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MINISTRY OF HEALTH, UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY
CHAIR OF ENDOCRINOLOGY
METHODOLOGICAL PROTOCOLS BY POST-AUDITORIUM
INDIVIDUAL WORK OF ENDOCRINOLOGY
FOR FOURTH - YEAR STUDENTS
OF FACULTY OF PREPARATION OF FOREIGN CITIZENS
WITH THE SPECIALITY “MEDICINE”
Theme # 1. DIABETES MELLITUS AND PREGNANCY. THE PREGNANCY FOR
THE DIABETIC PATIENTS. FEATURES IN THE TREATMENT OF DIABETES
MELLITUS TREATMENT IN PREGNANT WOMEN.
IFNMU
2010
Actually
Diabetes mellitus in pregnant women may be pregestational, where the diabetes mellitus (type 1 or
type 2) was diagnosed before pregnancy, or gestational, which refers to diabetes mellitus diagnosed during
pregnancy. Gestational diabetes accounts for 88 percent of diabetes mellitus in pregnancy, type 2 diabetes
mellitus comprises 8 percent, and type 1diabetes mellitus makes up the remaining 4 percent.
Complications are minimal in infants of mothers with gestational diabetes. In contrast,
hyperglycemia-induced teratogenicity occurs almost exclusively in pregestational diabetes. The most
difficult pregnancies for the mother and fetus occur in diabetic women with renal, cardiac, or retinal disease.
Study aim
To know:
1. To know terms and definition of gestational diabetes mellitus.
2. To know how to determine the diagnosis of gestational diabetes mellitus.
3. To know how to determine the criteria for either low risk or high risk development of gestational
diabetes mellitus.
4. To know classification of fetal complications for maternal diabetes mellitus.
5. To know about maternal risks in diabetic pregnancies.
6. To know fetal complications of maternal pregestational diabetes mellitus.
7. To know causes of fetal illnesses and death.
8. To know contraindication to pregnancy for patients with diabetes mellitus.
1.
2.
3.
4.
5.
6.
To be able:
To be able to prevalence of pregestational diabetes in pregnant women.
To be able to interpreted diagnostic criteria of gestational diabetes mellitus.
To be able to define pregnant women with the high risk of development of diabetes mellitus.
To determine a plan of treatment for pregnant patients with diabetes mellitus.
To be able to determine a plan of fetopathy monitoring.
To conduct the correction of insulin therapy during births and postpartum.
Base knowledges, abilities, skills, necessary are studying themes.
Discipline
Path. Physiology
Gynaecology
Paediatrics
To know
To be able
Features of exchange processes are in the
organism of woman in different periods of To estimate the state of compensation
diabetes mellitus.
pregnancy.
Role of carbohydrate changes.
State the diagnostic criteria for the
gestational diabetes mellitus.
The pregnant have requirements to
control of level of blood glucose.
To know the complications of mother
with diabetes mellitus and her child.
To conduct the correction of glucose
in the blood, control for sight, ECG
and body mass index in the pregnant
women with diabetes mellitus
To be able to conduct a woman with
diabetes mellitus in births.
Influence of pregnancy is on mental and
physical development of child.
To know about causes of fetal illnesses
and death.
To be able to determine a plan of
fetopathy monitoring.
Assessment questions:
1. Define gestational diabetes mellitus (GDM).
2. Describe the metabolic changes associated with the development of GDM.
3. List one potential risk of GDM on the fetus and one on the mother.
4. State the diagnostic criteria for the individual with GDM.
5. Propose the algorithm of diagnosing of GDM.
6. List one component of medical nutrition therapy for the individual with GDM.
7. State the criteria for initiating insulin as treatment for the individual GDM.
8. State two recommendations for post-partum care for GDM.
9. Clinical features of Diabetes Mellitus in pregnant women.
10. Features of the course of Diabetes Mellitus in pregnancy.
11. Treatment of Diabetes Mellitus in pregnant women in different stages of the disease.
12. Features in the treatment of Diabetes Mellitus treatment in pregnant women.
13. Build the scheme of treatment for pregnant women with diabetes mellitus.
Self-assessment examination:
# 1.
Which of the following statements is not true regarding gestational diabetes mellitus (GDM):
A. GDM affects up to 14% of pregnancies
B. Symptoms of GDM include increased thirst and frequent urination
C. GDM is typically found in the third trimester
D. If undetected, GDM can harm the mother and fetus
# 2.
Patient J. is a 24 year old woman. Her health care provider just confirmed she is 14 weeks pregnant. This
is her first pregnancy. She has a family history of diabetes and is overweight. What is her risk
assessment?
A. Low risk status. No need to test blood glucose levels
B. Average risk status and should be screened at 24-28 weeks
C. High risk status and should be screened at 24-28 weeks
D. High risk status and should be screened at this visit
E. High risk status and should be screened at this visit and at 24-28 weeks
# 3.
Which of the following is a fetal complication associated with GDM?
A. The infant will have hyperglycemia at birth
B. Pre-eclampsia
C. Macrosomia
D. Polyhydraminos
# 4.
Based on the following oral glucose tolerance test (GTT) results, which individual with the
following test results would be diagnosed with GDM?
A. Fasting: 4,9 mmol/L, 1 hour: 10,3 mmol/L, 2 hour: 8,6 mmol/L, 3 hour: 6,4 mmol/L
B. Fasting: 5,2 mmol/L, 1 hour: 9,9 mmol/L, 2 hour: 8,6 mmol/L, 3 hour: 7,7 mmol/L
C. Fasting: 4,6 mmol/L, 1 hour: 8,6 mmol/L, 2 hour: 6,2 mmol/L, 3 hour: 4,7 mmol/L
D. Fasting: 4,8 mmol/L, 1 hour: 10,8 mmol/L, 2 hour: 9,4 mmol/L, 3 hour: 7,7 mmol/L
E. Fasting: 3,6 mmol/L, 1 hour: 9,9 mmol/L, 2 hour: 6,9 mmol/L, 3 hour: 5,9 mmol/L
# 5.
In which situation should urine ketones be tested?
A. When nauseated and vomiting
B. 2 hours after every meal
C. When fasting blood glucose levels are less than 3,9 mmol/L
D. All of the above
# 6.
All of the following statements are true regarding insulin except:
A. Insulin needs are higher in the third trimester than in the first
B. Insulin needs are based solely on the fetal weight
C. Women with GDM requiring insulin should be educated on signs and symptoms of hypoglycemia
D. Insulin therapy is recommended when the meal plan and activity alone are unable to adequately
control blood glucose levels
# 7.
Post-partum counseling should include:
A. Elimination of all carbohydrates from the meal plan to facilitate weight loss
B. Avoidance of all oral contraceptive because they elevate blood glucose levels
C. Encouraging breastfeeding only for obese women to help them lose weight
D. Follow up with blood glucose testing at 6-week checkup
E. All of the above
# 8.
What kind of complications for diabetes mellitus in women is pregnancy contraindicated?
A. Background retinopathy
B. Maculopathy
C. Proliferative retinopathy
D. Neuropathic form of diabetic foot
E. Diabetic neuropathy
# 9.
Principles of treatment for pregnant women with diabetes mellitus are include:
A. Diet and insulin therapy
B. Oral antidiabetic drugs
C. Combinations of insulin therapy with oral antidiabetic drugs
D. Only insulin therapy
E. Diet
# 10.
What are preconditions must be preceded conception at women with diabetes mellitus?
A. Good and protracted compensation of diabetes mellitus
B. Good compensation of diabetes mellitus is on the day of conception
C. Only absence of glucosuria
D. Permanent indexes of metabolism are within the limits of norm
E. Not to use carbohydrates
Case # 1.
A 30 year old woman booked into the clinic at 17 weeks gestation. She was 165 cm tall and weighed
55,8 kg. Uterine ultrasound confirmed the gestational age and was otherwise unremarkable. She complained
of vaginal thrush and on routine testing had “++” glycosuria. There was no polydipsia or polyuria. She had a
past medical history of an operation for hiatus hernia at the age of 9 months. There was no relevant family
history. The thrush was treated. At 28 weeks gestation, she presented to again with pre-term labor. She was
noted to have marked polyhydramnios (an excess of amniotic fluid). She considered the polyhydramnios to
be due to gestational diabetes mellitus and performed a 75 g glucose tolerance test:
Time (min) Serum glucose concentration (mmol/L)
0
6,6
30
14,0
60
15,4
90
8,1
120
7,7
Question 1: Were correct in diagnosing gestational diabetes mellitus?
Question 2: If not, how may the glucose tolerance test be interpreted?
Question 3: How would you have treated the patient at the time of the presentation at 28 weeks gestation?
Case # 2.
Patient T., 28 year old with type 1 diabetes mellitus of 5 years duration was seen in the clinic. Daily
doses of insulin - 46 IU. She’s pregnant 16 weeks. During flu nausea, vomit, somnolence. The sick in the
evening gave up a meal, did’t get the duty dose of insulin, and unconsciousness a morning. Objectively: sick
without consciousness, a skin is dry. Strong smell of acetone from a mouth. Temperature - 36.6°, pulse – 100
beats per minute, weak; blood pressure (BP) is 90/50 mmHg. Lab studies: The reaction of the urine to acetone
is positive (+++). The glucose in blood - 23 mmol/L.
Question 1: Substantiate diagnosis.
Question 2: What therapy is needed first of all?
Standards of answers to the self- assessment examination.
Theme # 1. Diabetes Mellitus and pregnancy. The pregnancy for the diabetic patients. Features in the
treatment of Diabetes Mellitus treatment in pregnant women.
1.
2.
3.
4.
5.
Tests
C.
E.
C.
B.
D.
6. C.
7. E.
8. C.
9. A.
10. A.
Case # 1.
Answer 1: Diagnosis of gestational diabetes mellitus is correct.
Answer 2: The oral glucose tolerance test interpreted - gestational diabetes mellitus.
Answer 3: Insulin therapy.
Case # 2.
Answer 1: Type 1 diabetes mellitus, moderate form, the state of decompensation. Diabetic ketoacidotic
coma. Pregnancy 16 weeks.
Answer 2: Intensive insulin therapy. Rehydration and electrolyte balance recovery. Detection and
treatment of concomitant diseases.
