
symptoms, syndromes.
Pe dagogic tasks:
D results of training activities:
- To consider the causes of GP
polyuria and
should know:
polydipsia;
- Endocrine diseases associated
- Discuss the non-self- syndrome of polyuria and polydipsia;
diagnostic methods
- To understand the mechanisms of polydiabetes mellitus and the Uriah and polydipsia with endocrine violation
differential
sheniyah;
ing
diagnosed
with - Learn how to assess compensation criteria and
psychogenic
severity of diabetes;
polydipsia, enuresis, pyelitis - To analyze the data provided by endocrine
and
tious diseases with syndrome of polyuria and
glomerulonephritis;
polydipsia;
- To analyze the treatment of should be able to:
various
- Interpret the urine - a common and
forms of diabetes insipidus;
Zimnitskiy;
- To analyze the pathogenesis - Interpret blood sugar;
of nocturnal
- Interpretation of the data tolerance test glucosepolyuria
with
Conn's goat;
syndrome;
- Interpretation of the test with restrictions
- Discuss the differential diag- tion of the liquid;
nostiku Conn's syndrome with - Interpretation of the test with pituitridiabetic
Mr.
cal nephropathy;
must have skills:
- To consider the pathogenesis - Professional questioning, examination n atsienta,
of polyuria and
questioning relatives;
polydipsia
with - Interpretation of the clinical laboratory
hyperparathyroidism and
instrumental data;
diabetes;
- Clinical diagnosis on the classification 5
- To discuss the diagnosis of
diabetes diabeta, to make a differential
diagnostics
with
psevdoglyukozuriey,
renal glycosuria, diabetes
pregnant women;
- Analyze the severity, stage
compensation, complications
of diabetes
diabetes
control
and
prevention;
- To analyze the course and
treatment
Diabetes in Pregnancyand intercurrent diseases.
M Learning Methods
F orm training activities
With redstva training
Cn lady
feedback
and
means
of WHO;
- The basis of consultation with these patients
deseases;
- Master the skills of patients with diabetes
with diabetes and related conditions
in pregnancy.
le Ktsia, the method of "snowball", "weak link", exhibition,
entertainment experience, discussion, conversation, case.
of individuality work, group work, team, classroom, extracurricular.
Mr. Zdatochnye viziualnye training and materials, videos, models,
graphic organizers, kits medical charts, tables, stands, kits radiographs.
of Bl uu-survey, testing, presentation of the results of the training task,
filling medical records, execution of practical skills "professional
questioning"
2.Motivation
Diabetes affects a total of 6.6% of the population, and Uzbekistan - 3%. In industrialized countries,
every 10-15 years, the number of diabetic patients by an average of a factor of 2. In 11.2% of the
population in Western industrialized countries is determined by impaired glucose tolerance (IGT), a 15% every year they develop type 2 diabetes. Given the high prevalence of this disease and the need for
differential diagnosis of diseases that occur with the syndrome of polyuria and polydipsia with the
endocrine genesis to the actual session. In order to properly diagnose and treat these pathologies to the
GP should be able to properly assess the condition and choose the tactics of treatment.
During the development of the topic, to draw students' attention to the heterogeneity of diabetes for
reasons of occurrence, and on the pathogenetic mechanisms, which involves a variety of approaches to
treatment and prevention of this disease. Draw attention to the problems of diabetes can be, focusing
on the rapid spread of the disease in the world. Students should pay attention to the simplicity and
accessibility of diagnostic methods for diabetes doctors obshey practice. But the background can
move specific diagnostic markers SD SD different classification, listing the names of antidiabetic
drugs.
3.Intra and interdisciplinary communication
Teaching of the subject is based on the knowledge of the students major endocrine disease, received a
4th year in a cycle endocrinology, as well as therapy, which will continue to carry out differential
diagnosis of diseases with syndrome of polyuria and polydipsia. Acquired during the course
knowledge will be used during the passage of the cycle "internal medicine" on 6 and 7 course.
4.Contents classes
4.1 The theoretical part
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On practical training in the theoretical part series discusses the clinical features of polyuria and
polydipsia in diabetes mellitus, diabetes insipidus, Conn's syndrome, pheochromocytoma.
A list of the issues:
1. Osmoregulatory system
2. Causes of polyuria
3. Pathogenesis of polyuria and polydipsia in diabetes insipidus
- Methods of diagnosis of diabetes insipidus and differential diagnosis
psychogenic polydipsia, enuresis, pyelitis, and glomerulonephritis
- Causes and treatment of various forms of diabetes insipidus
4. The pathogenesis of nocturnal polyuria syndrome Conn
- Differential diagnosis of Conn's syndrome with enuresis, diabetic
nephropathy.
5. Pathogenesis of polyuria in gipeparatireoze
- Differential diagnosis of renal form of diabetes insipidus
- Diagnosis and treatment Conn's syndrome
6. Pathogenesis of polyuria and polydipsia in diabetes
- Diagnosis of diabetes mellitus manifest and latent
- Differential diagnosis with psevdoglyukozuriey, renal glycosuria,
Gestational diabetes
- Weight, stage of compensation, complications of diabetes and their prevention
- For and treatment of diabetes in pregnancy, intercurrent
diseases.
Diabetes mellitus (DM, diabetes mellitus) - heterogeneous system disease caused by the absolute (I
type) or relative (II type) insulin deficiency, which initially causes a disturbance of carbohydrate
metabolism, and then all kinds of metabolism, which ultimately leads to the defeat of functional
systems. SD-1 affects 0.25% of people under the age of 20 years. Children make up 54% of all
patients with DM-1. This form of diabetes is also referred to as juvenile diabetes or insulin-dependent
diabetes (IDDM). The concept of "insulin-dependent" is not equivalent to the concept of "insulin",
and means that the insulin these patients is vital. Another category of patients with DM-II insulin
administered after years of therapy sugar reducing tablets (TSP) when the D-cell depletion and
develops absolute deficit iisulina. DM-II - the most common form of diabetes - develops in the
presence of genetic predisposition and lifestyle factors. DM-II is also referred to as adult diabetes, or
insulin-dependent diabetes (NIDDM).
Impaired glucose tolerance (IGT) - a state of carbohydrate metabolism that is different from the norm,
but has not reached the values established for the SD. Regardless of the conditions under which IGT
was detected (a stressful situation, pregnancy, pancreatitis, diseases of the endocrine system, etc.), the
threat of developing diabetes in the future is very high. More than 25% of mature age with IGT and
obesity over the next five years developing DM-II. In children and young adults with normal body
weight and impaired glucose tolerance, especially when positive immunogenetic markers of SD-1,
there is a high risk of the latter. Diabetes during pregnancy (gestational diabetes) is caused by glucose
intolerance that occurs during pregnancy and usually the transmitted after birth. Gestational diabetes
occurs at an average of 2% of pregnant women, and usually develops in mid-trimester II. Treatment of
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gestational diabetes usually is that a low-calorie diet, increased physical activity regime, but about a
third of patients in need of insulin therapy appointment. The classes statistical risk is the category of
persons who have a threat of some type of diabetes. In patients with a history of previous NTG risk of
diabetes is higher than in the total population. Subjects with IGT potential despite normoglycemia, the
risk of diabetes was significantly higher, as in the previous group. For this group, the risk of
developing diabetes are primarily those with high titer antibodies antiostrovkovyh with HLA-identical
siblings with DM-I. In addition, this class of statistical risk include children born weighing more than
4.5 kg, and their mothers, as well as patients suffering from pancreatitis or metabolic syndrome.
The etimological classification of diabetes mellitus (WHO, 1999)
I.Diabetes mellitus type I (B-cell destruction, usually leading to absolute nnsulinovoy failure)
A. Hashimoto
B. Idiopathic
II.Diabetes mellitus type II (from primary insulin resistance with relative insulin deficiency to
predominantly secretory defect with insulin resistance or not)
III.Other specific types
A. Genetic defects in B-cell function
B. Genetic defects in insulin action
C. Diseases of the exocrine pancreas
D. Endokrnnopatii
E. Diabetes induced by drugs and chemicals
F. Infections
G. Unusual forms of immune-mediated diabetes
H. Other genetic syndromes sometimes combined with diabetes
IV.Gestational diabetes
Clinic. In DM there are two basic groups of symptoms. The first group includes Feature for all types
of diabetes symptoms, pathogenesis associated with hyperglycemia. These symptoms are thirst,
polyuria, itching, susceptibility to infectious processes. These symptoms should be seen as signs of
decompensation diabetes saharoponizhayuschimi against inadequate therapy. The second group of
symptoms are specific for CD-I and-II diabetes symptoms, diabetes-II, is generally characterized by a
milder course. These symptoms are mild, and often non-existent, and the diagnosis is made by chance
during a routine investigation of the level of blood glucose. For. DM-II generally not characteristic
weakness, and patients are generally maintains good working ability, they have normal, and often
increased appetite. Often the diagnosis of DM-II is established by dermatologists (chronic pustular
processes, lipoid necrobiosis, muco-cutaneous candidiasis, abrasions), urologists (chronic urinary tract
infections), ophthalmologist (chronic conjunctivitis, cataract), gynecologists (vaginal itching ("specific
inflammatory diseases of the genital bodies, dysmenorrhea). As mentioned, most of the patients were
overweight or obese, the disease manifests after 40 years, there is a positive family history of DM-II.
For CD-I are the specific complaints of weight loss (often considerable), marked weakness , decreased
performance, drowsiness. At the beginning of the disease sometimes there is an increased appetite,
which can then be replaced on the background of anorexia ketoacidosis. latter is characterized by the
appearance of the smell of acetone (or fruit odor) from the mouth, nausea, vomiting, abdominal pain
often (psevdoperitonit) severe dehydration and ends with the development of coma (coma
ketoatsidoticheskaya). pathogenetically these symptoms are associated with an absolute insulin
deficiency in the body. SD-I, as a rule, manifests acute medical history in most cases is a few months.
In some cases, the first manifestation of CD-I is a progressive disorder of consciousness up to coma
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amid comorbidities are usually infectious or acute surgical pathology. symptoms characteristic of CD-I,
in some cases, are found in DM-II. In DM-II symptoms of formation of absolute insulin deficiency
(weight loss , weakness, transient smell of acetone breath) may appear after a long period of
satisfactory compensation disease with TSP. When two groups of diabetic complications: acute and
chronic. Acute complications of diabetes are specific to different types of the disease. For SD-1
specific ketoatsidoticheskaya coma. When insulinpotrebnom SD-H may develop transient ketosis, but
ketoatsidoticheskaya coma due to always having her own insulin production is practically not
developed. hyperosmolar coma - a rare but specific complication. SD-P. hypoglycemia and
hypoglycemic coma may complicate the treatment of sugar reducing both types of diabetes. Late
complications developed in both types of diabetes, and they are specific. Clinically isolated 5 major
late complications of diabetes: macrovascular (large artery atherosclerosis), nephropathy, retinopathy,
neuropathy and diabetic foot syndrome.
Treatment of type I diabetes. When diagnosed IDDM installed immediately begin insulin therapy.
Timely and properly chosen dose allows for 75-90% of the time to achieve remission, and further
stabilize the disease and delay the onset of complications. Preferably, the insulin were carried out in
multiple co-injection, ie 4 times daily short-acting insulin (at meal and at bedtime) and intermediateacting insulin (25-30% of the dose obshey daily dose) or three meals rose short-acting insulin and
long-acting at bedtime. The total daily dose 0.6-1.0 edkg. 1-3 months from the start of insulin therapy,
you may receive a temporary remission (honeymoon) and the need for insulin is reduced to 0.1-0.3 U /
kg / day, or disappears, unit / kg / lpg, in subsequent years, it is reduced to 0.6-0.8 U / kg / day.
Complications of insulin therapy: hypoglycemia, Somogyi syndrome, allergy to insulin, postinjective
lipodystrophy. In order to prevent hypoglycaemia - 5-6 meals a day. When planning a diet, patient
preferences are taken into account, ethnic and family traditions, and should be well-balanced (carbs50-60%, protein 15-20%, fat - 25-30%). Physical activity - long planned for glycemic control and the
observer.
Principles of treatment of type 2 diabetes. Treatment should be individualized. Takes into account the
course and severity of NIDDM, lifestyle and nutrition patient, his response to diet therapy and oral
saharoponizhayuschie funds. The main treatment is diet therapy aimed at normalizing body weight,
blood sugar and blood lipids. Assigned a balanced low-calorie diet. Starvation is undesirable because
it can cause metabolic acidosis. In the appointment of physical activity, which reduces hyperglycemia
and improves insulin sensitivity, blood glucose levels should be considered, for the use of their high
hyperglycemia causes the opposite effect. Drug therapy is carried out in the event that diet and
exercise have not had the desired effect.
Patients with insulin resistance are assigned:
- Biguanides, they inhibit gluconeogenesis in the liver and increase the utilization of glucose by
muscles and adipose tissue do not cause hypoglycaemia in overdose;
- Inhibitors of intestinal a-glucosidases that cleave polysaccharides, thereby slowing down the
absorption of glucose
- Thiazolidinedione derivatives, reduce glucose production in the liver, lower triglyceride levels and
raise LPONL LPZP, but may have a hepatotoxicity deystvne (troglitazone, ciglitazone, darglitazon,
pioglitazone englitazone).
Patients with impaired insulin secretion appoint saharoponizhayuschie sulfonylureas (traditional 1, 2
and glimepiride generation third generation - Amar from 1.2 mg to 4.8 mg). The mechanism of action
of these drugs - they bind to the ATP-dependent potassium channels in the membrane of B-cells,
blocking these channels, and thereby stimulate insulin secretion, inhibit the production of glucose and
insulin in the splitting of the liver and increase insulin sensitivity.
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Indications for insulin therapy.
- Contraindications to oral sugar-reducing drugs;
- Ineffectiveness of diet and oral sugar-reducing drugs;
- High stress, trauma, surgery, pregnancy,
- Dramatic weight loss, accompanied by severe metabolic disturbances. Indications for
hospitalization of patients with diabetes:
- New-onset diabetes;
- Ketoacidosis and ketoatsidoticheskoe state hyperglycemic (ketoatsidoticheskaya, hyperosmolar,
giperlaktatsidemicheskaya) or hypoglycemic coma
- Pregnancy
- The inability to resolve decompensation of diabetes outpatient conditions (frequent hypoglycemic
state during labile diabetes);
- Allergy to insulin;
- Resistance to sugar-reducing drugs sulfonylureas;
- Syndrome of chronic insulin overdose or suspected him;
- Expressed vascular complications of diabetes.
Diabetes insipidus (LP, diabetes insipidus) - a clinical syndrome caused by decreased ability of the
kidneys to concentrate urine associated with a deficiency of antidiuretic hormone (central ND) or in
violation of the sensitivity of the renal tubules to its action (renal ND). Diabetes insipidus is classified
in the pathogenetic basis.
1. Central (hypothalamic-pituitary) ND
- Idiopathic (one third of all cases of ND)
- Symptomatic (two thirds of all cases of ND).
2. Renal diabetes insipidus.
Etimology. Approximately 1% of patients the etiology of the central ND (ND idiopathic). Part of
these observations can identify producing cells of neurohypophysis. ND occurs within Wolfram
syndrome (syndrome DIDMOAD - from the English. DI - diabetes insipidus, DM - diabetes mellitus,
OA - oculus atrophy, D - deafness), combined with diabetes mellitus, optic atrophy, deafness and
atony of the bladder. The above syndrome is inherited autosomal recessive and can be complete (there
are all manifestations) and incomplete (for example, the combination of diabetes and diabetes insipidus
and deafness in the absence of other components).
Diabetes insipidus - a relatively rare endocrine disorder that occurs with equal frequency in both sexes,
mostly aged 20 - 40 years, there are cases of the disease in any age. Congenital forms may be children
from the first months of life, but sometimes revealed much later. Diabetes insipidus may be preceded
by acute and chronic diseases: influenza, meningoencephalitis, sore throat, scarlet fever, whooping
cough, all kinds of fever, septic conditions, tuberculosis, syphilis, malaria, brucellosis, rheumatism.
The disease can occur after head trauma (accidental or surgical), electric shock, bleeding in the
appropriate area of the hypothalamus and pituitary. The cause of diabetes insipidus in children can be
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a birth trauma. Diabetes insipidus can be one of the first symptoms of primary or metastatic tumors of
the hypothalamus or pituitary gland.
Pathogenesis. ADH deficiency leads to disruption of urinary concentration at the level of the distal
tubules of the neuron, resulting in a significant amount of urine is released with a low relative density.
Stimulation of thirst center, preventing dehydration, leads to polydipsia. When abstinence fluid
develops hyperosmolar dehydration. Gastrointestinal fluid overload is manifested
ptosis of the stomach, biliary dyskinesia, irritable bowel syndrome. When long the current central ND
may develop secondary to the insensitivity of the kidneys injected exogenous ADH. LP, which
developed after neurosurgical intervention may be either permanent or transient with spontaneous
remission in a period of several days to several years.
The clinical picture. Severity of the disease, ie, severity of polyuria and polydipsia, depends on the
degree of deficiency of ADH. With a partial deficiency of ADH clinical symptoms may not be so
distinct. These forms are sometimes detected in drinking deprivation (hiking, expeditions) or after
receiving glucocorticoids. Fluid intake ranged from 3 to 18 liters a day, but sometimes with
excruciating thirst, do not leave the patients, day or night, you need 20-40 liters of water or more. In
children, frequent nighttime urination (nocturia) may be the initial sign of the disease. In small
children, severe polyuria instead of ND may show diarrhea. Released discolored urine contains no
pathological elements, the relative density of all the portions are very low (I.000-1,005). The onset is
usually acute, sudden, sometimes symptoms appear gradually and grow. Physical and mental asthenia
accompanied polyuria and polydipsia. Usually reduced appetite, weight decreased, sometimes with
hypothalamic disorders, on the contrary, develop obesity. There have dry skin and mucous
membranes, reduced salivation and sweating, Children are often stunted, physical and sexual
development. In patients with impaired gastric secretion, bile formation and motility of the
gastrointestinal tract, there are constipation, chronic hypoacid gastritis, colitis. Due to the chronic
volume overload the stomach is often stretched and lowered. With a Long-poor treatment diabetes
insipidus can be detected expansion of the bladder, ureter and pelvis. With sufficient supply of fluid in
the body's cardiovascular system is usually not affected (although there is a tendency to hypotension),
but with the rise in cases of dehydration when you lose urine liquid is not filled (reduced sensitivity
center thirst, lack of water, holding dehydration test xerophagy etc.), there are signs of dehydration:
sharp weakness, tachycardia, hypotension, collapse. With increasing dehydration in patients with
headache, nausea, vomiting (which aggravates the dehydration), fever, blood clots to increased levels
of sodium, red blood cells, hemoglobin, and residual nitrogen, convulsions, psychomotor agitation.
Even with severe dehydration, despite the decrease in blood volume and reduced glomerular filtration
rate, polyuria persists, the concentration of urine osmolality and almost do not increase. If ND caused
intracranial education, noted neurological symptoms, and headache, nausea and dizziness are signs of
dehydration rather than as intracranial hypertension.
Diagnostics. Typical laboratory findings include low OD relative density of urine (more than 1.005 for
the index diagnosis can be practically excluded), hyperosmolar plasma (> 290 mOsm / L),
gipoosmolyarnost urine (<300 mOsm / L).
Differential diagnosis. Diabetes insipidus differentiate from primary (psychogenic) polydipsia, but
diagnosis can be difficult. For the latter is characterized by functional or organic changes in the central
nervous system, a positive test with xerophagy. Diuresis with psychogenic polydipsia may
substantially exceed the diuresis in diabetes insipidus. When abstinence from fluid (test xerophagy)
maximum for 14 hours at LP urine osmolality, measured every hour, is low (<300 mOsm / L), and
psychogenic polydipsia it as normal, increases. The effect of the introduction of vasopressin excludes
nephrogenic diabetes insipidus.
Treatment. For the treatment of patients with LP used intranasal adiuretina (lysine, vasopressin,
desmopressin) 1 - 3 drops 1 - 3 times a day under the control of urine output and urine specific gravity.
In rhinitis adiuretin given sublingually. Treatment of nephrogenic diabetes insipidus is a difficult
11
problem. Restore sensitivity to endogenous vasopressin try using paradoxical antidiuretic effect of
thiazide diuretics (chlorpropamide), as well as the appointment of nonsteroidal anti-inflammatory
drugs, lithium, dimetilhlortetratsiklina. All patients with a first diagnosis of ND is necessary to
conduct imaging studies of pituitary and optimizing MRI study. In acute razvivshemsya ND elderly
patients require an active search of metastatic malignant tumors.
New educational technology: the method "Snezhkov," "The Weakest Link".
The method of "snowball"
To work needed:
1) a set of learning control tests
2) sheets of paper
Progress:
1) the group is divided into two subgroups.
2) The group is preparing for one sheet of paper.
3) is written on a piece of FI students, group, department, date.
4) one of the students taking the envelope issues that are the same for both groups.
5) Each correct answer is written in the score as "snowballs."
6) Rupp, received the maximum number of points is estimated excellent grades.
7) to conduct the method have 30 minutes.
1. Which electrolyte imbalance causes damage to the renal tubules and reduce sensitivity to
antidiuretic hormone receptors in Conn's syndrome
1) giperhloruriya
2)hypokalemia
3) chloropenia
4) hypercalciuria
5) hypercalcemia
6) giperkaliyuriya
2. Test with pituitrin with differential diagnostic purposes is used for what diseases:
1) diabetes
2) pituitary Cushing
3) diabetes insipidus renal form
4) Sheehan's syndrome
5) The central form of diabetes insipidus
6) Cushing's syndrome
3. Therapeutic measures used to derive the diabetic com
A. Ketoatsidoticheskaya
B. Hypoglycemic
1) 40% glucose solution
2) insulin
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3) mannitol
4) glucagon
5) 5% glucose pactvop
4. Select the complications of diabetes
A. Sharp
B. Chronic
1) coma
2) diabetic foot
3) retinopathy
4) nephropathy
5) autonomous nephropathy
5. Complications of diabetes include
A. makroangiopatnya
B. microangiopathy
1) retinopathy
2) nephropathy
3) Diabetic Foot
4) atherosclerosis
5) nephropathy
6. Used to treat diabetes
A. Type 1 diabetes
B. Type2 diabetes
1) ins. Actrapid
2) ins. Monotard
3) maninil
4) Siofor
5) ins. Mixtard
The method of "The Weakest Link"
To work needed:
1. A set of questions on endocrinology.
2. A sheet of paper with a list of games for logging.
3.Sekundomer.
Progress:
1. The game holds a teacher and an assistant from the students - the counter.
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2. Counter wrote on a sheet date, the group number, the faculty and the business name of the game
and a list of student groups.
3. Teacher hurt in series of questions from the students a set of questions.
4. The student must for 5 seconds to answer,
5. Teacher of the word "right" or "wrong" answer evaluates if the "wrong" he will give the correct
answer.
6. Counter puts opposite the name of the student, "+" or "-" depending on the correctness of the
answer.
7. Students are, therefore, two rounds of questions.
8. After 2 rounds of questions the game is suspended and students who have received, minus two out
of the game as the "weak link".
9. The game continues for a new circle with the rest of the students. Again, they are offered one new
round of questions, and again eliminated students who in the sum with the first two rounds turned
instrumentals.
10. Round by Round shown the strongest of the players, who responded to an increasing number of
issues.
11. Ha sheet against each name the teacher records - who in any round table and dropped the "weak
link".
12. Game estimated maximum of 100 points.
Students who withdrew after the first 2 rounds of the answers, get a game, "0" points,
after 3 rounds - "25" points,
after 4 rounds - "50" points,
after 5 rounds - "75" points,
the strongest participant receives 100 points.
13. The scoring on the sheet of the protocol to the count of the current total of occupation as an
estimate for the theoretical part.
14. At the bottom of the log free teacher records on a business game, the elder signs off.
15. Minutes of the game remains.
Set of questions.
1. What hormones are produced by the pancreas?
2. Enrolled patients with complaints of dry mouth, thirst, frequent urination to 15 liters per day. In a
study of a general analysis of urine density is 1001. Doctor diagnosed diabetes insipidus. What
diagnostic tests should be carried out for improvement of the form of the disease?
3. What is the duration of insulin used to treat diabetes?
4. A patient 32 years, complaints of dry mouth, thirst, frequent urination (up to 15-20 liters per day).
The complaints came after prostatectomy transfenoidalnoy pituitary. Your preliminary diagnosis.
5. What method of examination will confirm the diagnosis of diabetes insipidus?
6. What types of diabetes insipidus you know?
4.2 The analytical part
The decision of situational problems.
14
Students are given one task to the differential diagnosis of endocrine disease. Preparation time - 5
minutes. To answer - 2 minutes. Response is evaluated according to the criteria developed.
Considered amendments and judgments of students going into their asset. The group then divided into
2 groups and given a task with a difficult decision. Preparation time - 7 minutes. The solution
presented and discussed together with the other subgroups.
Objective number one. Male 21 years old. Complaints about dry mouth, weight loss, acute illness
began two weeks ago. Glycemia natoshak-18 mmol / L, daily glucosuria-4%, acetone "+", the density
of urine - 1038.
1. Your diagnosis
2. What complications occur in patients
3. Treatment of this condition
Objective number 2. Male 42 years. Height 168 cm, weight 88 kg. During the test, a fasting blood
glucose level of 6.8 mmol / L, 1 hour - 12.0 mmol / L, 2 hours, 8.2 mmol / l.
1. Preliminary diagnosis.
2. Recommendations.
Task number 3. Patient 18 years admitted to the department in a state of unconsciousness, the
installed ketoatsidoticheskaya coma. Patient derived from a coma. During the week, supported by
stable glycemia within 5.5 - b mmol / L glucose and 7.8 -12.0 mmol / l during the day. Is regular
insulin to 12 units, 16 units, 8 units, 6 units every 6 hours.
1. Diagnosed with type and severity of diabetes.
2. Tactics further treatment the patient
3. Which insulin is used in deriving from this coma
Objective number 4. Entered patient complaining of frequent urination, dry mouth, thirst. In the
history suffered a viral infection. The patient was diagnosed with diabetes insipidus, which receives
about adiuretin 1 drop 2 times a day. In urinalysis density 1001. Adjusting the dose did not lead to
improvement.
1. Your opinion about the diagnosis. That the patient?
4.3 The practical part
Performed at the bedside. Supervision is carried out under the supervision of a teacher. The student
must learn to practice proper medical history of patients with endocrine disorders, with ztom able to
differentiate primary and secondary information during the examination to focus on the endocrine
glands and the clinical features of dysfunction of these glands. When communicating with the patient
must be considered such psychological traits, such as irritability, fatigue, and during communication
exercise extreme tact and at the same time be confident and firm.
In conducting activities in the clinic, while outpatient care, to teach students to quickly, clearly
questioning and examination of the patient, proper filling patient card.
Practical skills for this occupation carried out in 3 phases and is estimated
maximum of 100 points
1.Glucose patience test in diabetics
Purpose: To test glucose patience in diabetics
Equipment: 75g. Glucose, 250-300 ml of water
Performs step (stage)
15
№
stage
Activities
Not
done
(0
points)
By
lnostyu
properly
executed
1.
That study of blood glucose
0
30
2.
Yes Th patient to drink 75 oz.glucose dissolved in 250-300 ml of 0
boiling water for 5 minutes.
40
3.
Used to follow glucose 2 hours after administration of glucose.The test 0
is positive if the fasting blood glucose levels> 6, 1 mmol / l.and after 2
hours> 11.1 mmol / l.
30
Sun it:
100
0
2.Calculation of the dose of insulin
Purpose: Calculation of the dose of insulin
Equipment: medical scales
Performs step (stage)
№
Me ropriyatie
stage
H e is n
satisfied Completely
(0 points) done
correctly
1.
Measure of patient weight and height to determine the ideal weight
0
20
2.
Ra sschet daily insulin dose per kg of patient weight: 1, in 0
overweight count on ideal body weight, 2, and underweight - the
actual weight
20
3.
Ra Thousands separator for bolus and basal dose ratio of 30/70 40/60
0
4. Thousands separator Ra bolus dose of insulin on meals and basal dose,
depending on the duration of the basic insulin
Sun it:
30
0
5.Forms of control knowledge, skills abilities m
- Oral
- Written
- Decision of situational problems;
- Demonstration of the developed skills
6.The evaluation criteria of the current control
16
30
100
№ Military
mustache
in points
Est. ENKA
Ka quality assessment
1. 86-100
Personally from
the "5"
Communicates about, think creatively, evaluates,
interprets.Applies knowledge in practice.Understands, knows,
says has no idea
2. 71-85
It is well "4"
Ra ssuzhdaet independently assess, interpret, apply knowledge
in practice, understands, knows, says has an idea
3. 55-70
Beats
Minimality know.Understand the essence, says
ovletvoritelno "3."
4
Not satisfactory,
"2"
0-54
Pl oxo know.Not thoroughly.Require additional training.
7.flow sheet studies
1. Checking the initial level of preparedness of students to engage in "Diseases of the endocrine
glands occurring polyuria and polydipsia." Explanation of the diagnosis and differential diagnosis.
2. Decision analysis and situational problems.
3. Supervision of patients. Clinical analysis of supervised patients.
4. Interactive games to assess knowledge on training.
№
fl ups lessons
Prospect
odolzhitelnost
classes
6 hours
1 Judgment of courses offered
8.30-10.05
2 Ca autonomy of patients Supervision attached houses, self Curation case
10.10-11.05
patients, participation in rounds of professors and associate professors
3 Ra Zborov the department examined case patients with the interpretation
11.10-11.55
of the survey data and treatment
4 ne reryv
11.55-12.40
5 On judgment tests, situational problems.
12.40-14.00
6 Pr Overcome digestibility.Ad evaluations homework
14.00-14.30
8.Test questions
1. What conditions are accompanied by acute and chronic polydipsia?
2. What endocrine disorders are accompanied by polyuria and nephropathy?
3. What are the symptoms, in addition to nocturnal polyuria, are common in patients with
Diabetic nephropathy and Conn's syndrome?
4. Whether the combination of two diseases - diabetes and diabetes insipidus?
5. What etiological variants of diabetes occur?
6. When assigned to insulin therapy in patients with diabetes mellitus?
7. How to conduct a glucose tolerance test in the polyclinic?
8. What is different from gestational diabetes diabetes?
9. How to determine the acetone in the urine rapid method?
10. How to determine the blood glucose rapid method?
9.Recommended Reading
Summary:
1.
Balabolkin MI Endocrinology. M., Medicine, 1998
17
2.
3.
4.
Vladimir Potemkin Endocrinology. M., Medicine, 1999
Grandparents II Endocrinology. M., Medicine, 2000
Melnichenko GA Tokmakova AY, deck DE, NV Lavrishcheva Endocrine
disease. M. Medicine, 2009
5.
Guidelines for Pediatric Endocrinology. Handbook of clinical Pediatric
Endocrinology. Edited by Charles G. Bouka, Rosalind S. Brown. 2009
6.
Shustov SB, Khalimov S, Trufanov GE Functional and topical diagnosis in endocrinology. M.
2010
7.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 1. Greenspan's Basic &
Clinical Endocrinology. 2010
8.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 2. Greenspan's Basic &
Clinical Endocrinology. 2011
9.
Clinical Endocrinology. Ed. EA Kholodova. Minsk. Belarus.
2011.
10. Melnichenko GA Udovichenko OV Shvedova AE Endocrinology.
Typical errors practitioner 2012
11. Endocrinology. National guidelines (+ CD-ROM). 2012
More:
1. Therapeutic Guide Washington, translated from English. (Section
"Endocrinology") 1996.
2. Laycock. Fundamentals of Endocrinology, Moscow 2000
3. Ty M. Mack - Dermott MD Secrets Endocrinology - Moscow 2000
4. Ketgayl VM, Arkin RA, Pathophysiology of endocrine system - Moscow, Medicine,
2001.
5. Balabolkin MI Diabetology - Moscow, Medicine, 2002
7. Fadeev PA. Endocrinology. Diabetes. A Reference Guide. 2009
8. Kartelishev Alexander Rumyantsev AG, Smirnova NS Actual problems of obesity
children and adolescents. 2010
9. Mkrtumyan AM, AA Nelaev. Emergency Endocrinology. 2010
10. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Diseases
Thyroid. Williams Textbook of Endocrinology. 2010
11. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Bark disease
Adrenal gland and endocrine hypertension. Williams Textbook of
Endocrinology, 11 th edition. 2010
12. AN hams Emergency Endocrinology. 2011
13. Petunina NA, AV Trukhina Thyroid disease. 2011
14. Manukhin IB Tumilovich LG, M. Gevorgyan Gynecological Endocrinology.
15. Lectures on gynecologic endocrinology. M. 2012
Journals:
15. Medical Journal of Uzbekistan, Tashkent.
16. "Problems of Endocrinology." Moscow.
17. "Therapeutic Archives", Moscow
18. "Clinical Medicine", Moscow
19. "Diabetes. Way of life ", Moscow
Internet sites:
1. "Internet Portal: Hunari»
2. Medscape.com
3. Alltheweb.com
4. Yahoo.com
5. E-medicine.com
6. Www tma. Uz
Ministry of Health of Uzbekistan
CENTRE FOR MEDICAL EDUCATION
18
TASHKENT MEDICAL ACADEMY
Department of Internal Medicine TRAINING GP endocrinologist
The subject of "Endocrinology"
Topic: "Latest complications of diabetes (neuropathy, micromacroangiopathy).The principles of treatment of diabetes and its complications.Assist
in the hospital and pre-hospital.GPs tactics. "
Educational and methodical development
(For teachers and students)
Tashkent - 2012
Flow chart lesson number 2
"Late complications of diabetes (neuropathy, micro19
Macroangiopathy).The principles of treatment of diabetes and its complications.Assist in the
hospital and pre-hospital.GPs tactics. "
stage practice session
№
f rma classes
Th e
m of esto
literature
classes
225 min.
1 Centuries odnaya part (study subject)
10
2 Judgment about topics practice session using marketing of op grew discussion
educational technology ("The Weakest Link"), as well as training room
demonstration material (boards, sets of medical records, tables,
poster, X-rays, situational problems glucometer, test strips,
instruments for determining the sensitivity) definition baseline.
3 You discuss water
40
4 The definition of reference for the practical part - n rofessionalny of judgment
questioning.Explanation of the provisions and recommendations
training room
for the job to fill medical records.
20
5 Military wasps practical training under the guidance of a teacher. Prospect ofes sional
questions, talk with
patients filling medical
records, case studies.
