Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
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. 2 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 6 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 7 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 8 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. 9 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 10 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 12 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. 13 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 131