REFERENCES
PRINCIPAL REFERENCES
1. Lectures.
2. Endocrinology. Textbook/ Study Guide for the Practical Classes. Ed. by prof. Petro M. Bodnar: Vinnytsya: NOVA KNYHA Publishers, 2008. – 496 pp.: Art.
3. Endocrinology Studie Guide for the Practical Classes Ed. by prof. Petro M. Bodnar, academician
APS of Ukraine Sergey D. Maksymenko. Kiev, 2007, 102 p.
4. Basic & Clinical Endocrinology. Seventh edition. Edited by Francis S. Greenspan, David G. Gardner.
– Mc Grew – Hill Companies, USA, 2004. – 976 p.
5. Oxford handbook of endocrinology and diabetes. Edited by Helen E. Turner, John A.H. Wass.
Oxford, University press. 2006. – 1005 p.
6. Harrison′s Endocrinology.Editor J. Larry Jameson. Mc Grew – Hill, USA, 2006. – 563 p.
7. International Textbook of Diabetes Mellitus Edited by R.A. Defronzo, E. Ferrannini, H. Keen, P.
Zimmet. John Wiley & Sons, Ltd. England, 2004. – vol. 1 – 1100 p., vol. 2 – 1913 p.
SUPPLIMENTARY REFERENCES:
1. The Diabetes Control and Complications Trial Research Group: Effect of pregnancy on
microvascular complications in the Diabetes Control and Complications Trial. Diabetes Care 2000,
23: 1084–1091.
2. Loukovaara S., Immonen I., Teramo K.A., Kaaja R.R. Progression of retinopathy during pregnancy
in type 1 diabetic women treated with insulin lispro // Diabetes Care. – 2003. - 26:1193–1198.
3. Larsen M., Colmorn L., Bonnelycke M., et al. Retinal artery and vein diameters during pregnancy in
diabetic women / Invest Ophthalmol Vis Sci. – 2005. - 46: 709–713.
4. Diabetic Retinopathy. Preferred Practice Patterns [pamphlet]. San Francisco, C.A.: The American
Academy of Ophthalmology; 2003.
5. American Diabetes Association, “Gestational Diabetes Mellitus,” Clinical Practice
Recommendations 2004: Diabetes Care, Jan. 2004; Volume 27, Supplement 1.
Prepared by MD, PhD, Associate of professor Kostitska I.O.
Adopted at the Chair Sitting №…… , …… . … . 2010 y.
MINISTRY OF HEALTH, UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY
CHAIR OF ENDOCRINOLOGY
METHODOLOGICAL PROTOCOLS BY POST-AUDITORIUM
INDIVIDUAL WORK OF ENDOCRINOLOGY
FOR FOURTH - YEAR STUDENTS
OF FACULTY OF PREPARATION OF FOREIGN CITIZENS
WITH THE SPECIALITY “MEDICINE”
Theme # 2. DIABETES MELLITUS IN CHILDREN. FEATURES IN THE COURSE
OF DIABETES MELLITUS IN CHILDREN. MAURIAC SYNDROME AND
NOBEKURA SYNDROME.
IFNMU
2010
Actually
Diabetes mellitus is typically perceived as a disorder of older adults; however, diabetes occurs in 1
out of 600 children under 18 years of age, and the incidence appears to be increasing. Unless children with
diabetes mellitus are diagnosed promptly and treated appropriately, they are at serious risk for acute and
long-term complications. Mauriac syndrome, also known as diabetic dwarfism, is a complication of diabetes
mellitus that causes enlarged liver, short stature and delayed puberty in children. The cause of the disorder is
believed to be related to low levels of insulin, inadequate diet and diabetes mellitus that has been poorly
controlled over a long period of time. It occurs most often in children, teens or young adults with type 1
diabetes mellitus.
Study aim
To know:
1. To know terms and definition of Diabetes Mellitus in children.
2. To know about peculiarity in development of Diabetes Mellitus in children.
3. To know definition of Mauriac syndrome and Nobekura syndrome.
4. To know causes of Mauriac syndrome and Nobekura syndrome.
1.
2.
3.
4.
5.
To be able:
To be able to prevalence of Mauric’s syndrome in children.
To be able to interpreted diagnostic criteria of type 1 and type 2 Diabetes Mellitus in children.
To be able to define children with the high risk of development of type 2 Diabetes Mellitus.
To determine a plan of treatment for children with type 1 Diabetes Mellitus.
To be able to determine a plan of glicemic control and lipid profile in children with type 2 Diabetes
Mellitus.
Base knowledges, abilities, skills, necessary are studying themes.
Discipline
Path. Physiology
Children diseases
Pharmacology
To know
Mechanism of interaction between
hormones, pathogenesis of Diabetes
Mellitus in children.
To be able
To examine glucose in blood and
urine and acetone in urine.
Carbohydrate, lipid and protein
metabolism in the children body.
To diagnose type, state, and stage of
difficulty of Diabetes Mellitus in
children.
Structure of visual analyzer
clinical symptoms of Diabetes Mellitus
in children.
Differential diagnosis and treatment of
Diabetes Mellitus in children.
To choose an adequate and
appropriate type of treatment of
Diabetes Mellitus in children.
Assessment questions:
1. Definition of term “Diabetes Mellitus” in children.
2. Epidemiological aspects of type 1 and type 2 Diabetes Mellitus in children.
3. The role of virus infection in Diabetes Mellitus in children development.
4. The role of autoimmune process and other damage factors of the pancreas in Diabetes Mellitus in
children development.
5. Pathogenesis of type 1 and type 2 Diabetes Mellitus in children.
6. Stages of severity of Diabetes Mellitus in children, diagnostic criteria of each stage.
7. The main signs and symptoms of Diabetes Mellitus in children and pathogenesis of them.
8. Pathogenetic mechanisms of development of chronic complications of Diabetes Mellitus in children.
9. Definition of Mauriac syndrome and Nobekura syndrome.
10. Etiology and pathogenesis of Mauriac syndrome and Nobekura syndrome.
11. The main principles of Diabetes Mellitus in children therapy.
12. Treatment of chronic complications of Diabetes Mellitus in children.
Self-assessment examination:
# 1.
Determining which type of diabetes mellitus a child has may be difficult because:
A. The signs and symptoms of each type may be similar
B. Recognition of the signs and symptoms is difficult
C. No exact lab test exists that can differentiate between them
D. Children are not reliable in reporting the signs and symptoms
# 2.
Initially, insulin dosages in children are determined primarily by:
A. The child’s age
B. The child’s weight
C. The physician’s preferences
D. How high the blood glucose was during the evening
E. The level of ketone bodies and child’s weight
# 3.
A child of ten years with diabetes mellitus of age could probably be expected to:
A. Be totally responsible for the management of the condition
B. Be able to check the blood sugar and record it accurately
C. Give insulin injections in an independent manner
D. Prepare appropriate meals
# 4.
The recent increase in type 2 diabetes mellitus in children is thought to be a response to which of
the following?
A. Diets high in fats and carbohydrates, combined with a sedentary lifestyle
B. A hereditary predilection for this type of diabetes mellitus
C. Ungrounded fears about diabetes mellitus
D. Better detection and diagnostic methods
# 5.
In a child with diabetes mellitus, if the morning fasting blood sugar is consistently elevated, which
insulin should be adjusted?
A. The a.m. short-acting insulin
B. The a.m. intermediate (rapid) acting insulin
C. The p.m. short-acting insulin
D. The p.m. intermediate (rapid) acting insulin
# 6.
In beginning education for the child and family who have just received a diagnosis of diabetes
mellitus, the educator should first determine:
A. The age of the affected child
B. The family history of diabetes
C. The child’s past medical history
D. What the child and family already know about diabetes mellitus
# 7.
The mother of a 14 year old girl complains that her daughter’s blood sugar values are frequently
elevated. She accuses the child of cheating on her diet plan. The best response would be to:
A. Discuss possible insulin resistance during puberty
B. Agree with the mother that her suspicions are probably true
C. Check the blood glucose yourself to see if it is elevated
D. Lecture the child on the importance of being honest about what she has eaten
# 8.
The child with diabetes mellitus who is involved in athletic activities should observe which of the
following recommendations?
A. Not to exercise when the insulin is peaking
B. To give additional insulin before exercise to meet the body’s metabolic demands
C. To check the blood sugar level one hour after exercising
D. To have a snack before or during strenuous exercise to prevent hypoglycemia
# 9.
A 18 years old man is diagnosed with diabetes mellitus. Which of the following findings would point
most convincingly to type 1 rather than type 2 diabetes?
A. He is not obese
B. Severe polydipsia and polyuria preceded the diagnosis
C. Ketoacidosis was present at the time of diagnosis
D. The serum C-peptide level was normal at the time of diagnosis
E. Glucose levels rose above 32 mmol/L before treatment was started
# 10.
A 21 years old female is diagnosed with diabetes mellitus. Type 1 diabetes mellitus is usually
associated with which one of the following?
A. Onset in middle age
B. Obesity
C. Insulin resistance
D. Requirement for insulin therapy
E. Absence of autoimmune manifestations
# 11.
In a boy of 5 years, after measles vaccination a temperature of the body is 37,8 0C, a big thirst,
polydipsia, polyuria. Weakness is increasing during 6 hours from the beginning of the disease, noisy
breathing, sleepy. Your preliminary diagnosis:
A. Type 1 diabetes mellitus
B. Postvaccination syndrome
C. Typical postvaccination reaction
D. Postvaccination allergy
E. Non of this variant
# 12.
A 9 year old boy had acute respiratory viral infection. After it there appeared polydipsia, polyuria,
weakness, nausea. Examination revealed the following symptoms: mental confusion, dry skin, soft eyeballs,
Kussmaul's respiration, acetone smell from the mouth, muffled heart sounds, soft and painless abdomen.
Blood sugar was 19 mmol/L. What acute condition is it?
A. Ketoacidotic coma
B. Hepatic coma
C. Cerebral coma
D. Acute renal insufficiency
E. Hyperosmolar coma
Case # 1.
A male, 19 years old with type 1 diabetic mellitus. In past history of multiple admissions to intensive
therapy unit (ITU) with diabetic ketoacidosis (DKA) in a period of 3 years was admitted to ITU with DKA.
On his examination protuberant abdomen with hepatomegaly, normal BMI and growth impairment were
seen. His sexual development was normal. He had background diabetic retinopathy. Labaratory: НвА1C 10.9%. His renal function was normal. Liver function test showed ALP, ALT and total bilirubin raise in 1.5
times. Your preliminary diagnosis.