Department of
Endocrinology Clinic 1TTA
6 John interpretation of the survey data of patients - complaints, tory studies of the
inspection, palpation, percussion and auscultation of patients as disease,
well as laboratory and instrumental studies
laboratory data
situational problems
Department of
Endocrinology Clinic 1TTA
7 Judgment on the theoretical and practical knowledge of the mustache tny survey,
students, fixing material, the level of learning assessment.
tests, discussion,
identification of practical
skills
Department of
Endocrinology Clinic 1TTA
8 The definition of output on practical training, evaluation of 100- infor mation, questions
point system, and ad evaluations.Homework the next practice for homework.
session (a collection of questions).
training room
20
10
25
75
25
Lesson number 2
"Late complications of diabetes (neuropathy, microMacroangiopathy).The principles of treatment of diabetes and its complications.Assist in the
hospital and pre-hospital.GPs tactics. "
20
uch ebnoe time: 6:00
Art ruktura training session
1. afedra to internal medicine training
GPs with an endocrinologist, endokrinologichessome branch 1 TTA clinic, clinical
1-clinic laboratory TTA;
2.set of tables, methodological recommendations
tion, laboratory and instrumental data,
video;
3.TCO: computer, video
The training session:
- The acquisition of knowledge and skills in students GPs to diagnose
and differential diagnosis of late complications of diabetes;
- To conduct early detection and prevention of late complications of diabetes
Pe dagogic tasks:
D results of training activities:
- Building knowledge and skills for
GP
diagnosis and differential
should know:
diagnostic stages of retinopathy;
- To understand the mechanisms of late
- To analyze the pathogenesis of diabetes
complications of diabetes;
cal foot;
- Learn to evaluate the criteria and the degree
- To discuss the differential diagnosis,
severity of late complications;
tic syndrome Conn with diabetic
- To analyze the data provided in diabetes
nephropathy;
diabetes.
- To analyze the treatment of complications - Learn the skills of patients with complications
Dr. iabeta;
tions of diabetes
- Building knowledge and skills for
should be able to:
prevention of complications of diabetes
- Interpret the urine - a common and
diabetes.
Zimnitskiy;
- Interpret the results of the sample Rehberg.
- Interpret blood sugar;
- Interpretation of the data tolerance test glucosegoat;
must have skills:
- Professional questioning, examination of the patient,
questioning relatives;
- Interpretation of the clinical laboratory
instrumental data;
- Clinical diagnosis for classical
fication of WHO;
- The basis of counseling patients with complications
tions of diabetes
Le Ktsia, the method of "weak link", exhibition,
Methods of training
entertainment experience, discussion, conversation, case.
Fo rms of training activities of individuality work, group work, team, classroom, extracurricular.
introduction training
Mr. zdatochnye viziualnye training and materials, videos, models,
graphic organizers, kits medical charts, tables, stands, kits radiograph.
21
Cn lady and means
of feedback
Bl uu-survey, testing, presentation of the results of the training task,
filling medical records, execution of practical skills "professional
questioning"
2.Motivation
Diabetes affects a total of 6.6% of the population, and Uzbekistan - 3%. In industrialized countries,
every 10-15 years, the number of diabetic patients by an average of a factor of 2. In 11.2% of the
population in Western industrialized countries is determined by impaired glucose tolerance (IGT), a 15% every year they develop type 2 diabetes. Given the high prevalence of this disease and the need for
differential diagnosis of diseases that occur with the syndrome of polyuria and polydipsia with the
endocrine genesis to the actual session. In order to properly diagnose and treat these pathologies to the
GP should be able to properly assess the condition and choose the tactics of treatment.
During the development of the topic, to draw students' attention to the heterogeneity of diabetes for
reasons of occurrence, and on the pathogenetic mechanisms, this involves a variety of approaches to
treatment and prevention of this disease. Draw attention to the problems of diabetes can be, focusing
on the rapid spread of the disease in the world. Students should pay attention to the simplicity and
accessibility of diagnostic methods for diabetes doctors’ practice. But the background can move
specific diagnostic markers SD SD different classification, listing the names of antidiabetic drugs.
3.Intra and interdisciplinary communication
Teaching of the subject is based on the knowledge of the students major endocrine diseases, received
a 4th year in a cycle endocrinology, as well as therapy, which will continue to carry out differential
diagnosis of diseases with syndrome of polyuria and polydipsia. Acquired during the course
knowledge will be used during the passage of therapy at 6 and 7 of the course.
4.Contents classes
4.1 The theoretical part
On practical training in the theoretical part series discusses the clinical features of neuropathy,
retinopathy, nephropathy, diabetic foot.
A list of the issues:
- Complications of diabetes and their prevention
- Principles of treatment of diabetes mellitus
The most important problem of diabetology, both medical and social, is the prevention and treatment
of late complications of diabetes, which largely determine high mortality, morbidity anddisability in
patients.By late complications include:

Macroangiopathy

Diabetic retinopathy
22

Diabetic nephropathy

Diabetic neuropathy

syndr omdiab etical ofthest ops.
In diabetes risk for such cardiovascular diseases such as stroke, myocardial infarction, obliterating
diseases of the arteries of the lower extremities, 4 times higher than in people without diabetes.Since
diabetes is associated 50% of all amputations, 15% of all cases of blindness.Among all patients on
chronic hemodialysis, 30% of patients with diabetes.
There is a clear link between the incidence of late complications of diabetes and the quality of his
compensation, according to existing criteria.This is most clearly observed in the case of intensive
insulin therapy in DM-1, which allows achieving the best performance compensation of
disease.Intensive, insulin SD-1 reduces the risk of:
- Proliferative retinopathy by about 50-70%;
- Clinically significant renal disease by about 60%;
- Severe neuropathy by 80%;
- Coronary and peripheral arteries by about 40%.
Diabetic retinopathy.Diabetes mellitus is the most common cause of blindness in adults.When
she develops diabetes is 25 times higher than in the general population.Retinopathy is present in 85%
of patients with DM-1 with a 20-year veteran of the disease, on average, it is diagnosed in 40% of
patients with DM-1.Blindness develops in about 2-4% of patients with DM-1.Retinopathy have a 20%
of patients with type-II at the moment of diagnosis of diabetes.Due to the fact that the development of
retinopathy pathogenesis associated with the duration of diabetes, the quality of its compensation and
hypertension, it is often associated with nephropathy.
Classification of diabetic retinopathy
I.Nonproliferative retinopathy
Microaneurysms, hemorrhages, edema, pleural lesions in the retina.Hemorrhage has the form of
small dots, lines or dark spots round, localized in the center of the fundus or in the course of the large
veins in the deeper layers of the retina.Hard and soft exudates usually located in the central part of
the fundus and are yellow or white.An important element of this phase is a swelling of the retina,
which is localized in the macular area, or in the course of the large vessels.
II.Preproliferative retinopathy.Venous Anomaly: beaded, winding, looped, double and marked
fluctuations caliber vessels.Large amounts of solid and "cotton" exudates.Intraretinalnye
microvascular abnormalities, large retinal hemorrhages.
III.Proliferative retinopathy.Neovascularization of the optic nerve and other parts of the retina,
vitreous hemorrhage, formation of fibrous tissue in the preretinal hemorrhage.The newly formed blood
vessels are very thin and fragile, so that often have repeated hemorrhages.Vitreoretinal traction leads to
retinal detachment.The newly formed blood vessels of the iris (rubeosis) are often the cause of
secondary glaucoma.
23
T r e a t m e n t . Basic principle of treatment of diabetic retinopathy, as well as other long-term
complications, diabetes is the optimal compensation.The most effective method for the treatment of
diabetic retinopathy and blindness prevention is laser photocoagulation.Her early holding to stabilize
the process at preproliferative and proliferative diabetic retinopathy.In later stages, it can preserve
vision in 60% of patients within 10-12 years.The purpose of laser photocoagulation is to stop the
functioning of newly formed vessels that predtavlyayut main threat of severe complications as
hemophthalmus, traction retinal detachment and secondary glaucoma.
Diabetic nephropathy.Specifically for diabetic renal disease is diabetic glom-ruloskleroz or proper
diabetic nephropathy (DN), which is approximately equal number of difficult for SD-1 and SD-P,
growing at 40-45% of patients.Approximately 30-50% of patients with DM-1 with a 40-year veteran of
the disease are diabetic nephropathy, which is an average of 10 years, leading to end-stage renal
failure.Mortality from uremia in DM-1 much higher than that in DM-II, respectively, accounting for
30-50% and 5-10.
T h e c l i n i c a l p i c t u r e . NAM is the main manifestations are proteinuria, hypertension, and
progressive renal failure.It is common today is the classification of diabetic nephropathy by
Mogensenu.
Diabetic nephropathy should be differentiated from other diseases of the kidneys, accompanied by
microalbuminuria or proteinuria.Up to 10% of patients with type-1 and 30% of patients with type-II
have proteinuria is not related to the NAM.
T r e a t m e n t . As already mentioned, the development of diabetic nephropathy is associated with
the pathogenesis of chronic hyperglycemia and hypertension (HT).Intensive insulin therapy with
normoglikemicheskoy compensation reduces the risk of NAM at 60%, inhibits its progressive course
and may prevent or at least significantly delay the onset of kidney failure.With poor compensation of
diabetes in patients with transplanted kidney NAM again develops in about 5 years.
Active treatment NAM should begin at leastIIIstage renal disease, which is characterized by
persistent microalbuminuria and in some cases the addition of moderate hypertension and
dislipidemin.
Diabetic neuropathy.Diabetic neuropathy is a combination of syndromes of the nervous system,
which can be classified according to the predominant involvement in its various departments
(sensorimotor, autonomic), and the prevalence and severity of the lesion.
Classification of diabetic neuropathy
I.Sensorimotor neuropathy
1.
2.
simmetric
focal ( mono neuropathy) polifocal (Motor, mononeuropathies limbs and trunk)
II. Autonomous (vegetative) neuropathy
1.cardiovaskulyary neuropathy (orthostatic hypotension, cardiac denervation syndrome)
2.gastrointestinal (atony of the stomach, biliary dyskinesia, diabetic enteropathy)
3.Urogenitaly (with dysfunction of the bladder ,with the violation of sexual function)
4 Disbalans patient ability
5. disbalans
gipoglikemy
Function pupil
24
6. disbalans Sweat gland function (distal anhidrosis,gipergidroz eating)
Diabetic neuropathy are equally common in both types SD Chastotf increases with age and
dlitelnost SD.Periferic neuropathy suffer an average 25% of all ill diabetes and 45% of patients
older than 60 years old.
A Whole structure etiologic polyneuropathy the fist place are diabetic (30%) and alcohol (30%) of
the form.
Sensorimotor neuropathy.Sensory and motor diabetic polyneuropathy manifested complex
motor and sensory disturbances (tactile, pain, temperature, vibration, and joint and muscle
sense).Process may be involved in the majority of departments as peripheral and central
nervous system.
Early manifestation of sensory neuropathy is a disorder of vibration sensitivity.Detection of vibration
sense with a graduated tuning fork is widely used in diabetes practice.Tuning fork is mounted on the
head of the first tarsal bones.The patient must first feel the vibration, and then say when it will
stop.Researcher at this point to read one of the tuning fork is applied to a scale of values in '/ &
octave.Abnormal values are less than 4 / & octave tuning fork.
Common symptoms of distal form of diabetic neuropathy are paresthesia and dysesthesia, which show
a sense of "pins and needles," numbness.Patients often complain of chilly feet, although they are still
warm to the touch, which is a sign that distinguishes polyneuropathy of ischemic changes, when the
feettouch the cold.
Autonomic neuropathy.Clinically, often to the fore are the manifestations of diabetic autonomic
neuropathy.It is important to understand that a diagnosis of dysfunction of an organ or system as a
result of autonomic neuropathy is a diagnosis of exclusion.First of all, should be excluded as a cause
of organ pathology existing symptoms.As indicated in the classification, identified a number of
clinical forms of autonomous diabetic neuropathy.
Cardiovascular shape.The vagus nerve is the longest nerve innervating the heart of all, and with
autonomic neuropathy, he struck first.As a result of the predominance of sympathetic influences
developed tachycardia rest.Later, when he joined a violation of sympathetic innervation, tachycardia
decreases somewhat.In a situation of persistent tachycardia with total vegetative doner-vatsii
compared with transplanted heart.Violation of the autonomic afferent dramatically reduces adaptive
potential cardiovascular system to physiological stress.
Gastrointestinal form.When gastrointestinal form of autonomic neuropathy symptoms is largely due
to the lack of regulation of the cholinergic function gastrointestinal tract:
- Gastroparesis with delayed or, conversely, upsetting gastric emptying, which creates considerable
difficulty
in
finding
insulin,
as
time
andvolume
absorption
of
carbohydrates
vary indefinitely;
- Atony of the esophagus, reflux esophagitis, dysphagia;
- Change of watery diarrhea (usually at night)
intestinal dysmotility, exocrine secretion PZHZHand
with
constipation
Joining dysbiosis, these manifestations by the term "diabetic enteropathy";
- Drooling;
- Biliary dyskinesia with a tendency to stone formation, reactive pancreatitis.
25
as
a
result
of
Urogenital form.This form of autonomic neuropathy develops as a result of involvement in the sacral
plexus and the autonomic regulation of the local features of the urogenital tract and is characterized by
the following symptoms:
- Atony ureters and bladder;
- Reflux and stasis of urine;
- The tendency to develop urinary tract infection;
- Erectile dysfunction (50% of patients with diabetes);
- Retrograde ejaculation pain and impaired innervation of the testicles;
- Violation of vaginal moisture.
Diabetic foot syndrome (SDS)- a pathological condition of the footin diabetes that
occursagainst the background of peripheral nerves, skin andsoft tissues, bones and joints and
manifested acute and chronic ulcers, bone and joint lesions and purulent necrotic processes.SDS is
observed in 10-25%, and according to some, in one form or another in 30-80% of patients with
diabetes.Amputation of the legs .
Pathogenesis SDSmulticomponent and presented a combination of neuropathic and perfusion
disorders with a strong propensity to infection.Based on the prevalence in the pathogenesis of any of
these factors distinguish three main forms of PIF.
I.Neuropathic form.
A. Without osteoarthropathy.
B. Diabetic osteoarthropathy.
II.Neuroischemic (mixed) form.
III. Coronary form.
The most common form of neuropathic SDS (60-70% of cases).Purely ischemic form SDS occurs in
3-7% of cases.In 15-20% of cases occur mixed form of the syndrome, which is clinically more or less
has the features of both.
T h e c l i n i c a l p i c t u r e . When neuropathic form PIF can distinguish at least three types of
lesions: neuropathic ulcers, osteoarthropathy (with the development of Charcot joints), neuropathic
edema.
Neuropathic ulcers are usually localized in the soles and interdigital spaces, iein areas of the foot with
the greatest pressure.Neuropathic osteoarthropathy is the result of the expression of dystrophic changes
in bones and joints of the foot unit (osteoporosis, osteolysis, and hyperostosis).Neuropathy masks
spontaneous bone fractures, which fifth of cases are painless.Palpable It may be noted hyperemia and
edema of the feet, compared with the other leg.If the fracture was only a few days, you may not have
the X-ray changes.For the diagnosis in this case it is advisable to conduct ultrasound bone.
An e h e n e.
1.Optimizing diabet.The need for insulin due to infectious and inflammatory process increases
significantly.In DM-II often need at least a temporary switch to insulin.
2.Systemic
antibiotics.Conducted
on
the
general
principles
tsipam
when
an
infected
ulcer,
involvement
of
the
subcutaneous
tissue and muscle.If there is only a violation of the integrity of the skin without
involvement of underlying tissues, the patient only requires unloading legs and hold local treatment
ulcer surface antiseptic kami.
26
P r e v e n t i o n . Primary method of prevention is to maintain an optimal SDS diabet.Inspection feet
of diabetic patients should be performed each time during a visit to the doctor, with no less than 1 time
a year.The volume of instrumental studies developed individually.
New educational technology: a method of "The Weakest Link"
To work needed:
1. A set of questions on endocrinology.
2. A sheet of paper with a list of games for logging.
3. Stopwatch
Progress:
1. The game holds a teacher and an assistant from the students - the counter.
2. Counter wrote on a sheet date, the group number, the faculty and the business name of the game
and a list of student groups.
3. Teacher hurt in series of questions from the students a set of questions.
4. The student must for 5 seconds to answer,
5. Teacher of the word "right" or "wrong" answer evaluates if the "wrong" he will give the correct
answer.
6. Counter puts opposite the name of the student, "+" or "-" depending on the correctness of the
answer.
7. Are the students are, therefore, two rounds of questions.
8. After 2 rounds of questions the game is suspended and students who have received, minus two out
of the game as the "weak link".
9. The game continues for a new circle with the rest of the students. Again, they are offered one new
round of questions, and again eliminated students who in the sum with the first two rounds turned
instrumentals.
10. Round by Round shown the strongest of the players, who responded to an increasing number of
issues.
11. Ha sheet against each name the teacher records - which in any round table and dropped the "weak
link".
12. Game estimated maximum of 100 points.
Students who withdrew after the first 2 rounds of the answers, get a game, "0" points,
After 3 rounds - "25" points, after 4 rounds - "50" points, after 5 rounds - "75" points,
The strongest participant receives 100 points.
13. The scoring on the sheet of the protocol to the count of the current total of occupation as an
estimate for the theoretical part.
14. At the bottom of the log free teacher records on a business game, the elder signs off.
15. Minutes of the game remains.
Set of questions.
1.
2.
Classification of diabetic retinopathy.
Name the form of diabetic foot.
4.2 The analytical part
The decision of situational problems.
Students are given one task to the differential diagnosis of endocrine disease. Preparation time - 5
minutes. To answer - 2 minutes. Response is evaluated according to the criteria developed.
Considered amendments and judgments of students going into their asset. The group then divided into
2 groups and given a task with a difficult decision. Preparation time - 7 minutes. The solution
presented and discussed together with the other subgroups.
Objective number one. Male 21 years old. Complaints about dry mouth, weight loss, and acute
illness began two weeks ago. Glycemia before meal-18 mmol / L, daily glucosuria-4%, acetone "+",
the density of urine - 1038.
1. Your diagnosis
2. What complications occur in patients?
27
3. Treatment of this condition
Objective number 2. Male 42 years. Height 168 cm, weight 88 kg. During the test, a fasting blood
glucose level of 6.8 mmol / L, 1 hour - 12.0 mmol / L, 2 hours, 8.2 mmol / l.
1. Preliminary diagnosis.
2. Recommendations.
4.3 The practical part
Performed at the bedside. Supervision is carried out under the supervision of a teacher. The student
must learn to practice proper medical history of patients with endocrine disorders, with ztom able to
differentiate primary and secondary information during the examination to focus on the endocrine
glands and the clinical features of dysfunction of these glands. When communicating with the patient
must be considered such psychological traits, such as irritability, fatigue, and during communication
exercise extreme tact and at the same time be confident and firm.
In conducting activities in the clinic, while outpatient care, to teach students to quickly, clearly
questioning and examination of the patient, proper filling patient card.
Practical skills for this occupation carried out in 3 phases and is estimated
maximum of 100 points
1.
Tes tt ole ran tno standtogl ow a r eEXAMPLEaandx andpn omd andab ete
Purpose: To test glucose tolerance in diabetes
Equipment: 75g. Glucose, 250-300 ml of water
Performs step (stage)
№ e Me ropriyatie
tapa
1.
2.
3.
Not
done
(0
points)
That schakovoe study of blood glucose
0
Yes Th patient to drink 75 oz.glucose dissolved in 250-300 ml of 0
boiling water for 5 minutes.
Used to follow glucose 2 hours after administration of glucose.The 0
test is positive if the fasting blood glucose levels> 6, 1 mmol / l.and
after 2 hours> 11.1 mmol / l.
Sun it:
0
2.
By
lnostyu
properly
executed
30
40
30
100
P ar ah e e s son sin and Silin
Purpose: Calculation of the dose of insulin
Equipment: medical scales
Performs step (stage)
№ e Me ropriyatie
tapa
1.
2.
Not
By
satisfied (0 lnostyu
points)
properly
executed
Measure of patient weight and height to determine the ideal weight 0
20
Ra sschet daily insulin dose per kg of patient weight: 1, in 0
20
28
3.
4.
overweight count on ideal body weight, 2, and underweight - the
actual weight
Ra Thousands separator for bolus and basal dose ratio of 30/70 0
40/60
Thousands separator Ra bolus dose of insulin on meals and basal
dose, depending on the duration of the basic insulin
Sun it:
0
30
30
100
5.Control forms of knowledge, skills and abilities
- Oral
- Written
- Decision of situational problems;
- Demonstration of the developed skills
6.The evaluation criteria of the current control
№ Military
Est. ENKA
mustache
in points
1. 86-100 Personally from
the "5"
Ka quality assessment
Communicates about, think creatively, evaluates,
interprets.Applies knowledge in practice.Understands, knows,
says has no idea
Ra ssuzhdaet independently assess, interpret, apply knowledge
in practice, understands, knows, says has an idea
Minimality know.Understand the essence, says
2. 71-85
It is well "4"
3. 55-70
Beats
ovletvoritelno "3."
Not satisfactory, Pl oxo know.Not thoroughly.Require additional training.
"2"
4
0-54
7.Flow chart classes
1. Checking the initial level of preparedness of students to engage in "Late
Complications of diabetes. Explanation of the diagnosis and differential
Diagnostics.
2. Decision analysis and situational problems.
3. Supervision of patients. Clinical analysis of supervised patients.
4. Interactive games to assess knowledge on training.
№
Training lessons
1 Judgment of courses offered
2 Ca autonomy of patients Supervision attached houses, self Curation case
patients, participation in rounds of professors and associate professors
3 Ra Zborov the department examined case patients with the interpretation of
the survey data and treatment
29
Prospect
classes
6 hours
8.30-10.05
10.10-11.05
11.10-11.55
4
5
6
ne reryv
On judgment tests, situational problems.
Pr Overcome digestibility.Ad evaluations homework
11.55-12.40
12.40-14.00
14.00-14.30
8.Test questions
1. What complications are common in diabetes mellitus type II?
2. What stages are distinguished in diabetic retinopathy?
3. What changes are observed in the phase III kidney disease?
4. List the forms of diabetic foot.
9.Recommended Reading
Summary:
1.
2.
3.
4.
Balabolkin MI Endocrinology. M., Medicine, 1998
Vladimir Potemkin Endocrinology. M., Medicine, 1999
Grandparents II Endocrinology. M., Medicine, 2000
Melnichenko GA Tokmakova AY, deck DE, NV Lavrishcheva Endocrine
disease. M. Medicine, 2009
5.
Guidelines for Pediatric Endocrinology. Handbook of clinical Pediatric
Endocrinology. Edited by Charles G. Bouka, Rosalind S. Brown. 2009
6.
Shustov SB, Khalimov S, Trufanov GE Functional and topical
diagnostics in endocrinology. M. 2010
7.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 1. Greenspan's
Basic & Clinical Endocrinology. 2010
8.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 2. Greenspan's Basic &
Clinical Endocrinology. 2011
9.
Clinical Endocrinology. Ed. EA Kholodova. Minsk. Belarus. 2011
10.
Melnichenko GA Udovichenko OV Shvedova AE Endocrinology. Typical
Error practitioner 2012
11.
Endocrinology. National guidelines (+ CD-ROM). 2012
More:
1. Therapeutic Guide Washington translated from English. (Section
"Endocrinology") 1996.
2. Laycock. Fundamentals of Endocrinology, Moscow 2000
3. Ty M. Mack - Dermott MD Secrets Endocrinology - Moscow 2000
4. Ketgayl VM, Arkin RA, Pathophysiology of endocrine system - Moscow, Medicine,
2001.
5. Balabolkin MI Diabetology - Moscow, Medicine, 2002
7. Fadeev PA. Endocrinology. Diabetes. A Reference Guide. 2009
8. Kartelishev Alexander Rumyantsev AG, Smirnova NS Actual problems of obesity
children and adolescents. 2010
9. Mkrtumyan AM, AA Nelaev. Emergency Endocrinology. 2010
10. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Diseases
thyroid. Williams Textbook of Endocrinology. 2010
11. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Bark disease
30
adrenal gland and endocrine hypertension. Williams Textbook of
Endocrinology, 11 th edition. 2010
12. AN hams Emergency Endocrinology. 2011
13. Petunina NA, AV Trukhina Thyroid disease. 2011
14. Manukhin IB Tumilovich LG, M. Gevorgyan Gynecological Endocrinology.
Lectures on gynecologic endocrinology. M. 2012
Journals:
15. Medical Journal of Uzbekistan, Tashkent.
16. "Problems of Endocrinology." Moscow.
17. "Therapeutic Archives", Moscow
18. "Clinical Medicine", Moscow
19. "Diabetes. Way of life ", Moscow
Internet sites:
1. "Internet Portal: Hunari»
2. Medscape.com
3. Alltheweb.com
4. Yahoo.com
5. E-medicine.com
6. www tma. uz
Ministry of Health Care of Uzbekistan
CENTRE FOR MEDICAL EDUCATION
TASHKENT MEDICAL ACADEMY
Department of Internal Medicine TRAINING GP endocrinologist
Subject: "Endocrinology"
31
Theme: "SCA"
Concept.Prevalence, the degree of increase to the WHO.Thyroid disease, accompanied
by an increase in: goiter (diffuse, nodular, mixed), diffuse toxic goiter, thyrotoxic
adenoma.
Educational and methodical development
(For teachers and students)
Tashkent - 2012
Flow chart lesson number 3
Goiter.The concept of prevalence, the degree of increase to the WHO.
Thyroid disease, accompanied by an increase in: goiter (diffuse, nodular, mixed), diffuse toxic
goiter, thyrotoxic adenoma.
№
fl ups practice session
PMA classes fo
venue
32
dl itTh
classes
270
min.
1 Centuries odnaya part (study subject)
10
2 Judgment about topics practice session with new educational op grew discussion
technologies
training room
("Gallery Tour"), as well as demonstration material (boards,
sets medical charts, tables, posters, hormonal and clinical tests,
X-rays, scans, situational problems, laser disc Tiroshkoloy,) to
determine the original level.
3 You discuss water
50
4 The definition of reference for the practical part - n
rofessionalny questioning.Explanation of the provisions and
recommendations for the job to fill medical records.
25
of judgment
training room
5 Military wasps practical training under the guidance of a Prospect ofes sional
teacher.
questions; talk with patients
filling medical records, case
studies.
Department of
Endocrinology Clinic 1-TTA
6 John interpretation of the survey data of patients - complaints, tory studies of the disease,
inspection, palpation, percussion and auscultation of patients as laboratory data situational
well as laboratory and instrumental studies
problems
Department of
Endocrinology Clinic 1-TTA
7 Judgment on the theoretical and practical knowledge of the mustache tny survey, tests,
students, fixing material, the level of learning assessment.
discussion, identification of
practical skills
Department of
Endocrinology Clinic 1-TTA
8 The definition of output on practical training, evaluation of Infor mation, questions for
100-point system, and ad evaluations.Homework the next homework.
practice session (a collection of questions).
training room
Lesson number three
1.Topic: Goiter.The concept of prevalence, the degree of increase to the WHO.
Thyroid disease, accompanied by an increase in:
Goiter (diffuse, nodular, mixed),
Diffuse toxic goiter, thyrotoxic adenoma.
uch ebnoe time: 7:00
Art ruktura training 1. afedra to internal medicine training
GPs with an endocrinologist, endokrinologichessession
some branch 1 TTA clinic, clinical
1-clinic laboratory TTA;
2.set of tables, methodological recommendations
33
15
30
35
80
25
tion, laboratory and instrumental data,
video, CD-ROM with Tiroshkoloy,
3.TCO: computer, video
The training session:
- Theacquisition of knowledge and skills in students GPs to diagnose
and differential diagnosis of endocrine diseases, accompanied by
Enlargement of the thyroid gland.
- Learn to use the modern classification of these diseases;
- To conduct early detection and disease prevention through individual
symptoms, syndromes.
Pe dagogicheskie tasks: D results of training activities:
- Build knowledge and GP
skills for
should know:
diagnosis and differential • to understand the causes of goiter
diagnosis of diseases of • determine the severity of iodine deficiency
the thyroid
and thyrotoxicosis
cancer caused by
• Be aware of the clinical symptoms of hyperthyroidism
iodine deficiency;
• Analyze data from laboratory tests and
- Build knowledge and instrumental studies
skills for
• assign a pathogenetic therapy for
prophylaxis deficit
goiter
iodine;
• differential diagnosis
- Discuss the clinical thyroid disease;
symptoms
• conduct pathogenetic therapy
thyrotoxicosis;
Thyroid Disease
- To consider the severity should be able to:
of the dash• to assess the functional status of the thyroid
toxicity
and
discuss cancer;
methods of treatment;
• interpret data Thyroid
- Form of knowledge on cancer;
treatment
• interpret data scans
Thyroid Disease
Thyroid.
must have skills:
- Professional questioning, examination of the patient;
- Interpretation of the clinical laboratory
instrumental data;
- Palpation of the thyroid gland and the definition
magnification;
- To identify the symptoms of eye-tireotok
sycosis;
- Clinical diagnosis for classical
fication of WHO;
- The basis of consultation with these patients
diseases;
- Learn the skills of patients with diseases
Tions of the thyroid gland during pregnancy.
le Ktsia, the method of "gallery tour", demonstration, entertainment
Me Toda training
experience, discussion, conversation, case
Fo rmy training activities of individuality work, group work, team, classroom, extracurricular.
Mr. zdatochnye viziualnye training and materials, videos, models, graphic
Wed edstva training
organizers, kits medical charts, tables, stands, kits radiograph.
34
Cn lady and means of Bl uu-survey, testing, presentation of the results of the training task, filling
medical records, execution of practical skills "professional questioning"
feedback
2.Motivation
Given the high prevalence of this disease and the need for differential diagnosis of diseases that occur
with an increase in thyroid cancer, having a basis of iodine deficiency is a need for this lesson. During
the development of the topic, to draw students' attention to the concept of "endemic", the geographical
location of Uzbekistan in the endemic area, mass distribution of goiter. To emphasize the importance
of iodine as a trace element for the formation of the central nervous system, intelligence and physical
development. Highlight the role of thyroid hormones in the body. In the background you can move
the assessment of the severity of endemic goiter. Be given to the possibilities of conservative
treatment nodal forms of endemic goiter.
In order to properly diagnose and treat these pathologies to the GP to be able to properly assess the
condition and choose the tactics of treatment. During the development of the topic, to draw students'
attention to the various forms of thyroid disease, for reasons of, and on pathogenetic mechanisms, this
involves a variety of approaches to treatment and prevention of this disease. To draw attention to the
thyroid can, focusing on the rapid spread of the disease in the world. Students should pay attention to
the simplicity and accessibility of diagnostic techniques for thyroid GPs. In the background you can
move specific diagnostic markers of thyroid, various classifications of increasing thyroid enumeration
of names of drugs used in the prevention of endemic goiter, hypothyroidism and diffuse toxic goiter.
3.Intra and interdisciplinary communication
Teaching of the subject is based on the knowledge of the students major endocrine diseases, received
a 4th year in a cycle endocrinology, as well as therapy, which will continue to carry out differential
diagnosis of diseases associated with an increase in thyroid cancer. Acquired during the course
knowledge will be used during the passage of therapy at 6 and 7 of the course.
4.Contents classes
4.1 The theoretical part
A list of the issues:
1. Iodine deficiency disease and methods of prevention.
2. Nodular and mixed craws
a) The diagnosis, treatment
b) Indications for strumectomy.
Z. diffuse toxic goiter
a) The differential diagnosis with NDC, tuberculosis, rheumatism,
Thyrotoxic adenoma, cachexia various origins
b) The pathogenesis of clinical symptoms
c) Methods of treatment, the selection of doses
35
d) Thyrotoxic goiter in pregnancy.
"Endemic goiter" - is iodine deficiency, which develops as a result of iodine deficiency in
people living in iodine-deficient regions. Iodine deficiency and endemic goiter is the area, if the
prevalence of thyroid enlargement even 1 degree is 5% or more in children and adolescents, or 30% or
more of adults in a given geographical area. The prevalence of iodine-deficient regions of the world is
very high. The total number of people living in iodine-deficient regions and, therefore, are at risk of
iodine deficiency is more than 1 billion
Iodine is a vital trace element, the bulk of its concentrates in the thyroid, blood. Iodine from the blood
gets to the various organs and tissues, as well as partially deposited in lipids and appears mainly
through the kidneys. The main role of iodine - involved in the formation of thyroid hormones.
The role of thyroid hormones in the thyroid gland:
- Determine the development of the fetal brain and intelligence of the child in later years
of life;
- Provide normal energy metabolism;
- Stimulate the synthesis of protein;
- Reduce the level of cholesterol in the blood;
- Affect the immune system;
- Provide a set of adaptive responses;
- Control the growth and maturation of skeleton;
- Determine the quality of reproductive health services.
To determine the size of the thyroid gland, there are two methods:
1. Palpable and visual method - is the most accessible and easily manageable, but it has its drawbacks,
since it is based on subjective data, depending on the anatomy of the neck, the age of the subject, the
location of the thyroid gland, the experience of the researcher. In our country, since 1955, has acted
and acts
Classification proposed by OV Nikolayev, under which stands 5 degrees of thyroid enlargement. However,
the use of this extremely detailed classification leads to an overestimation of the frequency of goiter in the
population. Since 1994, the world recommended by the WHO uses a more simplified and accessible to
physicians of all specialties of the international classification of the size of the thyroid gland:
0-degree goiter not.
Grade 1 - goiter is not visible, but palpable, and the size of each of the segments more distal phalanx of the
subject.
Stage 2 - goiter palpable and visible to the eye. This classification is very useful in epidemiological surveys.
2. Ultrasound (U.S.), which is considered a more accurate method. Using ultrasound determine the volume of
the thyroid gland by the formula - (WS • AP • TA + SHL • DL • TL) • 0,479. According to international
36
standards using ultrasonography in adults (over 18 years) goiter is diagnosed when the amount of cancer in
women is more than 19 ml, 25 ml of men.
The severity of iodine deficiency. The International Council for Control of iodine deficiency diseases
recommends that you make three degrees of severity of iodine deficiency:
Mild iodine deficiency goiter (all forms of thyroid enlargement) occurs between 10 and 30% of the population,
and the median urinary iodine excretion is 50-99 mg / l. Hypothyroidism and cretinism are missing,
At moderate - frequency of goiter and 50%, the average urinary iodine excretion is reduced to 20-49 mg / l.
there may be cases of hypothyroidism;
In severe goiter rate may reach almost 100% of the average level of urinary iodine excretion - below 20 mg / l.
Cretinism occur with a frequency of 1 to 10%. Pathogenesis of iodine deficiency. Iodine deficiency in the
environment affects the functional state of the thyroid gland, in particular reducing its functional activity. But at
the same time the possibility of compensatory thyroid in terms of functional recovery in iodine deficiency is
extremely high; in the course of centuries of human evolution have developed mechanisms of adaptation to
iodine deficiency:
• In response to iodine deficiency and reduced levels of thyroid hormone (TH) on the law of feedback increased
levels of TSH, which leads to increased capture of iodine and synthesis of triglycerides with subsequent
hyperplasia of parenchymal cells;
• Increased synthesis and metabolism of triglycerides in response to an increase in TSH enhances the process of
circulation of iodine, which allows the body to do smaller amounts of iodine;
• The character of the synthesis of TG. Under physiological conditions, the main hormone that is synthesized
by the thyroid gland, is the PM. Given the shortage of iodine by the thyroid gland begins to actively produce Ts.