Standards of answers to the self- assessment examination.
Theme # 2. Diabetes mellitus in children. Features in the course of Diabetes Mellitus in children.
Mauriac syndrome and Nobekura syndrome.
1.
2.
3.
4.
5.
6.
A.
E.
B.
A.
D.
D.
7. B.
8. D.
9. C.
10. D.
11. A.
12. A.
Case # 1.
Type 1 Diabetes Mellitus. Mauriac syndrome.
REFERENCES
PRINCIPAL REFERENCES
1. Lectures.
2. Endocrinology. Textbook/ Study Guide for the Practical Classes. Ed. by prof. Petro M. Bodnar: Vinnytsya: NOVA KNYHA Publishers, 2008. – 496 pp.: Art.
3. Endocrinology Studie Guide for the Practical Classes Ed. by prof. Petro M. Bodnar, academician
APS of Ukraine Sergey D. Maksymenko. Kiev, 2007, 102 p.
4. Basic & Clinical Endocrinology. Seventh edition. Edited by Francis S. Greenspan, David G. Gardner.
– Mc Grew – Hill Companies, USA, 2004. – 976 p.
5. Oxford handbook of endocrinology and diabetes. Edited by Helen E. Turner, John A.H. Wass.
Oxford, University press. 2006. – 1005 p.
6. Harrison′s Endocrinology.Editor J. Larry Jameson. Mc Grew – Hill, USA, 2006. – 563 p.
7. International Textbook of Diabetes Mellitus Edited by R.A. Defronzo, E. Ferrannini, H. Keen, P.
Zimmet. John Wiley & Sons, Ltd. England, 2004. – vol. 1 – 1100 p., vol. 2 – 1913 p.
SUPPLIMENTARY REFERENCES:
Manual of Endocrinology and Metabolism edited by Norman Lavin. Lippincott Williams & Wilkins.
2009. – 837 p.
Prepared by MD, PhD, Associate of professor Kostitska I.O.
Adopted at the Chair Sitting №…… , …… . … . 2010 y.
MINISTRY OF HEALTH, UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY
CHAIR OF ENDOCRINOLOGY
METHODOLOGICAL PROTOCOLS BY POST-AUDITORIUM
INDIVIDUAL WORK OF ENDOCRINOLOGY
FOR FOURTH - YEAR STUDENTS
OF FACULTY OF PREPARATION OF FOREIGN CITIZENS
WITH THE SPECIALITY “MEDICINE”
Theme # 3. METABOLIC SYNDROME
IFNMU
2010
Actually
The contemporary definition of the Metabolic Syndrome refers to a cluster of metabolic
abnormalities related to a state of insulin resistance which is often associated with a high-risk
overweight/obesity phenotype. Because such cluster increases the risk of coronary heart disease (CHD) and
type 2 diabetes mellitus, numerous consensus groups have attempted to provide recommendations to identify
in clinical practice patients with these atherogenic/diabetogenic metabolic abnormalities.
Study aim
 To understand the various theories of Metabolic Syndrome development and research studies
that support these theories.
 To know about the etiology, pathogenesis and clinical presentation of Metabolic Syndrome.
To know:
1. To know about definition of Metabolic Syndrome (Syndrome X, Insulin Resistance Syndrome).
2. To know about pathogenesis of insulin resistance.
3. To determine the diagnosis of Metabolic Syndrome and build the scheme of clinical and laboratory
diagnostic.
To be able:
1. To find out the clinical and laboratory criteria of the Metabolic Syndrome.
2. To be able to conduct differential diagnostics between of the Metabolic Syndrome and cardio
metabolic syndrome.
3. To be able build the scheme principle of treatment of Insulin Resistance Syndrome.
Base knowledges, abilities, skills, necessary are studying themes.
Discipline
Path. Physiology
Internal medicine
Pharmacology
1.
2.
3.
4.
5.
6.
7.
8.
9.
To know
To be able

Mechanism of interaction between To explain the action of antagonists
of insulin, violation, at cellular level
insulin resistance and compensate
(defect of receptors) and postreceptor
hyperglycemia;
levels.

Mechanisms of development of
atherosclerosis.
Causes of development of cardio vascular To explain the role of risk factors for
diseases and hypertension.
development of metabolic syndrome.
Pharmacology effects of oral antidiabetic
To conduct the correction of
drugs, antihypertension medicine and
dyslipidemia, hypertension and other
lipidmodifications therapy.
metabolic changes.
Assessment questions:
Definition of Metabolic Syndrome (MS).
The role of insulin resistance and hyperinsulinemia in pathogenesis of MS.
The diagnostic criteria of MS.
Build the scheme of pathogenesis of MS.
Name three laboratory values that indicate possible MS.
Define insulin resistance (IR).
Discuss the two most serious consequences of developing MS.
Describe two major lifestyle changes that can help treat and prevent MS.
Treatment approaches to MS.
Self-assessment examination:
# 1.
Insulin resistance is:
A. Fear of changing from oral medications to insulin injections
B. Abnormal difficulty body cells have in using insulin
C. Abnormal difficulty beta cells have in making insulin
D. The difficulty kidneys have in secreting insulin
# 2.
Insulin resistance can be caused by:
A. Excessive thirst (polydipsia)
B. Excessive urination (polyuria)
C. Excess visceral fat
D. Excessive sweating
# 3.
Weight loss for people with metabolic syndrome:
A. Cannot be recommended if the person has heart or kidney disease
B. Can reduce insulin resistance
C. Is generally dangerous to the person's general health
D. Is the least important lifestyle change
# 4.
A high level of blood cholesterol:
A. Protects people with type 2 diabetes mellitus from kidney damage
B. Lowers the risk of cardiovascular disease
C. Is not a problem unless people also have hypertension
D. Is a type of dyslipidemia
# 5.
In people with type 2 diabetes mellitus, hypertension:
A. Doubles the risk of developing cardiovascular disease
B. Occurs rarely
C. Increases the risk of neuropathy but not of cardiovascular disease
D. Cannot be controlled
# 6.
People with metabolic syndrome need to:
A. Use protein as their main source of calories
B. Reduce proteins to less than 10% of total calories
C. Choose bacon, steak, sausage, and ground beef as potent protein sources
D. Get their protein from poultry, fish, cheese, and soy products
# 7.
Hyperinsulinemia is:
A. Decreased sensitivity to the action of insulin
B. Elevated levels of plasma insulin
C. Elevated blood glucose levels
D. Elevated blood glucose levels and levels of plasma insulin
E. Insulin resistance
# 8.
Metabolic syndrome is a cluster of problems including impaired fasting glucose, dyslipidemia, and:
A. Hyperadrenalism
B. Hypercapnia
C. Hyperthyroidism
D. Hypertension
E. Hypercortisolemia
# 9.
The patient Q., 53 years old during random checkup has the fasting level glycemia – 8,2 mmol/L, the
glucosuria – 1,5 g/L. Body height -172 cm, body weight - 106 kg. Body mass index – 35,8 kg/m2. Define
initial tactics of treatment:
A. Insulin
B. Biguanides
C. Diet with carbohydrate restriction
D. Sulfonylureas of 1 generation
E. Sulfonylureas of 2 generation
# 10.
The patient W., 66 years old, the diabetes mellitus is revealed random during checkup. It was not
treated. Objectively: body height - 170 cm, weight -112 kg. Body mass index – 38,8 kg/m2. Ps - 76 /minutes,
regular. The blood pressure - 160/90 mm Hg. The fasting level of glycemia – 8,2 mmol/L. What is primary tactics of treatment:
A. Diet recommendations
B. Prescribe Repaglinide
C. Prescribe Metformin
D. Prescribe Glibenklamide
E. Prescribe Insulin
# 11.
Which of the following is associated with the use of prescription omega-3 fatty acids for dyslipidemia?
A. Bleeding
B. Hypervitaminosis
C. Reduction in LDL (low density) cholesterol
D. Reduction in triglycerides
# 12.
Which of the following statements about the use of lipid-modifying drug therapy is correct?
A. Empiric dosage reductions should be made for all agents in the elderly solely on the basis of age
B. Empiric dosage reductions should be made for selected agents in the elderly solely on the basis of
age
C. Empiric dosage reductions should be made for selected agents on the basis of renal insufficiency in
patients of all ages
D. Empiric dosage reductions should be made for selected agents on the basis of renal insufficiency only
in the elderly
# 13.
Which combination of metabolic syndrome criteria can be used to estimate future risk of chronic
heart disease (CHD), cardiovascular mortality, and all-cause mortality in women?
A. Triglyceride level and waist circumference
B. HDL (high density) level and waist circumference
C. Triglyceride and HDL (high density) levels
D. HDL (high density) level and blood pressure
E. Triglyceride level and blood pressure
# 14.
The body shape most closely associated with metabolic syndrome is:
A. Gynecoid (pear shaped)
B. Ovoid (egg shaped)
C. Android (apple shaped)
D. Droid (star shaped)
# 15.
Which pair of serious health problems are the most common results of metabolic syndrome?
A. Colon cancer and stroke
B. Coronary heart disease and type 2 diabetes mellitus
C. Pulmonary hypertension and portal hypertension
D. Breast cancer and prostatic cancer
Standards of answers to the self- assessment examination.
Theme # 3. Metabolic syndrome.
1.
2.
3.
4.
5.
6.
7.
B.
C.
B.
D.
A.
D.
B.
8. D.
9. C.
10. A.
11. D.
12. C.
13. B.
14. A.
15. B.
REFERENCES
PRINCIPAL REFERENCES
1. Lectures.
2. Endocrinology. Textbook/ Study Guide for the Practical Classes. Ed. by prof. Petro M. Bodnar: Vinnytsya: NOVA KNYHA Publishers, 2008. – 496 pp.: Art.
3. Endocrinology Studie Guide for the Practical Classes Ed. by prof. Petro M. Bodnar, academician
APS of Ukraine Sergey D. Maksymenko. Kiev, 2007, 102 p.
4. Basic & Clinical Endocrinology. Seventh edition. Edited by Francis S. Greenspan, David G. Gardner.
– Mc Grew – Hill Companies, USA, 2004. – 976 p.
5. Oxford handbook of endocrinology and diabetes. Edited by Helen E. Turner, John A.H. Wass.
Oxford, University press. 2006. – 1005 p.
6. Harrison′s Endocrinology.Editor J. Larry Jameson. Mc Grew – Hill, USA, 2006. – 563 p.
7. International Textbook of Diabetes Mellitus Edited by R.A. Defronzo, E. Ferrannini, H. Keen, P.
Zimmet. John Wiley & Sons, Ltd. England, 2004. – vol. 1 – 1100 p., vol. 2 – 1913 p.
SUPPLIMENTARY REFERENCES:
1. Grundy S.M., Brewer H.B., Jr., Cleeman J.I., Smith S.C., Jr., Lenfant C. Definition of metabolic
syndrome: Report of the National Heart, Lung, and Blood Institute/American Heart Association
conference on scientific issues related to definition. Circulation 2004; 109: 433-438.
2. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults:
Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP)
Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult
Treatment Panel III). JAMA. 2001;285:2486-2497.
3. Lakka H.M., Laaksonen D.E., Lakka T.A., et al. The metabolic syndrome and total and
cardiovascular disease mortality in middle-aged men. JAMA. 2002; 288:2709-2716.
4. Laaksonen D.E., Lakka H.M., Niskanen L.K., Kaplan G.A., Salonen J.T., Lakka T.A. Metabolic
syndrome and development of diabetes mellitus: application and validation of recently suggested
definitions of the metabolic syndrome in a prospective cohort study. Am. J. Epidemiol.
2002;.156:1070-1077.
5. Mc.Cormack J. New approaches to treat insulin resistance. In Symposium: Targeting Insulin
Resistance and Defective Insulin Secretion. Presented at the 18th International Diabetes Federation
Congress; August 24-29, 2003; Paris, France.
Prepared by MD, PhD, Associate of professor Kostitska I.O.
Adopted at the Chair Sitting №…… , …… . … . 2010 y.
MINISTRY OF HEALTH, UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY
CHAIR OF ENDOCRINOLOGY
METHODOLOGICAL PROTOCOLS BY POST-AUDITORIUM
INDIVIDUAL WORK OF ENDOCRINOLOGY
FOR FOURTH - YEAR STUDENTS
OF FACULTY OF PREPARATION OF FOREIGN CITIZENS
WITH THE SPECIALITY “MEDICINE”
THEME # 4. THE SURGICAL TREATMENT FOR DIABETIC PATIENTS.
IFNMU
2010
Actually
There is a permanent increase of amount of patients with diabetes mellitus, frequent development of
complications, which quite often are completed lethally, require implementation of surgical interferences.
Therefore knowledge of mechanisms of development of features of clinical picture of disease, pathogenic
therapy of the exigent states, will provide the rational passing to treatment of patients with diabetes mellitus
and concomitant surgical pathology.
Study aim
To know:
1. To know pathogenesis in development of surgical complications in patients with diabetes mellitus
2. To know to receive the planned surgical treatment of patients with diabetes mellitus
3. To know about methods of anaesthetizing, which apply at small and large operations for patients
with diabetes mellitus
To be able:
1. To be able to conduct differential diagnostics of surgical complications of diabetes mellitus with
nosology of other etiology
2. To be able to execute complex therapy for patients with diabetes mellitus and surgical pathology
3. To be able to choose the methods of anaesthetizing for every patient
4. To be able to warn possible complications at implementation of surgical interferences for patients
with diabetes mellitus
Base knowledges, abilities, skills, necessary are studying themes.
Discipline
Path. Physiology
Surgery
Fist aid and anaestheology
To know
To know about pathological mechanisms
of development surgical complications in
patients with diabetes mellitus.
To know about pathophysiological
mechanisms of tissues regeneration in
patients with diabetes mellitus.
To find out the pathological links of
mechanism with the purpose of
setting of pathogenic treatment.
To know new methods of treatment of
surgical pathology in patients with
diabetes mellitus.
To conduct differential diagnostics
of surgical complications of diabetes
mellitus with similar nosologies of
other etiology.
To choose the method of surgical
interference.
To know principles of anaesthetizing for
patients with diabetes mellitus and
surgical pathology.
To know principles of complex therapy
of the exigent states are at diabetes
mellitus.
To be able
To conduct surgical preparation of
patient with diabetes mellitus.
To provide the correction during an
operation and after that.
Assessment questions:
1. To know about surgical complications of diabetes mellitus and tell about the pathological
mechanisms of their development.
2. To conduct differential diagnostics of veritable “sharp stomach” and diabetic pseudoperitonitis.
3. To describe the features of flowing of sharp festering-inflammatory diseases on a background
diabetes mellitus.
4. To describe the role of violations of the immune system for patients with diabetes mellitus and
concomitant hyperthyroidism and features of surgical preparation of such patients.
5. To tell for violation of stasis of blood for patients with diabetes mellitus and concomitant surgical
pathology.
6. To describe the clinical picture of diabetic gangrene and diabetic osteoartropathy. To know methods
of their diagnostics and treatment.
7. To build the scheme of surgical preparation of patient with diabetes mellitus.
8. To transfer contraindication to implementation of surgical interferences for a patient with diabetes
mellitus.
9. To describe facilities of complex medicinal therapy, which apply for the correction of the broken
metabolism during surgical treatment.
10. To tell about influence on the carbohydrate exchange of accumulated drugs of different
pharmacological groups.
11. To transfer possibilities of complication, which arise up for patients with diabetes mellitus after
surgical preparation, and measures, for their warning.
Self-assessment examination:
# 1.
At suspicion on diabetic pseudoperitonitis which from the indicated examination will you do fist of all?
A. Determination of glycemia
B. Determination of glucosuria
C. Determination of ketone body in urine
D. Determination of activity of alpha amylase
E. Determination of leukocytosis
# 2.
Patient 21 years of age, suffering from diabetes mellitus for 2 years. Compensation of diabetes mellitus is
not satisfactory. Complains that turned blue feet, chilliness in both legs. Objective review: foot cold to the
touch, bluishred color on the little finger of both feet ulcer with pus. Ripple in the dorsal arteries of the foot
is good. Substantiate diagnosis:
A. Diabetes mellitus type 1, neurotrophic ulcers
B. Diabetes mellitus type 1, diabetic microangiopathy and macroangiopathy low extremites
C. Diabetes mellitus type 1, diabetic ishemic angiopathy low extremites, diabetic gangrene
D. Diabetes mellitus type 1, acute diabetic foot ulcers
# 3.
How to treat diabetic blister?
A. Immediately cut, cut the epidermis and put a bandage poluspirtnuyu
B. Immediately cut, cut the epidermis and put a bandage with an antiseptic solution
C. Immediately cut, cut the epidermis and put dry aseptic bandage
D. Remove the syringe contents puhirya and put dry aseptic bandage
E. Do not shoot blister, put a gauze bandage on it and recommend shoes that do not sting blister
# 4.
Which listed symptoms distinguish diabetic ketoacidosis with clinic "acute abdomen" from present
"acute abdomen"?
A. Availability acetonuria
B. Vomiting precedes pain
C. Indeterminate localization pain
D. Reducing pain in result of intensive therapy diabetic ketoacidosis
E. Impetuous development symptoms
# 5.
Abdominal pain with ketoacidosis predetermined:
A. Enhanced peristalsis of small intestine
B. Loosening of peristalsis of the colon
C. Violation egestion function of the pancreas
D. Increasing the stomach
E. Paresis of the ileum
Clinical cases
Case 1. Male 23 years old, suffers from type 1 diabetes mellitus. During the party with friends did not
impose insulin. On the second day began to disturb nausea, vomiting, a bulging belly. Feebleness. Caused by
the ambulance. The patient reported that he suffers from diabetes. Emergency doctor decided to hospitalize
the patient to the duty surgical department with a diagnosis of acute pancreatitis. What is substantiate
diagnosis in patient?
Case 2. In the surgical department of hospitalized patients 46 years old and diagnosed with exacerbation of
chronic cholecystitis. From history we know that the patient suffers from diabetes mellitus type 2. Treatment
by maninil a dose of 20 mg per day. Diets are not followed. Glycemia, usually within 15-17 mmol / L. The
last week did not take maninil and significantly violated diet. Objective review: contact, slightly inhibited,
accelerated respiration, noisy, sharp smell of acetone in the air. Pulse - 142 beats/ min. In order to prepare
for the surgery the patient is assigned: 10% glucose solution 500.0 ml of sodium chloride 0.8% to 500,0 ml.
Insulin 32 IU. Do you think that if this therapy requires correction?
Case 3. Patient 50 years preparing for operations in connection with calculous cholecystitis. 5 years
suffering from diabetes mellitus, treated maninil 3 tables / day. Fasting blood glucose - 5,5 mmol / L.
Glycosuria abstent. What treatment should be nominated?
Case 4. Type 2 diabetic patients suffering carbunculosis. Could this serve as indications for insulin
therapy?
Standards of answers to the self- assessment examination.
Theme # 4. The surgical treatment for diabetic patients.
1.
2.
3.
4.
5.
Answers the tests:
C.
C.
E.
A.
E.
Answers the clinical cases:
CASE 1. Diabetic psevdoperitonit.
CASE 2. The patient needs intensive care because of her diabetic ketoacidosis.
CASE 3. Insulin therapy.
CASE 4. Insulin therapy.
REFERENCES
PRINCIPAL REFERENCES
1. Lectures.
2. Endocrinology. Textbook/ Study Guide for the Practical Classes. Ed. by prof. Petro M. Bodnar: Vinnytsya: NOVA KNYHA Publishers, 2008. – 496 pp.: Art.
3. Endocrinology Studie Guide for the Practical Classes Ed. by prof. Petro M. Bodnar, academician
APS of Ukraine Sergey D. Maksymenko. Kiev, 2007, 102 p.
4. Basic & Clinical Endocrinology. Seventh edition. Edited by Francis S. Greenspan, David G. Gardner.
– Mc Grew – Hill Companies, USA, 2004. – 976 p.
5. Oxford handbook of endocrinology and diabetes. Edited by Helen E. Turner, John A.H. Wass.
Oxford, University press. 2006. – 1005 p.
6. Harrison′s Endocrinology.Editor J. Larry Jameson. Mc Grew – Hill, USA, 2006. – 563 p.
7. International Textbook of Diabetes Mellitus Edited by R.A. Defronzo, E. Ferrannini, H. Keen, P.
Zimmet. John Wiley & Sons, Ltd. England, 2004. – vol. 1 – 1100 p., vol. 2 – 1913 p.