This hormone gives a more pronounced effect than the PM, and the synthesis of the hormone uses less iodine;
• Given the lack of iodine in the accelerated conversion of Ah Ts, ie increases the activity of thyroid hormones.
These mechanisms are in most cases can successfully adapt to the light of iodine deficiency. In this case, the
iron is slightly increased in size, but the function of the body is not affected. With more severe deficits, as well
as the presence in the environment of other goitrogen, amplifying the effect of iodine deficiency, compensatory
mechanisms are not completely eliminate the harmful effects of iodine deficiency. In these circumstances, the
thyroid gland is greatly increased in size, the possible development of subclinical and, in some cases, and
clinical hypothyroidism
Methods of iodine prophylaxis. For satisfactory use of the body for iodine following recommended daily
intake of iodine standards (WHO, 1996):
Infants - 50 mcg;
From 2 to 6 years - 90 mg;
From 7 to 12 years - 120 mg;
12 years and older - 150 mg;
Pregnant and breastfeeding - 200 micrograms.
Actual average intake of iodine iodine deficiency regions residents, including Uzbekistan, is 40-80 mg per day,
ie 2-3 times lower than the recommended level. To overcome the lack of iodine in the diet used methods of
individual, group and mass iodine prophylaxis.
Mass iodine prophylaxis is the most effective and economical method of replenishment of iodine deficiency.
Achieved by adding potassium salts (iodide or potassium iodate) in the most common foods: salt (for mild
iodine deficiency is 10-25 mg / kg, with an average weight - 25-40 mg / kg, with a heavy - up to 60 mg / kg ),
bread and water.
37
Collective iodine prophylaxis is carried out by organized the drugs containing iodine, populations most at risk
of IDD (children, adolescents, pregnant and lactating women). With mild to moderate iodine deficiency is
assigned daily additional amount of iodine:
Children age dopubertatnogo - 100 mcg
Teens - 200 micrograms;
Adults-150 mg,
Pregnant and breastfeeding - 200 micrograms.
Individual iodine prophylaxis involves the use of preventive medicines that capture physiological iodine.
Assigned antistrumin or potassium iodide in a dose to iodine per day is at least 150-200 mg.
Treatment of endemic (iodine deficiency) goiter. In the presence of diffuse goiter according to palpation and /
or ultrasound after exclusion of autoimmune goiter appointed supplementation of iodine in a daily dose of 200
mg course of at least 6 months. If after 6 months showed a significant reduction or normalization of the size of
the thyroid, then continue taking the drugs in the prevention of iodine dose of 100-200 mg for the prevention of
recurrent goiter. If the intake of iodine preparations during this period happened normalizing thyroid size, it is
assigned to levothyroxine vine 2,6-3 mg per 1 kg of body weight per day alone or in combination of iodine
intake in a dose of 100-150 mg per laziness. Adequate dose of thyroxine is selected according to the level of
TSH.
Evolved in the presence of nodal forms of thyroid goiter used drugs - levothyroxine dose of 150 - 200 mg per
day. The optimal dose is determined by the level of Ts, T 4 and TSH in serum and the absence of signs of
overdose. If, five - month therapy was ineffective, surgery is recommended.
Tactics GPs.
- Set up a system of iodine prophylaxis (group, individual)
- For those with a low level of thyroid enlargement to organize and carry out treatment with iodine, as the basis
of the elimination and prevention of diffuse nodular goiters forms of goiter.
New educational technology: a method of "Tour Gallery»
To work needed:
1. A set of questions that have been printed on a separate sheet.
2. A set of case and diagnostic tasks, printed on separate sheets,
3. Blank sheets of paper
4. Pens with colored bars (blue, red, black, green)
5. Number plates for the draw, the number of students per class
6. Speedometer or clock.
Course of the business game:
1. A group of students is divided into subgroups 3.4 na draw of 2-3 people in each
2. Each subgroup sits alone, takes a sheet of paper and on one of the colored pens.
3. on a sheet date, number of gaming title, name of student participants in this subgroup.
4. One of the players takes the envelope question or problem, depending on the choice of the teacher.
5. For each sub-question its departments or task, the complexity of their subgroups for all about the same.
6. Takes the time to 10 minutes.
7. Small groups (subgroups) each for 10 minutes to discuss the job, write a judgment at the end of the game
and share the sheets with another sub-group of the circle.
38
8. The next subgroup assesses previous answer and if the answer is not complete or supplement it offers its
own version, if they value as the correct answer at this stage is given a time of 10 minutes.
9. At the end of processing (30 minutes or 40 minutes) depending on the number of sub-groups (3 or 4) on a
piece of writing is 3.4 different color pens.
10. The works shall be the teacher
11. All participants will discuss the results and choose the most correct answers are worth points.
12. for discussion of play time of 15 minutes
13. Subgroup, which gave the most correct answers will receive the maximum score of 100% on the rating of
the theoretical part of the training.
Subgroup, who took 2nd place - 85.9% rating.
Subgroup, who took 3rd place - 70.9% rating
14. Students with scores recorded for billing ongoing evaluation sessions.
15. The works are signed by the teacher and students elder group and remain a teacher.
Appendix:
1. Complex test questions
2. Situational and complex diagnostic problems.
4.2 The analytical part
1. Checking the initial level of preparedness of students to engage in "Diseases accompanied by enlargement of
the thyroid gland." Explanation of the diagnosis and differential diagnosis of diseases associated with an
increase in thyroid cancer.
2. Decision analysis and situational problems.
3. Supervision of patients with diseases that are accompanied with impaired consciousness.
Clinical analysis of supervised patients
4. Interactive games to assess knowledge on training.
Problem number 1. Patient 49 years at a reception at the endocrinologist complains of weight loss, tremors in
the body, disruption of the heart, dry mouth and thirst. Complaints emerged two months ago after the stress and
move to another job. Inspection: the skin is soft, normal humidity, elastic. Tongue dry, coated with white
bloom. Heart sounds loud, irregular, atrial fibrillation heart rate 96-118 beats per minute, blood pressure 140/40
mm Hg. Art. Stool after every meal, unformed. Swelling in the legs. The thyroid gland is located low, small,
in the right lobe palpable nodules the size of a walnut. Marked bilateral proptosis, scleral injection, lacrimation.
Of analyzes: Ts - 3.4 nmol / L (normal 1,2-2,8), T4 - 209 nmol / L (normal 60-160). Thyroid cancer - nodular
goiter. ECG - atrial fibrillation, heart rate 100-126 beats per minute.
1. What additional research is needed?
A. Thyroid gland
B. Postgrad T3, T4, TSH
B. thyroid scan
D. CT scan of the thyroid gland
D. determination of iodine bound to blood proteins
2. What is the severity of hyperthyroidism?
A. Thyroid gland
B. research level T3, T4, TSH
B. thyroid scan
39
D. CT scan of the thyroid gland
D. determination of iodine bound to blood proteins
3. Treatment
A thyroid drugs
B. conservative
B. Treatment with radioactive iodine
G. rapid
D. thyreostatics
Objective number 2. Female 58 years. Complaints of shortness of breath, palpitations, weakness, weight loss.
Within 5 years, coronary heart disease, competent treatment which does not lead to success. OBJECTIVE:
satisfactory condition, height 176 cm, weight 62 kg. The skin is warm, normal humidity, tremor of the fingers.
Blood pressure 130/60, pulse 110 in 1 minute, atrial fibrillation, heart sounds are muffled, the lungs in the lower
fine moist rales are heard. The liver was not palpable. Swelling in the legs to the upper third. In the right lobe
of the thyroid gland is palpable tight knot, painless, mobile, 3x3 cm
1. Preliminary diagnosis.
A. Diffuse enlargement of the thyroid gland 2 degrees
B. Nodular Goiter
B. Thyrotoxic adenoma
G. thyroid cyst
D. Thyroid Cancer
2. What instrumental examination of the thyroid gland to be performed.
A thyroid ultrasound
B. research level T3, T4, TSH
B. thyroid scan
D. CT scan of the thyroid gland
D. determination of iodine bound to blood proteins
3. Treatment policy.
A. thyroid drugs
B. conservative
B. treatment with radioactive iodine
G. rapid
D. thyreostatics
Task number 3. Patient C., 46 years old. Complaints of a feeling of suffocation, and compression of the neck,
shortness of breath, hair loss, sensitivity to cold, swelling. On examination: the skin on the legs dry, dense,
poorly collected in the crease. In the lungs, respiratory depression, cardiac rhythmic, significantly suppressed,
heart rate 54 per minute, blood pressure 115/60 mm Hg. Art. Stomach increased through the subcutaneous
tissue. Chair prone to constipation. Having hard swelling in the legs. The thyroid gland is enlarged to 2
degrees, dense, heterogeneous' consistency inactive. Thyroid scan: mosaic capture iodine. TSH - 11 mIU / L
(normal 0.5 - 5.0). Thyroglobulin antibodies 1:100 (normal 1:10000).
1. Diagnosis.
A. Alimentary-constitutional obesity grade 2
B. Autoimmune thyroiditis, hypothyroidism
40
B. Primary hypothyroidism
G. Secondary hypothyroidism
A grade 3 Endemic goiter, hypothyroidism
2. Treatment strategy.
A treatment with radioactive iodine
B. Conservative
B. thyroid drugs
G. iodine
D. thyreostatics
4.3 The practical part
Endocrinology mastering each skill is carried out in two phases and is estimated maximum of 100 points.
Breath holding test on inspiration.
Purpose: The sample of breath holding at inspiration
Equipment: stopwatch
Performs step (stage)
№e
tapa
Me ropriyatie
Not done
(0 points)
By lnostyu
properly
executed
1.
To measure the pulse of the patient for 1 minute (and for 5 seconds)
0
25
2.
Ask for the patient to hold his breath after a deep inspiration
0
35
3.
Measure of the pulse during and 5-10 seconds. If no pulse slows test
is considered positive.
0
45
Sun it:
0
100
Palpation of the thyroid gland and determine the degree of enlargement of the thyroid
cancer.
Purpose: palpation of the thyroid gland and determine the degree of enlargement of the thyroid gland.
Equipment: patient
Performs step (stage)
№ e tapa
Me ropriyatie
Not done
(0 points)
By lnostyu
properly
executed
1.
Wasps Motril neck
0
30
2.
Wasps Motril thyroid is tilted head back when swallowing saliva
0
30
41
3.
Pa lpatsiya thyroid
Sun it:
0
0
40
100
5.Control forms of knowledge, skills and abilities
- Oral;
- Written
- Decision of situational problems
- Demonstration of the developed skills
6.The evaluation criteria of the current control
№ Military
Est. ENKA
Ka quality assessment
mustache
in points
1. 86-100 Personally from Communicates about, think creatively, evaluates,
the "5"
interprets.Applies knowledge in practice.Understands, knows,
says has no idea
2. 71-85 It is well "4"
Ra ssuzhdaet independently assess, interpret, apply knowledge in
practice, understands, knows, says has an idea
3. 55-70
Beats
Minimality know.Understand the essence, says
ovletvoritelno "3."
4 0-54
Not satisfactory, Pl oxo know.Not thoroughly.Require additional training.
"2"
7.Chronological map classes
1. Checking the initial level of preparedness of students to engage in "Diseases of the endocrine
glands occurring thyroid enlargement." Explanation of the diagnosis and differential diagnosis.
2. Decision analysis and situational problems.
3. Supervision of patients. Clinical analysis of supervised patients.
4. Interactive games to assess knowledge on training.
№
practical lessons
1 Judgement of courses offered
2 Ca autonomy of patients Supervision attached houses, self Curation case
3
4
5
6
patients, participation in rounds of professors and associate professors
Ra Zborov the department examined case patients with the interpretation
of the survey data and treatment
ne reryv
Prospectowe
classes
7-hour ace
8.30-10.05
10.10-11.05
11.10-11.55
11.55-12.40
On judgment tests, situational problems.
12.40-14.40
Pr Overcome digestibility.Ad evaluations homework
14.40-15.10
8.Test questions
1. Indications for thyroid and iodine preparations
42
2. Status and performance of the hypothalamic-pituitary-thyroid system in Graves.
3. Skanograficheskaya picture sites with various active absorption.
4. Indications strumectomy
5. Status and performance of the hypothalamic-gilofizarno-thyroid system in hypothyroidism
6. How is the severity of hyperthyroidism?
7. For what purpose the breath holding test on inspiration?
8. Treatment of hyperthyroidism.
9.Recommended Reading
Summary:
1. Balabolkin MI Endocrinology. M., Medicine, 1998
2. Vladimir Potemkin Endocrinology. M., Medicine, 1999
3. Grandparents II Endocrinology. M., Medicine, 2000
4. Melnichenko GA Tokmakova AY, deck DE, NV Lavrishcheva Endocrine
disease. M. Medicine, 2009
5. Guidelines for Pediatric Endocrinology. Handbook of clinical Pediatric
Endocrinology. Edited by Charles G. Bouka, Rosalind S. Brown. 2009
6. Shustov SB, Khalimov S, Trufanov GE Functional and topical
diagnostics in endocrinology. M. 2010
1.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 1. Greenspan's Basic &
Clinical Endocrinology. 2010
2.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 2.
Greenspan's Basic & Clinical Endocrinology. 2011
3.
Clinical Endocrinology. Ed. EA Kholodova. Minsk. Belarus.
2011.
10.Melnichenko GA Udovichenko OV Shvedova AE Endocrinology.
Typical errors practitioner 2012
11.Endokrinologiya. National guidelines (+ CD-ROM). 2012
More:
1. Therapeutic Guide Washington, translated from English. (Section
"Endocrinology") 1996.
2. Laycock. Fundamentals of Endocrinology, Moscow 2000
3. Ty M. Mack - Dermott MD Secrets Endocrinology - Moscow 2000
4. Ketgayl VM, Arkin RA, Pathophysiology of endocrine system - Moscow, Medicine,
2001.
5. Balabolkin MI Diabetology - Moscow, Medicine, 2002
6. Fadeev PA. Endocrinology. Diabetes. A Reference Guide. 2009
7. Kartelishev Alexander Rumyantsev AG, Smirnova NS Actual problems of obesity
in children and adolescents. 2010
43
8. Mkrtumyan AM, AA Nelaev. Emergency Endocrinology. 2010
9. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Diseases
thyroid. Williams Textbook of Endocrinology. 2010
4.
Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Bark disease
adrenal gland and endocrine hypertension. Williams Textbook of
Endocrinology, 11 th edition. 2010
11. AN hams Emergency Endocrinology. 2011
12. Petunina NA, AV Trukhina Thyroid disease. 2011
13. Manukhin IB Tumilovich LG, M. Gevorgyan Gynecological
endocrinology.
14. Lectures on gynecologic endocrinology. M. 2012
Journals:
15. Medical Journal of Uzbekistan, Tashkent.
16. "Problems of Endocrinology." Moscow.
17. "Therapeutic Archives", Moscow
18. "Clinical Medicine", Moscow
19. "Diabetes. Way of life ", Moscow
Internet sites:
1. "Internet Portal: Hunari»
2. Medscape.com
3. Alltheweb.com
4. Yahoo.com
5. E-medicine.com
6. www tma. uz
Ministry of Health Care of Uzbekistan
CENTRE FOR MEDICAL EDUCATION
TASHKENT MEDICAL ACADEMY
Department of Internal Medicine TRAINING GP endocrinologist
Subject: "Endocrinology"
44
Theme: "SCA"
Thyroiditis: acute, subacute, Riedel's struma.Etiology, pathogenesis, clinical
features.The differential diagnosis of thyroid cancer, treatment, prognosis.Hashimoto's
thyroiditis.Clinical manifestations and stages, forms, differential diagnosis with
endemic goiter, treatment, prognosis.
Educational and methodical development
(For teachers and students)
Tashkent - 2012
Process chart classes № 4
Goiter.Thyroiditis: acute, subacute, Riedel's struma.Etiology, pathogenesis, clinical features.The
differential diagnosis of thyroid cancer, treatment, prognosis.Hashimoto's thyroiditis.Clinical
manifestations and stages, forms, differential diagnosis with endemic goiter, treatment,
prognosis.
№
fl ups practice session
PMA classes fo
venue
45
lasts
hour270
min.
1 Centuries odnaya part (study subject)
10
2 Judgment about topics practice session with new educational op grew discussion
technologies
training room
("Gallery Tour"), as well as demonstration material (boards,
sets medical charts, tables, posters, hormonal and clinical
tests, X-rays, scans, situational problems, laser disc
Tiroshkoloy,) to determine the original level.
3 You discuss water
50
4 The definition of reference for the practical part - n
of judgement
rofessionalny questioning.Explanation of the provisions and
training room
recommendations for the job to fill medical records.
25
5 Military wasps practical training under the guidance of a Prospect ofesionally
teacher.
questioning, conversation with
patients filling medical
records, case studies.
Department of Endocrinology
Clinic 1-TTA
6 John interpretation of the survey data of patients - tory studies of the disease,
complaints, inspection, palpation, percussion and laboratory data situational
auscultation of patients as well as laboratory and problems
instrumental studies
Department of Endocrinology
Clinic 1-TTA
7 Judgment on the theoretical and practical knowledge of the mustache tny survey, tests,
students, fixing material, the level of learning assessment.
discussion, identification of
practical skills
Department of Endocrinology
Clinic 1-TTA
8 The definition of output on practical training, evaluation of infor mation, questions for
100-point system, and ad evaluations.Homework the next homework.
practice session (a collection of questions).
training room
30
15
35
80
25
Lesson number three
Goiter.Thyroiditis: acute, subacute, Riedel's struma.Etiology, pathogenesis, clinical features.The
differential diagnosis of thyroid cancer, treatment, prognosis.Hashimoto's thyroiditis.Clinical
manifestations and stages, forms, differential diagnosis with endemic goiter, treatment,
prognosis.
uch ebnoe time: 7:00
Art
ruktura
training 1. afedra to internal medicine training
session
GPs with an endocrinologist, endokrinologichessome branch 1 TTA clinic, clinical
1-clinic laboratory TTA;
2.set of tables, methodological recommendations
tion, laboratory and instrumental data,
video, CD-ROM with Tiroshkoloy,
46
3.TCO: computer, video
Tse eh training session:
- Theacquisition of knowledge and skills in students GPs to diagnose
and differential diagnosis of thyroiditis;
- Learn to use the modern classification of these diseases;
- To conduct early detection and disease prevention through individual
symptoms, syndromes.
Pe dagogicheskie tasks: D results of training activities:
- Build knowledge and GP
skills for
should know:
diagnosis and differential • to understand the causes of tireoidiagnosis of thyroiditis; dits;
- Build knowledge and • Know the classification of severity
skills for
thyroiditis;
identifying
clinical • Analyze data from laboratory tests and
symptoms
instrumental studies at
thyroiditis;
thyroiditis;
- To consider the severity • assign a pathogenetic therapy
of the dashthyroiditis;
toxicity
and
discuss • differential diagnosis with
methods of treatment;
other diseases of the thyroid gland;
- Form of knowledge on should be able to:
treatment
• to assess the functional status of the thyroid
thyroiditis
cancer;
• interpret data Thyroid
cancer;
• interpret data scans
thyroid.
must have skills:
- Professional questioning, examination of the patient;
- Palpation of the thyroid gland, the definition
severity;
- Interpretation of the clinical laboratory
instrumental data;
- Clinical diagnosis for classical
fication of WHO;
- The basis of consultation with these patients
diseases;
- Learn the skills of patients with
thyroiditis in pregnancy
Me Toda training
le Ktsia, the method of "gallery tour", demonstration, entertainment
experience, discussion, conversation, case.
Fo rmy training activities of individuality work, group work, team, classroom, extracurricular.
Wed edstva training
Mr. zdatochnye viziualnye training and materials, videos, models, graphic
organizers, kits medical charts, tables, stands, kits radiographs.
Cn lady and means of b-people survey, testing, presentation of the results of the training task,
feedback
filling medical records, execution of practical skills "professional
questioning"
2.Motivation
47
Given the high prevalence of this disease and the need for differential diagnosis of diseases that occur
with an increase in thyroid cancer, having a basis of iodine deficiency is a need for this lesson. During
the development of the topic, to draw students' attention to the concept of "endemic", the geographical
location of Uzbekistan in the endemic area, mass distribution of goiter. To emphasize the importance
of iodine as a trace element for the formation of the central nervous system, intelligence and physical
development. Highlight the role of thyroid hormones in the body. In the background you can move
the assessment of the severity of endemic goiter. Be given to the possibilities of conservative
treatment nodal forms of endemic goiter.
In order to diagnose and treat these pathologies properly to the GP to be able to properly assess the
condition and choose the tactics of treatment. During the development of the topic, to draw students'
attention to the various forms of thyroid disease, for reasons of, and on pathogenetic mechanisms, this
involves a variety of approaches to treatment and prevention of this disease. To draw attention to the
thyroid can, focusing on the rapid spread of the disease in the world. Students should pay attention to
the simplicity and accessibility of diagnostic techniques for thyroid GPs. In the background you can
move specific diagnostic markers of thyroid, various classifications of increasing thyroid enumeration
of names of drugs used in the prevention of endemic goiter, hypothyroidism and diffuse toxic goiter.
3.Intra and interdisciplinary communication
Teaching of the subject is based on the knowledge of the students major endocrine diseases, received
a 4th year in a cycle endocrinology, as well as therapy, which will continue to carry out differential
diagnosis of diseases associated with an increase in thyroid cancer. Acquired during the course
knowledge will be used during the passage of therapy at 6 and 7 of the course.
4.Contents classes
4.1 The theoretical part
A list of the issues:
1. Thyroiditis: acute, subacute, Riedel's struma
a) The etiology, pathogenesis
b) Clinic
c) The differential diagnosis of thyroid cancer
d) Methods of treatment, prognosis.
2. Hashimoto's thyroiditis
a) The clinical presentation and stage forms
b) The differential diagnosis with endemic goiter
c) Treatment, prognosis.
Subacute thyroiditis - (de Quervain's thyroiditis) - an inflammatory disease of the thyroid gland
viral nature, accompanied by destruction of thyrocytes.
Etiology. Disease is caused by a viral infection, but is specific to the virus of the disease is not checked,
subacute thyroiditis may be caused by the Coxsackie virus, adenovirus, measles, mumps, influenza.
Contributing factors are:
- Connection with a previous medical history of viral infection;
- Increase in the number of cases during the outbreak of viral infection;
- The presence of high titers in patients with antibodies to Coxsackie, adenovirus, influenza viruses.
Pathogenesis. Matter following pathogenetic factors:
48
- A damaging effect on the thyroid gland virus infection;
- The development of autoimmune reactions, the formation of antibodies to the antigens of the thyroid
gland, the formation of immune complexes, complement activation and development of immune
inflammation.
Clinic. Local symptoms:
- Intense pain in the thyroid gland, irradiruyuschie in the head, ears, jaw, back of the neck, throat;
- Pain increases when turning your head, swallowing, chewing, head bowed, holding pain 2-3 weeks;
- Swallowing difficult;
- Thyroid gland is enlarged, firm, sometimes in the early enlarged and painful right lobe, later in the
disease process involved other departments cancer;
- The skin over the iron is hot, flushed, painful;
Common symptoms are:
- A significant increase in body temperature;
- Chills, weakness, sweating, headache;
- Effects of hyperthyroidism in the early, most bonyh irritability, sweating, hot flashes, palpitations,
weight loss, hot, moist, flushed, elastic skin, bright eyes, trembling fingers outstretched hands.
Diagnostics. Perhaps higher blood IgM, a temporary increase in titers of antibodies to thyroglobulin
and microsomal fractions. The change in the blood of thyroid hormones. Thyroid cancer: a slight
decrease in uniform echogenicity, over at least 1 \ 3 thyroid lobe. Biopsy of the thyroid gland: a
punctate defined giant multinucleated cell against oxyphilic colloid substance.
Differential diagnosis.
Graves' disease. For Graves' disease is not characterized by the presence of hyperthyroidism against
high fever, severe pain when swallowing, pain on palpation of the thyroid gland, the link with a history
of viral infection, a significant increase in ESR.
Acute suppurative thyroiditis. For acute suppurative thyroiditis is characterized by a growing general
intoxication, hectic high body temperature, stunning chills, pronounced leukocytosis, fluctuation in the
thyroid gland.
Thyroid cancer.
Cancer characterized by density, low morbidity, raised glands, regional
lymphadenopathy, failure of treatment with glucocorticoids, the presence of atypical cells in the biopsy
of the thyroid gland.
Treatment program in subacute thyroiditis.
1.
Treatment of glucocorticoid drugs.
2.
NSAIDs.
3.
Treatment with metronidazole.
4.
Treatment of thyroid medication.
5.
Immunomodulatory therapy.
6.
Local treatment.
7.
Symptomatic treatment of hyperthyroidism.
49
Corticosteroid treatment is the mainstay of treatment of subacute thyroiditis. The most frequently used
prednisolone; it is prescribed in doses of 30-40 mg per day (6-8 tablets). The duration of treatment of
the timing of pain relief in the thyroid gland and the normalization of ESR. Indications in the
appointment of NSAIDs are mild forms of subacute thyroiditis, severe pain in the thyroid gland. The
most pronounced effect was observed in indomethacin (indomethacin). He is appointed to 0,025 g 3-4
times a day after meals. In rare cases, subacute thyroiditis may be called anaerobic flora. In such
cases assigned metronidazole 0.25 g four times a day after meals for 10-14 days. Thyroid drugs are
prescribed in 3-4 weeks of treatment with glucocorticoids. Assign L - thyroxine at 50-100 mg per day,
for 1-1.5 months. Of immunomodulatory drugs used timalin 20 mg intramuscularly for 5 days, or Tactivin, 100 mg intramuscularly for 5 days.
Autoimmune thyroiditis (AIT) - a chronic inflammation of the thyroid autoimmune origin.
Hashimoto's autoimmune thyroiditis was first described in 1912.
Etiology. Internal etiological factors are hereditary and predisposing factors. AIT is a genetic marker
specific antigen HLA. Predisposing factor is the internal disorders of the immune and endocrine
homeostasis in puberty, menopause, pregnancy, childbirth, and aging. The external causative factors
include:
1. Pollution of the environment with waste industry, which could have a negative impact on the
human immune homeostasis and promote AIT.
2. The use of pesticides in agriculture.
3. Treatment with lithium.
4. Prolonged intake of excessive amounts of iodine increases the frequency of AIT, including in
individuals genetically predisposed to it, as induces the production of anti-thyroid autoantibodies.
5. Exposure to low doses of ionizing radiation.
6. Viral, bacterial, Yersinia infection may induce the development of AIT. 7. Treatment with
interferon induces expression of molecular HLA-II-class thyrocytes and may trigger autoimmune
reactions. AIT can accompany other diseases of the thyroid gland and to be "the second disease."
This is possible with diffuse toxic, endemic, sporadic goiter, adenoma and carcinoma of the thyroid
gland.
Pathogenesis. Underlying diseases are deficiency of T-suppressor function of lymphocytes, the release
of thyroid antigens, entering into the blood and the appearance of antibodies.
Clinic. Disease in women is 4-7 times more likely than men, can develop at any age, most often after
age 60. The main complaints of patients: an enlarged thyroid gland, difficulty in swallowing, there
may be weakness, a feeling of compression of the neck. About 5% of patients with hypertrophic form
there is an increase in thyroid function, which gives a picture of hyperthyroidism - the so-called
"hashi-toxicosis." Patients concerned palpitations hot flashes, sweating, weight loss, irritability.
Atrophic form has its own characteristics: The thyroid gland is not palpable, with defined clinical
hypothyroidism. This is a situation that used to be called "idiopathic hypothyroidism." Focal (focal)
form of autoimmune thyroiditis is characterized by lesions of one share (the proportion is small, dense).
Biopsy reveals in this share signs of autoimmune thyroiditis. Latent form is characterized by the
presence of only the immunological characteristics of the disease without clinical manifestations. Size
of the thyroid gland was normal. Latent form is often associated with nodular goiter. Depending on
the functional state of the thyroid in any case (form) of autoimmune thyroiditis may be: euthyroidism,
hyperthyroidism (rare) or hypothyroidism.
A group of persons at high risk for AIT
- Undergone toxic goiter
- Have undergone thyroid surgery
50
- Patients with any form of endemic goiter
- Patients with the syndrome galactorrhea-amenorrhea
- Patients with diabetes mellitus
- Patients with Stein-Leventhal syndrome (sklerokistozom ovaries)
- Allergic and autoimmune diseases
- Women age 40 and older
- Relatives of patients with Hashimoto's thyroiditis, Graves' disease and other autoimmune and
allergic diseases.
Differential diagnosis.
Euthyroid nodular goiter. Nodular AIT has to differentiate with euthyroid nodular goiter. Particulars
of euthyroid nodular goiter:
- In the blood no antithyroid antibodies
- In no punctate thyroid lymphoma and plasma cell infiltration, cell Ashkenazi.
Thyroid cancer. AIT and nodular thyroid cancer have common characteristics - the presence of units
and density of the thyroid gland.
The distinguishing features of cancer - low mobility or immobility site, unity with the surrounding
tissues, regional lymphadenopathy, the presence of punctate site of undifferentiated cells with signs of
proliferation.
Graves' disease. AIT patients in the early stages of the disease may be clinical signs of
hyperthyroidism (hashi-toxicosis). However, unlike the DTG in AIT symptomatic hyperthyroidism
smaller, no progression of thyrotoxicosis without thyrostatic therapy, perhaps even self-restoring
euthyroid status, have high titers of anti-thyroid antibodies.
The treatment program at AIT.
1.
2.
3.
4.
5.
6.
7.
Treatment of thyroid medication.
Treatment with glucocorticoids.
Combined therapy elektrodregingom taking prednisolone and thyroid medications.
Immunomodulatory therapy and treatment with heparin.
Efferent therapy.
Surgical treatment.
Clinical examination.
Thyroid drugs are used: L-thyroxine (in tablets of 100 mg), triiodothyronine (tablets of 25 and 50 mg).
Treatment is carried out over many months and years, and the development of hypothyroidism - for
life. Treatment of glucocorticoid therapy is conducted on continued treatment with thyroid hormones,
the initial dose of prednisone 30-40 mg per day, and reduced by 5 mg every 10-12 days. One of the
most common is the immunomodulator levamisole (Decaris) - given at a dose of 150 mg 1 time a week
for 2-6 months.
New educational technology: a method of "Tour Gallery»
To work needed:
1. A set of questions that have been printed on a separate sheet.
2. A set of case and diagnostic tasks, printed on separate sheets,
3. Blank sheets of paper
4. Pens with colored bars (blue, red, black, green)
51
5. Number plates for the draw, the number of students per class
6. Speedometer or clock.
Course of the business game:
1. A group of students is divided into subgroups 3.4 Na draw of 2-3 people in each
2. Each subgroup sits alone, takes a sheet of paper and on one of the colored pens.
3. On a sheet date, number of gaming title, name of student participants in this subgroup.
4. One of the players takes the envelope question or problem, depending on the choice of the teacher.
5. For each sub-question its departments or task, the complexity of their subgroups for all about the
same.
6. Takes the time to 10 minutes.
7. Small groups (subgroups) each for 10 minutes to discuss the job write a judgment at the end of the
game and share the sheets with another sub-group of the circle.
8. The next subgroup assesses previous answer and if the answer is not complete or supplements it
offers its own version, if they value as the correct answer at this stage is given a time of 10 minutes.
9. At the end of processing (30 minutes or 40 minutes) depending on the number of sub-groups (3 or
4) on a piece of writing is 3.4 different color pens.
10. The works shall be the teacher
11. All participants will discuss the results and choose the most correct answers are worth points.
12. for discussion of play time of 15 minutes
13. Subgroup, which gave the most correct answers will receive the maximum score of 100% on the
rating of the theoretical part of the training.
Subgroup, who took 2nd place - 85.9% rating.
Subgroup, who took 3rd place - 70.9% rating
14. Students with scores recorded for billing ongoing evaluation sessions.
15. The works are signed by the teacher and students elder group and remain a teacher.
4.2 The analytical part
Checking the initial level of preparedness of students to engage in "Diseases involving the thyroid
gland." Explanation of the diagnosis and differential diagnosis of diseases associated with an increase
in thyroid cancer.
2. Decision analysis and situational problems.
3. Supervision of patients. Clinical analysis of supervised patients
4. Interactive games to assess knowledge on training.
Problem number 1. Patient C., 46 years old. Complaints about a feeling of suffocation, and
compression of the neck, shortness of breath, hair loss, sensitivity to cold, swelling. On examination:
the skin on the legs dry, dense, poorly collected in the crease. In the lungs, respiratory depression,
cardiac rhythmic, significantly suppressed, heart rate 54 per minute, blood pressure 115/60 mm Hg.
Art. Stomach increased through the subcutaneous tissue. Chair prone to constipation. Having Hard
swelling in the legs. The thyroid gland is enlarged to 2 degrees, dense, heterogeneous' consistency
inactive. Thyroid scan: mosaic captures iodine. TSH - 11 mIU / L (normal 0.5 - 5.0). Thyroglobulin
antibodies 1:100 (normal 1:10000).
1. Diagnosis.
A. Alimentary-constitutional obesity grade 2
B. Autoimmune thyroiditis, hypothyroidism
B. Primary hypothyroidism
G. Secondary hypothyroidism
A grade 3 Endemic goiter, hypothyroidism
2. Treatment strategy.
A treatment with radioactive iodine
B. Conservative
B. thyroid drugs
G. iodine
52
D. thyreostatics
Objective number two. Went to the clinic the patient complained of pain in the neck, worse when
turning the head, smack in the back of the neck and lower jaw. A few weeks ago suffered a severe flu.
Now worry the increase in body temperature up to 38 °, weakness, sweating, palpitations, headache.
Skin covers moist, warm, tongue coated with a brown film. Cardiac rhythmic, tachycardia, heart rate
84 per minute. The thyroid gland is not enlarged, sharp pain on palpation; the patient pushes the
doctor's hands. The skin over it hyperemic. In general, the analysis of blood Hb • 120 g / L, white
blood cells - 8,0 x109, ESR - 28 mm / h Thyroid gland - a small increase in parenchymal echogenicity,
swelling capsule.
1. What kind of diseases can think of?
A. Subacute thyroiditis
B. Acute thyroiditis
B. Hashimoto's thyroiditis, hypothyroidism
G. diffuse toxic goiter
D. Diffuse enlargement of the thyroid gland 2 degrees, hypothyroidism
2. Treatment strategy.
A. treatment with radioactive iodine
B. Antibiotics
B. thyroid drugs
G. iodine
D. thyreostatics
Task number 3. Patient B., 31 years. Admitted to the emergency room complaining of a sharp pain in
the front of the neck, difficulty in swallowing, headache. The thyroid gland is enlarged, palpation
sharply painful, over her skin hyperemic, enlarged and painful cervical and submandibular lymph
nodes. Neck swelling. The body temperature rises 38.7 C, symptoms of intoxication.
1. What kind of disease you can think of?
A. Subacute thyroiditis
B. Acute thyroiditis
B. Hashimoto's thyroiditis, hypothyroidism
G. diffuse toxic goiter
D. Diffuse enlargement of the thyroid gland 2 degrees, hypothyroidism
2. What changes need to be in this disease in the general analysis of blood?
A. increase lymphocyte
B. increase in leukocyte
B. increase of eosinophils
The decline of ESR
D. increase in ESR
4.3 The practical part
Endocrinology mastering each skill is carried out in two phases and is estimated maximum of 100
points.
Breathe holding test on inspiration.
Purpose: The sample of breath holding at inspiration
Equipment: stopwatch
Performs step (stage)
№e
Me ropriyatie
Not
By
tapa
satisfied (0 lnostyu
points)
properly
executed
1.
To measure the pulse of the patient for 1 minute (and for 5
0
25
seconds)
53
2.
3.
Ask for the patient to hold his breath after a deep inspiration
Of measured pulse for 5-10 seconds.If no pulse slows test is
considered positive.
Sun it:
0
0
35
45
0
100
Palpation of the thyroid gland and determine the degree of enlargement of the thyroid
Cancer.
Purpose: palpation of the thyroid gland and determine the degree of enlargement of the thyroid gland.
Equipment: patient
Performs step (stage)
№e
tapa
Me ropriyatie
1.
2.
Wasps Motril neck
Wasps Motril thyroid is tilted head back when swallowing
saliva
Pa lpatsiya thyroid
Sun it:
3.
Not satisfied By lnostyu
(0 points)
properly
executed
0
30
0
30
0
0
40
100
5.Control forms of knowledge, skills and abilities
- Oral;
- Written
- Decision of situational problems
- Demonstration of the developed skills
6.The evaluation criteria of the current control
№ Military
Est. ENKA
Ka quality assessment
mustache
in points
1. 86-100 Personally from Communicates about, think creatively, evaluates,
the "5"
interprets.Applies knowledge in practice.Understands, knows,
says has no idea
2. 71-85 It is well "4"
Ra ssuzhdaet independently assess, interpret, apply knowledge in
practice, understands, knows, says has an idea
3. 55-70
Beats
Minimality knows.Understand the essence, says
ovletvoritelno "3."
4 0-54
Not satisfactory, Pl oxo know.Not thoroughly.Require additional training.
"2"
7.Chronological map classes
1. Checking the initial level of preparedness of students to engage in "Diseases of the endocrine
glands occurring thyroid enlargement." Explanation of the diagnosis and differential diagnosis.
2. Decision analysis and situational problems.
3. Supervision of patients. Clinical analysis of supervised patients.
4. Interactive games to assess knowledge on training.
№
fl ups lessons
Prospect
odolzhitelnost
classes
54
1 Judgment of courses offered
2 Ca autonomy of patients Supervision attached houses, self Curation case
patients, participation in rounds of professors and associate professors
3 Ra Zborov the department examined case patients with the interpretation
of the survey data and treatment
4 ne reryv
5 On judgment tests, situational problems.
6 Pr Overcome digestibility.Ad evaluations homework
7-hour ace
8.30-10.05
10.10-11.05
11.10-11.55
11.55-12.40
12.40-14.40
14.40-15.10
8.Checklists.
1. The incidence of autoimmune thyroiditis in the "clean" and "dirty"
Iodine-deficient areas.
2. Indications for thyroid and iodine preparations
3. Status and performance of the hypothalamic-pituitary-thyroid system in
Thyroiditis.
4. Skanograficheskaya picture sites with various active absorption.
5. Indications strumectomy
9.Recommended Reading
Summary:
1.
2.
3.
Balabolkin MI Endocrinology. M., Medicine, 1998
Vladimir Potemkin Endocrinology. M., Medicine, 1999
Grandparents II Endocrinology. M., Medicine, 2000
4. Melnichenko GA Tokmakova AY, deck DE, NV Lavrishcheva Endocrine
disease. M. Medicine, 2009
5.
Guidelines for Pediatric Endocrinology. Handbook of clinical Pediatric
Endocrinology. Edited by Charles G. Bouka, Rosalind S. Brown. 2009
6.
Shustov SB, Khalimov S, Trufanov GE Functional and topical
diagnostics in endocrinology. M. 2010
7.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 1.
Greenspan's Basic & Clinical Endocrinology. 2010
8.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 2. Greenspan's Basic &
Clinical Endocrinology. 2011
9.
Clinical Endocrinology. Ed. EA Kholodova. Minsk. Belarus. 2011
10. Melnichenko GA Udovichenko OV Shvedova AE Endocrinology. Typical
Error practitioner 2012
11. Endocrinology. National guidelines (+ CD-ROM). 2012
More:
1. Therapeutic Guide Washington, translated from English. (Section
"Endocrinology") 1996.
2. Laycock. Fundamentals of Endocrinology, Moscow 2000
3. Ty M. Mack - Dermott MD Secrets Endocrinology - Moscow 2000
4. Ketgayl VM, Arkin RA, Pathophysiology of endocrine system - Moscow, Medicine,
2001.
5. Balabolkin MI Diabetology - Moscow, Medicine, 2002
7. Fadeev PA. Endocrinology. Diabetes. A Reference Guide. 2009
55
8.
Kartelishev Alexander Rumyantsev AG, Smirnova NS Actual problems of obesity in children and
adolescents. 2010
9. Mkrtumyan AM, AA Nelaev. Emergency Endocrinology. 2010
10. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Diseases
thyroid. Williams Textbook of Endocrinology. 2010
11. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Bark disease
adrenal gland and endocrine hypertension. Williams Textbook of
Endocrinology, 11 th edition. 2010
12. AN hams Emergency Endocrinology. 2011
13. Petunina NA, AV Trukhina Thyroid disease. 2011
14.Manuhin IB Tumilovich LG, M. Gevorgyan Gynecological Endocrinology. Lectures on gynecologic
endocrinology. M. 2012
Journals:
15. Medical Journal of Uzbekistan, Tashkent.
16. "Problems of Endocrinology." Moscow.
17. "Therapeutic Archives", Moscow
18. "Clinical Medicine", Moscow
19. "Diabetes. Way of life ", Moscow
Internet sites:
1.
"Internet Portal: Hunari»
2. Medscape.com
3. Alltheweb.com
4. Yahoo.com
5. E-medicine.com
6. www tma. uz
Ministry of Health Care of Uzbekistan
CENTRE FOR MEDICAL EDUCATION
TASHKENT MEDICAL ACADEMY
Department of Internal Medicine TRAINING GP endocrinologist
The subject of "Endocrinology"
56
Topic: "Arterial hypertension"
Endocrine diseases, accompanied, arterial hypertension: Conn's syndrome, the disease
and Cushing's syndrome, pheochromocytoma, hypophyseal syndrome, pubertal and
youth dispituitarizm (PYUD), diabetic nephropathy, acromegaly.Diagnosis, differential
diagnosis.Principles of treatment.Tactics GPs.
Educational and methodical development
(For teachers and students)
Tashkent - 2012
Flow chart classes № 5
Hypertension.Endocrine diseases, accompanied, arterial hypertension: Conn's syndrome, the disease and
Cushing's syndrome, pheochromocytoma, hypophyseal syndrome, pubertal and youth dispituitarizm
(PYUD), diabetic nephropathy, acromegaly.Diagnosis, differential diagnosis.Principles of
treatment.Tactics GPs.
№
fl ups practice session
PMA classes fo
venue
dl itTh
classes
270
min.
1 Centuries odnaya part (study subject)
10
57
2 Judgment about topics practice session with new educational op grew discussion
technologies
training room
("Snowballs", "swarm"), as well as demonstration material (boards,
sets medical charts, tables, posters, hormonal and clinical tests, Xrays, situational problems, blood pressure, balance), the definition of
the initial level.
50
3 You discuss water
15
4 The definition of reference for the practical part - n rofessionalny of judgment
questioning. Explanation of the provisions and recommendations for
the job to fill medical records.
training room
25
5 Military wasp’s practical training under the guidance of a teacher.
30
Prospect ofes sional questions;
talk with patients filling medical
records, case studies.
Department of Endocrinology
Clinic 1-TTA
6 John interpretation of the survey data of patients - complaints, tory studies of the disease,
inspection, palpation, percussion and auscultation of patients as well
laboratory data situational
as laboratory and instrumental studies
problems
35
Department of Endocrinology
Clinic 1-TTA
7 Judgment on the theoretical and practical knowledge of the students, mustache tny survey, tests,
fixing material, the level of learning assessment.
discussion, identification of
practical skills
80
Department of Endocrinology
Clinic 1-TTA
8 The definition of output on practical training, evaluation of 100- infor mation, questions for
point system, and ad evaluations. Homework the next practice homework.
session (a collection of questions).
training room
25
Lesson number five
Hypertension.Endocrine diseases, accompanied, arterial hypertension: Conn's syndrome, the disease and
Cushing's syndrome, pheochromocytoma, hypophyseal syndrome, pubertal and youth dispituitarizm
(PYUD), diabetic nephropathy, acromegaly.Diagnosis, differential diagnosis.Principles of
treatment.Tactics GPs.
uch ebnoe time: 7:00
58
Art ruktura training session
1. afedra to internal medicine training
GPs with an endocrinologist, endokrinologichessome branch 1 TTA clinic, clinical
1-clinic laboratory TTA;
2. set of tables, methodological recommendations
tion, laboratory and instrumental data,
video;
3. TCO: computer, video
Tse eh training session:
- The acquisition of knowledge and skills in students GPs to diagnose
and differential diagnosis of diseases associated with arterial
hypertension;
- Learn to use the modern classification of these diseases;
- To conduct early detection and disease prevention through individual
symptoms, syndromes.
Pe dagogicheskie tasks:
D results of training activities:
- Form of knowledge on the GP
etiology,
should know:
pathogenesis
of
endocrine
- To understand the causes of endocrine hypertension genesis
diseases,
by high blood
- Be able to identify the symptoms of endocrine
hypertension;
patients with hypertension,
- Form of knowledge, skills and - Analyze laboratory results and
skills in identifying clinical
instrumental studies
symptoms of the disease;
- Appoint pathogenetic therapy for hypertension,
- Analyze laboratory data
- Be able to differentiate between the endocrine and
GOVERNMENTAL
instrumental analyzes
- To make
diagnosis,
a
and Neendokrinnuyu hypertension.
should be able to:
differential 1. assess the functional status of adrenal
nicknames;
59
tic diseases associated
2. make a differential diagnosis
hypertension;
hypertension between different
- Form
methods
of
knowledge
on genesis;
3. interpret urine;
treatment of hypertension in
4. interpret data interpretation diagnosed
endocrine patients;
Elliptic samples and hormone research.
- Form of knowledge, skills and
must have skills:
skills for emergency
- Professional questioning, examination of the patient;
help with arterial
- Interpretation of the clinical laboratory
hypertension
instrumental data;
- Clinical diagnosis for classical
fication of WHO;
- The basis of consultation with these patients
diseases;
- Learn the skills of patients with arterytial hypertension in pregnancy
Me Toda training
Fo rmy training activities
Wed edstva training
le Ktsia, the method of "snowball", "swarm" demonstration, entertainment
experience, discussion, conversation, case.
individuality work, group work, team, classroom, extracurricular.
Mr. zdatochnye viziualnye training and materials, videos, models, graphic
organizers, kits medical charts, tables, stands, kits radiograph.
Cn lady and means of feedback bl uu-survey, testing, presentation of the results of the training task, filling
medical records, execution of practical skills "professional questioning"
2.Motivation
In preparation for the GP specialty endocrinology study of the subject dictated by the need to conduct timely
diagnosis, differential diagnosis and treatment of hypertension in diseases of the endocrine system With the
development of the topic, to pay attention to the students as to the causes, and on pathogenetic mechanisms,
which involves a variety of approaches to treatment and prevention of these diseases.
60
3.Intra-called interdisciplinary communication
Teaching of the subject is based on the knowledge of the students’ major endocrine
Disease received a 4th year in a cycle endocrinology, as well as therapy, which will continue to carry out
differential diagnosis of diseases associated with hypertension. Acquired during the course knowledge will be
used during the passage of therapy at 6 and 7 of the course.
4.Contents classes
4.1.The theoretical part
On practical training in the theoretical part series discusses the clinical features of Conn's syndrome,
pheochromocytoma, Cushing's syndrome.
A list of the issues:
1.
Pheochromocytoma.
a) clinical forms;
b) The differential diagnosis of GB and hypertension neendokrinnogo
of origin;
c) Diagnosis;
d) Methods of treatment, prognosis.
2. Conn's syndrome
a) The etiology and pathogenesis of the main clinical symptoms;
b) The differential diagnosis of secondary aldosteronism;
c) Treatment, prognosis.
3. Cushing's syndrome
a) The differential diagnosis of Cushing's disease, voucher, diabetes PYUD,
Acromegaly;
b) The principles of treatment.
Pheochromocytoma (FHTS) (hromofinoma) - functioning tumor originating from the adrenal
medulla and extraadrenal hromoffinnoy tissue. Vnenadpochechnnkovye hromoffinnoy of tumor tissue
is sometimes called paragangliomas.
Hromoffinnoy tissue tumors secrete catecholamines.
Pheochromocytomas are benign or malignant.
In 90% of cases FHTS located in the adrenal glands (usually the right), in 10% of cases are bilateral,
approximately 10% are identified in one family, 10% of registered children and therefore FHTS
sometimes called "Ten percent tumor." Frequency of pheochromocytoma is 3.1 per 1,000 population.
Extraadrenal FHTS most frequently located in the sympathetic chain along the abdominal aorta, and
then the organ Zuckerkandl (hromoffinovaya tissue located anterior to the abdominal aorta), in the
lower mesenteric artery in the chest cavity, the bladder, head and neck. FHTS refers to tumors APUD
- systems and is often combined with tumors in the syndrome of multiple endocrine neoplasia type 2A
(MEN-2A), combined with a medullary thyroid cancer and hyperparathyroidism (Cipla syndrome) is
much less common (MEN-2B joins them neuropathy, mucosal neuromas, the pathology of the muscles
and skeleton (Gorlin syndrome). In both cases there is an autosomal dominant inheritance.
61
FHTS pathogenesis due to the action of catecholamines on alpha and beta adrenergic receptors, a
violation of the vascular and metabolic disorders. The clinical picture may be grouped into the
following syndromes:
- Syndrome of hypertension (paroksizmallnoy or permanent)
- Neuropsychiatric syndrome (nervous irritability, fatigue, headache, paresthesia)
- Neurovegetative syndrome (violation of sweating, tremors, dilated pupils);
- Gastrointestinal syndrome (abdominal pain, nausea, vomiting);
- Cardiac syndrome (dyspnea, palpitation, the phenomenon of cardiac asthma)
- Exchange of endocrine syndrome (symptomatic diabetes).
Clinical, symptoms depend on the clinical form FHTS. Distinguish Distinguish
1. 1. Paroxysmal
2. 2. Permanent permanent
3. 3. Mixed
Paroxysmal crises manifested. Feohromotsitarny (adrenal) crisis - sudden weight increase during
FHTS caused massive and rapid release of catecholamines and the tumor into the blood flow.
The reasons could be:
1. 1. Supercooling
2. 2. Physical and emotional stress
Z. flick
4. 4. Trauma of the lumbar region
5. 5. Smoking and alcohol intake
6. 6. Rough palpation of the abdomen
7. 7. The use of such drugs, such as insulin, histamine, sympathomimetic agents;
8. 8. Balanced meal, laughing, sneezing, etc.
Pathogenesis FHTS crisis is a surplus into the blood catecholamines, especially adrenaline. Crises
begin suddenly, but some are harbingers, dizziness, hot flashes, numbness in the hands and feet. At
the height of a crisis there are the following symptoms:
- Headache, pain in the heart contracts the nature and often abdominal pain unspecified nature, pain in
the lumbar region
- Reduction of
- Frequent urination
62
- Anxiety, tremor, sweating, rapid heartbeat
- Pale skin (sometimes red), bright eyes, dilated pupils
- Reduction of spasmodic muscles of the upper limb
- Pulse to 160 170ud. in min., rarely bradycardia
- Blood pressure (BP) were significantly increased, systolic 200-300 mm. Hg. Art., and 180 mm Hg
diastolic
- Crisis often accompanied by nausea, vomiting,
- Possible ischemic ECG changes
- Increase in body temperature (sometimes up to 40 ° C)
- A blood test revealed hyperglycemia, leukocytosis, eosinophilia, and lymphocytosis
During and after the crisis increases the blood levels and urinary excretion of catecholamines.
Crisis ends as suddenly as the beginning, blood pressure normalizes. At the end of the crisis there
profuse sweating, hypersalivation, stands up to 3-5 liters of light incontinence with low relative density.
After attack patients feel overwhelmed, sometimes lethal crisis end. Death may end later ventricular
fibrillation, stroke, and acute left ventricular failure with pulmonary edema. The frequency of crises in
patients with pheochromocytoma crises varies from 5-15 per day to one in a few months. Duration from a few minutes to a few hours, but most of crisis lasts several minutes.
The most difficult to distinguish from the hypothalamic feohromotsitarny crisis crisis, in which the
possibility of secondary hyperfunction of the adrenal medulla. Unlike hypothalamic crisis psychiatric
symptoms (fear of death, depression) has been fairly typical, but may be present. Also shows no
delirious state with visual and auditory hallucinations, which can be observed in the hypothalamic
crisis. Blood pressure at at FHTS can reach 300 and 160 mm Hg, and at gipotalamicheokom Stroke
not exceed 240 and 120 mm Hg It should be noted that the crisis is not typical of the hypothalamic
modified orthostatic test and an increase in the blood levels of catecholamines. The ultrasound showed
normal adrenal size in hypothalamic adrenal Stroke, also unstable effect of phentolamine.
In the differential diagnosis of hypothalamic crisis amid essential hypertension and FHTS crisis,
consider the following distinguishing features:
- For patients suffering FHTS crisis, characterized by weight loss 6-10 pounds or more from the time
of pheochromocytoma;
- An early period and duration of hypertension is not more than 2 years
- Feohromatsitarny crisis is accompanied by a bowl carbohydrate metabolism (hyperglycemia,
glycosuria, impaired glucose tolerance), with hypertensive crisis of no violations;
- For FHTS crisis characterized by positive test with an alpha-adrenergic blocker phentolamine
(redzhetinom) after i / v administration of 5 mg phentolamine is a decrease in blood pressure for 5
minutes to 40/25 mm Hg or more compared to baseline;
- For FHTS crisis characterized by high concentrations of catecholamines in the 3-hour urine sample
collected after the crisis, with hypertensive crisis this figure does not change
- Ultrasound in hypertensive crisis adrenal size is not changed, at FHTS Stroke detected by an
increase in adrenal tumors.
Permanent form
This form is characterized by persistent arterial hypertension without constant crises. This form is
difficult to distinguish from essential hypertension without crises. It should be recognized that at
63
FHTS patients lose weight and in addition, there is usually no effect on ongoing antihypertensive
therapy.
Mixed form
This form is characterized by the fact that with the constant high blood pressure there are typical
crises described above.
Abdominal shape
Abdominal shape resembles a picture of "acute abdomen":
- Severe abdominal pain with no clear localization;
- Nausea, vomiting
- Abdominal symptoms are accompanied by a hypertensive crisis, pallor, sweating
- Possible worn pattern of abdominal symptoms (blurred abdominal pain, chronic constipation)
Dumb tumor.
These tumors are not clinically manifest, they are found incidentally at autopsy of patients dying from
any other cause. In history there is no indication of hypertension. Bolnyya suffering from this form of
FHTS suddenly die from the first and only severe hypertensive crisis. To differentiate FHTS adrenal
genesis of extraadrenal considers the following features:
- The kind produced by catecholamine
- The nature of hypertension
- The state of the pupils
- Blood Sugar
Primary aldosteronism (PG) - a clinical syndrome that develops as a result of excessive production
of aldosterone by the adrenal cortex and shown by arterial hypertension and hypokalemia, and was
first described by Jerome Conn in 1954, currently there is no single standard classification syndrome
PG.
Etiology. Reasons PG for different variants syndrome are different. More common single
aldosteronoma, insensitive to angiotensin II. Malignant forms are rare. The tumor usually is small in
size up to 3 cm in diameter.
Idiopathic primary hyperaldosteronism (IPGA) is characterized by non-tumor bilateral hyperplasia
glomerular zone of the adrenal cortex to the micro-or makronodulyarnymi or without changes. IPGA
is found in 30-40% of all GHG emissions. The principal difference is the preservation of the
sensitivity of IPGA hyperplastic glomerular zone to the stimulating effect of angiotensin II. Also
distinguish ACTH - dependent (repressed glucocorticoid therapy) tumor.
When glyukokortikoidpodavlyaemom hyperaldosteronism produced "defective" genes enzyme 11hydroxylase A and aldosteronsintetazy. Both of these genes are located on chromosome 8, and about
90% homologous. Normally, the gene encoding aldosteronsintetazu, expressed only in the glomerular
zone and that zone is synthesized aldosterone. Gene 11-p-hydroxylase expressed under the influence
of ACTH, whereas the main stimulant of gene expression is aldosteronsintetazy aigiotenzin II and
potassium ions. As a result of this mutation beam area, which is a major regulator of ACTH, acquires
the ability to synthesize aldosterone. In addition to the excessive secretion of aldosterone beam area at
this form of hyperaldosteronism produces 20-30 times higher than the norm of 18 oksikortizola
gidroksikortizola and 18, which are formed from 11-dezoksikortizola, under the action of a "defective"
enzyme that is of great importance in the differential diagnosis glyukokortikoidpodavlyaemoy
aldosteromas of IPGA. Urinary excretion of 18-oksokortizola more than 15 mg / day and 18gidroksikortizola over 60 mg / day allow a high probability to distinguish adenoma from hyperplasia.
64
Pathogenesis. Excessive secretion of aldosterone leads to increased levels of sodium in the blood and
an increased excretion of potassium in urine - giperkaliurii. The resulting severe hypokalemia
secondary causes of renal tubules. Prolonged hypokalemia contributes to the defeat of renal tubules,
which in turn leads to an impaired ability of the kidneys to concentrate urine, as a result, developed
polyuria, polydipsia and gipostenuriya. Due to the low level of serum potassium decreases the effect
of antidiuretic hormone (ADH) in the reabsorption of water in the renal tubules, resulting in increased
polyuria. As a result of hyponatremia is water retention and develops hypervolemia, resulting in an
arterial hypertension. At PG, despite hypernatremia, never develop edema. This phenomenon is
called "uskalzyvaniya of aldosterone." At the beginning of the high content of aldosterone leads to
increased cardiac output due to sodium retention and then develops hypertension and hypertensive
diuresis. Strengthening the excretion of potassium in the urine leads to hypokalemia in violation of
neuromuscular excitability. Clinic. GHG bowl occurs in individuals between the ages of 35 to 50 years,
but aldosteromas observed in children. Clinical manifestations of GHG: hypertension (headache,
dizziness, the emergence of "fly" before the eyes), conduction disorders and neuromuscular
excitability (muscle weakness, paresthesias, seizures, bradycardia, rarely - Titania), changes in renal
function (polyuria, polydipsia, nocturia) . These symptoms are not always present simultaneously:
frequently observed oligosymptomatic or asymptomatic. According to Conn, hypertension is
diagnosed in 96% of patients, muscle weakness - 73% -72% polyuria, headache 51%, polydipsia - 46%,
paresthesia - 24%, tetany - 21%, muscular discomfort - 16%, fatigue - in 19% of patients with enough
common symptom of GHG is saluretics intolerance, although this reaction appears in the application
of drugs.
The main role in the diagnosis belongs to laboratory methods.
Diagnostics. Certain value in the diagnosis of the following laboratory and instrumental data:
- CBC - no specific changes;
- Urinalysis - gipoizostenuriya, alkaline reaction, sometimes proteinuria;
- Blood chemistry - hypernatremia, hypokalemia;
- High levels of aldosterone in the blood and reduced levels of renin;
- ECG - bradycardia, arrhythmia, atrioventricular conduction slowing, reducing the interval ST
downward from the isoline interval prolongation QT, abnormal tooth U. The above changes are due to
hypernatremia, hypokalemia;
- Ultrasound and computed tomography of the adrenal glands - reveal the presence of adenomas
ili.giperplazii adrenal
- Scanning the adrenal 19-yodholesterolom labeled with I
adrenal glands in the presence of a tumor.
131
- reveals an asymmetry - uptake in the
Functional Tests. Diagnostic tests based on the stimulation or
Suppression of the renin - angiotensin - aldosterone system, 10 days before the study is canceled all
drug therapy, especially antihypertensives, diuretics. Veroshpiron canceled 2-4 weeks prior to the
survey with high blood pressure can be applied only clonidine and dibazol.
Sample 1 - hour walking.
Against the background of this sample of healthy and hypertensive patients with secondary
hyperaldosteronism is stimulation of renin. Growth of plasma renin is 1 mg / ml / h. Based on this
sample of patients with isolated secondary hyperaldosteronism. For distinguishing patients with PH
conduct additional tests.
65
Test with veroshpirona
Patients can veroshpiron 100 mg 4 times daily for 3 days, increasing the level of potassium in the
blood at day 4 for more than 1 mmol / L indicates the overproduction of aldosterone.
Test with furosemide.
Inside the patient give 0.08 g of furosemide and 3 hours determine blood levels of aldosterone and
renin in the blood. Increased aldosterone and renin decrease indicative of primary hyperaldosteronism.
PG differentiates with different diseases or conditions that cause secondary hyperaldosteronism.
Secondary hyperaldosteronism (VG) is accompanied by increased plasma levels of aldosterone and
combined with adequate elevated renin. When HS unlike PG maintain normal regulatory interactions
within the renin-angiotensin-aldosterone system, ie Aldosterone production is not offline, and in
response to stimulation with angiotensin II, which corresponds adequately elevated levels of renin.
Marching and other specimens used for the investigation of autonomous aldosterone secretion, with
secondary hyperaldosteronism negative. In arterial any origin, heart failure, renal artery stenosis, etc.
reduced perfusion pressure in the kidney per unit time, which is the physiological stimulus of renin
secretion juxtaglomerular apparatus. Often it is necessary to differentiate PG with essential
hypertension (EH) and chronic glomerulonephritis.
Unlike PG for GB is not typical progressive myasthenic syndrome, thirst, polyuria, with a
predominance of nocturnal urine, hypokalemia. Content is usually normal aldosterone, renin and may
be normal, high, and sometimes reduced. Test with veroshpirona and furosemide negative. CT scan
adrenal glands are not enlarged in contrast to PG. The differential diagnosis of chronic
glomerulonephritis and PG should pay attention to the relationship with streptococcal infection, which
is not the case with PG. BP corrected various antihypertensive agents, and with PG only veroshpirona.
During the march, and the sample with furosemide aldosterone content in GHG increases significantly,
and especially in glomerulonephritis not change from baseline. On CT were not enlarged adrenal
glands in chronic glomerulonephritis, kidney size on ultrasound reduced.
New educational technology: a method of "snowball", "swarm"
Method of "snowball"
To work needed:
1) A set of learning-control tests
2) Sheets of paper
Progress:
1) The group is divided into two subgroups.
2) Each team wills one sheet of paper.
3) On a sheet of written FI students, group, department, date.
4) One of the students taking the envelope issues that are the same for both groups.
5) Each correct answer is recorded as a credit in the form of "snowballs"
6) Group, has received the maximum number of points is estimated excellent grades.
66
7) To hold the method has 30 minutes.
Tests
1) Specify the location of hormone
A. Adenohypophysis
B. Neurohypophysis
1) ACTH
2) ADH
3) TSH
4) Prolactin
5) Vasopressin
2) Select the clinical - laboratory changes characteristic of the disease
A pituitary - Cushing
B. Itsenko - Cushing
1) 2-sided adrenal hyperplasia
2) Unilateral adrenal hyperplasia
3) Headaches
4) Hyperglycemia
5) Reduction of ACTH
3) What are the hormones produced by the adrenal glands:
A. Cortical layer
B. Medulla
1) Noradrenaline
2) Cortisol
3) Aldosterone
4) Dopamine
5) Androgens
4) Specify the etiological cause of adrenal insufficiency
A. Addisonichesky crisis
B. Acute adrenal insufficiency
1) Addison's Disease
2) Mt. adequacy of adrenal cortical insufficiency
3) Withdrawal
4) 2-sided adrenalectomy
5) Myocardial adrenal
5) List the adrenal disease, associated with the topical diagnosis:
A. Cortical layer
67
B. Medulla
1) Pheochromocytoma
2) Conn's syndrome
3) Addison's disease
4) Disease Itsengo - Cushing 6) List the clinical symptoms of the disease
A. Addison's disease
B. Conn's syndrome
1) Hypotension
2) Hypertension
3) Polyuria
4) Hyperpigmentation
5) muscle weakness
7) Differentiate disease and Cushing's syndrome by clinical and laboratory parameters:
A BIC
B. SIC
1) 2-sided adrenal hyperplasia
2) Unilateral adrenal hyperplasia
3) Hirsutism
4) Increased ACTH
5) Reduction of ACTH
6) Hypertension
The method of "swarm"
To work needed:
1. A set of setting and situational problems that have been printed on a separate page.
2. Number plates for the draw in the number of students in each subgroup.
3. Blank sheets of paper, pens.
Progress:
1. All the students are divided into groups by lot 3 subgroups of 2-3 students each.
2. Each subgroup sits at a separate table, preparing the paper and pen.
3. Written on a sheet date, the group number, department, name, name of participating students in
this subgroup and the name of the business game.
4. One of the participants in each subgroup takes the envelope of setting that is used for all
subgroups.
5. One of the students in each subgroup rewrites on the job list.
6. All subgroups of students together to discuss the job, and then one of them writes his decision.
7. The decision set to 15 minutes.
68
8. The teacher watches the game.
9. after the time of the surrender teacher.
10. All the players discuss the results; choose the most appropriate solution for which to set the
maximum score.
11. on the decision to 15 minutes.
12. Students get points for answering the theoretical part of the rating classes.
13. Subgroup, which gave the most correct answers will receive the maximum score - 100 points,
the subgroup took 2nd place - 85 points, 3 subgroup - 70 rating points.
14. On the answer sheet scores and teacher puts his signature.
15. by students score recorded for billing Estimates for the current session.
16. In the lower part of the magazine is free to note on the game with a signature
Elder group.
17. Student work saved teacher.
Complex issues for the business game:
1. The structure of the adrenal gland.
2. Regulation of glucocorticoid biosynthesis.
3. Regulation of mineralocorticoid biosynthesis.
4. The mechanism of action of glucocorticoids
5. The mechanism of action of mineralocorticoids.
6. The mechanism of action of adrenal androgens.
7. Methods of examination of patients with diseases of the adrenal glands.
8. Methods of diagnosis of chronic adrenal insufficiency.
9. The clinical picture of pheochromocytoma.
10. Treatment of pheochromocytoma.
11. Conn's syndrome etiology.
12. Diagnosis of Conn's syndrome.
13. Treatments for Conn's syndrome.
14. The clinical picture of Cushing's syndrome.
15. Diagnosis of Cushing's syndrome.
16. Test diagnosis Cushing's syndrome.
17. Differential diagnosis of the syndrome and Cushing's disease
4.2 the analytical part
The decision of situational problems
Objective number one. Patient A., 47 years old. For 15 years suffered systemic lupus erythematosus.
He takes prednisolone 15 mg per day. On examination, I used high-power, thin limbs, face
lunoobraznoe, signs of hirsutism. BP 160/100 mm Hg, pulse 82 beats • min., Heart tones are muffled,
rhythmic, two accent colors of the aorta. In the lungs, vesicular breathing. Question: What
complications develop in the patient?
69
Objective number two. Patient 38 years complains of severe headaches, palpitations. A few years
had been under surveillance cardiologists. A / D is increased to 220/170 mm Hg Usual
antihypertensive therapy. Ineffective. Endocrinologist patient suspected pheochromocytoma, but
indicators of hormonal studies of catecholamines were within normal limits. To confirm the
diagnosis, which should still check endocrinologist?
Objective number 3. A woman 29 years there paroxysmal increase in blood pressure 220/120 mm
Hg accompanied by palpitations, sweating, trembling and fear of death. Ends attack a great amount
of colorless urine. At the time of the attack was taken blood sugar is the result of 12 mmol / l.
Questions:
1. Your diagnosis.
2. Assign the survey.
3. Which antihypertensive drugs are used in this case.
4.3 The practical part
Performed at the bedside. Supervision is carried out under the supervision of a teacher. The student
must learn to practice proper medical history of patients with endocrine disorders, thus able to
differentiate between primary and secondary information during the examination to focus on the
endocrine glands and the clinical features of dysfunction of these glands. When communicating with
the patient should consider the mental state such as irritability, fatigue, and during communication
exercise extreme tact and at the same time be confident and firm.
In conducting activities in the clinic, while outpatient care, to teach students to quickly, clearly
questioning and examination of the patient, proper filling patient card.
5.Control forms of knowledge, skills and abilities
- Oral
- Written
- Testing
- Decision of situational problems
- Demonstration of the developed skills'
Monitoring the activity of the students in the discussion, analysis of case-patients and situational
problems, making tests for the diagnosis and differential diagnosis.
6.
K pandm epand on en te k and w toyero aon tr il
№ Military
Est. ENKA
Ka quality assessment
mustache
in points
1. 86-100 Personally from Communicates about, think creatively, evaluates,
the "5"
interprets.Applies knowledge in practice.Understands, knows,
says has no idea
2. 71-85 It is well "4"
Ra ssuzhdaet independently assess, interpret, apply knowledge
in practice, understands, knows, says has an idea
3. 55-70
Beats
Minimality know.Understand the essence, says
ovletvoritelno
"3."
4. 0-54
Not satisfactory, Pl oxo know.Not thoroughly.Require additional training.
"2"
7.Flow chart classes
1. Checking the initial level of preparedness of students to engage in "Diseases of the endocrine
glands occur with hypertension." Explanation of the diagnosis and differential diagnosis of diseases
associated with hypertension.
2. Decision analysis and situational problems.
3. Supervision of patients with diseases that are accompanied by hypertension. Clinical analysis of
supervised patients.
70
4. Interactive games to assess knowledge on training.
№
fl ups lessons
1 Judgment of courses offered
2 Ca autonomy of patients Supervision attached houses, self Curation
case patients, participation in rounds of professors and associate
professors
3 Ra Zborov the department examined case patients with the
interpretation of the survey data and treatment
4 ne reryv
5 On judgment tests, situational problems.
6 Pr Overcome digestibility.Ad evaluations homework
8.Test questions:
Prospect
odolzhitelnost
classes
7-hour ace
8.30-10.05
10.10-11.05
11.10-11.55
11.55-12.40
12.40-14.40
14.40-15.10
1. Modern classification of arterial hypertension
2. Particulars of hypertension and adrenal norepinephrine crises
3. under any endocrine diseases with hypertension observed
weight loss and weight gain on the contrary?