1.
2.
3.
4.
5.
SUPPLIMENTARY REFERENCES:
Novella S.P., Inzucchi S.E., Goldstein J.M. The frequency of undiagnosed diabetes and impaired
glucose tolerance in patients with idiopathic sensory neuropathy. Muscle Nerve. - 2001;24:1229-31.
McCrimmon R. The mechanisms that underlie glucose sensing during hypoglycaemia in
diabetes. Diabet Med. May 2008;25(5):513-22.
Clinical Endocrinology and Diabetes: An Illustrated Color Text by Sheru L. Chew, David Leslie.
Churchill Livingstone, 2006. – 120 p.
Diabetic Medicine Philip Wright Blackwell Publishing Ltd. Oxford, UK, 2007.
А. Veves, J.M. Giurini, F.W. LoGerfo (ebs). The diabetic foot (second edn). Humana Press. Totowa,
New Jersey, 2006, 696 p.
Prepared by MD, PhD, Associate of professor Kostitska I.O.
Adopted at the Chair Sitting №…… , …… . … . 2010 y.
MINISTRY OF HEALTH, UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY
CHAIR OF ENDOCRINOLOGY
METHODOLOGICAL PROTOCOLS BY POST-AUDITORIUM
INDIVIDUAL WORK OF ENDOCRINOLOGY
FOR FOURTH - YEAR STUDENTS
OF FACULTY OF PREPARATION OF FOREIGN CITIZENS
WITH THE SPECIALITY “MEDICINE”
Theme # 5. DIFFERENTIAL DIAGNOSIS OF KETONURIA.
IFNMU
2010
Actually
Mortality rates for DKA are between 1 and 10%. Shock or coma on admission indicates a worse
prognosis. Main causes of death are circulatory collapse, hypokalemia, and infection. Among children with
cerebral edema, 57% recover completely, 21% survive with neurologic sequelae, and 21% die. The
knowledge of etiological factors that contribute to the development ketoacidosis states pathogenetic
mechanisms that cause metabolic disturbances in the patient with diabetes mellitus, diagnostic features and
basic elements of immediate treatment of diabetic coma to save the life of the patient and prevent
complications.
1.
2.
3.
4.
Study aim
To know:
The causes and mechanisms of decompensation of diabetes mellitus;
Early signs ketoatsydotychnyh states;
Principles of timely diagnosis and emergency care;
Prevention of diabetic coma.
To be able:
1. Explain the possible causes of decompensation;
2. To the differential diagnosis of the complications of the disease;
3. Assign adequate medical therapy.
Base knowledges, abilities, skills, necessary are studying themes.
Discipline
To know
To be able
- The main pathogenetic mechanisms of
diabetes mellitus;
- The main etiological factors leading to
decompensation of the disease;
- Biosynthesis, secretion, mechanism of
action of insulin.
- Detect abnormal levels of ketone
bodies;
- To correct violations of
metabolism.
Resuscitation and
anesthesiology
Urgent measures to prevent diabetic
coma.
Perform correction of acid-alkaline
balance and damaged metabolism.
Pharmacology
Pharmacodynamic and pharmacokinetic
features of drugs that eliminate the state
ketoacidosis.
Apply the medication to the impact
of abnormal levels of disease.
Path. Physiology
Assessment questions:
1. To define the notion of ketosis, ketoacidosis and ketoacidic coma.
2. Visit the cause of decompensation of diabetes mellitus.
3. An algorithm to compute intermediate care at ketoacidosis condition.
4. Tell about the possible complications damaged metabolism and list the measures to prevent them.
5. Perform differential diagnosis hyperglycemic state with ketonuria.
6. Explain the mechanism of these symptoms ketoacidosis as: Kussmaul's breathing, "acute abdomen", etc.
7. List the early signs of diabetic ketoacidosis.
8. Describe the main laboratory parameters, confirming ketoacidosis.
9. Terming the basic principles of management of patients with decompensated diabetes mellitus and
concomitant surgical pathology.
10. Tell about the tactics of elderly patients with ketosis and pathology of the cardiovascular system.
Self-assessment examination:
# 1.
When suspected diabetic psevdoperytonit with which these surveys will you do first?
A. determining glycemia;
B. determine glycosuria;
C. determination of ketonuria;
D. determine the activity of alpha-amylase;
E. determine the presence of leukocytosis
# 2.
The manifestations of hypoglycemia associated with the level of glycemia:
A. if glycemicemia is 4 mmol / L;
B. if glycemicemia - 3 mmol / L;
C. not related;
D. yes, but with a period of days;
E. yes, but the nature of the physical work
# 3.
Which of these measures is necessary to hold in the case of hypoglycemia?
A. insulin therapy;
B. 40% glucose solution;
C. 10% glucose solution;
D. 5% fructose solution
# 4.
Healing diabetic ketoacidosis applying:
A. insulin short action;
B. introduction solution with kalii from the very beginning of treatment;
C. input soalt solutions;
D. the introduction of 40% glucose solution;
E. introduction of 10% glucose solution
# 5.
Episodic hypoglycemia characteristic of these diseases:
A. insulinoma;
B. pheohromotsytoma;
C. Itsenko-Cushing's syndrome;
D. diffuse toxic goiter;
E. diabetes insipitus
# 6.
Development ketoacidic coma and promote these factors:
A. reducing unnecessary dose of insulin;
B. physical and mental injury;
C. short-term reduction of caloric food;
D. alcohol;
E. abuse of simple carbohydrates
# 7.
In decompensated diabetes mellitus, high lever blood sugar characteristic symptoms:
A. no drought;
B. a great thirst;
C. severe famine;
D. dry skin;
E. wet skin
# 8.
Which of the listed measures to bring to ketoacidic coma should be started at the prehospital stage:
A. rehydration;
B. insulin therapy;
C. prevention of iatrogenic hypoglycemia;
D. restoration of acid-base status;
E. prevention of infectious complications
# 9.
"Ketone bodies" defined in reaction to:
A. ortotoluyidyn;
B. glucose oxidase
C. nitrosynim tetrazolin
D. nitroprusyd sodium
E. acetic acid
# 10.
Pain in the abdomen due to ketoacidosis:
A. increased peristalsis of the large intestine;
B. violation of excretory function of the pancreas;
C. expansion of the stomach;
D. fever intestine
CASE 1.
The patient U., 28 years old, during 5 years treated diabetes mellitus, takes insulin in daily dose
38 IU. He was hospitalized with signs of ketoacidosis. What the scheme of insulin therapy is indicated for
patient with ketoacidotic state?
CASE 2.
The patient E., 24 years, is suffering from diabetes mellitus type 1 during 3 years. Several days ago she
canceled the insulin. Patient lost consciousness in the evening. She is hospitalized. Objectevly: the skin is
dry. Kussmaul's respiration, the odor of acetone from the mouth, tongue is dry, with fur of brown colour.
Pulse 120 /minutes, the arterial pressure 80/45 mmHg. The abdomen does not react to the palpation. The liver
is + 3 cm. The reaction of urine to acetone is positive, the glucose of blood - 28 mmol/L. What is the
preliminary diagnosis?
CASE 3.
A girl 9 years old has been suffering from diabetes mellitus for 3 years. The patient has fallen ill with
acute respiratory infection. Her state became worse during the last two days, the temperature reached 38 0 C,
the thirst and the frequency of urination increased. General weakness enlarged. Nausea and vomiting
appeared. General condition is grave. Consciousness is dizzy. Rubeosis. The tungue is dry. Heart tones are
rythmic, accelerated. What is your diagnosis?
Standards of answers to the self- assessment examination.
Theme # 5. Differential diagnosis of ketonuria.
Answers of the tests:
1.
2.
3.
4.
5.
C.
B.
B.
C.
A.
6. A.
7. B.
8. B.
9. E.
10. D.
Answers of the cases:
CASE 1. The scheme of insulin therapy is short or ultrashort action insulin (intensifyed).
CASE 2. The preliminary diagnosis is diabetic ketoacidotic coma.
CASE 3. Type 1 Diabetes mellitus, stage of decompensation. Diabetic ketoacidosis.
REFERENCES
PRINCIPAL REFERENCES
1. Lectures.
2. Endocrinology. Textbook/ Study Guide for the Practical Classes. Ed. by prof. Petro M. Bodnar: Vinnytsya: NOVA KNYHA Publishers, 2008. – 496 pp.: Art.
3. Endocrinology Studie Guide for the Practical Classes Ed. by prof. Petro M. Bodnar, academician
APS of Ukraine Sergey D. Maksymenko. Kiev, 2007, 102 p.
4. Basic & Clinical Endocrinology. Seventh edition. Edited by Francis S. Greenspan, David G. Gardner.
– Mc Grew – Hill Companies, USA, 2004. – 976 p.
5. Oxford handbook of endocrinology and diabetes. Edited by Helen E. Turner, John A.H. Wass.
Oxford, University press. 2006. – 1005 p.
6. Harrison′s Endocrinology.Editor J. Larry Jameson. Mc Grew – Hill, USA, 2006. – 563 p.
7. International Textbook of Diabetes Mellitus Edited by R.A. Defronzo, E. Ferrannini, H. Keen, P.
Zimmet. John Wiley & Sons, Ltd. England, 2004. – vol. 1 – 1100 p., vol. 2 – 1913 p.
SUPPLIMENTARY REFERENCES
1. Gunnerson K.J., Saul M., He S., Kellum J.A. Lactate versus non-lactate metabolic acidosis: a
retrospective outcome evaluation of critically ill patients // Crit. Care. – 2006. -10(1). – P.R22.
2. Manual of Endocrinology and Metabolism edited by Norman Lavin. Lippincott Williams & Wilkins.
2009. – 837 p.
Prepared by MD, PhD, Associate of professor Kostitska I.O.
Adopted at the Chair Sitting №…… , …… . … . 2010 y.
MINISTRY OF HEALTH, UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY
CHAIR OF ENDOCRINOLOGY
METHODOLOGICAL PROTOCOLS BY POST-AUDITORIUM
INDIVIDUAL WORK OF ENDOCRINOLOGY
FOR FOURTH - YEAR STUDENTS
OF FACULTY OF PREPARATION OF FOREIGN CITIZENS
WITH THE SPECIALITY “MEDICINE”
Theme # 6. INSULINOMA. EARLY DIAGNOSIS,
CLINICAL PRESENTATION, TREATMENT.
IFNMU
2010
Actually
Insulinomas are rare neuroendocrine tumours with an incidence estimated at 1 to 4 new cases per
million persons per year. Insulinoma is one of the most common types of tumour arising from the islets of
Langerhans cells (pancreatic endocrine tumours). Estimates of malignancy (metastases) range from 5% to
30%. Over 99% of insulinomas originate in the pancreas, with rare cases from ectopic pancreatic tissue.
About 5% of cases are associated with tumours of the parathyroid glands and the pituitary (Multiple
endocrine neoplasia type 1) and are more likely to be multiple and malignant.
Study aim
To know:
1. Causes of hypoglycemia;
2. Sings and symptoms of hypoglycemic states;
3. Principles of diagnosis hypoglycemic states;
4. Principles of treatment of patients with hypoglycemia.
To be able:
1. To identify of causes in anamnesis of hypoglycemic states;
2. To identify pathology of pancreas and other organs, which led to a hypoglycemic state;
3. Provide differentiated treatment to such patients.
Base knowledges, abilities, skills, necessary are studying themes.
Discipline
Oncology
Histology
Anatomical Pathology
To know
- Key performance indicators of
oncological employment;
- Principles of cancer care.
-Histological variants of insulinomas and
other pancreatic endocrine tumors.
- Histological forms of insulinomas;
- Histological variants of pancreatic cells.
To be able
- Conduct early diagnostic of
insulinoma;
- Choose the right of treatment
tactics.
- Microscopy of preparations.
- Macroexamination of endocrine
pancreatic tumors;
- Microscopic study of pancreatic
tumors.
Assessment questions:
1. Definition of terms “hyperinsulinemia” and “insulinoma”.
2. Etiology and pathogenesis of pancreatic hypoglycemia.
3. Stages of hypoglycaemia development.
4. Pathological anatomy of insulinomas.
5. Classification of endocrine pancreatic tumors.
6. Classification of hypoglycemic states.
7. Classification of primary hyperinsulinemia (hypoglycemic diseases).
8. Diagnosis of hypoglycemic states.
9. The main signs and symptoms of hypoglycemia and pathogenesis of them.
10. Clinical characteristics of the hyperinsulinemia.
11. Differential diagnosis of endocrine hypoglicemia.
12. Principle of treatment of hypoglycemic states.
Self-assessment examination:
Case 1.
A 32 year old male had episodic confusion and blackouts progressing over 2 years. Lab tests
demonstrated true hypoglycemia at time of episodes. Two admissions at a local hospital for 72 hour fast
showed hypoglycemia without definite hyperinsulinemia. CT scan of the pancreas was normal. Arterial
calcium stimulation did not localize an insulin secreting mass. A trial of diazoxide did not improve his
symptoms. On a repeat 72 hour fast, admission blood glucose was 3,2 mmol/L, insulin - 4.6 uU/mL (normal
5-25 uU/mL), C-peptide - 1.4 ng/mL (normal 1,6-3,6 ng/mL), proinsulin - 86.0 pmol/L (normal 0,35-4,50
pmol/L), negative sulfonylurea screen, with mild confusion present. After 1 hour, glucose was 4,1 mmol/L,
insulin - 5.9 uU/mL, C-peptide - 1.5 ng/mL, proinsulin - 103.7 pmol/L, with severe neuroglycopenic
symptoms. What is your diagnosis?
Case 2.
The patient 27 years old, complains on regular morning headache, which is present when he awakes.
Patient has type 1 Diabetes Mellitus and takes 82 units of insulin/day. What is your previous diagnosis?
Case 3.
The patient, 42 years old, has Diabetes Mellitus for 12 years, takes 62 unites of insulin daily,
complains on early-morning headache. Fast serum glucose level is 13,2 mmol/l. What is your diagnosis and
treatment?
Case 4.
A 59 years old woman had experienced intermittent fatigue, diaphoresis, and tremors for 6 weeks.
The signs and symptoms characteristically occurred several hours after a meal and would abate as soon as
the patient ate. Two episodes of syncope prompted her to seek medical attention. Because of her medical
history, insulinoma was suspected. Blood analysis revealed a serum glucose level of 1,7 mmol/L (normal,
3.3-6.6 mmol/L) and corresponding serum insulin level of 62 pmol/L (normal 5-25 pmol/L). Proinsulin level
at that time was 0.78 ng/mL (normal <0.2 ng/mL). What is your previous diagnosis?
Case 5.
A 62 years old female patient defines hypoglycemic attacks for 1.5 years. In physical examination the
body mass index (BMI) was 24 kg/m2, initial glucose level was 2,72 mmol/L, plasma insulin level was
17 μIU/ml (5–25 μIU/ml), C-peptide level was 12.9 ng/ml (1.6–3.6 ng/ml). Prolonged supervised fast test
was applied and at the sixth hour of the test hypoglycemic symptoms were occurred. The CT scan showed
no pathology. In the EUS scanning at the pancreas uncinate process, there was a hypoechoic 11 mm nodular
lesion. It was in homogenous echo and well shaped. It was toughed as neuroendocrine tumor. She was
examined for multiple endocrine neoplasia. Magnetic resonance imaging (MRI) of hypophysis, hypophysial
hormonal analysis and intact parathormone levels were normal. What is the best principle of treatment?
Case 6.
A 43 years old female patient defines hypoglycemic attacks for two years. In physical examination
the body mass index (BMI) was 27 kg/m2, initial glucose level was 3,0 mmol/L, plasma insulin level was
16 μIU/ml (5–25 μIU/ml), C-peptide level was 2.7 ng/ml (1.6–3.6 ng/ml). Prolonged supervised fast test was
applied and at the sixteenth hour of the test hypoglycemic symptoms were occurred. Simultaneously taken
blood samples showed the glucose 2,3 mmol/L, plasma insulin 12.7 μIU/ml, insulin/glucose ratio was 0,52.
What should be your next diagnostic step?
Standards of answers to the self- assessment examination.
Theme # 6. Insulinoma. Early diagnosis, clinical presentation, treatment.
Case 1.
In this case, a proinsulinoma resulted in severe hypoglycemia in an otherwise healthy, young patient.
Case 2.
Hypoglycemic status. (You have to investigate blood glucose level at 3 o’clock in the morning and if the
level is low decrease the dose of insulin.)
Case 3.
Somogyi phenomenon. Treatment: gradual reduction of insulin dose.
Case 4.
This led to a diagnosis of insulinoma.
Case 5.
The best principle of treatment is the surgical operation.
Case 6.
The next diagnostic tests are CT scan and magnetic resonance imaging (MRI) of hypophysis,
hypophysial hormonal analysis and intact parathormone levels.
REFERENCES
PRINCIPAL REFERENCES
1. Lectures.
2. Endocrinology. Textbook/ Study Guide for the Practical Classes. Ed. by prof. Petro M. Bodnar: Vinnytsya: NOVA KNYHA Publishers, 2008. – 496 pp.: Art.
3. Endocrinology Studie Guide for the Practical Classes Ed. by prof. Petro M. Bodnar, academician
APS of Ukraine Sergey D. Maksymenko. Kiev, 2007, 102 p.
4. Basic & Clinical Endocrinology. Seventh edition. Edited by Francis S. Greenspan, David G. Gardner.
– Mc Grew – Hill Companies, USA, 2004. – 976 p.
5. Oxford handbook of endocrinology and diabetes. Edited by Helen E. Turner, John A.H. Wass.
Oxford, University press. 2006. – 1005 p.
6. Harrison′s Endocrinology.Editor J. Larry Jameson. Mc Grew – Hill, USA, 2006. – 563 p.
7. International Textbook of Diabetes Mellitus Edited by R.A. Defronzo, E. Ferrannini, H. Keen, P.
Zimmet. John Wiley & Sons, Ltd. England, 2004. – vol. 1 – 1100 p., vol. 2 – 1913 p.
1.
2.
3.
4.
5.
SUPPLIMENTARY REFERENCES:
Cryer P.E. Glucose homeostasis and hypoglycemia. In: Kronenberg H.M., Shlomo M., Polonsky
K.S., Larsen P.R., eds. Williams Textbook of Endocrinology. 11th ed. Philadelphia, Pa: Saunders
Elsevier; 2008:chap 33.
Dhumbe V.M., Amarapurkar A.D., Rege J.D. et al. Insulinoma- a case report. Indian Journal
Pathology Microbiology 2004; 47: 540-1.
Fajans S.S., Vinik A.I.: Diagnosis and treatment of insulinoma. In Diagnosis and Management of
Endocrine Related Tumors. Fanten R.J., Manni A., Eds. Boston, Martinus Nijhoff, 1984, p. 235.
Starke A., Saddig C., Kirch B., Tschahargane C., Goretzki P.: Islet hyperplasia in adults: challenge to
preoperatively diagnose non-insulinoma pancreatogenic hypoglycemia syndrome. World J. Surg.
30:670-679, 2006.
Yao M.M., Reynertson R.H. Insulinoma: a case report and review of the clinical features and
diagnosis. Gundersen Lutheran Medical Journal 2005; 3: 73-6.
Prepared by MD, PhD, Associate of professor Kostitska I.O.
Adopted at the Chair Sitting №…… , …… . … . 2010 y.
MINISTRY OF HEALTH, UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY
CHAIR OF ENDOCRINOLOGY
METHODOLOGICAL PROTOCOLS BY POST-AUDITORIUM
INDIVIDUAL WORK OF ENDOCRINOLOGY
FOR FOURTH - YEAR STUDENTS
OF FACULTY OF PREPARATION OF FOREIGN CITIZENS
WITH THE SPECIALITY “MEDICINE”
Theme # 7. ATYPICAL FORMS OF HYPOTHYROIDISM.
DIFFERENTIAL DIAGNOSIS, CLINICAL PRESENTATION.
IFNMU
2010
Actually
Hypothyroidism is defined as the insufficient production of thyroid hormone. Secondary
hypothyroidism as a result of dysfunction of hypothalamic and pituitary hormone secretion are much less
common but should be suspected in a patient with a history suggestive of Sheehan syndrome or with
symptoms or signs of a tumor in the region of the sella. Ninety-five percent of cases of hypothyroidism are
caused by primary thyroid gland failure, resulting in insufficient thyroid hormone production. The most
common cause of hypothyroidism is lymphocytic (Hashimoto) thyroiditis, in which cytotoxic antibodies are
produced, which leads to thyroid atrophy and fibrosis. The next most common cause is surgical or
radioactive iodine treatment for hyperthyroidism, or Graves disease. Worldwide, iodine deficiency is the
most common cause of goiter (enlarged thyroid) hypothyroidism. Most hypothyroid patients present with
vague and nonspecific symptoms.