4. The mechanism of hypertension in the application of hormonal
contraceptives.
9.Recommended Reading:
Summary:
1.
2.
3.
4.
Balabolkin MI Endocrinology. M., Medicine, 1998
Vladimir Potemkin Endocrinology. M., Medicine, 1999
Grandparents II Endocrinology. M., Medicine, 2000
Melnichenko GA Tokmakova AY, deck DE, NV Lavrishcheva Endocrine
disease. M. Medicine, 2009
5.
Guidelines for Pediatric Endocrinology. Handbook of clinical Pediatric
Endocrinology. Edited by Charles G. Bouka, Rosalind S. Brown. 2009
Shustov SB, Khalimov S, Trufanov GE Functional and topical
diagnostics in endocrinology. M. 2010
6.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 1.
Greenspan's Basic & Clinical Endocrinology. 2010
7.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 2.
Greenspan's Basic & Clinical Endocrinology. 2011
8.
Clinical Endocrinology. Ed. EA Kholodova. Minsk.
Belarus. 2011
9.
Melnichenko GA Udovichenko OV Shvedova AE Endocrinology. Typical
Error practitioner 2012
10.
Endocrinology. National guidelines (+ CD-ROM). 2012
More:
1. Therapeutic Guide Washington, translated from English. (Section
"Endocrinology") 1996.
2. Laycock. Fundamentals of Endocrinology, Moscow 2000
3. Ty M. Mack - Dermott MD Secrets Endocrinology - Moscow 2000
4. Ketgayl VM, Arkin RA, Pathophysiology of endocrine system - Moscow, Medicine,
2001.
5. Balabolkin MI Diabetology - Moscow, Medicine, 2002
7. Fadeev PA. Endocrinology. Diabetes. A Reference Guide. 2009
71
8. Kartelishev Alexander Rumyantsev AG, Smirnova NS Actual problems of obesity
in children and adolescents. 2010
9. Mkrtumyan AM, AA Nelaev. Emergency Endocrinology. 2010
10. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Diseases
thyroid. Williams Textbook of Endocrinology. 2010
11. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Bark disease
adrenal gland and endocrine hypertension. Williams Textbook of
Endocrinology, 11 th edition. 2010
12. AN hams Emergency Endocrinology. 2011
13. Petunina NA, AV Trukhina Thyroid disease. 2011
14. Manukhin IB Tumilovich LG, M. Gevorgyan Gynecological
endocrinology. Lectures on gynecologic endocrinology. M. 2012
Journals:
15. Medical Journal of Uzbekistan, Tashkent.
16. "Problems of Endocrinology." Moscow.
17. "Therapeutic Archives", Moscow
18. "Clinical Medicine", Moscow
19. "Diabetes. Way of life ", Moscow
Internet sites:
1. "Internet Portal: Hunari»
2. Medscape.com
3. Alltheweb.com
4. Yahoo.com
5. E-medicine.com
6. www tma. uz
Ministry of Health Care of Uzbekistan
CENTRE FOR MEDICAL EDUCATION
TASHKENT MEDICAL ACADEMY
Department of Internal Medicine TRAINING GP endocrinologist
Subject: "Endocrinology"
72
Topic:"obesity"
Diseases associated with obesity.Classification.Constitutional-exogenous
obesity.Cerebro-hypothalamic (PYUD, AGD, Barker-Simmonds syndrome), obesity
and endocrine (hypothyroidism, Cushing, acromegaly).Differential diagnosis.Treatment
principles, tactics GPs.
Educational and methodical development
(For teachers and students)
Tashkent - 2012
Process chart classes № 6
Disease accompanied by obesity.Classification.Constitutional-exogenous obesity.Cerebrohypothalamic (PYUD, AGD, Barker-Simmonds syndrome), obesity and endocrine
(hypothyroidism, Cushing, acromegaly).Differential diagnosis.Treatment principles, tactics
GPs.
№
fl ups practice session
PMA classes fo
venue
73
dl itTh
classes
270
min.
1 Centuries odnaya part (study subject)
10
2 Judgment about topics practice session with new educational op grew discussion
technologies
training room
("Snowballs", "weak link"), as well as demonstration material
(boards, sets medical charts, tables, posters, hormonal and
clinical tests, X-rays, situational problems, tonometer,
stadiometer, scales, measuring tape), the definition of the initial
level.
3 You discuss water
50
4 The definition of reference for the practical part - n rofessionalny of judgment
questioning.Explanation of the provisions and recommendations
training room
for the job to fill medical records.
25
15
30
5 Military wasp’s practical training under the guidance of a Prospect ofes sional
teacher.
questions; talk with patients
filling medical records,
case studies.
Department of
Endocrinology Clinic 1TTA
35
6 John interpretation of the survey data of patients - complaints, tory studies of the disease,
inspection, palpation, percussion and auscultation of patients as laboratory data situational
well as laboratory and instrumental studies
problems
Department of
Endocrinology Clinic 1TTA
7 Judgment on the theoretical and practical knowledge of the mustache tny survey, tests, 80
students, fixing material, the level of learning assessment.
discussion, identification of
practical skills
Department of
Endocrinology Clinic 1TTA
8 The definition of output on practical training, evaluation of 100- infor mation, questions for
25
point system, and ad evaluations.Homework the next practice homework.
session (a collection of questions).
training room
Lesson number 6
Disease accompanied by obesity.Classification.Constitutional-exogenous obesity.Cerebrohypothalamic (PYUD, AGD, Barker-Simmonds syndrome), obesity and endocrine
(hypothyroidism, Cushing, acromegaly).Differential diagnosis.Treatment principles, tactics
GPs.
1.
uch ebnoe time: 7:00
Art ruktura
session
training 1. afedra to internal medicine training
GPs with an endocrinologist, endokrinologiches74
some branch 1 TTA clinic, clinical
1-clinic laboratory TTA;
2.set of tables, methodological recommendations
tion, laboratory and instrumental data,
video;
3.TCO: computer, video
Tse eh training session:
- Theacquisition of knowledge and skills in students GPs to diagnose
and differential diagnosis of diseases associated with obesity;
- Learn to use the modern classification of these diseases;
- To conduct early detection and disease prevention through individual
symptoms, syndromes.
Pe dagogicheskie tasks:
D results of training activities:
• to consider the causes of GP
obesity
should know:
• analyze the mechanisms • the causes of obesity;
of development
• Be aware of the degree of obesity;
obesity
• Be aware of the clinical symptoms of the various forms
• compare the different
obesity;
types of obesity
• discuss options for the • Analyze data from laboratory tests and
treatment of obesity
instrumental studies
• demonstrate a patient • assign a pathogenetic therapy for
with
obesity.
obesity
should be able to:
• discuss the diagnostic
• conduct professional inquiries, inspection
algorithms
the patient;
obesity.
• interpret clinical laboratory
instrumental data;
• put on a clinical diagnosis of classical
fication of WHO;
• advise patients with data
diseases;
• master the skills of patients with obesity
Pregnancy
must have skills:
75
• Determine the degree of obesity formula Brock
• Body mass index
• Determine abdominal index
Me Toda training
le Ktsia, the method of "snowball", "weak link" of the demonstration,
entertainment experience, discussion, conversation, case.
Fo rmy training activities of individuality work, group work, team, classroom, extracurricular.
Wed edstva training
Mr. zdatochnye viziualnye training and materials, videos, models, graphic
organizers, kits medical charts, tables, stands, kits radiograph.
Cn lady and means of bl uu-survey, testing, presentation of the results of the training task, filling
medical records, execution of practical skills "professional questioning"
feedback
2.Motivation
Obesity is one of the most common diseases in the world. According to WHO, overweight have about
Z0% of our planet? Despite the prevalence of obesity and the proven role of obesity in the
pathogenesis of diseases such as diabetes, atherosclerosis, hypertension, has not yet developed a single
pathogenetic classification of obesity, the minimum number of relatively safe drugs that are used for
the treatment of obesity, and in the minds of most human obesity is more a cosmetic problem, not the
disease. This is partly explained by the fact that the current understanding of normal body weight were
formed only in the 30s of XX century, and before that the so-called diseases of civilization did not
represent a significant problem for medicine, fought hard against infectious diseases. With an average
life expectancy of less than 40 years the effect of excess body weight could not be the subject of study.
In order to properly diagnose and treat these pathologies to the GP to be able to properly assess the
condition and choose the tactics of treatment.
During the development of the topic, to draw students' attention to the various forms of obesity, for
reasons of, and on pathogenetic mechanisms, this involves a variety of approaches to treatment and
prevention of this disease. Draw attention to the problems of obesity can be, focusing on the rapid
spread of the disease in the world. Students should pay attention to the simplicity and accessibility of
diagnostic methods for obesity in general practice. In the background you can move specific
diagnostic markers of metabolic syndrome, different classifications of obesity, list of names of drugs
used in the treatment of obesity.
3.Intra and interdisciplinary communication
Teaching of the subject is based on the knowledge of the students major endocrine diseases, received
a 4th year in a cycle endocrinology, as well as therapy, which allows further differential diagnosis of
diseases associated with obesity. Acquired during the course knowledge will be used during the
passage of therapy at 6 and 7 of the course.
4.Contents classes
4.1 The theoretical part
76
A list of the issues:
1. Constitutional-exogenous obesity
a) The reasons, the degree of
b) Methods of determining excess weight
c) Current treatments
2. Hypothyroidism
a) Clinical and etiological forms
b) The differential diagnosis with anemia of various origins, voucher
Kidney, intestine
c) The characteristics of the course and treatment of pregnancy
d) Hormone replacement therapy, selection of doses
3. Cushing's Disease
a) The differential diagnosis of various forms of Cushing
b) The pathogenesis of obesity and the clinical symptoms of Cushing
c) Treatment
4. Adipozo-genital dystrophy
a) The etiology and pathogenesis of the main clinical symptoms
b) The differential diagnosis with primary hypogonadism, with a false-adipozo
Genital dystrophy
c) The prevention, treatment.
Obesity - excessive deposition of fat - can be an independent disease is chronic and requires lifelong
treatment. According to the WHO, obesity is about 30% of the inhabitants of the earth. Proved the
role of nutritional obesity in atherosclerosis, hypertension, disorders of carbohydrate metabolism.
Uniform classification of obesity is not used for classification of the etiology, nature of the distribution
of fat on the degree of weight gain. In alimentary obesity distinguish ginoidny, android and mixed
types, with the metabolic syndrome or its components: the upper type of obesity, glucose intolerance,
hyperlipidemia, hypertension. The most obvious causes of obesity - excess calories write, lack of
physical activity. Energy balance is regulated by leptin - the hormone of adipose tissue and insulin,
noradrenaline, and serotonin. The ability to store energy as fat is one of the basic vital functions of
adipose tissue, especially when restricted energy intake. In adipose tissue metabolic processes
occurring fatty acids, carbohydrates, and fat formation from carbohydrate. Since the decay of the fat is
released large amounts of water, adipose tissue is also a kind of shed body water. Adipose tissue plays
an important role in the regulation of calcium-phosphorus metabolism (the initial stages of the
formation of vitamin D), and metabolism of sex steroids (aromatase fat cells contributes to the
transformation of adrenal androgens to estrogens). Adipose tissue is the primary site of action of
insulin and is more sensitive to this hormone than other fabrics. Obesity can be a stable, progressive
and residual (residual effects after sustained reduction in body weight). Distinguish between general
and local (local lipohypertrophy) obesity. Obesity, anorexia nervosa and bulimia nervosa are
classified as eating disorders. Strategically more properly considered emaciated obese patient is not
cured, but are in remission of obesity ("thin thick"). Despite the fact that a visual inspection and
measurement of total body weight can assess the degree of obesity, more informative measure is body
mass index (BMI), calculated as weight in kilograms divided by the height of a man in meters squared
(kg / m 2). Ideal BMI of 18-25 kg / m 2. The higher the BMI, the higher morbidity and mortality. The
77
normative content of adipose tissue in men is 15-20% of body weight in women-25-30%. To assess
the type of fat deposits using the ratio of waist to hips. This figure is normally not exceed 0.8 for
women and 0.95 for men. Exceeding these indicators suggests an upper type of obesity in the presence
of increased BMI.
The clinical picture. Obesity is often accompanied by depressive disorders, anxiety, impaired
interpersonal and social contacts. An obese person is exposed to varying degrees of discrimination,
particularly severe in adolescence. Low self-esteem hinders the harmonious social and personal
development. Complaints range is large, from overweight as an aesthetic problem to the characteristic
manifestations of obesity is often associated disease (CHD, diabetes, circulatory failure) and nonspecific symptoms (apathy, drowsiness, fatigue tendency to constipation, joint pain). Despite the fact
that patients are almost never complain about the increased appetite, we should try to clarify the nature
of the patient's nutrition. Possible solutions to the problem - ask the patient to talk about the food
eaten and the frequency of its methods, as well as the last meal for the day, the patient can be asked to
provide a record of the food eaten in the last 2-5 days. This is a longer but more effective way.
History, the typical patient with exogenous-constitutional obesity, as follows. Patients believe that
they eat little, and point out that in the morning they do not eat. Drink a cup of coffee with sugar (80
calories) and a sandwich with cheese and butter (300 calories) is usually not considered as food. At
work, patients begin to "bite." Usually it is calorie foods with high fat content. Often patients chew at
work automatically, without noticing it, eating with waves, and at night before bed. For reasons not
entirely clear in individuals with insulin resistance and their immediate families reduced exercise
capacity, which creates conditions for the development of obesity. In patients with android type
obesity with advanced ginoidnym obesity often enhanced function of sweat and sebaceous glands, so
the skin of patients with wet, greasy, with pustules, eczematization, pyoderma, furunculosis. Typical
inguinal and umbilical hernia. Obesity is accompanied by insulin resistance, which lowers the ability
of insulin to ensure the utilization of glucose, suppress the release of glucose by the liver. Often
detected in obesity hyperinsulinemia is a factor of the pathogenesis of hypertension and polycystic
ovary syndrome. Hypertrichosis is quite typical for obesity and explains the formation of the
secondary polycystic ovarian anovulation. Requires an active search for these satellites obesity,
coronary heart disease, hypertension, atherosclerosis, diabetes mellitus type II, circulatory failure,
pulmonary heart, gallstones, osteoarthritis, impaired purine metabolism, venous insufficiency and
trophic ulcers of the lower extremities. One of the complications of obesity is the formation of right
ventricular failure due to pulmonary hypertension with hypoventilation, daytime sleepiness and sleep
apnea syndrome, secondary polycythemia and hypertension. This is a very serious condition called Pickwick syndrome, after the fat man-servant of the Charles Dickens novel "The Pickwick Papers",
constantly sleeping at work. Identification of cyanosis, orthopnea, dyspnea, marks the formation of
heart failure. Obesity is part of the so-called metabolic syndrome or syndrome X. This syndrome was
also called the "deadly quartet" (the top type of obesity, impaired carbohydrate tolerance,
hyperlipidemia, hypertension). Other components of the metabolic syndrome are hyperuricemia,
atherosclerosis, coronary heart disease, diabetes. Laboratory research is also aimed at the exclusion of
organic causes of obesity, as well as to identify possible long-term complications of existing obesity.
For individuals with excess body weight is typically high cholesterol, atherogenic lipoproteins, uric
acid. Coagulation often indicates a tendency to hypercoagulability (increased fibrinogen levels,
inhibition of fibrinolysis). Traditionally in obese patients in search of nonexistent (most often) the
endocrine pathologist examines the level of certain hormones. It is important to remember that obesity
is the typical secondary hyperaldosteronism, the violation ratio of LH and FSH elevated estradiol.
Current approaches to the treatment of obesity - a recognition long-term treatment, and safe methods
of prevention-oriented.
Need to develop the concept of reasonable eating. The diet should not be less than 1000 - 1200
calories a day. Limited to animal fats, use sweeteners, add more fiber.
78
Physical activity should be equivalent to the, but rather long, because only in this case, spent reserves
fat depots.
Medications prescribed for BMI greater than 30, with no effect of diet and exercise.
Options for drug therapy: effects on hunger and satiety center - drug "Izolipan", blocking fat
absorption - the drug "Xenical", increased lipolysis - the drug "Siofor."
Pituitary - Cushing (BIC) - neuroendocrine disease pathogenetic basis of which is the formation or
hyperplasia kortikotropinomy kortikotrofov pituitary gland, combined with an increase in the
sensitivity of the hypothalamic-pituitary axis to the inhibitory effects of glucocorticoids, which leads to
disruption of the daily dynamics of ACTH secretion secondary to the development of bilateral cortical
hyperplasia adrenal and clinically total of Cushing's syndrome. The most common form of Cushing is
exogenous hypercortisolism caused by prolonged glucocorticoid, whereas the most frequent variant of
endogenous Cushing's is pituitary - Cushing. The incidence of pituitary - Cushing of 2 new cases per
year per 1 million populations. For every 5 cases, 1 case of BIC has kortikosteromy. As BIC and
kortikosteroma more common in women (approximate ratio 8:1). Suffer mainly aged 20 - 40 years.
Syndrome, ectopic ACTH production occurs in approximately 15% of patients with endogenous
Cushing, he observed an older age of 40 - 60 years, more frequently in men (ratio 1: 3).
Bilateral ACTH - independent nodular hyperplasia have been observed mainly in childhood and
adolescence, and in this form (the only one of all forms of Cushing) is the accumulation of family
cases, most affected siblings ..
Etiology and pathogenesis. If the etiology and pathogenesis of Cushing's syndrome due
vnegipofizarnymi tumors, whether kortikosteroma or ACTH-producing tumors, in general seem to
understand (or rather, they are similar to the etiology and pathogenesis of tumors in general), for
Cushing's disease, these issues remain controversial. Currently, the most accepted pituitary theory that
morphological and pathogenic substrate BIC is a pituitary adenoma (90% of microadenoma - a tumor
diameter of less than 1 cm). Adenoma is a monoclonal tumor, which is the cause of the local mutation
that leads to hyperplasia kortikotrofov, which in some cases do not reach the stage of microadenomas.
Much less common macroadenomas. As it follows from the definition of the BIC formation
kortikotropinomy combined with disruption of the normal control mechanism for the secretion of
ACTH, which increases the threshold of sensitivity to glucocorticoids pituitary, ie despite sometimes
significant hyperproduction of cortisol, combined with jetlag secretion, the latter does not suppress the
production of ACTH, as is the norm. Thus, there is a violation of the negative feedback mechanism of
secretion of corticosteroids. However, the BIC (in contrast to the ectopic ACTH - syndrome)
production of ACTH pituitary adenoma is not fully autonomous. This is based on a large
dexamethasone at which, in the case of the appointment of BIC 8 mg of dexamethasone to suppress the
secretion of ACTH and cortisol, respectively. Violation of the dynamics and control of ACTH
secretion in the BIC combined with reduced dopaminergic influences the hypothalamus, inhibiting the
secretion of ACTH, and increased serotonergic effects. The latter fact is the basis of the theory of the
pathogenesis of hypothalamic BIC. In addition, the argument in favor of a primary hypothalamic
defect is a violation of not only the dynamics of secretion of ACTH and prolactin and growth hormone.
The clinical picture. Physical examination of the patient data is critical in the diagnosis of Cushing’s
total, but rarely allows him to suspect a specific form (or Cushing's disease). In some cases, based on a
clinical picture may be suspected ectopic ACTH syndrome. Obesity occurs in 90% of patients and is
one of the highlights of clinical signs. When fat is stored Cushing dysplasia (cushingoid type of
obesity) on the abdomen, chest, neck, face (moon face purplish-red in color, sometimes with cyanotic
tinge, "matronizm") and back ("menopausal hump"), at the same time there is atrophy hand muscles
("spider fingers") and legs ("oblique buttocks"). On the back of the hand and the fat of the skin
noticeably thinner, with other forms of obesity is not observed. Even in the absence of obesity (in very
severe cases) a redistribution of subcutaneous fat. Selectivity obesity explains different sensitivities fat
body parts to glucocorticoids. Catabolic action of glucocorticoids leads to muscle atrophy, which is
79
particularly evident in the large muscles of the shoulder girdle and lower limbs. Muscle atrophy is
especially noticeable when you try to sit down and get sick: both these movements will be much more
difficult, especially getting up. Atrophy of the muscles of the anterior abdominal wall ("frog belly")
results in a hernial protrusion on the white line of the abdomen. Skin is thinned, a kind of marble with
a marked vascular pattern, dry, with lots of regional sweating, scaly. Characterized by the specific
"sheep" smell. The combination of obesity and the progressive collapse of collagen explain banding
stretch - stretch marks. Stretch marks are purplish-red or purple color on the skin are the abdomen,
inner thighs, breasts, upper arms, and their width can be up to several centimeters, The treatment of the
disease fade stretch marks. Often depend on the skin type of acne lesions, numerous minor bruising.
Hyperpigmentation is mainly observed in the BIC SA %) and ectopic ACTH-snndrome AOS %). For
ectopic ACTH syndrome is characterized by a pronounced myasthenic syndrome associated with
severe hypokalemia and muscular dystrophy. In addition, the natural pigmentation of the skin occurs
in patients who are at the BIC was performed bilateral adrenalectomy. A serious complication of
Cushing, which on the one hand, largely determines the severity of the disease and on the other - is a
very important diagnostic feature {80 - 90%), is osteoporosis, which develops due to destruction under
the influence of glucocorticoids protein matrix of bone with subsequent leaching of calcium. Excess
corticosteroid promotes sodium retention, hypokalemia, alkalosis gipokaliemicheskoe. Evolving
myocardial electrolyte-steroid, during which exacerbated the development of hypertension, diastolic
mainly on giperkinetncheskomu type. The latter is a constant and early symptom of Cushing's
syndrome. Myocardial often manifested arrhythmias (atrial fibrillation, arrhythmias). At the end of
these processes inevitably develops heart failure, which in most cases is the direct cause of death in
patients. Symptoms such as drowsiness, polyphagia with night hunger, polydipsia, impaired
thermoregulation, mental depression or aggression, induced by the action of an excess of
corticosteroids. Excess steroids also explain mental changes of patients (from lethargy and depression
to euphoria and steroid psychosis). Often scarce mismatch complaints severity. Due to the small size
of corticotropin-specific neurological symptoms of pituitary adenomas (chiasmal) is usually not
detected.
Gain under the influence of excess glucocorticoid gluconeogenesis and peripheral insulin resistance
leads to the development of steroid diabetes, which manifest in the form occurs in 10-20% of patients.
Increasingly determined by breach of tolerance to carbohydrates. The special features of the steroid
diabetes are ease of flow and compensation against the diet and use of sugar reducing tablets, a rare
development of ketoacidosis. Immunosuppressive action of corticosteroids reduces the body's
resistance to infection, including specific. At Cushing decrease the total number and activity of
lymphocytes, there is a general involution of the lymphoid tissue. During infectious processes in
Cushing is atypical, oligosymptomatic, excess secretion of sex steroids results in the development of
women hypertrichosis (excessive hair growth), hirsutism (hirsutism). Virilization (hirsutism in
combination with hypertrophy of the clitoris and defeminizatsiey) is more common in mixed tumors
(kortikoandrosteromah), lipid-cell tumors of the gonads, or "clean" androsteromah. At the last clinical
signs of Cushing missing. Violation under the influence of androgen excess cyclic release of GnRH
causes the development of amenorrhea. After successful treatment of patients with BIC often develop
autoimmune tireopatii - autoimmune thyroiditis, rolling in primary hypothyroidism.
Diagnostics. In the diagnostic finding in Cushing's syndrome can be divided into several stages:
1. Clinical stage. Includes a medical history, physical and routine clinical
Examination of the patient. At this stage, can be suspected, and in most cases is safe to conclude that
the presence of Cushing's syndrome.
2. Hormonal studies. In patients with suspected Cushing's syndrome is first necessary to prove or
refute the presence of Cushing as such (urinary free cortisol excretion, small deksametazonovy test).
In individuals with a proven way of Cushing syndrome total, as well as overt clinical signs of the last
80
differential diagnosis to determine the causes of Cushing: Cushing's disease, ectopic ACTH or
kortikosteroma syndrome (large deksametazonovaya test, ACTH level).
3. Topical diagnosis. At this stage, the morphological substrate of the disease: pituitary adenoma and
bilateral adrenal hyperplasia with BIC; kortikosteroma adrenal or ACTH - producing ectopic tumor at
CIC. To confirm the presence of Cushing's syndrome is the main method was to determine daily
urinary free cortisol excretion. The specificity of this study was 98%, sensitivity - 95 - 100%. Small
deksametazonovaya test has a specificity of 80% (see section 7.3.2) and is used less and less. Despite
the high specificity of the daily urinary free cortisol, remember that conditions involving relative
giperkortizolemiey.
New educational technology: the method "Snezhkov," "The Weakest Link".
The method of "snowball"
To work needed:
1) a set of training - control tests
2) sheets of paper
Progress:
1) The group is divided into two subgroups.
2) Each team will one sheet of paper.
3) On a sheet of written FI students, group, department, date.
4) One of the students taking the envelope issues that are the same for both groups.
5) Each correct answer is recorded as a credit in the form of "snowballs."
6) Group, has received the maximum number of points is estimated excellent grades.
7) to hold the method have 30 minutes.
1. What type of obesity exists?
Ginoidny
Mixed
Android
2. What is the degree of obesity is characterized by BMI (body mass index) 35.5?
Obesity 2 tbsp.
3. By what formula determined BMI (body mass index?
Kg / m 2
4. What research should be carried out for the differential? Diagnosis of disease and syndrome of
pituitary - Cushing?
Dexamethasone test
The method of "The Weakest Link"
To work needed:
1. A set of questions on endocrinology.
2. A sheet of paper with a list of games for logging.
3. Stopwatch.
Progress:
81
1. The game holds a teacher and an assistant from the students - the counter.
2. Counter wrote on a sheet date, the group number, the faculty and the business name of the game
and a list of student groups.
3. Teacher hurt in series of questions from the students a set of questions.
4. The student must in 5 seconds. to answer.
5. Teacher of the word "right" or "wrong" answer evaluates if the "wrong" he gives the correct
answer.
6. Counter puts opposite the name of the student, "+" or "-" depending on the correctness of the
answer.
7. Students are thus two rounds of questions. '
8. After 2 rounds of questions the game is suspended and the students who were minus two out of the
game as the "weak link".
9. The game continues for a new circle with the rest of the students. Again, they are offered one new
round of questions and again eliminated students who in the sum with the first two rounds turned
instrumentals.
10. Round by Round shown the strongest of the players, who responded to an increasing number of
issues.
11. On a sheet against each name the teacher records - who in any round was eliminated and became
the "weakest link".
12. Game estimated maximum of 100 points.
Students who withdrew after the first 2 rounds of the answers, get a game of "0" points,
after 3 rounds answers - "25" points,
after 4 rounds answers - "50" points,
after 5 rounds answers - "75" points,
the strongest participant receives 100 points.
13. The scoring on the sheet of the protocol to the count of the current total of occupation as an
estimate for the theoretical part.
14. At the bottom of the log free teacher records on a business game, the elder signs off.
15. Minutes of the game remains.
1. Patient T. 49. Complaints against the overweight, dry mouth, headaches,
high blood pressure, white stretch marks on the skin of the abdomen. Diet - mainly eating food after
19.00, the last meal at 22:00.
On examination: height - 170cm and weighs 100kg, waist - 90cm, Hips - 125cm. BMI (body mass
index - 34.6 kg/m2, abdominal nndeks-0, 72).
1. What is the degree of obesity is characterized by BMI (Body Mass Index)?
A. Obesity 2 tbsp.
B. normal weight
B. obesity 1 tbsp.
G. low body weight
D. Obesity W Art.
2. What type of obesity in the patient?
A. android
82
B. ginoidny
V. uniform
G. Mixed
D. subcutaneous
3. Preliminary diagnosis:
A pituitary Kushnnga.
B. hypophyseal syndrome
B. Cushing's syndrome
G. alimentary-constitutional obesity
D. hypothyroidism
2. A man of 38 years. Clerk. Complained of weight gain, shortness of breath, recurrent palpitations,
sleepiness, fatigue. The patient prefers greasy meats.
On examination - preferential deposition of fat in the abdominal area. P-170cm, B - 101kg, BMI
(body mass index, 34 9kg/m2, abdominal index-1, 07).
1. What is characteristic of obesity BMI (body mass index?
A. 1st.
B. 2cT.
B. normal weight
G. W power.
D. low body weight
2. By what formula defined abdominal index?
A. hips / waist
B. bust / waist
B. kg/m2
G. waist / hips
D. growth-100cm
3. What type of obesity in a patient?
A. hypoid
B. Mixed
B. android
G. gipoovarialny
D. central
4.2 The analytical part
The decision of situational problems. Students are given one task to the differential diagnosis of
endocrine disease. Preparation time - 5 minutes. To answer - 2 minutes. Response is evaluated
according to the criteria developed. Accounted
Additions and judgments of students going into their asset. The group then divided into 2 groups and
given a task with a difficult decision. Preparation time - 7 minutes. The solution presented and
discussed together with the other subgroups.
Problem number 1. Patient KA 32 years, with growth of 162 cm has a weight of 118 kg. Complains
of excessive sweating, especially after eating, periodic menstrual cycle as polimenorei and raises blood
pressure in an emotional outburst. Of history - grew up in a family where everyone was indifferent to
foodies and sweets, baked goods. Father, mother, brothers and sisters all have different expressions of
obesity. On examination - uniform distribution of p / fat, belly droops as "apron", stretch marks on the
skin are "stretching" whitish. BP within the permissible limits, a small tachycardia, increased left
border of the heart, to listen to accent 2 tone of the aorta. In the lungs - a slight lengthening of
expiration (a history of frequent colds as bronchitis). Percussion liver and spleen were not enlarged,
the chair is prone to constipation, but readily respond to laxative herbal remedies. For 10 years
working as an economist in a shoe factory. She is married and has 2 of their children.
83
1. What type and degree of obesity in this patient?
2. Explain the mechanism of menstrual disorders, hypertension
3. Why is sweating, especially after a meal?
4. The differential diagnosis on objective criteria other
types of obesity of endocrine origin
5. What method of treating obesity assign the patient?
Objective number two. Turning you a woman of childbearing age complaining of constant headaches,
aggravated by the rise in blood pressure, thirst and polyuria. These phenomena are observed for 2
years. Has your gynecologist about opsomenorei and oligomenorrhea, but because of hypertension
that advised to consult a cardiologist or district physician. On examination notes - red moon face, fat
deposits on the body and its absence on the buttocks and legs. Skin covers acne; stretch marks are
purple-red color on the sides of the chest, abdomen, inner arms and thighs.
1. For what disease is characterized tsentropitalny type of obesity?
2. Whether examination of the patient in a specialized center and how this
Center will be named?
C Explain the mechanism of the above symptoms (headache, blood pressure menstrual disorders,
thirst, polyuria, re p / fat, formation of stretch marks)
4. Spend the diagnostic algorithm of this disease
Task number 3. Medical department in the direction of admissions clinic with complaints of weight
gain, difficulty bending in all large and small joints, frequent "radicular" pain in the neck, back, hair
loss, brittle nails. However, negative acute phase (revmoproby), ASO, normal ESR excluded
inflammation in the bones and joints. On radiographs of joints showed little effects of osteoarthritis,
which could give the difficulty of movements. Anamnesis revealed that the gradual weight gain
observed for 6 years, and with his relatives increased appetite and overeating, the patient was not, but
she was lazy and the last 2 years is very sleepy. On examination, paying attention - it is dry, thick skin,
swelling of the face, thick lips, enlarged tongue, hoarseness, slurred speech, slow movements,
bradycardia. The absence of menstruation is celebrated all these years. This woman was called an
endocrinologist.
1. For any endocrine disease characterized this syndrome?
2. What is obesity nutritional or endocrine?
3. Explain the mechanism of obesity unmotivated
4. What is the plan of inspection sick?
5. Is it possible without hormonal measurements put the diagnosis?
4.3 The practical part
Performed at the bedside. Supervision is carried out under the supervision of a teacher. GPs must
learn to practice proper history taking in patients with obesity, with the know how to differentiate
between primary and secondary information during the examination to focus on the type of obesity,
clinical symptoms of thyroid and adrenal glands. When communicating with the patient should
consider the mental state such as shyness obese, irritability, fatigue, and during communication
exercise extreme tact and at the same time be confident and firm.
In conducting activities in the clinic, while outpatient care, to teach students to quickly, clearly
questioning and examination of the patient, proper filling patient card.
Students are taught correct measurement of anthropometric indices and calculating BMI.
1.Determination of ideal body weight
Objective: To determine the ideal body weight
Equipment: stadiometer, scales
Performs step (stage)
№
e
Me ropriyatie
Not
By
tapa
satisfied (0 lnostyu
points)
properly
executed
84
1.
2.
3.
Measure the growth of the patient's stadiometer, in meters
OT weigh the patient's medical scales in kg
Prospect Ovest calculation using the formula: height (cm) -100 =
ideal body weight
Sun it:
0
0
0
25
25
50
100
2.The definition of obesity according to the formula Quetelet
Objective: To determine the degree of obesity formula Quetelet
Equipment: stadiometer, medical scales
Performs step (stage)
№
e
Me ropriyatie
tapa
1.
2.
3.
Not
By
satisfied (0 lnostyu
points) properly
executed
Measure the growth of the patient's stadiometer, in meters
0
30
OT weigh the patient's medical scales in kg
0
30
Prospect Ovest calculation using the formula: height (cm) -100 =
0
40
ideal body weight
Sun it:
100
3.Determination of the index of abdominal
Objective: To determine the index of abdominal
Equipment: measuring tape
Performs step (stage)
№ E tapa
Me ropriyatie
1.
2.
3.
Measure the circumference of talin patient - waist
Of hip circumference measured patient - hips
Ra OF PRODUCTS View / OB, abdominal get index
N men: 0.9
women: 0.85
Sun it:
Not
satisfied (0
points)
0
0
0
By lnostyu
properly
executed
30
30
40
100
5.Control forms of knowledge, skills and abilities
- Oral;
- Written
- Decision of situational problems
- Demonstration of the developed skills
6.The evaluation criteria of the current control
№ Military
Est. ENKA
Ka quality assessment
mustache
in points
1. 86-100 Personally from Communicates about, think creatively, evaluates,
the "5"
interprets.Applies knowledge in practice.Understands, knows,
says has no idea
2. 71-85 It is well "4"
Ra ssuzhdaet independently assess, interpret, apply knowledge
in practice, understands, knows, says has an idea
3. 55-70
Beats
Minimality knows.Understand the essence, says
85
ovletvoritelno "3."
4 0-54
Not satisfactory, Pl oxo know.Not thoroughly.Require additional training.
"2"
7.Flow chart classes
1. Checking the initial level of preparedness of students to engage in "Diseases of the endocrine
glands occur with obesity." Explanation of the diagnosis and differential diagnosis.
2. Decision analysis and situational problems.
3. Supervision of patients with diseases that are accompanied by obesity. Clinical analysis of
supervised patients.