1.
2.
3.
4.
Study aim
To know:
The place of hypothyroidism in the structure of endocrinology diseases;
To the differential diagnosis of hypothyroidism with other diseases;
The etiology, pathogenesis of hypothyroidism;
The modern methods of treatment of hypothyroidism.
To be able:
Clinical and pathogeneses substantiation of hypothyroidism, laboratory and instrumental methods;
Principle of palpation of thyroid gland;
Timely to diagnostic atypical forms of hypothyroidism.
Base knowledges, abilities, skills, necessary are studying themes.
Discipline
Physiology
Pathology Physiology
Functional Diagnostics
To know
Physiological role of thyroid hormones
Changes in the amount of thyroid
hormones, their causes
Diagnostic methods of patients with
hypothyroidism
To be able
Determination (laboratory
diagnostic) of thyroid hormones
Definition of metabolism in humans
with hypothyroidism
Dates interpretation of thyroid
ultrasound, determine the
concentration of thyroid hormones
in the blood
Assessment questions:
1.
2.
3.
4.
5.
6.
Definition of atypical forms of hypothyroidism.
Classification of hypothyroidism.
Causes of atypical forms of hypothyroidism.
Primary, secondary hypothyroidism: etiology and pathogenesis.
Changes of the skin and subcutaneous adipose tissue in patients with hypothyroidism.
Changes of cardiovascular system, nervous system and gastrointestinal tract in patients with
hypothyroidism.
7. Clinical peculiarities of congenital hypothyroidism.
8. Syndrome of galactorhea - amenorhea.
9. Laboratory and instrumental signs of atypical forms of hypothyroidism.
10. Differential diagnosis of atypical forms of hypothyroidism.
11. Principle of treatment of atypical forms of hypothyroidism.
Self-assessment examination:
# 1.
An individual with cirrhosis who has decreased production of thyroid-binding globulin (TBG) yet clinically
is euthyroid would most likely have which one of the listed sets of laboratory values?
A.
B.
C.
D.
E.
Serum T4
Normal
Decreased
Normal
Decreased
Decreased
Serum T3
Normal
Normal
Decreased
Normal
Decreased
Serum TSH
Normal
Normal
Normal
Decreased
Normal
# 2.
An 8-month-old infant is being evaluated for growth and mental retardation. Physical examination reveals a
small infant with dry, rough skin; a protuberant abdomen; periorbital edema; a flattened, broad nose; and a
large, protuberant tongue. Which one of the listed disorders is the most likely cause of this infant’s signs
and symptoms?
A. Graves’ disease
B. Cretinism
C. Toxic multinodular goiter
D. Toxic adenoma
E. Struma ovarii
# 3.
A perimenopausal woman presents with increasing swallowing difficulty and fatigue. Physical examination
reveals that her thyroid is enlarged (palpable goiter). Laboratory examination of her serum reveals T4 of 4.9
mg/dL, free T4 of 2.5 ng/dL, and TSH of 5.5 mIU/mL. No thyroidstimulating immunoglobulins are
identified in the serum, but antimicrosomal antibodies are present. Which one of the listed histologic
findings, if present in a thyroid biopsy from this individual, would be most consistent with a diagnosis
of Hashimoto’s thyroiditis?
A. Lymphocytic infiltrate without follicle formation
B. Intense lymphoplasmacytic infiltrate with lymphoid follicles and scattered oxyphilic cells
C. Hyperplasia of follicular cells with scalloping of colloid at the margin of follicles
D. Granulomatous inflammation with multinucleated giant cells surrounding fragments of colloid
E. Dense fibrosis within the thyroid gland extending into adjacent soft tissue
# 4.
Histologic sections of a follicular carcinoma of the thyroid would characteristically reveal:
A. An amyloid stroma intermixed with neoplastic C cells
B. Blood vessel and capsular invasion by malignant thyroid follicles
C. Diagnostic nuclear changes including “Orphan Annie eyes,” nuclear grooves, and intranuclear
inclusions
D. Papillary fronds with fibrovascular cores and psammoma bodies
E. Undifferentiated anaplastic cells with occasional giant cells
# 5.
A 37 years old man presents with a single, firm mass within the thyroid gland. This patient’s father
developed a tumor of the thyroid gland when he was 32 years of age. Histologic examination of the mass in
this 37 years old male reveals organoid nests of tumor cells separated by broad bands of stroma, as seen in
the photomicrograph below. The stroma stains positively with Congo red stain and demonstrates yellowgreen birefringence.The most likely diagnosis of this lesion is:
A. Follicular carcinoma
B. Papillary carcinoma
C. Squamous cell carcinoma
D. Medullary carcinoma
E. Anaplastic carcinoma
# 6.
A 42 years old woman presents to your office for her annual physical. On examination, you note neck
fullness. When you palpate her thyroid, it is enlarged, smooth, rubbery, and nontender. The patient is
asymptomatic. You send her for thyroid function testing: her T4, free T4, and T3 are normal, but her TSH is
slightly elevated. Which of the following is the most likely diagnosis?
A. Iodine deficiency
B. Thyroid cancer
C. Hashimoto thyroiditis
D. Graves disease
E. Multinodular goiter
# 7.
Which of the following laboratory tests could be performed to confirm your diagnosis of the patient in
Question 6?
A. Repeat thyroid function tests
B. Thyroid ultrasound
C. Nuclear thyroid scan
D. Antithyroid antibody tests
E. Complete blood count with differential
# 8.
A 19 years old gymnast active in national competition is brought to your office by her mother because the
daughter’s menses have ceased for the last 3 months. Prior to this, she was always regular. She denies excess
dieting, although she does work out with her team 3 hours daily. Her physical examination is normal except
for her body mass index (BMI) of 20 kg/m2. Which of the following laboratory tests should be ordered
first?
A. Thyroid function tests
B. Complete blood count
C. Luteinizing hormone (LH)/follicle-stimulating hormone (FSH)
D. Prolactin
E. Beta-hCG
# 9.
A 35 years old woman who was diagnosed with hypothyroidism 4 weeks ago presents to your office
complaining of persistent feelings of fatigue and sluggishness. After confirming your diagnosis with a
measurement of the TSH, you started her on levothyroxine 50 μg daily. She has been reading about her
diagnosis on the Internet and wants to try desiccated thyroid extract instead of the medicine you gave her.
On examination, she weighs 95 kg, her heart rate is 64 bpm at rest, and her blood pressure is normal. Which
of the following is the best next step?
A. Tell her that this delay in resolution of symptoms is normal and schedule a follow-up visit with
her in 2 months
B. Change her medication, as requested, to thyroid extract and titrate
C. Increase her dose of levothyroxine and have her come back in 4 weeks
D. Tell her to start a multivitamin with iron to take with her levothyroxine
Case 1.
A 38 years old woman presents to your office for evaluation of menstrual irregularity. She states that her
periods started when she was 12 years old, and they have been fairly regular ever since, coming once every
28 to 30 days. She has had three previous uncomplicated pregnancies and deliveries. However,
approximately 9 months ago, her cycles seemed to lengthen, and for the last 3 months she has not had a
period at all. She stopped breast-feeding 3 years ago, but over the last 3 months she noticed that she could
express a small amount of milky fluid from her breasts. She had a bilateral tubal ligation after her last
pregnancy, and she has no other medical or surgical history. She takes no medications except multivitamins.
Over the last year or so, she thinks she has gained about 10 kg, and she feels as if she has no energy despite
adequate sleep. She has noticed some mild thinning of her hair and slightly more coarse skin texture. She
denies headaches or visual changes. Her physical examination, including pelvic and breast examinations, are
normal. She is not obese or hirsute. You elicit slight whitish nipple discharge. Her pregnancy test is negative.
What is the most likely diagnosis?
What is the most likely etiology for the condition?
Case 2.
The patient, 35 years old, 3 month ago has subtotal thyroidectomy. She complaints on fatigue,
somnolence, constipation, edema on the face, changing of the voice. During examination was found: skin
pale, thick and cold, face enlarged, pulse – 58/minute, blood pressure is decreased.
What is the most likely diagnosis?
What is the most likely the plan of examination?
Standards of answers to the self- assessment examination.
Theme # 7. Atypical forms of hypothyroidism. Differential diagnosis, clinical presentation.
1.
2.
3.
4.
B.
B.
B.
B.
5.
6.
7.
8.
9.
D.
C.
D.
E.
C.
Case 1.
Most likely diagnosis: Oligomenorrhea and galactorrhea due to hypothyroidism.
Most likely etiology: In this patient with symptoms of weight gain, fatigue, thinning hair, and galactorrhea
in the setting of previously normal menses, hypothyroidism is the most likely diagnosis.
Case 2.
Most likely diagnosis: Primary, postoperative hypothyroidism.
Most likely of plan of examination: Level of thyroid hormones T4, T3, TSH and fat metabolism cholesterol.
REFERENCES
PRINCIPAL REFERENCES
Lectures.
Endocrinology. Textbook/ Study Guide for the Practical Classes. Ed. by prof. Petro M. Bodnar: Vinnytsya: NOVA KNYHA Publishers, 2008. – 496 pp.: Art.
Endocrinology Studie Guide for the Practical Classes Ed. by prof. Petro M. Bodnar, academician APS of
Ukraine Sergey D. Maksymenko. Kiev, 2007, 102 p.
Basic & Clinical Endocrinology. Seventh edition. Edited by Francis S. Greenspan, David G. Gardner. –
Mc Grew – Hill Companies, USA, 2004. – 976 p.
Harrison′s Endocrinology.Editor J. Larry Jameson. Mc Grew – Hill, USA, 2006. – 563 p.
1.
2.
3.
4.
SUPPLIMENTARY REFERENCES:
Cooper D.S.: Clinical practice. Subclinical hypothyroidism. N. Engl. J. Med. 2001; 345:260–265.
Dillman W.H.: The thyroid. In Goldman L., Bennett J.C. (eds): Cecil Textbook of Medicine, 21st ed.
Philadelphia, WB Saunders, 2000, p.p. 1231–1250.