4. Interactive games to assess knowledge on training.
№
fl ups lessons
Prospect
odolzhitelnost
classes
7-hour ace
1 Judgment of courses offered
8.30-10.05
2 Ca autonomy of patients Supervision attached houses, self Curation case
10.10-11.05
patients, participation in rounds of professors and associate professors
3 Ra Zborov the department examined case patients with the interpretation
11.10-11.55
of the survey data and treatment
4 ne reryv
11.55-12.40
5 On judgment tests, situational problems.
12.40-14.40
6 Pr Overcome digestibility.Ad evaluations homework
14.40-15.10
8.Test questions
1. Obesity - a disease or physiological condition?
2. Which diseases are prone obese?
3. What is metabolic syndrome and that it is characteristic?
4. Modern surgical methods (pros and cons of these methods)
5. What features of the patients with PYUD And ADGD?
6. How is the BMI?
7. How is the ideal body weight formula Brock?
8. Special diet for obesity
9. What are the characteristics of obesity in with-me Cushing?
10. List the causes of hypophyseal syndrome.
9.Recommended Reading
Summary:
1.
Balabolkin MI Endocrinology. M., Medicine, 1998
2.
Vladimir Potemkin Endocrinology. M., Medicine, 1999
3.
Grandparents II Endocrinology. M., Medicine, 2000
4.
Melnichenko GA Tokmakova AY, deck DE, NV Lavrishcheva Endocrine
disease. M. Medicine, 2009
5.
Guidelines for Pediatric Endocrinology. Handbook of clinical Pediatric
Endocrinology. Edited by Charles G. Bouka, Rosalind S. Brown. 2009
86
6.
Shustov SB, Khalimov S, Trufanov GE Functional and topical
diagnostics in endocrinology. M. 2010
7.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 1. Greenspan's Basic &
Clinical Endocrinology. 2010
8.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 2. Greenspan's Basic &
Clinical Endocrinology. 2011
9.
Clinical Endocrinology. Ed. EA Kholodova. Minsk. Belarus.
2011
10. Melnichenko GA Udovichenko OV Shvedova AE Endocrinology.
Typical errors practitioner 2012
11. Endocrinology. National guidelines (+ CD-ROM). 2012
More:
1. Therapeutic Guide Washington, translated from English. (Section
"Endocrinology") 1996.
2. Laycock. Fundamentals of Endocrinology, Moscow 2000
3. Ty M. Mack - Dermott MD Secrets Endocrinology - Moscow 2000
4. Ketgayl VM, Arkin RA, Pathophysiology of endocrine system - Moscow, Medicine,
2001.
5. Balabolkin MI Diabetology - Moscow, Medicine, 2002
7. Fadeev PA. Endocrinology. Diabetes. A Reference Guide. 2009
8. Kartelishev Alexander Rumyantsev AG, Smirnova NS Actual problems of obesity
children and adolescents. 2010
9. Mkrtumyan AM, AA Nelaev. Emergency Endocrinology. 2010
10. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Diseases
thyroid. Williams Textbook of Endocrinology. 2010
11. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Bark disease
adrenal gland and endocrine hypertension. Williams Textbook of
Endocrinology, 11 th edition. 2010
12. AN hams Emergency Endocrinology. 2011
13. Petunina NA, AV Trukhina Thyroid disease. 2011
14. Manukhin IB Tumilovich LG, M. Gevorgyan Gynecological Endocrinology.
Lectures on gynecologic endocrinology. M. 2012
Journals:
15. Medical Journal of Uzbekistan, Tashkent.
16. "Problems of Endocrinology." Moscow.
17. "Therapeutic Archives", Moscow
18. "Clinical Medicine", Moscow
87
19. "Diabetes. Way of life ", Moscow
Internet sites:
1. "Internet Portal: Hunari»
2. Medscape.com
3. Alltheweb.com
4. Yahoo.com
5. E-medicine.com
6. www tma. uz
Ministry of Health Care of Uzbekistan
CENTRE FOR MEDICAL EDUCATION
TASHKENT MEDICAL ACADEMY
88
Department of Internal Medicine TRAINING GP endocrinologist
Subject: "Endocrinology"
Theme: "hypotension"
Diseases of the endocrine system, leading to hypotension: chronic and acute adrenal
insufficiency, hypothyroidism, Sheehan syndrome, cachexia Simmonds.Addisonichesky
crisis and pituitary coma.Diagnosis, differential diagnosis.Tactics GPs.
Educational and methodical development
(For teachers and students)
Tashkent - 2012
Process chart classes № 7
Diseases associated with arterial hypertension: chronic and acute adrenal insufficiency,
hypothyroidism, Sheehan syndrome, cachexia Simmonds.Addisonichesky crisis and pituitary
coma.Diagnosis, differential diagnosis.Tactics GPs.
№
fl ups practice session
PMA classes fo
venue
89
dl itTh
classes
270
min.
1 Centuries odnaya part (study subject)
10
2 Judgment about topics practice session with new educational op grew discussion
technologies
training room
("Swarm", "Gallery Tour"), as well as demonstration material
(boards, sets medical charts, tables, posters, hormonal and
clinical tests, X-rays, situational problems, tonometer,
stadiometer, scales, measuring tape), to determine the original
level.
3 You discuss water
50
4 The definition of reference for the practical part - n rofessionalny of judgment
questioning.Explanation of the provisions and recommendations
training room
for the job to fill medical records.
25
5 Military wasps practical training under the guidance of a teacher. Prospect ofes sional
questions, talk with patients
filling medical records,
case studies.
Department of
Endocrinology Clinic 1TTA
6 John interpretation of the survey data of patients - complaints, tory studies of the disease,
inspection, palpation, percussion and auscultation of patients as laboratory data situational
well as laboratory and instrumental studies
problems
Department of
Endocrinology Clinic 1TTA
7 Judgment on the theoretical and practical knowledge of the mustache tny survey, tests,
students, fixing material, the level of learning assessment.
discussion, identification of
practical skills
Department of
Endocrinology Clinic 1TTA
8 The definition of output on practical training, evaluation of 100- infor mation, questions for
point system, and ad evaluations. Homework next practice homework.
session (a collection of questions).
training room
30
15
35
80
25
Lesson number 7
Diseases associated with arterial hypertension: chronic and acute adrenal insufficiency,
hypothyroidism, Sheehan syndrome, cachexia Simmonds.Addisonichesky crisis and pituitary
coma.Diagnosis, differential diagnosis.Tactics GPs.
1.
uch ebnoe time: 7:00
Art ruktura training 1. afedra to internal medicine training
90
session
GPs with an endocrinologist, endokrinologichessome branch 1 TTA clinic, clinical
1-clinic laboratory TTA;
2.set of tables, methodological recommendations
tion, laboratory and instrumental data,
video;
3.TCO: computer, video
Tse eh training session:
- Theacquisition of knowledge and skills in students GPs to diagnose
and differential diagnosis of diseases associated with arterial
hypertension;
- Learn to use the modern classification of these diseases;
- To conduct early detection and disease prevention through individual
symptoms, syndromes.
Pe dagogicheskie tasks: D results of training activities:
• consider endocrine GP
diseases
should know:
system, leading to
• understand the causes of hypotension,
hypotension;
know the rules of hormone
• to consider the causes therapy;
of
• Analyze data from laboratory tests and
diseases of the endocrine instrumental studies;
system,
• writing of drugs in
by high blood
Depending on the etiology of diseases
hypotension;
Accompanied by hypotension.
• Discuss the clinical
symptoms
should be able to:
Sheehan
syndrome, • conduct professional inquiries, inspection
Addison's disease,
the patient;
• analyze the laboratory • interpret clinical laboratory
Data in these diseases, instrumental data;
• Discuss ways to treat • put on a clinical diagnosis of classical
endocrine hypotension. fication of WHO;
• counseling of patients with data
diseases;
• master the skills of patients with
hypotension in pregnancy
must have skills:
• Identify symptoms of Sheehan disease
Addison;
• distinguish between primary and secondary gipokortitsizm;
• make a differential diagnosis
diseases that occur with arterial
hypotension
le Ktsia, the method of "swarm", "Gallery Tour", demonstration,
Methods of training
entertainment experience, discussion, conversation, case.
Forms of
training of individuality work, group work, team, classroom, extracurricular.
activities
Mr. zdatochnye visual training and materials, videos, models, graphic
Wed edstva training
organizers, kits medical charts, tables, stands, kits radiographs.
91
Cn lady and means of bl uu-survey, testing, presentation of the results of the training task, filling
medical records, execution of practical skills "professional questioning"
feedback
2.Motivation
Conducting this training allows the learner time and correctly diagnose and to provide emergency
assistance in cases involving hypotension.
3.Intra and interdisciplinary communication
Teaching of the subject is based on the knowledge of the students major endocrine diseases, received
a 4th year in a cycle endocrinology, as well as therapy, which will continue to carry out differential
diagnosis of diseases associated with hypotension. Acquired during the course knowledge will be used
during the passage of therapy used and 7 course.
4.Contents classes
4.1 The theoretical part
On practical training in the theoretical part series discusses the clinical features of the syndrome and
Addison's disease Sheehan.
A list of the issues:
1.Simmonds-Sheehan syndrome
a) The pathogenesis of the main clinical manifestations, shape, weight
b) Hormone replacement therapy
a) The prevention, prognosis.
2.Chronic and acute adrenal insufficiency
a) The reasons, the pathogenesis of hypotension and other clinical symptoms
b) The differential diagnosis with NDCs, hemochromatosis, scleroderma, enteritis, malabsorption
syndrome, pellagra.
Simmonds-Sheehan syndrome. Hypothalamic-pituitary failure (panhypopituitarism) - a
clinical syndrome that develops as a result of degradation, followed by persistent decreased production
of tropic hormones and disorders of the peripheral endocrine glands. One variety of the hypothalamicpituitary insufficiency is panhypopituitarism, which refers to postpartum septikoembolichesky
adenohypophyseal necrosis leading to severe cachexia and involution of organs and tissues. When
syndrome Simmonds, the clinical picture is dominated by steadily increasing weight loss. In patients
with cachexia and the prevalence of symptoms gipokortitsizma observed the progression of symptoms,
resulting in a short time to death.
Sheehan's disease - the most common and more benign current and evolving gradually option
postpartum panhypopituitarism. If a marked loss of tropic hormones, then it is an isolated failure. In
operation, 10% of pituitary cells developed panhypopituitarism.
Etiology. Most common cause of hypopituitarism is the circulatory disturbances in the hypothalamicpituitary region (hemorrhage, ischemia), developing after birth, complications of massive (> 1 L)
hemorrhage, thrombosis, and sepsis. Repeated frequent pregnancy and childbirth as factors of
functional stress predispose to pituitary hypopituitarism. Rarely, but sometimes ischemic changes in
the pituitary gland may occur after gastrointestinal, nasal bleeding. Rarer causes include: pituitary
adenoma with hemorrhage or infarction, metastases (lung cancer, breast cancer), granulomatous
92
diseases, inflammatory diseases (encephalitis, meningitis, tuberculosis, and abscess), cranial trauma,
hypophysectomy, congenital aplasia or hypoplasia.
Pathogenesis. Panhypopituitarism The pathogenesis is tropic hormone deficiency and growth
hormone (GH). The result comes secondary hypoadrenalism, thyroid and gonads. In rare cases, the
simultaneous involvement of the posterior lobe of the pituitary gland or the legs may reduce the level
of vasopressin with the development of diabetes insipidus. Decrease in production of GH with its
universal effect on protein synthesis leads to progressive atrophy of the smooth and skeletal muscles
and internal organs. Loss of production of prolactin causes agalactia.
The clinical picture. Clinic panhypopituitarism determined by the speed of development and the
amount of destruction of the adenohypophysis. Often affects women young and middle-aged (20-40
years), but there are cases of the disease in the elderly and younger age. Disease often develops slowly
over several years. Most often the first down and somatotropic gonadotropic activity, then thyrotropic
and adrenocorticotropic function. There is even exhaustion, muscle atrophy, reduction in the volume
of the internal organs. Weight loss can be mild, ie 2-6 kg per month, in severe cases, 25-30 pounds
per month. Edema usually does not happen. The characteristic changes of the skin: thinning, dryness,
wrinkling, scaling, combined with pale waxy icteric coloring. Fade hair in the armpits and pubic hair.
General view of the original. Due to the reduction of melanin synthesis (deficit MSH) depigmenting
nipples and the skin in the perineal area, sweating and sebaceous glands weaken. Marked loss and
brittle hair, early graying of them, decalcification of bones, teeth fall out. Rapidly developing
phenomenon senility and senile involution.
Characterized rezchayshaya weakness, lethargy, weakness until the complete immobility,
hypothermia, collapse (orthostatic), coma, which without specific treatment leads to patient's death.
Reduction of thyroid stimulating hormone (TSH) leading to a rapid or gradual development of
hypothyroidism. There are drowsiness, sensitivity to cold, fatigue, weakness, bradycardia. Develops
atony of the gastrointestinal tract, and constipation. In severe picture of hypothyroidism and
hypogonadism may experience swelling. One of the leaders in clinical disorders occupy the sexual
sphere. Sexual disorders often precede the appearance of other symptoms. Lost libido, reduced
potency, external and internal genital organs gradually atrophy. The women stopped menstruating,
breast cancer reduced in volume. With the development of the disease after birth and is characterized
by agalactia amenorrhea. Men disappear secondary sexual characteristics
(Pubic, axillary body hair, mustache, beard), atrophied testicles, prostate, seminal vesicles, penis,
reduced testosterone levels.
Diagnostics. Typically panhypopituitarism diagnosis is not difficult. Appearance after difficult birth,
or in connection with another cause of the complex of symptoms of adrenal insufficiency, thyroid and
gonads favor of the hypothalamic-pituitary failure.
Common laboratory findings in disease Simmonds - Sheehan is hypochromic and normochromic
anemia, particularly in patients with severe hypothyroidism, sometimes with zoeinofiliey leukopenia,
lymphocytosis. Blood glucose level is low, cholesterol increased. With hormonal study determined
the combination of low levels of hormones of peripheral endocrine glands (T 4, testosterone, daily
urinary free cortisol excretion) with reduced or low-tropic hormone and GH. To clarify the provisions
of pituitary hormone stimulating tests show releasing - hormone (thyroliberin, gonadotropin - releasing
hormone).
Differential diagnosis of panhypopituitarism - Sheehan had to spend the whole series of diseases that
lead to weight loss (malignant tumors, tuberculosis, enterocolitis, etc.). Depletion of the indicated
disease occurs gradually, is the outcome of the disease, anemia its dominant manifestations. Severity
of anemia gives rise to differential diagnosis of diseases of the blood. Hypoglycaemia with
hypopituitarism can simulate organic giperinsulinnzm (insulin).
In clinical practice,
93
panhypopituitarism often have to differentiate with psychogenic (nervous), anorexia, occurring in
young girls with an active desire to lose weight and stubborn refusal of food. Crucial in the
differential diagnosis are the history, preservation of physical, intellectual, creative activity with
extreme exhaustion, the preservation of secondary sexual characteristics in combination with atrophy
of the reproductive organs and the propensity hypertrichosis. Tropic hormone levels may be normal,
slightly elevated or reduced. However, is determined by their normal release to stimulating hormone
test, which speaks in favor of functional disturbances in anorexia nervosa.
Treatment of hypopituitarism should be directed to refund hormone deficiency, and, where possible, to
eliminate the cause of the disease. Used primarily by hormones of peripheral endocrine glands and to
a lesser extent of missing anterior pituitary tropic hormones.
Hormone replacement therapy usually begins with the preparations of adrenal, thyroid and sex
hormones. Glucocorticoids are assigned: hydrocortisone (50-200 mg / day), and when the symptoms
go gipokortitsizma of prednisolone (5-15 mg / day) or cortisone (25-75 mg / day). Mineralocorticoid
deficiency persists 0.5% deoxycorticosterone acetate (Doxil) - 0,5-1 ml intramuscular injection daily,
every other day or 1 to 2 times a week, then move on sublingual tablets 5 mg 1 to 2 times a day.
Against the background of corticosteroid replacement therapy (after 10-15 days from the beginning) is
added ACTH (corticotropin), short or long-acting. Start with small doses - ml/7-10 0.3-0.5 units) and
20 units / day for courses repeated after 6-12 months - 400-1000 units.
Gonadal failure compensated female estrogens and progestins, and men - androgens. 15-20 days is
administered estrogen (eg mikrofollin 0.05 per day) and the next day b - progestins (pregnin 10 mg * 3
times a day or 1-2.5% solution of 1.0 progesterone daily turinal on 1t * 3p per day) after pre-treatment
of sex hormone HCG is prescribed, it is also desirable in cycles - the first 2 weeks of menopausal
gonadotropin follikullyarny 300-400 IU a day, and the next 2 weeks lyuteiniziruyushy (chorionic) - for
1000-1500 units with partial or functional failure to stimulate the use of 50-100 mg of Clomid for 5-9
or 5-11 days cycle.
Men with substitution to use methyltestosterone 5 mg * 3p per day under the tongue, testosterone
propionate - 25 mg * 3 times a week intramuscularly or sustanon 1.0 intramuscularly in 3-4 weeks. 1
time.
Thyroid deficiency of thyroid hormone is eliminated; the treatment begins with L-thyroxine in a dose
of 100-150 mg or Tireokomb 1-1.5 tablets a day with a very slow increase of the dose, respectively,
under the control of the heart rate and ECG.
Gipopituitarnoy coma treatment includes high doses of parenteral corticosteroids actions intravenous
drip or subcutaneous administration of 5% - 500,0-1000,0 glucose / day, vascular and cardiac facilities.
Panhypopituitarism patients needed vitamins, anabolic hormones, and high-energy protein diet.
Targeted hormone therapy - cycles or continuously carried throughout life. Disabled patients are
usually reduced.
Chronic insufficiency of the adrenal cortex. Chronic adrenal insufficiency is associated with
primary adrenal cortical lesions and reduced as a result of their hormonal activity or secondary her
defeat.
Etiology
- An autoimmune destruction of the adrenal cortex (80-85%)
- Tuberculosis adrenal (5-10%)
- Adrenoleukodystrophy (5%)
- Adrenal metastases
- Suprarenalopathy with disseminated fungal infections
94
- HIV-related complex
- Iatrogenic primary gipokortitsizm (after bilateral adrenalectomy) and other rare causes
In the serum of patients with chronic adrenal insufficiency (HNN) is defined organ specific
autoimmune genesis autoantibodies to the adrenal cortex. Specific autoimmune markers are
autoantibodies to adrenal steroidogenic enzymes P-450 with 21, P-450 and P 17 450scc.
- TB is caused by adrenal hematogenous spread of mycobacteria. In the lungs of patients are traces
left over or active tuberculosis. The tubercular process involved and the adrenal medulla, in contrast to
idiopathic autoimmnogo process
- Adrenoleukodystrophy (ALD) is an X-linked recessive inherited disease that may affect the white
matter lesions of the brain and spinal cord, and the adrenal cortex. The underlying mutation on the
long arm of the X chromosome (Xq28).
Pathogenesis. The pathogenesis of any form of adrenal insufficiency is an inadequate secretion of
hormones by the adrenal cortex, and especially cortisol and aldosterone, which leads to disruption of
all types of metabolism. Loss of secretion of catecholamines (tuberculosis, metastases) pathogenetic
significance has little.
Diagnosis:
Three stages
1. Clinical stage
2. Hormonal studies
3. Topical diagnosis
The key role played by medical history, characterized by: hyperkalemia, high hematocrit,
hypoglycemia, hyponatremia, eosinophilia, lymphocytosis, hypercalcemia, and metabolic acidosis. In
the diagnosis of certain values has a complaint history and objective data. In the laboratory diagnosis
is important determining the level of free cortisol excretion and daily urine. Against the background of
the expanded clinical Addison's disease low urinary free cortisol confirms the diagnosis. Additionally,
you can explore the blood electrolytes - Na *, K +, Cl, Ca **, of H *. Also conducted functional tests
with ACTH, with insulin hypoglycemia and orthostatic test. ACTH stimulation test is the "gold
standard" of a diagnosis of primary adrenal insufficiency. After blood in / injected ACTH 250mkg,
after 60 minutes produced a second blood sample.
Interpretation: The maximum emission occurs in healthy after administration of 10 mg. Increased
cortisol levels at 60 min after injection of less than 20 micrograms (550nmol / L) indicates a failure of
the adrenal cortex.
Of necessity used in the diagnosis of CT and MRI, chest X-ray, specific tuberculin.
Differential diagnosis
Addison's disease is often necessary to differentiate from a number of diseases occurring melasma,
hypotension and other similar clinical symptoms. Most often when melasma hypadrenia differentiate
from bronze diabetes (gemahromatoza), pellagra, systemic sclerosis and other hypotension and other
symptoms of diarrheal disease of the gastrointestinal tract and neuro dystonia, etc. For
hemochromatosis, unlike Addison's disease is characterized by the following symptoms: hepatomegaly,
splenomegaly, cirrhosis of the pancreas and other organs in combination with diabetes and deposition
in the skin pigment containing iron (hemosiderin) and free of its (gemofustsin), which gives the skin a
slate-gray color.
In contrast to Addison's disease is characterized by a triad of pellagra: dermatitis preceding
pigmentation dementia (dementia), and diarrhea. In pellagra pigmentation occurs only on the exposed
areas of the body (hands, arms, face, neck).
95
In systemic scleroderma in contrast to Addison's disease are widespread swelling of the skin tight or
seal and atrophy. Characteristic pustules, expressions and other trophic skin changes. Pigmentation of
the skin is often associated with areas of depigmentation. There are additional specific laboratory
findings characteristic of scleroderma (revmoproby, skin biopsy, etc.)
Often have to differentiate from Addison's disease neuro dystonia (NCD) flowing through the
hypotonic type. In contrast to Addison's disease at NDC a primary or secondary hypertension,
particularly increased with emotional stress, also reported normal levels of electrolytes (K +, Na * and
chloride), as the content of hormones (cortisol, aldosterone, ACTH). These clinical manifestations as
gastrointestinal dyspeptic symptoms, weakness sometimes necessary to distinguish from the
gastrointestinal tract (pancreatitis, enteritis, gastritis, etc.). Addison's disease against gastro-intestinal
diseases characterized by history, seasonality, and localization of a relationship over the meal, etc., as
well as the specific changes observed in gastrofibroskopicheskih and radiological investigation, normal
values hormonal parameters.
Treatment. For newly diagnosed adrenal insufficiency and decompensated treatment process should
begin with the intramuscular administration of hydrocortisone acetate and hemisuccinate scheme: 8 ° °
- 75 mg, 13 ° ° - 50 mg, 17 ° ° - 25 mg for 3 - 7 days. Then clean the evening dose gradually over 3-5
days to reduce the total dose of 75 mg (8 ° ° - 50 mg, 14 ° ° - 25 mg), and then, if conditions allow the
patient is transferred to the tablet formulations.
There are several schemes alternate therapies:
- With the use of short-acting drugs.
Hydrocortisone - 20 mg 10 mg in the morning in the afternoon in conjunction with 0.05-0.2 mg
kortinefa morning
- Using drugs average duration of prednisolone - 5-7.5 mg in the morning, 2.5 mg in the afternoon in
conjunction with 0.05-0.2 mg kortinefa morning
- Using drugs long night of action
Dexamethasone 0.5 mg at bedtime in combination 0,005-0,2 mg kortinefa morning
- Various combinations of HA in conjunction with a 9-ftorkortizolom
Thus, with concomitant diseases (colds) and severe stress dose corticosteroids should be increased by
1.5-2 times. To small surgical interventions (gastroscopy, extractions) the patient must enter
intramuscularly 25-50 mg of hydrocortisone, with severe somatic diseases (pneumonia), the patient is
transferred to treatment with hydrocortisone.
For large surgery or childbirth treatment is as follows: before surgery (early labor) intramuscularly
injected 75 mg hydrocortisone during surgery (birth) is injected intramuscularly 75-100 mg
hydrocortisone hemisuccinate 5-10% glucose solution. The first 3 days after surgery, intramuscular
100-150 mg / day, followed by 75-100 mg / day, then transferred to the tablet formulations in the usual
way.
New educational technology: the method "swarm", "Gallery Tour"
The method of "swarm"
To work needed:
1. A set of setting and situational problems that have been printed on a separate page.
2. Number plates for the draw in the number of students in each subgroup.
3. Blank sheets of paper, pens.
Progress:
1. All the students are divided into groups by lot 3 subgroups of 2-3 students each.
96
2. Each subgroup sits at a separate table, preparing the paper and pen.
3. Written on a sheet date, the group number, department, name, name of participating students
the sub-group and the name of the business game.
4. One of the participants in each subgroup takes the envelope of setting that is used for all subgroups.
5. One of the students in each subgroup rewrites on the job list.
6. All subgroups of students together to discuss the job, and then one of them writes his decision.
7. The decision set to 15 minutes.
8. The teacher watches the game.
9. after the time of the surrender teacher.
10. All the players discuss the results; choose the most appropriate solution for which to set the
maximum score.
11. on the decision to 15 minutes.
12. Students get points for answering the theoretical part of the rating classes.
13. Subgroup, which gave the most correct answers will receive a maximum score of -100 points
subgroup took 2nd place 85 points, 3 subgroup of 70 points rating
14. On the answer sheet scores and teacher puts his signature.
15. by students score counted in the scoring for the current session.
16. In the lower part of the magazine is a free stamp on the game with a signature
Elder group.
17. Student work saved teacher.
Complex issues for the business game:
1. The structure of the adrenal gland.
2. Regulation of glucocorticoid biosynthesis.
3. Regulation of biosynthesis mnneralokortikoidov.
4. The mechanism of action of glucocorticoids.
5. The mechanism of action of mineralocorticoids.
6. The mechanism of action of adrenal androgens.
7. Methods of examination of patients with diseases of the adrenal glands.
8. The causes of acute adrenal insufficiency.
9. The causes of chronic adrenal insufficiency.
10. Methods of diagnosis of chronic adrenal insufficiency.
11. The clinical picture of pheochromocytoma.
12. Diff. diagnosis of primary and secondary adrenal insufficiency.
13. Causes of Addisonicheskogo crisis.
The method of "Tour Gallery»
To work needed:
97
1. A set of questions that have been printed on the fin. sheets.
2. Set of spokes and diagnostic tasks, printed on separate sheets.
3. Blank sheets of paper
4. Pens with colored bars (blue, red, black, green)
5. Number plates for the draw, the number of students per class
6. Speedometer or clock.
Course of the business game:
1. A group of students is divided into 3-4 draw subgroups of 2-3 people in each
2. Each subgroup sits alone, takes a sheet of paper and on one of the colored pens.
3. on a sheet date, number of gaming title, name of student participants in this subgroup.
4. One of the players takes the envelope question or problem, depending on the choice of the teacher.
5. For each sub-question its departments or task, the complexity of their subgroups for all about the
same.
6. Takes the time to 10 minutes.
7. Small groups (groups), each for 10 minutes to discuss the job, write down your judgment, and at
the end of the time sheets are exchanged with another subgroup of the circle.
8. The next subgroup assesses previous answer and if the answer is not the full complement of his or
offer your own version. At this stage will have 10 minutes.
9. At the end of the work (30 minutes or 40 minutes) depending on the number of sub-groups (3 or 4)
on a piece of writing is 3.4 different color pens.
10. The works shall be the teacher.
11. All participants will discuss the results and choose the most correct answers are worth a
maximum score.
12. for discussion of play time of 15 minutes
13. Subgroup, which gave the most correct answers will receive the maximum score of 100% on the
rating of the theoretical part of the training.
Subgroup, who took 2nd place - 85.94% rating.
Subgroup, who took 3rd place - 70.9% rating.
14. Students with scores recorded for billing ongoing evaluation sessions.
15. Work of students counted teacher and elder group, and saved a teacher.
Appendix:
1. Complex test questions
2. Situational and complex diagnostic problems.
Test questions for the online game "City gallery»
1. ACTH biological effect.
2. STG, the biological effect.
3. FSH, LH, prolactin: biological effects.
4. TSH: biological effects.
98
5. Simmonds-Sheehan syndrome: etiology and pathogenesis, clinic.
6. Simmonds-Sheehan's syndrome: diagnosis and treatment.
7. Chr. Adrenocortical insufficiency - etiopathogenesis.
8. Chr. Adrenocortical insufficiency - clinical, diagnostic.
9. Chr. Adrenocortical insufficiency - differential diagnosis and treatment.
10. Acute adrenal insufficiency - etiology, clinical signs, first aid.
11. Criteria for severity of chronic adrenal insufficiency.
12. Scheme of glucocorticoids in Addison's disease.
13. Differential diagnosis between primary and secondary and secondary adrenal insufficiency.
14. What hormones are produced in the cortex and the adrenal medulla?
15. Addisonichesky crisis: causes, first aid.
4.2.The analytical part of
Conducted analysis of the clinical case patient with Sheehan's syndrome and patients with XP.
insufficiency of the adrenal cortex. Proposed to solve situational problems in differential diagnosis of
these diseases with hemochromatosis and other for individual and pair solutions.
Practical skills that require incremental development, in this session there.
The decision of situational problems. Students are given one task to the differential diagnosis of
endocrine disease. Preparation time - 5 minutes. To answer - 2 minutes. Response is evaluated
according to the criteria developed. Considered amendments and judgments of students going into
their asset. The group then divided into 2 groups and given a task with a difficult decision.
Preparation time - 7 minutes. The solution presented and discussed together with the other subgroups.
Objective number one. 40th patient complains of constant muscle weakness with periodic
amplification, sharp pains in the muscles, numbness and cramps in the legs, nocturnal polyuria and
polydipsia, increased blood pressure permanent. Periodically there are heartaches without irradiation,
shortness of breath, palpitations and irregular. Such a state with a gradual increase continued for 1
year. Noticed that salty foods worsen the condition, that is, cause increased muscle weakness. On
examination: blood pressure - 180/100 mmHg, heart sounds are muffled, accent 2 tone of the aorta, the
ECG-gipokaliemicheskoe symptoms.
1. What endocrine disorder is accompanied by hypertension, polyuria and severe myasthenia?
2. That should be investigated in the first place?
3. Make a diagnostic algorithm
4. Describe the electrocardiographic signs of hypokalemia
4. Your preliminary diagnosis.
Object number 2. A woman is 27 years. Complains of weakness, sensitivity to cold, dry skin,
amenorrhea. Three years ago, labor, complicated by severe postpartum hemorrhage, collapse. Soon
she stopped breastfeeding, monthly not resumed, increasing weakness, feeling of chilliness, and
constipation. Satisfactory condition, the figure is correct. Height is 168 sm, weight is 66 kg. The skin
is dry and cold, normal color. Pulse is 62 a minute, rhythmic. BP - 100/70 mm. Hg. Art., the
internal organs abnormalities were found. Laboratory data: Hb - 10.2 g%, WBC 3.5 thousand,
lymphocytosis, blood cholesterol - 4.8 mmol / l. Concentration of TSH, ACTH, growth hormone in
the blood is reduced. The value of urinary excretion of 17 ACS and 17 CS - decreased.
99
1. Diagnosis
2. The expected level of thyroid hormones in the blood?
3. The expected level of cortisol in the blood?
4. Explain the mechanism of pathogenesis and clinical symptoms
5. Treatment policy.
Task number 3. A dark man of 27 years. Illness - for 2 years a tendency to a prolonged duration of
colds, fatigue in the 2nd half of the day, especially after exercise, dizziness when getting up from bed.
Losing appetite. She lost 10 pounds. Against the backdrop of the darkening of the skin appeared
white spots of various sizes on the face, back and limbs. About vitiligo seen by a dermatologist. On
the mucosa of the mouth and tongue are dark spots, pigmentation palmar lines, scars, lips, nipples and
areola of the breast, the linea Alba. Reduced blood pressure, with a change in body position (lying to
standing) there was a decrease in blood pressure of 20 - 25 mm Hg. Carpal dynamometer showed low
numbers do not correspond to age and sex.
1. Preliminary diagnosis
2. The mechanism of development of pigmentation, rapid muscle fatigue, weight loss and
hypotensive
3. Expected blood glucose, lipids, minerals, and hormones
4. What hormonal research you should assign?
5. What accounts for the appearance of depigmented patches on the background of the darkening of
the skin?
4.3.The practical part
Performed at the bedside. Supervision is carried out under the supervision of a teacher. The student
must learn to practice proper medical history of patients sendokrinnoy pathology, thus to be able to
differentiate between primary and secondary information during the examination to focus on the
endocrine glands and the clinical features of dysfunction of these glands. When communicating with
the patient should consider the mental state such as irritability, fatigue, and during communication
exercise extreme tact and at the same time be confident and firm.
In conducting activities in the clinic, while outpatient care, to teach students to quickly, clearly
questioning and examination of the patient, proper filling patient card.
Supervision of patients. On first contact with the sick student has to gain the most patient. Achieve
this may have a serious attitude towards their work, talk to the patient confidence, articulate questions.
Listen carefully to the patient, at the same time firmly directing the conversation back on track. It is
important to have a neat appearance. When collecting complaints to be able to identify major
complaints associated with damage to the endocrine system (can be active after self-questioning story
patient). When collecting history focuses on the relationship of the disease to damaging factors, acute
or latent onset, family history of endocrine diseases, it is associated with periods of onset of hormonal
changes, etc. The physical examination to draw attention to the clinical signs of disorders of the
endocrine glands (mass body build, hair growth, secondary sexual characteristics, the condition of the
skin, thyroid, etc.). The student must know the normal common blood and urine tests, blood glucose is
normal, to be able to interpret the results of studies of hormonal data.
Supervision is carried out in the presence of the teacher and supervision results are then evaluated and
analyzed in the group.
The student must keep a journal of practical classes, and writes some
moments theoretical section and the data about the patient.
100
5.Control forms of knowledge, skills and abilities
- Oral
- Written
- Testing
- Decision of situational problems;
- Demonstration of the developed skills
Monitoring the activity of the students in the discussion, analysis of case-patients and situational
problems, making tests for the diagnosis and differential diagnosis.
6.The evaluation criteria of the current control
№ Military
mustache
in points
Est. ENKA
Ka quality assessment
1. 86-100 Personally from
the "5"
Communicates about, think creatively, evaluates,
interprets.Applies knowledge in practice.Understands, knows,
says has no idea
2. 71-85
It is well "4"
Ra ssuzhdaet independently assess, interpret, apply knowledge
in practice, understands, knows, says has an idea
3. 55-70
Beats
Minimality know.Understand the essence, says
ovletvoritelno "3."
4
Not satisfactory, Pl oxo know.Not thoroughly.Require additional training.
"2"
0-54
7.Flow chart classes
1. Checking the initial level of preparedness of students to engage in "Diseases
endocrine glands occur with arterial hypertension. " Explanation
diagnosis and differential diagnosis of diseases involving
hypotension.
2. Decision analysis and situational problems.
3. Supervision of patients with diseases that are accompanied by hypotension.
Clinical analysis of supervised patients.
4. Interactive games to assess knowledge on training.
№
fl ups lessons
Prospect
odolzhitelnost
classes
7-hour ace
1 Judgment of courses offered
8.30-10.05
101
2 Ca autonomy of patients Supervision attached houses, self Curation case
patients, participation in rounds of professors and associate professors
10.10-11.05
3 Ra Zborov the department examined case patients with the interpretation
of the survey data and treatment
11.10-11.55
4 ne reryv
11.55-12.40
5 On judgment tests, situational problems.
12.40-14.40
6 Pr Overcome digestibility.Ad evaluations homework
14.40-15.10
8.Checklists.
1. The biological effect of gklyuko and mineralocorticoids.
2. The pathogenesis of the major clinical manifestations of the syndrome Simmonds-Sheehan.
3. Causes of hypotension and other clinical symptoms of chronic and acute
adrenocortical insufficiency.
4. Criteria for severity of chronic adrenal insufficiency.
5. Differential diagnosis of hypotension.
9.Suggested Reading.
Summary:
1.
Balabolkin MI Endocrinology. M., Medicine, 1998
2.
Vladimir Potemkin Endocrinology. M., Medicine, 1999
3.
Grandparents II Endocrinology. M., Medicine, 2000
4.
Melnichenko GA Tokmakova AY, deck DE, NV Lavrishcheva Endocrine
disease. M. Medicine, 2009
5.
Guidelines for Pediatric Endocrinology. Handbook of clinical Pediatric
Endocrinology. Edited by Charles G. Bouka, Rosalind S. Brown. 2009
6.
Shustov SB, Khalimov S, Trufanov GE Functional and topical
diagnostics in endocrinology. M. 2010
7.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 1. Greenspan's Basic &
Clinical Endocrinology. 2010
8.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 2. Greenspan's Basic &
Clinical Endocrinology. 2011
9.
Clinical Endocrinology. Ed. EA Kholodova. Minsk. Belarus.
2011
10. Melnichenko GA Udovichenko OV Shvedova AE Endocrinology.
Typical errors practitioner 2012
11. Endocrinology. National guidelines (+ CD-ROM). 2012
More:
1. Therapeutic Guide Washington, translated from English. (Section
102
"Endocrinology") 1996.
2. Laycock. Fundamentals of Endocrinology, Moscow 2000
3. Ty M. Mack - Dermott MD Secrets Endocrinology - Moscow 2000
4. Ketgayl VM, Arkin RA, Pathophysiology of endocrine system - Moscow, Medicine,
2001.
5. Balabolkin MI Diabetology - Moscow, Medicine, 2002
7. Fadeev PA. Endocrinology. Diabetes. A Reference Guide. 2009
8. Kartelishev Alexander Rumyantsev AG, Smirnova NS Actual problems of obesity
children and adolescents. 2010
9. Mkrtumyan AM, AA Nelaev. Emergency Endocrinology. 2010
10. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Diseases
thyroid. Williams Textbook of Endocrinology. 2010
11. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Bark disease
adrenal gland and endocrine hypertension. Williams Textbook of
Endocrinology, 11 th edition. 2010
12. AN hams Emergency Endocrinology. 2011
13. Petunina NA, AV Trukhina Thyroid disease. 2011
14. Manukhin IB Tumilovich LG, M. Gevorgyan Gynecological Endocrinology.
Lectures on gynecologic endocrinology. M. 2012
Journals:
15. Medical Journal of Uzbekistan, Tashkent.
16. "Problems of Endocrinology." Moscow.
17. "Therapeutic Archives", Moscow
18. "Clinical Medicine", Moscow
19. "Diabetes. Way of life ", Moscow
Internet sites:
1. "Internet Portal: Hunari»
2. Medscape.com
3. Alltheweb.com
4. Yahoo.com
5. E-medicine.com
6. www tma. uz
Ministry of Health Care of Uzbekistan
CENTRE FOR MEDICAL EDUCATION
TASHKENT MEDICAL ACADEMY
103
Department of Internal Medicine TRAINING GP endocrinologist
Subject: "Endocrinology"
Theme: "Dysplasia"
The causes of dysplasia.Diseases of the endocrine system, leading to high-and short
stature: pituitary dwarfism, Turner syndrome, chondrodystrophy, prepubescent teens
hypogonadism, late puberty, thyrogenic dwarfism, primordial dwarfism.Differential
diagnosis.Tactics GPs.
Educational and methodical development
(For teachers and students)
Tashkent - 2012
Process chart classes № 8
Dysplasia.The causes of dysplasia.Diseases of the endocrine system, leading to high-and short stature:
pituitary dwarfism, Turner syndrome, chondrodystrophy, prepubescent teens hypogonadism, late
puberty, thyrogenic dwarfism, primordial dwarfism.Differential diagnosis.Tactics GPs.
№
fl ups practice session
PMA classes fo
dl itvenue
Th
104
classes
270
min.
1 Centuries odnaya part (study subject)
10
2 Judgment about topics practice session with new educational op grew discussion
technologies
training room
("Gallery Tour"), as well as demonstration material (boards,
sets medical charts, tables, posters, hormonal and clinical tests,
X-rays, situational problems, stadiometer, scales, measuring
tape), the definition of the initial level.
3 You discuss water
50
4 The definition of reference for the practical part - n
rofessionalny questioning.Explanation of the provisions and
recommendations for the job to fill medical records.
25
of judgment
15
training room
5 Military wasps practical training under the guidance of a Prospect ofes sional
teacher.
questions, talk with patients
filling medical records, case
studies.
Department of
Endocrinology Clinic 1-TTA
6 John interpretation of the survey data of patients - complaints, tory studies of the disease,
inspection, palpation, percussion and auscultation of patients as laboratory data situational
well as laboratory and instrumental studies
problems
Department of
Endocrinology Clinic 1-TTA
7 Judgment on the theoretical and practical knowledge of the mustache tny survey, tests,
students, fixing material, the level of learning assessment.
discussion, identification of
practical skills
Department of
Endocrinology Clinic 1-TTA
8 The definition of output on practical training, evaluation of 100- infor mation, questions for
point system, and ad evaluations.Homework the next practice homework.
session (a collection of questions).
training room
30
35
80
25
Lesson number 8
Dysplasia.The causes of dysplasia.Diseases of the endocrine system, leading to high-and short stature:
pituitary dwarfism, Turner syndrome, chondrodystrophy, prepubescent teens hypogonadism, late
puberty, thyrogenic dwarfism, primordial dwarfism.Differential diagnosis.Tactics GPs.
uch ebnoe time: 7:00
Art ruktura training session 1. afedra to internal medicine training
GPs with an endocrinologist, endokrinologichessome branch 1 TTA clinic, clinical
1-clinic laboratory TTA;
2.set of tables, methodological recommendations
tion, laboratory and instrumental data,
105
video;
3.TCO: computer, video
Tse eh training session:
- Theacquisition of knowledge and skills in students GPs to diagnose
and differential diagnosis of diseases associated with impaired growth;
- Learn to use the modern classification of these diseases;
- To conduct early detection and disease prevention through individual
symptoms, syndromes.
Pe dagogicheskie tasks:
D results of training activities:
• consider the disease is GP
accompanied
should know:
Giver dysplasia;
• understand the causes of dysplasia.
• to consider the causes of • symptoms of diseases associated with
endocrine disorders,
dysplasia.
accompanied by dysplasia; • methods of diagnosis,
• Discuss the clinical associated with impaired growth.
symptoms
• Analyze data from laboratory tests and
diseases associated with
instrumental studies of diseases
dysplasia;
associated with impaired growth
• analyze the laboratory data • assign therapy in disorders of growth.
nye in these diseases,
should be able to:
• consider the differential • diagnose acromegaly and to
diagnosis of diseases which differential diagnosis akromegaloidare accompanied by
GOVERNMENTAL syndromes.
Giver dysplasia;
• diagnose gigantism.
• Discuss ways to treat • diagnose dwarfism and to the differential
diseases
cial diagnosed with short stature
tions involving violation
various origins (syndrome Shereshevskygrowth
Turner Chondrodystrophy, congenital
.
hypothyroidism, hereditary short stature)
• diagnose hypogonadism and to conduct
hormone replacement therapy
Depending on the clinical and pathogenic forms
must have skills:
• to assess the functional state of the pituitary gland.
• to assess the state of the secondary sex
signs.
• assess the skull radiographs.
• evaluate radiographs of the hand.
• calculate the projected growth in the final
children.
Me Toda training
le Ktsia, method "Tour Gallery", demonstration, entertainment
experience, discussion, conversation, case.
Fo rmy training activities of individuality work, group work, team, classroom, extracurricular.
Wed edstva training
Mr. zdatochnye viziualnye training and materials, videos, models,
graphic organizers, kits medical charts, tables, stands, kits radiographs.
Cn lady and means of bl uu-survey, testing, presentation of the results of the training task,
feedback
filling medical records, execution of practical skills "professional
questioning"
2.Motivation
106
Of endocrine diseases take a percentage of diseases associated with impaired growth. Determine the
causes of the pathogenesis of these conditions, knowledge of the clinical symptoms and diagnostic
criteria and methods of examination are necessary GP for timely diagnosis and further management of
patients.
Conducting this training allows the learner time and correctly diagnose diseases associated with
impaired growth, make a differential diagnosis, carry pathogenic therapy and prevention.
3.Intra and interdisciplinary communication
Teaching of the subject is based on the knowledge of the students major endocrine diseases, received
a 4th year in a cycle endocrinology, as well as therapy, which will continue to carry out differential
diagnosis of diseases associated with impaired growth. Acquired during the course knowledge will be
used during the passage of therapy at 6 and 7 of the course.
4.The content of the practical classes.
1. Checking the initial level of preparedness of students to engage in "diseases associated with
impaired growth." Explanation of the diagnosis and differential diagnosis of diseases associated with
impaired growth.
2. Decision analysis and situational problems.
3. Supervision of patients with diseases associated with impaired growth. Clinical analysis of
supervised patients.
4. Interactive games to assess knowledge on training.
A list of the issues:
1. Gigantism
a) The differential diagnosis with Klinefelter's syndrome, a hereditary tall.
2. Acromegaly
a) The differential diagnosis with akromegaloidnymi syndromes.
3. Hypogonadism (male)
a) Etiology
b) Clinical and pathogenic forms
c) Diagnosis
d) Hormone replacement therapy
d) Prediction, prevention.
4. Nanizm
a) The differential diagnosis with short stature of various origins (Turner's syndrome,
chondrodystrophy, congenital hypothyroidism, hereditary short stature, etc.)
4.1.The theoretical part.
Diseases accompanied by tall.
Gigantism - neuroendocrine syndrome that occurs as a result of excessive production and / or
increased biological activity of growth hormone (GH). Disease occurs in children and adolescents with
incomplete physiological growth. Characterized by exceeding the physiological limits, relatively
proportional increase of the epiphyseal and periosteal bone, soft tissue and organs. Abnormal growth
is greater than 200 cm for men and 190 cm for women. After ossification of the epiphyseal cartilage
gigantism usually goes to acromegaly.
Gigantism differentiated from other forms of tall - Klinefelter's syndrome and hereditary tall.
Klinefelter's syndrome - a form of chromosomal birth defects sexual development, deterministic at
fertilization. Usually only diagnosed in adolescence. Characterized by immaturity, moderate
hypogonadism and progressive with age hyalinosis seminiferous tubules with degeneration of
testicular germ cell elements. Sex chromatin positive, some patients have two or more cells Bara in a
single core. Karyotype-47, XXY, 46, XY/47, XXY; 48 XXXY in blood.
Gonads reduced in size, sealed the testicles, usually located in the scrotum. Gistologncheski hyalinosis seminiferous tubules of varying severity, degeneration or absence (in adults) of germ cells.
Internal genitalia of male type, prostate normal size or slightly reduced. External genitalia - male.
The penis of normal size or slightly behind in development. The scrotum is formed correctly. The
testicles are located in the scrotum, at least - in the inguinal canal, reduced in size. Secondary sexual
107
characteristics are not well developed, lean body hair, most female type. More than half of patients
have true gynecomastia. Patients with above-average growth. Differentiation of skeletal age
appropriate or slightly behind the age norm.
Acromegaly - a disease that is associated with increased secretion of growth hormone. It
occurs usually in people an out of physiological growth. Characterized by abnormal bone growth
disproportionately, soft tissue and internal organs, as well as breach of various types of metabolism.
Acromegaly is usually a consequence of eosinophilic or mixed, rarely chromophobe pituitary
adenoma, and the question of the etiology of the disease is associated with the problem of the etiology
of cancer. In acromegaly always a tumor, not hyperplasia adenohypophysis.
The pathogenesis of acromegaly is increased production of growth hormone pituitary adenoma.
Adults with epnfizarnymi ossified cartilage and finish the physiological growth of excess growth
hormone is exclusively periosteal bone growth to their thickening and disproportionate increase.
Simultaneously, there is an abnormal growth of cartilage, all soft tissues.
The disease occurs usually in middle age (30-50 years), more often in women and is very rare in
children. Clinical signs of the disease develop slowly.
Complaints of patients with acromegaly are diverse: general weakness, fatigue, headache, different in
nature and intensity. Occasionally headaches are very strong, resistant.
In some cases a single complaint of patients is to change the external appearance (increase the nose,
ears, hands, feet).
On examination, the patient attract attention coarsening. features, increase the hands and feet,
kyphoscoliosis, voice changes, hair and skin. Increase eyebrows, cheekbones and chin. Hypertrophy
of soft tissues, the skin thickens, the skin is oily. Increased language and interdental spaces, develops
prognathism. There is a growth of the skull bones, particularly facial. The men - is reduced potency,
libido and spermatogenesis and testicular atrophy in women - menstrual cycle until amenorrhea.
Differential diagnosis. Pachydermoperiostosis differentiate from acromegaly, severe hypothyroidism,
Paget's disease, disease Marie-Bamberger.
Paget's disease (deforming osteodystrophy) selectively thicken and become deformed proximal long
bones. For the disease characterized by a decrease of the facial skeleton, the formation of a "tower
skull." Dimensions sella not changed.
Pachydermoperiostosis is an inherited abnormality of the skin and bones, characterized by thickening
of the periosteum of the facial bones and limbs, enlargement of hands and feet. For the disease
characterized by the development of hyperostosis of long bones.
Marie-Bamberger syndrome is characterized by a system of large and small lesions of the long
bones. This disease is secondary, being a reaction to the bone flowing chronic disease.
Severe hypothyroidism is characterized by thick mucoid swelling, severe dry skin, slow speech and
movements. There has been increasing strain and facial bones, increasing the size of the sella.
Treatment. Therapeutic measures in acromegaly address the increased secretion of growth hormone
by the pituitary gland. This is achieved by surgical removal of the pituitary irradiation mezhutochnopituitary region, pituitary implantation of radioactive yttrium, gold, cryogenic fracture pituitary
stereotactic electrocoagulation high and drug therapy.
Hypogonadism or testicular failure, pathological condition, the clinical picture is caused by a
decline in the body androgen levels, and is characterized by underdeveloped genitals, secondary sex
characteristics and are usually infertile.
Clinical and pathogenic forms.
Primary hypogonadism:
I. congenital
1. - Anorhizm;
2. - Klinefelter's syndrome;
3. - XX male syndrome;
4. - Shereshevsky syndrome - Turner in men;
5. - Syndrome del Castillo (Sertoli cell syndrome);
6. - Syndrome of incomplete masculinization.
108
P. Acquired
1. - Infektsinno - inflammation of the testicles;
2. - Hypogonadism caused by exposure neblagopriyanyh external factors;
3. - Tumors of the testicles;
4. - Injury.
Secondary hypogonadism:
I - Congenital
1 Kallmena syndrome;
2 isolated LH deficiency;
3-pituitary dwarfism;
4 craniopharyngiomas;
5 Medloka syndromes.
II - Acquired
I-infection - inflammation of the hypothalamic-pituitary region;
2-hypophyseal syndrome;
3 tumors of the hypothalamic-pituitary region;
4-loss isotropic function as a result of traumatic or surgical injury of the hypothalamic-pituitary
region;
5 - Gilerprolaktinemichesky syndrome.
Primary hypogonadism accompanied by hypersecretion of gonadotropins and gipergonadotropnym
called hypogonadism. In secondary hypogonadism there is decreased secretion of gonadotropinreleasing hormone - is hypogonadotropic hypogonadism. Established forms of hypogonadism are
important for the doctor, as it affects the assignment of adequate treatment. Less common
normogonadotropny hypogonadism, this is characterized by low production of T at normal levels of
gonadotropins.
Postpubertal forms of hypogonadism are characterized by the disappearance of secondary sexual
characteristics in initially healthy adult men: decrease in body hair on the face and body, thinning hair,
testicular hypoplasia, and sexual dysfunction (decreased libido, fall and weak erection, changes in the
duration of intercourse, attenuation, sometimes and the disappearance of orgasm).
To detect abnormalities in the male phenotype of rigor needed in refining history. Malpresentation of
the fetus, prematurity. Pay attention to cryptorchidism. Malformation of external genitalia often
indicates a genetic pathology and requires not only clinical, but also the genetic examination of the
patient. However, some defects in the development of the external genitalia can be detected in men
without symptoms of testicular failure. For example, hypospadias is possible and in the absence of any
symptoms of testicular failure.
Hypogonadism may be accompanied by gynecomastia, which is found in other pathological
conditions not related to the pathology of the male sex glands, such as cirrhosis of the liver. The
defeat of the testicles may be associated with impaired sense of smell.
Diagnostics. Hypofunction testicles diagnosed besides anamnesis, based on X-ray examination, skull
and arm with wrist joint, determining sex chromatin and karyotype, morphological and chemical
analysis of ejaculate. And if necessary, testicular biopsy. Most useful in the direct determination of
plasma levels of gonadotropins (LH and FSH). testosterone (T), and, when indicated, prolactin (PRL).
Less informative indicators of urinary excretion of 17-ketosteroids (17-KS). The increasing use of
ultrasound scanning method finds the pelvic organs that would reveal the location of the testicles with
cryptorchidism, as well as their value.
The simplest and most affordable way to diagnose hypogonadism indirectly is to determine the socalled bone age by x-ray method. Androgens influence the structure of the bone tissue and cause the
sexual differentiation of the skeleton. At puberty, under the direct influence of androgens completes
the process of meta-epiphyseal ossification zones. Androgen deficiency, which for hypogonadism,
leads to inhibition of cartilage ossification and osteoporosis. Therefore, almost all of these patients the
changes in bones and joints. Since the bone age of the organism depends on the saturation of sex
hormones, the bone age directly reflects the degree of maturity of the body. There are several methods
109
for determining the radiological bone age, which take into account the maturity of the skeleton, the
degree of differentiation and synostosis. The most significant of these processes in the bones of the
wrist and hand. Bone age can accurately determine the onset of puberty corresponds to bone age 13.514 years and puberty activate gonad synostosis occurs in the metaphysis to the epiphysis of the first
metacarpal bone. Full sexual maturity is characterized by the disappearance of the X-ray crossstriation in long tubular bones of the forearm in place the closed epiphyseal lines. This will
immediately tell prepubescent biological age of puberty, as the appearance of sesamoid bones in the
first metacarpophalangeal joint (bone age corresponds to 13.5 years) in the absence of synostosis in the
first metacarpophalangeal joint of the preservation of evidence is an infantile state. The presence of
synostosis in the first metacarpophalangeal joint of evidence of active inclusion of the sex glands.
This should take into account the state of the other endocrine glands, also affect the differentiation of
the skeleton (adrenals, thyroid, etc.) Treatment. In congenital secondary hypogonadism treatment is
long-term administration of human chorionic gonadotropin or horiogonina on 1500-2000 IU twice a
week for a month courses at monthly intervals. With a sharp testicular hypoplasia, along with human
chorionic gonadotropin administered and male sex hormones (testenat 10% 2-3 times a month or
Sustanon-250 in 1 ml once a month for a year). In the future, perhaps only one treatment chorionic
gonadotropin.
Methods of implementation of the issues: traditional didactic form survey. Of new teaching
technologies appropriate to apply the methods: on the topic, case studies, interactive game "gallery
tour"
New educational technology: a method of "Tour Gallery»
To work needed:
1. A set of questions that have been printed on a separate sheet.
2. A set of case and diagnostic tasks, printed on separate sheets.
3. Blank sheets of paper
4. Pens with colored bars (blue, red, black, green)
5. Number plates for the draw, the number of students per class
6. Speedometer or clock.
Course of the business game:
1. A group of students is divided into 3-4 draw subgroups of 2-3 people in each
2. Each subgroup sits alone, takes a sheet of paper and on one of the colored pens.
3. on a sheet date, number of gaming title, name of student participants in this subgroup.
4. One of the players takes the envelope question or problem, depending on the choice of the teacher.
5. For each sub-question its departments or task, the complexity of their subgroups for all about the
same.
6. I time - 10 minutes.
7. Small groups (subgroups) each for 10 minutes to discuss the job write down its judgment, sharing
the sheets with another subgroup of the circle.
8. The next subgroup assesses previous answer and if the answer is not the full complement of his or
offer your own version. At this stage it will be given a time of 10 minutes.
9. At the end of processing (30 minutes or 40 minutes) depending on the number of sub-groups (3 or
4) on a piece of writing is 3.4 different color pens.
10. The works shall be the teacher
11. All participants will discuss the results and choose the most correct answers are worth points.
12. For discussion of play time of 15 minutes
13. Subgroup, which gave the most correct answers will receive the maximum score of 100% on the
rating of the theoretical part of the training.
Subgroup, 2nd place - 85, 9% rating. Subgroup, who took 3rd place - 70.9% rating
14. Students with scores recorded for billing ongoing evaluation sessions.
15. Student work sow teacher and elder group, and saved a teacher.
110
Appendix:
1. Complex test questions
2. Situational and complex diagnostic problems.
4.2.The analytical part of
Conducted analysis of a patient with a clinical case of a patient with short stature and vysokoroslostyu.
Proposed to solve situational problems for differential diagnosis of diseases associated with high and
low growth for the individual and pair solutions.
Problem number 1. In the Family Advice to Patient A., 16 years with complaints of lack of
menstruation and stunting of peers.
Anamnesis: a healthy child was born on the third pregnancy at term. Pregnancy and childbirth was
normal, without complications, the other children are healthy They note that little girl behind the
growth and development of their peers, which became particularly evident in the 14 - 15 years, the
nation's underdevelopment of the mammary glands, the absence of the characteristic body hair pubic
and axillary depressions, lack of menstruation.
Objectively: general condition is satisfactory, the figure is correct. Height 140 cm, weight 50 kg,
there is a rare pubic and body hair in the armpits, low position of the lower boundary of the hair
growth. Marked shortening of the neck, the skin fold triangular shape, extending from the head to the
shoulders. The chest is broad, the nipples separated by a considerable distance. In the mammary
glands of the subcutaneous adipose tissue is well developed.
Auscultation of the heart: a systolic murmur on the basis of the sternum. Examination of reproductive
organs: underdevelopment of small and large labia.
Talking girl inactive, questions answers in monosyllables, can not tell the meaning of proverbs.
1. Preliminary diagnosis.
2. Plan Survey.
Object number two. Boy 17 years old went to a doctor complaining of delay in sexual development,
breast enlargement, obesity.
Of history: the growth and development in early childhood was normal. Since 14 years, began to
celebrate breast enlargement, rapid increase in growth.
Inspection: height 185 cm, weight 7S kg. Not proportionally increase in mammary glands, body hair
on the female type, the lack of hair on the face, increasing the testicles. On palpation of the breast
marked presence of glandular tissue, palpation testicles enlarged sealed. When speaking to a high tone
voice notes
1. Preliminary diagnosis.
2. Survey
Task number 3. Patient 16 complained of slow development and low growth. From history: born a
normal child, birth weight 3500 g, height - 50 cm It developed according to the age of 4.5 years, when
suffered meningitis, then noted a slowdown in development.
OBJECTIVE: Build correct, proportional, 120 cm height, skin pale, and yellowish, dry. Subcutaneous
adipose tissue is poorly developed muscular system is not developed enough, the body hair in the
pubic and underarm meager. Auscultation: Cardiac clear, pulse rate 40 beats per minute, blood
pressure 90/60 mm Hg. Art. Urogenital: penis and testicles dimensions correspond to age 7-8 years.
Child in the school has good intelligence is not disrupted.
1. Preliminary diagnosis
2. Examination.
4.3 The practical part
Performed at the bedside. Supervision is carried out under the supervision of a teacher. The student
must learn to practice proper history taking in patients with impaired growth, while able to
differentiate primary and secondary information during the examination to focus on the figure, the
clinical signs of the thyroid and adrenal glands, secondary sexual characteristics.
When
communicating with the patient should consider the mental state such as shyness patients with growth
retardation, irritability, and while talking to exercise maximum tact and at the same time be confident
and firm.
111
In conducting activities in the clinic, while outpatient care, to teach students to quickly, clearly
questioning and examination of the patient, proper filling patient card.
Practical skills that require incremental development
1) Determination of the projected growth in children
2) Measure the growth of the child's mother
3) Measure the growth of the child's father
4) calculate the projected growth for the girls: mother + growth (growth father - 13 cm) / 2 10 cm, and
for the boy, his father + growth (growth of mother + 13 cm) / 2 +10
5.Control forms of knowledge, skills and abilities
- Oral
- Written
- Testing
- Decision of situational problems;
- Demonstration of the developed skills.
Monitoring the activity of the students are in the process of discussion, analysis of case-patients and
situational problems, making tests for the diagnosis and differential diagnosis.
6.The evaluation criteria of the current control
№ Military
Est. ENKA
Ka quality assessment
mustache
in points
1. 86-100 Personally from Communicates about, think creatively, evaluates,
the "5"
interprets.Applies knowledge in practice.Understands, knows,
says has no idea
2. 71-85 It is well "4"
Ra ssuzhdaet independently assess, interpret, apply knowledge
in practice, understands, knows, says has an idea
3. 55-70
Beats
Minimality know.Understand the essence, says
ovletvoritelno "3."
4 0-54
Not satisfactory, Pl oxo know.Not thoroughly.Require additional training.
"2"
7.Flow chart classes
1. Checking the initial level of preparedness of students to engage in "Diseases of the endocrine
glands occur with arterial hypertension." Explanation of the diagnosis and differential diagnosis
associated with impaired growth.
2. Decision analysis and situational problems.
3. Supervision of patients with diseases associated with impaired growth.
Clinical analysis of supervised patients.
4. Interactive games to assess knowledge on training.
№
fl ups lessons
Prospect
odolzhitelnost
classes
7-hour ace
1 Judgment of courses offered
8.30-10.05
2 Ca autonomy of patients Supervision attached houses, self Curation case
10.10-11.05
patients, participation in rounds of professors and associate professors
3 Ra Zborov the department examined case patients with the interpretation
11.10-11.55
of the survey data and treatment
4 ne reryv
11.55-12.40
5 On judgment tests, situational problems.
12.40-14.40
6 Pr Overcome digestibility.Ad evaluations homework
14.40-15.10
112
8.Checklists.
1. The distinguishing features of gigantism from family Tall
2. At what age is celebrated intense stretch of growth?
3. How is the projected final height?
4. Indications for hypophysectomy
5. What is different from gigantism, acromegaly?
6. Conservative treatment of gigantism
7. Treatment nanizma
8. Methods of treatment of acromegaly
9. Diagnosis nanizma
10. Differential diagnosis of short stature and constitutional nanizma
9.Suggested Reading.
Summary:
1.
2.
3.
4.
Balabolkin MI Endocrinology. M., Medicine, 1998
Vladimir Potemkin Endocrinology. M., Medicine, 1999
Grandparents II Endocrinology. M., Medicine, 2000
Melnichenko GA Tokmakova AY, deck DE, NV Lavrishcheva Endocrine
disease. M. Medicine, 2009
5.
Guidelines for Pediatric Endocrinology. Handbook of clinical Pediatric
Endocrinology. Edited by Charles G. Bouka, Rosalind S. Brown. 2009
6.
Shustov SB, Khalimov S, Trufanov GE Functional and topical
diagnostics in endocrinology. M. 2010
7.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 1. Greenspan's Basic &
Clinical Endocrinology. 2010
8.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 2. Greenspan's Basic &
Clinical Endocrinology. 2011
9.
Clinical Endocrinology. Ed. EA Kholodova. Minsk. Belarus.
2011.
10. Melnichenko GA Udovichenko OV Shvedova AE Endocrinology.
Typical errors practitioner 2012
11. Endocrinology. National guidelines (+ CD-ROM). 2012
More:
1. Therapeutic Guide Washington, translated from English. (Section
"Endocrinology") 1996.
2. Laycock. Fundamentals of Endocrinology, Moscow 2000
3. Ty M. Mack - Dermott MD Secrets Endocrinology - Moscow 2000
4. Ketgayl VM, Arkin RA, Pathophysiology of endocrine system - Moscow, Medicine,
2001.
5. Balabolkin MI Diabetology - Moscow, Medicine, 2002
7. Fadeev PA. Endocrinology. Diabetes. A Reference Guide. 2009
8. Kartelishev Alexander Rumyantsev AG, Smirnova NS Actual problems of obesity
children and adolescents. 2010
9. Mkrtumyan AM, AA Nelaev. Emergency Endocrinology. 2010
10. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Diseases
thyroid. Williams Textbook of Endocrinology. 2010
11. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Bark disease
adrenal gland and endocrine hypertension. Williams Textbook of
Endocrinology, 11 th edition. 2010
12. AN hams Emergency Endocrinology. 2011
113
13. Petunina NA, AV Trukhina Thyroid disease. 2011
14. Manukhin IB Tumilovich LG, M. Gevorgyan Gynecological Endocrinology.
Lectures on gynecologic endocrinology. M. 2012
Journals:
15. Medical Journal of Uzbekistan, Tashkent.
16. "Problems of Endocrinology." Moscow.
17. "Therapeutic Archives", Moscow
18. "Clinical Medicine", Moscow
19. "Diabetes. Way of life ", Moscow
Internet sites:
1. "Internet Portal: Hunari»
2. Medscape.com
3. Alltheweb.com
4. Yahoo.com
5. E-medicine.com
6. www tma. uz
Ministry of Health Care of Uzbekistan
CENTRE FOR MEDICAL EDUCATION
TASHKENT MEDICAL ACADEMY
114
Department of Internal Medicine TRAINING GP endocrinologist
Subject: "Endocrinology"
Topic: "Thedisturbance of consciousness"
Coma in endocrinology: Hypoglycemic coma.Hyperglycaemic coma (ketoatsidotic,
hyperosmolar, laktatatsidemic).Thyrotoxic and addisonic crises.Reasons.Differential
diagnosis.Tactics GPs.
Educational and methodical development
(For teachers and students)
Tashkent - 2012
Process chart classes № 9
115
Coma in endocrinology: Hypoglycemic coma.Hyperglycaemic coma (ketoatsidoticheskaya,
hyperosmolar, laktatatsidemicheskaya).Thyrotoxic and addisonicheskie
crises.Reasons.Differential diagnosis.Tactics GPs.
№
fl ups practice session
PMA classes fo
venue
dl itTh
classes
270
min.
1 Centuries odnaya part (study subject)
10
2 Judgment about topics practice session with new op grew discussion
educational technologies
training room
("Round Table", "weak link"), as well as demonstration
material (boards, sets medical charts, tables, posters,
hormonal and clinical tests, radiographs, case studies), the
definition of the initial level.
3 You discuss water
50
4 The definition of reference for the practical part - n
of judgment
rofessionalny questioning.Explanation of the provisions and
training room
recommendations for the job to fill medical records.
25
5 Military wasps practical training under the guidance of a Prospect ofessionalny
teacher.
questioning, conversation with
patients filling medical records,
case studies.
Department of Endocrinology
Clinic 1-TTA
6 John interpretation of the survey data of patients - tory studies of the disease,
complaints, inspection, palpation, percussion and laboratory data situational
auscultation of patients as well as laboratory and problems
instrumental studies
Department of Endocrinology
Clinic 1-TTA
7 Judgment on the theoretical and practical knowledge of the mustache tny survey, tests,
students, fixing material, the level of learning assessment. discussion, identification of
practical skills
Department of Endocrinology
Clinic 1-TTA
8 The definition of output on practical training, evaluation of infor mation, questions for
100-point system, and ad evaluations.Homework the next homework.
practice session (a collection of questions).
training room
30
Lesson № 9
116
15
35
80
25
Coma in endocrinology: Hypoglycemic coma.Hyperglycaemic coma (ketoatsidoticheskaya,
hyperosmolar, laktatatsidemicheskaya).Thyrotoxic and addisonicheskie
crises.Reasons.Differential diagnosis.Tactics GPs.
1.
uch ebnoe time: 7:00
Art
ruktura
training 1. afedra to internal medicine training
GPs with an endocrinologist, endokrinologichessession
some branch 1 TTA clinic, clinical
1-clinic laboratory TTA;
2.set of tables, methodological recommendations
tion, laboratory and instrumental data,
video;
3.TCO: computer, video
Tse eh training session:
- Theacquisition of knowledge and skills in students GPs to diagnose
and differential diagnosis of diseases associated with comatose
states;
- Learn to use the modern classification of these diseases;
- To conduct early detection and disease prevention through individual
symptoms, syndromes.
Pe dagogicheskie tasks:
D results of training activities:
• consider the disease is GP
accompanied
should know:
Giver
impairment
of
• understand the causes of disorders of consciousness;
consciousness;
• symptoms of diseases associated with
• to consider the causes of
impairment of consciousness;
diseases associated with
• methods of diagnosis,
impairment
of
associated with impaired consciousness;
consciousness;
• Discuss
symptoms
the
clinical • Analyze data from laboratory tests and
instrumental studies of diseases
com and crises;
associated with impaired consciousness;
• consider the severity and • Be aware of rapid diagnosis, analyze data
com
nye laboratory and instrumental
crises;
GOVERNMENTAL research;
• analyze the laboratory data
• appoint an emergency therapy for komah and
nye in coma
crises.
• consider the differential
should be able to:
diagnosis of diseases which
• diagnose hypoglycemic coma.
are accompanied by
Giver
impairment
of • diagnose ketoatsidoticheskuyu coma.
consciousness;
• diagnose thyrotoxic crisis.
117
• discuss
diagnosis
methods
of • diagnose addisonichesky crisis.
must have skills:
states of emergency and • determine acetone in urine express method.
urgent
• determine blood glucose express method.
help.
• provide emergency care to patients with
• Discuss ways to treat
impairment of consciousness.
diseases
tions involving violation
consciousness
Me Toda training
le Ktsia, the method of "round table", "weak link", exhibition,
entertainment experience, discussion, conversation, case.
Fo rmy training activities of individuality work, group work, team, classroom, extracurricular.
Wed edstva training
Mr. zdatochnye viziualnye training and materials, videos, models,
graphic organizers, kits medical charts, tables, stands, kits radiographs.
Cn lady and means of bl uu-survey, testing, presentation of the results of the training task,
filling medical records, execution of practical skills "professional
feedback
questioning"
2.Motivation
Conducting this training allows the learner time and correctly diagnose and to provide emergency
assistance in cases involving violation of consciousness
3.Intra and interdisciplinary communication
Teaching of the subject is based on the knowledge of the students major endocrine diseases, received
a 4th year in a cycle endocrinology, as well as therapy, which will continue to carry out differential
diagnosis of diseases associated with impaired consciousness. Acquired during the course knowledge
will be used during the passage of therapy at 6 and 7 of the course.
4.Contents classes
4.1 The theoretical part
Coma in diabetes. Diabetes mellitus (DM) is a chronic disease. In certain cases, a sharp increase or
decrease in plasma glucose, the increase or decrease of ketone bodies or lactic acid can endanger the
patient's life. These acute complications of diabetes require special attention, because without
immediate and accurate diagnosis and treatment are rapidly fatal outcome.
Hypoglycemic coma. Most common serious complication of diabetes therapy is hypoglycemia. It
develops when excessive doses of insulin administration in relation to the entry of glucose from
endogenous or exogenous (food) sources.
Hypoglycemia of rapid-acting insulin occurs within 3 hours after the administration of drugs
poluprodlennyh - 5-7 hours, from a long-acting - at night and in the early morning hours. Heavy
118
prolonged hypoglycemia occur when using Manin, chlorpropamide, diabeneza. Physical activity has a
hypoglycemic effect in 1 hour.
Hypoglycemia - a clinical syndrome characterized by signs of activation of the sympathetic nervous
system and / or dysfunction of the central nervous system, which are caused by abnormally low levels
of blood glucose and plasma. Hypoglycemia as a laboratory phenomenon (reduced plasma glucose
concentrations below 2.2 - 2.8 mmol / L) is not identical to the concept of hypoglycemic symptoms, as
laboratory data and clinical symptoms are not always identical.
On the other hand, in patients with diabetes, who for many years are in a constant state of
hyperglycemia, hypoglycemic symptoms may occur even at the level of glucose 6.8 mmol / l.
Etiology. In DM, there are many reasons and prerequisites for the development of hypoglycaemia.
Thus a key cause of hypoglycemia in diabetes
Not eating enough
High physical activity
For example, an insufficient number of Xe on the dose of insulin with
a reference blood glucose.
An overdose of insulin or While maintaining the same dose of insulin or TSP
TSP
For example, receiving a constant dose of glibenclamide, despite a
decrease in body weight.
Autonomic neuropathy
Acceleration of resorption Normally, emergency adaptation to hypoglycemia
of insulin.
Provided by the parasympathetic stimulation PZHZH (glucagon is
released) and sympathetic activation of the adrenal medulla
Cumulation TSP
(adrenaline).In addition, the neuropathy
Alcohol
suffers stomach innervation to the development of gastroparesis and
Development
of impaired evacuation write.
associated
For example, intramuscular, subcutaneous instead of insulin.
endocrinopathies
For example, with the progression of renal failure.
Suppression of gluconeogenesis
Hypothyroidism, adrenal insufficiency
The clinical picture. Hypoglycemic symptoms are highly variable on a set of symptoms as well as
their severity. By severity emit light and severe hypoglycaemia. Mild hypoglycemia believe that the
patient, regardless of the severity or duration of subjective symptoms, suppresses self-administration of
carbohydrate. Severe hypoglycemia is accompanied by loss of consciousness, and its treatment
requires intravenous glucose.
In other words, in addition to the severity and duration of hypoglycaemia, is important
Individualized response to her patients. Progressive hypoglycemia leads to hypoglycemic coma.
Classically, two groups of symptoms: adrenergic resulting
Compensatory activation of the autonomic nervous system, and neyroglikopenicheskie that result
from dysfunction of the CNS in insufficient intake of its main
Substrate
Symptoms: anxiety, agitation, palpitations, sweating, trembling, hunger, angina, headache, fatigue,
inability to concentrate, inappropriate behavior, hallucinations, seizures, impaired consciousness,
transient visual disturbances.
119
If hypoglycemia begins during sleep, its symptoms include nightmares, sweating and headache in the
morning waking. Special studies have shown that asymptomatic nocturnal hypoglycemia with plasma
glucose levels below 3.5 mmol / L may be found in almost 30-40% of patients treated with insulin.
Seizures may be local and generalized, the elderly may be a hemiplegia and aphasia, which creates the
impression of acute cerebrovascular accidents. Repeated prolonged hypoglycemia lead to lower
intelligence.
For typical episodic hypoglycemia, the duration of her few minutes or hours. Short duration due to
the fact that the level of glucose can be restored to normal and above because of the "trigger"
mechanism kontrregulyatornyh: eating quickly cease the attack, or the violation occurs consciousness
and coma.
If symptoms similar to hypoglycemia last for days, weeks or months - it's not hypoglycemia.
Treatment. For the treatment of mild hypoglycemia in which the patient is conscious and can itself
provide help themselves, usually enough to write containing carbohydrates in the amount of 1-2 BU
(10-20 g of glucose).
If symptoms continue to grow despite the ongoing carbohydrate, intravenous glucose should or
intramuscular - glucagon. Similarly treated and severe hypoglycemia occurring with loss of
consciousness.
Le chenie severe hypoglycemia
40% solution Centuries odyat 50 ml of 40% solution intravenously.Administration of glucose
of
glucose should continue until treat an attack, and more generally is not required.Wrong to
astvor
draw conclusions about the absence of hypoglycemia, if there was no improvement
after the administration of only 10 ml.
glucagon
Injected 10 mL intramuscularly or subcutaneously.After a few minutes due to
induction of glucagon, glucose glycogenolysis normal.However, this does not
always happen.
Diabetic hyperglycemic, ketoatsidoticheskaya coma. Diabetic ketoacidosis (DKA) in the past was
the main cause of death in patients with diabetes, is now due to DKA mortality of 5-15%.
Thus a key cause of ketoacidosis
Prospect Ichin
For diseases and conditions
You fall in insulin Ma nifestatsiya DM1, DM2 insulinpotrebny (krayredko).
secretion - cells Lack of insulin, the introduction of expired or improperly stored insulin
PZHZH
cessation insulin with suicidal intent.
Errors in insulin
Urinary tract infections, osteomyelitis, dermatitis, pneumonia, diabetic foot
Infections
syndrome, infected necrosis angiopathy
Myocardial
infarction, stroke
Pregnancy
10-25% in 10 patients with diabetes - heart attacks painless.Stroke can be
both a cause and a consequence of ketotsidoza exhibit significant increase
in the need for insulin and nnsulinorezistentnost.
The state of stress
Shock, sepsis, trauma, surgery
120
Etiology. Ketoacidosis - typical complications of DM-1. With a relative lack of insulin in the
background of insulin resistance, ie, in DM-2 with even minimal preservation of insulin secretion, for
decompensated metabolic ketoacidosis is not typical. Thus, the cause of diabetic ketoacidosis is an
absolute deficiency of insulin. DKA is associated with a pronounced insulin deficiency due to lack of
insulin administration or termination of its administration, a violation of the diet, addition of stress,
acute inflammatory diseases. A sharp increase in insulin deficiency leads to increased hyperglycemia,
glycosuria, polyuria, leading to dehydration. Enhanced with the development giperketonemii
ketogenesis and ketonuria. Acid-base balance shifts to the acidosis. Coma is a result of dehydration of
brain cells, acidosis, hyperventilation, hypoperfusion and failure mechanisms of intracellular energy
supplies. Actually coma precede symptoms such as nausea, vomiting, weakness, dizziness.
Clinical symptoms of DKA occur due to poisoning of the body ketone bodies, dehydration, acidosis.
This coma usually develops gradually over 1-3 days.
In the development of coma
gnperketonemicheskoy distinguish 3 stages: precoma starting coma, deep (full) coma. Clinical signs
prekomatoznoe states are increased symptoms of diabetes: thirst, polyuria, and loss of appetite,
lethargy, drowsiness, nausea with repeated vomiting, can be a pain in the abdomen 6ez precise locality,
and signs of irritation of the peritoneum. In exhaled air and vomit smells of acetone. Consciousness is
preserved. Hyperglycemia than 16.6 mmol / L, giperketonemiya (over 10 mg%), acetonuria,
glucosuria.
When starting a coma increases dehydration, which manifests dry skin and mucous membranes,
hypotension eyeballs and muscles, sharp-featured face, flushing of the skin, oliguria, tachycardia,
hypotension. Drowsiness, stupor, deep, noisy breathing Kussmaul. Glycemia usually over 22.2 mmol
/ L, blood clots, neutrophilic leukocytosis, high hemoglobin. In urine, proteinuria, cylindruria. Then
comes complete coma. Patients are in a state of hypovolemic shock with a pronounced acidosis in
unconsciousness state. Blood pH 73-7,1.
Diagnostic criteria: pronounced glycosuria, acetonuria, hyperglycemia, blood pH below 7.3 P C0 2 40
mm Hg. or lower. Laboratory diagnosis of hyperglycemia, glycosuria, giperketonemiya, acetonuria,
acidosis, increase in serum creatinine, neutrophilic leukocytosis.
In the differential diagnosis should include all types of metabolic acidosis and coma.
Alcoholic ketoacidosis can occur in alcoholic patients with malnutrition, with frequent bouts of
vomiting. In moderately severe blood giperketonemiya and acidosis, the positive reaction of urine for
acetone. Blood glucose levels below 11.1 mmol / L, 30% of the apparent hypoglycemia, glycosuria
not.
When uremic acidosis, or acidosis, developing a case of poisoning acidosis without ketosis.
DFA is very different from hypoglycemic coma. DKA develops gradually and is accompanied by
symptoms of acidosis, dehydration. Hypoglycemic coma develops rather quickly, there are no signs of
dehydration and acidosis. If in doubt, even before the results of laboratory tests can be introduced 25 g
of glucose. When hypoglycemic coma after glucose condition improves.
When hyperosmolar coma there is a pronounced dehydration, hypovolemic shock, very high
hyperglycemia, but no acidosis and ketonuria.
When there is a sharp lactic acidosis metabolic acidosis in the absence of ketosis.
Patients are able to DFA urgently need treatment. Therapeutic measures aimed at ensuring adequate
amounts of insulin to normalize the day to day exchange, restoration of water and electrolyte loss,
correction of acidosis and identify the causes which led to the development of the ECU to increase
sensitivity to the treatment measures and avoid a recurrence.
Tactics GPs prehospital:
121
a) diagnosis of ketoacidosis (by clinical signs, medical history, testing, special test strips blood sugar
levels, the presence of sugar and acetone in the urine), take a blood sample from a vein to determine
the Express Lab RN, AAR, urea, creatinine, coagulation blood levels of potassium, sodium.
b) Identification of the causes of decompensation and ketoacidosis;
c) The detection of early signs of stage 1 patients received ketoacidosis:
- Excessive drinking (mineral alkaline water, fresh fruit and vegetable juices, green tea, juice from
fresh or dried fruit)
- Daily dose of long-acting insulin is not changed; it is entered as usual;
- Jokes short-acting insulin every 2-3 hours in the glycemic control (for example: when blood sugar
6.9 mmol / l - 1 cm, 9.12 mmol / l - 2 points, 12-15 mmol / l - 4 units, more mmol/l-8 15 units.)
- Every 2-3 hours determine blood sugar (using a glucometer and test strips);
- Diet, which prevents animal fats;
d) in the diagnosis of 2, 3 stages and developed coma - urgent hospitalization in the intensive care unit.
All patients with DKA should only fast insulin. Initially, insulin is administered intravenously IOEDb, then 6ED / h intravenous infusion (or / m) while plasma glucose drops to 13.6 mmol / l. Children
can be introduced in Part O.1ED/kg
Every 2 hours to determine the level of glucose in the blood, and shall adjust the insulin dose
depending on the degree of reduction of glucose. General lack of fluid in patients with DKA is
approximately 4.8 liters. To fill this gap to isotonicity (or poluizotonicheskim) saline (sodium chloride
solution "Disol", "Atsesol.) For 1h, enter 1 liter, and then introduce it at a rate of 300-500 ml / h
volume of fluid administration depends on the degree of dehydration and the cardiovascular system,
especially in elderly patients, and is usually 3-6 liters.
After reaching the glucose 13.5 mmol / L saline infusion should be replaced by infusion of 5%
glucose solution, which prevents hypoglycemia and cerebral edema.
With moderate acidosis pH 7.3 - 7.2, no additional administration of sodium bicarbonate, because it is
a rapid increase in the pH of arterial blood, which can cause excessive decrease in the pH of
cerebrospinal fluid and a concomitant deterioration of the central nervous system. enter only patients
with severe metabolic acidosis with a pH below 7.1 and PCO 2 level of less than 5 mEq / l. In such
cases, the first liter of hypotonic saline (0.45%)
3 hours after the infusion of insulin to prevent hypokalemia, add potassium chloride (if the patient is
not anuria) at a dose of 40 mEq / L, total lead 120-160 mEq of potassium in the first 12-18 hours of
treatment,
Few patients (less than 5%) from the beginning there is hypokalemia, potassium (40-60 mEq / L KCI)
is added to the first portions of the injected fluid. Monitoring the ECG may help to identify hypo-or
hyperkalemia, but should not replace frequent measurements of the concentration of potassium in the
serum to determine the need for potassium and rate of administration.
Hyperosmolar coma without ketoacidosis usually occurs in patients of middle and old age with
nnsulinzavisimym type of diabetes, but more often with non-insulin dependent diabetes. Characterized
by a pronounced hyperglycemia 33.3 - 66.6 mmol, hyperosmolarity blood to 350 mOsm / L (normal
315-320 mOsm / L) and dehydration in the absence of ketoacidosis.
Mining can be a cause of long-term treatment with glucocorticoids or diuretics, vomiting, diarrhea.
Polydipsia and polyuria symptoms usually develop within a few days (7-10 days) growing, they cause
a disturbance of consciousness. Retardation ranging from drowsiness to coma. Unlike DFA mine
accompanied by neurological and meningeal symptoms, hemiparesis, dysphagia, local and generalized
122
convulsions, hyperthermia, nystagmus, psychomotor agitation sometimes. Breathing deeply in these
patients, but without the smell of acetone, the skin becomes parchment, tachycardia, arrhythmia often
type beats, and blood pressure decreases up to vascular collapse.
Increased blood viscosity, leukocytosis, hematocrit, blood pH changes and alkaline reserve. Sugar in
the blood is very high above 33.3 mmol / L increased the residual nitrogen in the blood. Changes in
the level of electrolytes in the blood: hypokalemia, hypernatremia, hyperchloremia, hypercoagulability
of blood.
Sodium levels in serum may be elevated, normal or even reduced. This is due to the redistribution of
body fluids due to hyperglycemia yield of water from within the extracellular space. For every (5.5
mmol / L) increase in the level of glucose in serum is reduced by 1.6 m) q / l. Therefore, in patients
with severe hyperglycemia, normal and high sodium content. When hyperosmolar coma: higher
hyperglycemia, normal ketonemiya, no smell of acetone in breath, no acetone in the urine. Mortality
from mine is about 50%.
Laboratory diagnosis of hyperglycemia high, hyperosmolar 310 mol / L, hypo-, normo-, hypernatremia,
hypokalemia, giperkaogulyatsiya blood, azotemia, blood pH 7.3-7.4; acetonuria no glycosuria high.
Tactics GPs prehospital:
a) Diagnosis of mine (clinical symptoms, testing blood glucose and glycosuria), take a blood sample
from a vein to determine in the laboratory Express-osmolarity, blood coagulation system, the levels of
potassium, sodium
b) Identification of the causes;
c) The urgent hospitalization in a specialized intensive care unit.
Treatment of mine is continuous drip intravenous short-acting insulin, 6-10 U-corrected dose every 2
hours, depending on the degree of reduction of glucose levels. Polyglukin, reopoliglyukin / O, to
prevent blood clots - anticoagulants of direct action, as well as heart medications. IV fluids should be
in the amount of 6-10 l.
Basically it is a hypotonic solution of sodium 0.45%. It is obligatory to filling potassium resources of
the body.
Laktatatsidemic coma. Occurs when the type 1 and type 2 diabetes in combination with DFA in 10%
of patients, in conjunction with the mine - at 40-60%, as a complication of treatment phenformin, in
the presence of significant renal failure, cardiogenic, septic, hypovolemic shock, as well
as spontaneous exchange.
Laktatsidemicheskaya coma develops in patients taking drugs biguanides: phenformin, rarely adebit.
Believe that metilbiguanidy not cause lacticemia.
LAC develops gradually. At the beginning of the patient usually disturb weakness, vomiting, weight,
pain, and muscle cramps: pain in the heart, stomach then nausea, motor and mental excitement,
delirium, decreased body temperature, dehydration develops. Reduced blood pressure, heart rhythm is
disturbed, there comes a transition to oliguria anuria. Kussmaul breathing type, no smell of acetone.
Blood glucose levels are relatively low, small glucosuria. Acetone in the urine, no. Reduction of
reserve alkalinity and reducing blood pH below 7.2. Giperketonemii not. Lactate levels are high (up
to 10 mg% or higher). Ratio lactate / pyruvate ratio is high (in the norm of 12:1). Azotemia is present
in patients with kidney disease.
Treatment is aimed at combating acidosis, lactic acid excretion, rehydration patient.
Enter the 2-4 liters of alkaline solutions consisting of isotonic sodium chloride solution, 4% sodium
bicarbonate, 5% glucose solution at a ratio of 1:1:2 or solution "Trisol." They added 100 mg
cocarboxylase. Introduced simple insulin in small doses of 6-10 units of s / c every 3-4 hours. To
123
neutralize the lactic acid is introduced into / drip 50-100 ml% methylene blue. Inhalation of oxygen,
cardiovascular agents. Hemodialysis.
Tactics GPs prehospital:
a) Diagnosis giperlaktatsidemicheskoy coma
b) Determination of glycemia and glycosuria special test strip, take a blood sample from a vein for the
determination of rapid laboratory pH, AAR, lactic acid.
c) Identification of the causes
d) Removal of biguanide, giving oxygen, low blood pressure - hydrocortisone (40 - 100 mg) and
urgent hospitalization in a specialized intensive care unit.
Thyrotoxic crisis. Graves' Disease, especially its severe form, in some cases, and the average severity
of thyrotoxic crisis may worsen. It is more common in females and is developed mainly in the
summer season. For its formation requires the following two conditions:
a) Undiagnosed or inadequately treated hyperthyroidism;
b) precipitating factors: mental trauma, rough palpation of the thyroid, toxemia of pregnancy, abrupt
withdrawal of antithyroid drug therapy, response to medication (insulin, glycosides, salicylates,
clofibrate), radioactive iodine therapy, any small or major surgery (extraction of a tooth, a laparotomy ,
appendectomy and TA)
Pathogenesis. Sharp intakes of thyroid hormones from the thyroid gland into the blood enhances
catabolic processes (protein, fat, carbohydrate) and accelerate the oxidation processes within the cell
that has a direct toxic effect on the heart muscle.
Clinic thyrotoxic crisis is accompanied by a dysfunction of the central nervous system, cardiovascular,
gastrointestinal, hypothalamic-pituitary-adrenal system, liver and kidneys. Symptoms: mental and
restlessness; possible drowsiness (rarely), disorientation, high fever (above 38 degrees), asthma, heart
pain, tachycardia of 200 beats I5O in I min is possible paroxysmal atrial fibrillation, arrhythmias,
congestive heart failure , systolic and diastolic blood pressure or reduction of both, abdominal pain,
diarrhea, nausea and sometimes jaundice and hepatomegaly.
Treatment:
a) Drugs that block the biosynthesis of thyroid hormones;
b) Drugs that reduce sensitivity to catecholamines;
c) Inhibitor activity kallikreininovoy system;
d) Glucocorticoids;
e) Antipyretics;
c) Cardiac glycosides, diuretics, oxygen
Tactics GPs prehospital:
a) Diagnosis of thyrotoxic crisis;
b) Identification of the causes of a crisis;
a) Giving oxygen, wrap a wet cold sheets in the presence of hypotension, kordiamin, mezaton (1-2 ml
/ m), and if necessary (collapse) - hydrocortisone (40-100 mg / in) and urgent hospitalization in a
specialized intensive care department.
Acute adrenocortical insufficiency. Are 2 of its kind: a primary syndrome (Waterhouse-Friderichsen)
and addisonichesky crisis.
124
Conditions for the development of a coma:
1. Primary
a) Absence of chronic adrenal insufficiency
b) Bleeding in the adrenal cortex and its central vein thrombosis
2. Addisonic crisis
a) The presence of chronic adrenal insufficiency
b) Stress (triggers) factors.
The reasons:
a) Bleeding in the adrenal cortex: infection (influenza, measles, scarlet fever, diphtheria, dysentery,
etc.), or staphylococcal meningococcal sepsis, bleeding diathesis, DIC, hemophilia, severe,
complicated delivery, surgical removal of the adrenal gland,
b) Central venous thrombosis of the adrenal glands, SLE, periarthritis nodosa
c) Adrenal injury: physical injury, especially in various accidents, extensive surgery on the abdominal
and retroperitoneal
d) Stress (triggers) factors: heavy physical exertion, mental (acute, chronic) injury
Pathogenesis. Sharp deficit gluco - and mineralocorticoid reduces glycogen stores in the liver,
decreased ability to maintain normal blood glucose levels, slowing the formation of glycogen from
carbohydrates and fats. Also disrupted by phosphorylation, water and mineral metabolism (loss of
chlorine and sodium, potassium delay) changes the ionic balance, the content of nitrogenous wastes,
ketone bodies in the blood, disturbed osmotic intra-and extracellular pressure.
Clinic. Conditionally are the following clinical types of acute adrenal insufficiency:
- Cardiovascular (hypotension prevails until the zero digits, collapse)
- Gastrointestinal (nausea, vomiting, anorexia, diarrhea, abdominal pain, simulating acute abdominal
disease);
- Neuro-psychological (irritability, delirium with visual hallucinations or fatigue, weakness,
depression);
- Mixed.
Treatment. Replacement therapy with corticosteroids, anti-dehydration, correction of electrolyte
abnormalities, restoring glucose, stimulation of high blood pressure, eliminating the causative factor.
Tactics GPs prehospital
a) Diagnosis on clinical grounds syndrome Waterhouse - Friderichsen or addisonicheskogo crises in
patients with chronic adrenal insufficiency;
b) Identification of the causes;
c) investigate the glycemic acetonuria special test strips, take blood from a vein for the determination
of rapid laboratory levels of potassium, sodium, chloride and nitrogen impurities, pH, AAR;
c) Enter in / hydrocortisone 40-100 mg and lying to hospital patients in the intensive care unit.
New educational technology: a method of "round table", "weak link"
method of the "Round Table"
To work needed:
1.
2.
3.
A set of questions and situational problems that have been printed on a separate sheet
Number plates for the draw in the number of students per class
Blank sheets of paper, pens
Progress:
1. All residents of a toss divided into 3 groups of 4 students each.
2. Each subgroup sits at a separate table, prepare a blank sheet of paper and a pen.
3. Written on a sheet date, FI residents of the sub-group (the name of the business game).
4. One of the participants in each group takes the question out of the envelope. The level of
complexity of tasks for all subgroups is about the same.
5. Students rewrite their job on a sheet.
6. Embarks on a circle that sheet.
7. Each student writes down the answer sheet and sends another.
125
8. The response of each student is given 3 minutes.
9. after the time of the surrender teacher.
10. All participants will discuss results, choose the most correct answers are put maximum Bayaly.
11. for discussion to 15 minutes.
12. Students receive a score from the ranking answers the theoretical part of the training.
13. Students with scores counted in the scoring taken.
14. In the lower part of the magazine is a free stamp on the game with the signature of elders.
15. Student work saved teacher.
Tests
1.
When there ketoatsidoticheskaya coma?
1) Type 1 diabetes
2) Type 2 diabetes
3) Obesity
4) Metabolic Syndrome
5) insulin resistance
6) Diabetes, LADA
2. What drugs are used tireotoksicheskom Stroke:
1) Lugol's solution
2) L-thyroxine
3) Merkazolil
4) Hydrocortisone in /
5) Insulin in /
6) iodide
3. That does not apply to hypoglycemic coma?
1) Insulin
2) 40% glucose
3) adrenaline
4) 5% glucose
5) mannitol
6) maninil
The method of "The Weakest Link"
To work needed:
1. A set of questions on endocrinology.
2. A sheet of paper with a list of games for the introduction of the protocol.
3. Stopwatch.
Progress:
1. Igpy conducts teacher and an assistant from the students - the counter.
2. Counter wrote on a sheet date, the group number, the faculty and the business name of the game
and a list of student groups.
3. Teacher hurt in series of questions from the students a set of questions.
4. The student must in 5 seconds. to answer.
5. Teacher of the word "right" or "wrong" answer evaluates if the "wrong" he gives the correct
answer.
6. Counter puts opposite the name of the student, "+" or "-" depending on the correctness of the
answer.
7. Students are, therefore, two rounds of questions.
8. After 2 rounds of questions the game is suspended and students who have received 2 minus
out of the game as the "weak link".
9. The game continues for a new circle with the rest of the students. Again, they are offered one new
round of questions and again eliminated students who in the sum with the first two rounds turned
instrumentals.
126
10. Round by Round shown the strongest of the players, who responded to an increasing number of
issues.
11. Ha sheet against each name the teacher records - who in any round was eliminated and became
the "weakest link".
12. Game estimated maximum of 100 points.
Students who withdrew after the first 2 rounds of the answers, get a game, "0" points,
after 3 rounds answers - "25" points,
after 4 rounds answers - "50" points,
after 5 rounds answers - "75" points,
the strongest participant receives 100 points.
13. The scoring on the sheet of the protocol to the count of the current total employed as an estimate
for the theoretical part.
14. B bottom of the log free teacher records on a business game, Mayor signs off.
15. Minutes of the game remains.
Set of questions.
1. Describe how hypoglycemia syndrome:
Is a clinical syndrome characterized by signs of activation of the sympathetic nervous system and / or
dysfunction of the central nervous system, which are caused by abnormally low levels of plasma
glucose?
2. Hypoglycemia - reduced plasma glucose concentration below ...
2.2-2.8 mmol / l.
3. Causes of hypoglycemia in diabetic patients:
Inadequate food intake, high physical activity, an overdose of insulin or TSP, autonomic neuropathy,
accelerated resorption of insulin accumulation TSP.
alcohol, the development of related
zndokrinopaty.
4. Severity of hypoglycemia:
Light and heavy.
5. What are two groups of symptoms during hypoglycemia?
Adrenergic and neyroglikopenic.
6. Typical clinical symptoms of hypoglycemia:
Agitation, palpitations, seizures.
7. Characterized whether hypoglycemia acidosis and dehydration of the body?
No.
8. Treatment for hypoglycemia:
Admission write (10-20 g glucose) in / spacers 40% glucose solution, a / m 1 ml of glucagon
9. The causes of ketoacidosis in diabetic patients:
Loss of insulin p-cells PZHZH, errors insulin, infection, myocardial infarction, stroke, pregnancy,
stress.
10. How quickly develops ketoatsidoticheskaya coma?
Gradually over 1-3 days.
4.2 The analytical part
1. Checking the initial level of preparedness of students to engage in "diseases associated with
impaired consciousness." Explanation of the diagnosis and differential diagnosis of diseases
associated with impaired consciousness.
2. Decision analysis and situational problems.
3. Supervision of patients with diseases that are accompanied with impaired consciousness. Clinical
analysis of supervised patients
4. Interactive games to assess knowledge on training.
Problem number 1. Patient 42 years in the clinic at the doctor suddenly lost consciousness. The
doctor knows that the patient has diabetes since his youth and all the years of taking insulin, 6 days
makes poluprodlenny insulin two times a day. 36 units before breakfast and before dinner 14. Regular
visits to the doctor due to the fact that a few days during the day began to appear excessive sweating,
127
accompanied by palpitations and compressive pain in the heart. The appearance of pain in my heart is
not related to exercise or negative emotions. On examination, attracted attention - is sweaty skin and
motor stimulation patient. BP - 160/100 mm Hg (working pressure - 130/70-75), pulse - 102 beats per
minute. Immediately glucometer was examined blood sugar.
1. What type of diabetes (prove)?
2. Expected blood glucose levels?
3. Enter the reason for the loss of consciousness?
4. Correctly were selected morning and evening dose of insulin?
5. Explain the mechanism of appearance of tachycardia and pain in his heart?
6. Tactics physician clinics:
7. Your advice to the patient in the future.
4.3 The practical part
Performed at the bedside. Supervision is carried out under the supervision of a teacher. The student
must learn to practice proper history taking in patients with impaired consciousness, while able to
differentiate between primary and secondary information during the examination to focus on the type
of house, in conducting studies in the clinic, while outpatient care, to teach students to quickly, clearly
questioning and examination of the patient, proper filling patient card.
Supervision of patients. On first contact with the sick student has to gain the most patient. Achieve
this may have a serious attitude towards their work, talk to the patient confidence, articulate questions.
Listen carefully to the patient, at the same time firmly directing the conversation back on track. It is
important to have a neat appearance. When collecting complaints to be able to identify major
complaints associated with damage to the endocrine system (can be active after self-questioning story
patient). When collecting history focuses on the relationship of the disease to damaging factors, acute
or latent onset, family history, endocrine disease, whether due to the onset of disease with periods of
hormonal changes, etc. The physical examination to draw attention to the clinical signs of disorders of
the endocrine glands (body weight, body type, hair growth, secondary sexual characteristics, the
condition of the skin, thyroid, etc.). The student must know the normal common blood and urine tests,
blood glucose is normal, to be able to interpret the results of studies of hormonal data.
Supervision is carried out in the presence of the teacher and supervision results are then evaluated and
analyzed in the group.
The student must keep a journal of practical classes, and writes some
moments theoretical section and the data about the patient.
5.Control forms of knowledge, skills and abilities
- Oral
- Written
- Testing
- Decision of situational problems;
- Demonstration of the developed skills
Monitoring the activity of the students in the discussion, analysis of case-patients with situational
problems, making tests for the diagnosis and differential diagnosis.
6.The evaluation criteria of the current control
№ Military
Est. ENKA
Ka quality assessment
mustache
in points
1. 86-100 Personally from Communicates about, think creatively, evaluates,
the "5"
interprets.Applies knowledge in practice.Understands, knows,
says has no idea
2. 71-85 It is well "4"
Ra ssuzhdaet independently assess, interpret, apply knowledge
in practice, understands, knows, says has an idea
3. 55-70
Beats
Minimality know.Understand the essence, says
ovletvoritelno "3."
128
4
0-54
Not satisfactory, Pl oxo know.Not thoroughly.Require additional training.
"2"
7.Flow chart classes
1. Checking the initial level of preparedness of students to engage in "Diseases of the endocrine
glands occurring impairment of consciousness." Explanation of the diagnosis and differential
diagnosis associated with impaired consciousness.
2. Decision analysis and situational problems.
3. Supervision of patients. Clinical analysis of supervised patients.
4. Interactive games to assess knowledge on training.
№
fl ups lessons
1 Judgment of courses offered
2 Ca autonomy of patients Supervision attached houses, self Curation case
patients, participation in rounds of professors and associate professors
3 Ra Zborov the department examined case patients with the interpretation
of the survey data and treatment
4 ne reryv
5 On judgment tests, situational problems.
6 Pr Overcome digestibility.Ad evaluations homework
Prospect
odolzhitelnost
classes
7-hour ace
8.30-10.05
10.10-11.05
11.10-11.55
11.55-12.40
12.40-14.40
14.40-15.10
8.Test questions:
1. Mechanism to reduce blood glucose when taking alcohol?
2. Clinical symptoms of "hidden hypoglycaemia '?
3. Clinical symptoms of hypokalemia in patients during injection of
Ketoatsidotic coma?
4. Causes of mortality in hypo-and hyperglycemic komah?
5. Does the self-development of hypo - or hyperglycemic whom?
6. Clinical manifestations of adrenal insufficiency in tireotoksicheskom
Stroke?
7. Distinguishing features of acute and chronic insufficiency of the adrenal cortex?
8. Prevention of comatose states in DM.
9. Differential diagnosis of hyperglycemic com.
10. Tactics excretion of thyrotoxic crisis.
9.Recommended Reading:
Summary:
1.
Balabolkin MI Endocrinology. M., Medicine, 1998
2.
Vladimir Potemkin Endocrinology. M., Medicine, 1999
3.
Grandparents II Endocrinology. M., Medicine, 2000
129
4.
Melnichenko GA Tokmakova AY, deck DE, NV Lavrishcheva Endocrine
disease. M. Medicine, 2009
5.
Guidelines for Pediatric Endocrinology. Handbook of clinical Pediatric
Endocrinology. Edited by Charles G. Bouka, Rosalind S. Brown. 2009
6.
Shustov SB, Khalimov S, Trufanov GE Functional and topical
diagnostics in endocrinology. M. 2010
7.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 1. Greenspan's Basic & Clinical
Endocrinology. 2010
8.
Gardner, D., D. Shobek Basic and Clinical Endocrinology Book 2. Greenspan's Basic & Clinical
Endocrinology. 2011
9.
Clinical Endocrinology. Ed. EA Kholodova. Minsk. Belarus.
2011.
10. Melnichenko GA Udovichenko OV Shvedova AE Endocrinology.
Typical errors practitioner 2012
11. Endocrinology. National guidelines (+ CD-ROM). 2012
More:
1. Therapeutic Guide Washington, translated from English. (Section
"Endocrinology") 1996.
2. Laycock. Fundamentals of Endocrinology, Moscow 2000
3. Ty M. Mack - Dermott MD Secrets Endocrinology - Moscow 2000
4. Ketgayl VM, Arkin RA, Pathophysiology of endocrine system - Moscow, Medicine,
2001.
5. Balabolkin MI Diabetology - Moscow, Medicine, 2002
7. Fadeev PA. Endocrinology. Diabetes. A Reference Guide. 2009
8. Kartelishev Alexander Rumyantsev AG, Smirnova NS Actual problems of obesity
children and adolescents. 2010
9. Mkrtumyan AM, AA Nelaev. Emergency Endocrinology. 2010
10. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Diseases
thyroid. Williams Textbook of Endocrinology. 2010
11. Cronenberg GM, Melmed S., Polonsky KS, Larsen PR Bark disease
adrenal gland and endocrine hypertension. Williams Textbook of
Endocrinology, 11 th edition. 2010
12. AN hams Emergency Endocrinology. 2011
13. Petunina NA, AV Trukhina Thyroid disease. 2011
14. Manukhin IB Tumilovich LG, M. Gevorgyan Gynecological Endocrinology.
Lectures on gynecologic endocrinology. M. 2012
Journals:
130
15. Medical Journal of Uzbekistan, Tashkent.
16. "Problems of Endocrinology." Moscow.
17. "Therapeutic Archives", Moscow
18. "Clinical Medicine", Moscow
19. "Diabetes. Way of life ", Moscow
Internet sites:
1. "Internet Portal: Hunari»
2. Medscape.com
3. Alltheweb.com
4. Yahoo.com
5. E-medicine.com
6. www tma. uz
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