Santiago-Fernandez P., Torres-Barahona R., Muela-Martinez J.A., et al. Intelligence quotient and
iodine intake: a cross-sectional study in children. J. Clin. Endocrinol. Metab. Aug 2004; 89(8):
3851-7.
Romanchishen A.F., Lakovlev P.N. Special surgical treatment of patients with nodular tumors of the
thyroid gland against the background of diffuse toxic goiter. Vestn. Khir. Im. I. I. Grek. 2005;
164(1): 21-4.
Prepared by MD, PhD, Associate of professor Kostitska I.O.
Adopted at the Chair Sitting №…… , …… . … . 2010 y.
MINISTRY OF HEALTH, UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY
CHAIR OF ENDOCRINOLOGY
METHODOLOGICAL PROTOCOLS BY POST-AUDITORIUM
INDIVIDUAL WORK OF ENDOCRINOLOGY
FOR FOURTH - YEAR STUDENTS
OF FACULTY OF PREPARATION OF FOREIGN CITIZENS
WITH THE SPECIALITY “MEDICINE”
Theme # 8. TOXIC ADENOMA. EARLY DIAGNOSIS,
CLINICAL PRESENTATION, TREATMENT.
IFNMU
2010
Actually
Hyperthyroidism has no uniform etiology. Of three patients, only two fit the picture of the syndrome
described first by Graves and later, in more detail, by Basedow. The third patient's hyperthyroidism is caused
by a toxic thyroid adenoma. Toxic adenoma accounted for 9.5 % of a series of 680 thyrotoxic patients.
Comparison of the 65 cases of toxic adenoma with the 615 cases of Graves disease revealed that the former
group presented a milder clinical picture, without overt toxicity in about 40 % of the cases. Approximately 1
in 10, to 1 in 20 solitary nodules present with hyperthyroidism. This varies from country to country, being
more common in Europe than in the USA. The problem is 5 times more common in women than men. The
proportion of cases of thyroid toxic adenoma with hyperthyroidism was 33% in males, but only 17% in
females.
1.
2.
3.
4.
5.
6.
Study aim
To know:
Risk factors for thyroid adenoma;
Early detection of disease;
Learn the complications of thyrotoxicosis, including thyroid storm;
Understand the evaluation of a patient with a thyroid nodule;
Histological of thyroid adenoma;
Principle of treatment of toxic thyroid adenoma.
1.
2.
3.
4.
To be able:
Show a history of risk factors of thyroid adenoma;
Be able to discuss the causes of hyperthyroidism, including Graves disease and toxic nodule;
To identification of thyroid pathology;
Differentiated to provide to treatment the patients with thyroid adenoma.
Base knowledges, abilities, skills, necessary are studying themes.
Discipline
Oncology
Histology
Human pathology
To know
To be able
Key indicators of service of patients with To conduct early diagnosis of toxic
thyroid adenoma;
thyroid adenoma;
Principles of cancer care.
Right-to guide patient treatment.
Histological variants of toxic thyroid
To study preparation (puncture,
adenoma.
biopsy), microscopy.
Groups of thyroid neoplasms;
Macroexamination of thyroid
Histological forms of toxic
tumors;
thyroid adenoma.
Microscopic study of thyroid tumors.
Assessment questions:
1. To define a toxic thyroid adenoma.
2. Etiology and pathogenesis of toxic thyroid adenoma.
3. Histological picture of toxic thyroid adenoma.
4. The clinical presentation of toxic thyroid adenoma.
5. Laboratory diagnostic of toxic thyroid adenoma.
6. Instrumental diagnostic of toxic thyroid adenoma.
7. Diagnosis and differential diagnosis of toxic thyroid adenoma.
8. Prediction of this disease.
9. Principle of treatment of toxic thyroid adenoma.
Self-assessment examination:
# 1.
A 58 years old woman is noted to have Graves disease, and has a nodule toxic goiter. Which of the
following is the best therapy?
A. Long-term propranolol
B. Lifelong oral propylthiouracil (PTU)
C. Radioactive iodine ablation
D. Surgical thyroidectomy
# 2.
Which of the following distinguishes hyperthyroidism from thyroid storm?
A. Tachycardia to heart rate 120 bpm
B. Weight loss
C. Fever and delirium
D. Large goiter
# 3.
A 44 years old woman is noted to be nervous and has heat intolerance. Her thyroid gland is diffusely
enlarged, nontender, with an audible bruit. Her TSH level is very low. Which of the following is the most
likely etiology?
A. Lymphocytic thyroiditis
B. Hashimoto thyroiditis
C. Graves disease
D. Multinodular toxic goiter
# 4.
Graves’ disease is characterized clinically by finding:
A. Central obesity, “moon” face, and abdominal striae
B. Hyperthyroidism, exophthalmus, and pretibial myxedema
C. Polyuria, polydipsia, and hyponatremia
D. Polyuria, polydipsia, and polyphagia
E. Progressive lethargy, cold intolerance, and myxedema
# 5.
The term goiter refers to
Any enlargement of the thyroid regardless of the etiology
Any involution of the thyroid regardless of the etiology
Enlargement of the thyroid secondary to Graves’ disease
Enlargement of the thyroid secondary to the ingestion of goitrogens
Involution of the thyroid secondary to Hashimoto’s thyroiditis
Case 1.
A 37 years old previously healthy woman presents to your clinic for unintentional weight loss. Over
the past 3 months, she has lost approximately 8 kg without changing her diet or activity level. Otherwise, she
feels great. She has an excellent appetite, no gastrointestinal complaints except for occasional loose stools, a
good energy level, and no complaints of fatigue. She denies heat or cold intolerance. On examination, her
heart rate is 108 bpm, blood pressure 142/82 mm Hg, and she is afebrile. When she looks at you, she seems
to stare, and her eyes are somewhat protuberant. You note a large, smooth, nontender thyroid gland, a 2/6
systolic ejection murmur on cardiac examination, and her skin is warm and dry. There is a fine resting
tremor.
What is the most likely diagnosis?
How could you confirm the diagnosis?
What are the options for treatment?
Standards of answers to the self- assessment examination.
Theme # 8.
1.
2.
3.
4.
5.
D.
C.
C.
B.
A.
Case 1.
Most likely diagnosis: Thyrotoxicosis/Graves disease.
Confirming the diagnosis: A low serum thyroid-stimulating hormone (TSH) level and an increased free
thyroxine (T4) level with this clinical presentation would be confirmatory of hyperthyroidism. However,
other tests that would define the etiology would be thyroid-stimulating immunoglobulins or diffusely
elevated uptake of radioactive iodine on thyroid scan.
Treatment options: Antithyroid drugs, radioactive iodine ablation, or less commonly, surgical ablation of
the thyroid.
REFERENCES
PRINCIPAL REFERENCES
1. Lectures.
2. Endocrinology. Textbook/ Study Guide for the Practical Classes. Ed. by prof. Petro M. Bodnar: Vinnytsya: NOVA KNYHA Publishers, 2008. – 496 pp.: Art.
3. Endocrinology Studie Guide for the Practical Classes Ed. by prof. Petro M. Bodnar, academician
APS of Ukraine Sergey D. Maksymenko. Kiev, 2007, 102 p.
4. Singer P.A. Thyroiditis. In: Lavin N., ed. Manual of Endocrinology and Metabolism. Boston, M.A:
Little Brown; 2002:386-395.
5. Basic & Clinical Endocrinology. Seventh edition. Edited by Francis S. Greenspan, David G. Gardner.
– Mc Grew – Hill Companies, USA, 2004. – 976 p.
6. Harrison′s Endocrinology.Editor J. Larry Jameson. Mc Grew – Hill, USA, 2006. – 563 p.
SUPPLIMENTARY REFERENCES
1. American Association of Clinical Endocrinologists. Medical guidelines for clinical practice for the
evaluation and treatment of hyperthyroidism and hypothyroidism. Endocrine Pract. 2002;8:457-469.
2. Belfiore A., Sava L., Runello F., Tomaselli L., Vigneri R. 1983 Solitary autonomously functioning
thyroid nodules and iodine deficiency. J Clin Endocrinol Metab. 56:283–287.
3. Davies D.F., Larsen T.F. Thyrotoxicosis. In: Wilson J.D., Foster D.W., Kronenberg H.M., et al., eds.
Williams Textbook of Endocrinology. 9th ed. Philadelphia, PA: WB Saunders; 2003: 372-421.
4. Hay I.D., Morris J.C. 1996 Toxic adenoma and toxic multinodular goiter. In: Braverman L.E., Utiger
R.D., eds. Werner and Ingbar’s the thyroid. Philadelphia: Lippincott-Raven; 566–572.
5. McDermott M.T. Thyroid emergencies. In: Endocrine Secrets. Philadelphia, P.A: Hanley and Belfus;
2002: 302-305.
6. MacFarlane I. 2000 Thyroid disease. Pharm. J. 265; 240-244.
7. Wiener J.D. 1987 Plummer’s disease: localized thyroid autonomy. J. Endocrinol. Invest. 10:207–224.
Prepared by MD, PhD, Associate of professor Kostitska I.O.
Adopted at the Chair Sitting №…… , …… . … . 2010 y.
MINISTRY OF HEALTH, UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY
CHAIR OF ENDOCRINOLOGY
METHODOLOGICAL PROTOCOLS BY POST-AUDITORIUM
INDIVIDUAL WORK OF ENDOCRINOLOGY
FOR FOURTH - YEAR STUDENTS
OF FACULTY OF PREPARATION OF FOREIGN CITIZENS
WITH THE SPECIALITY “MEDICINE”
Theme # 9. ADRENO-GENITAL SYNDROME.
EARLY DIAGNOSIS, CLINICAL PRESENTATION, TREATMENT.
IFNMU
2010
Actually
Adreno - genital syndrome is a group of disorders caused by adrenocortical hyperplasia or malignant
tumors, resulting in abnormal secretion of adrenocortical hormones and characterized by masculinization of
women, feminization of men, or precocious sexual development in children. About 1 in 10,000 to 18,000
children are born with congenital adrenal hyperplasia. A newborn screening test is available for the most
common form of congenital adrenal hyperplasia and can be done on heelstick blood (as part of the routine
screenings done on newborns).
Study aim
To know:
1. Control mechanism at the level of sex hormones hypothalamus-pituitary-adrenal-ovarian;
2. Menstrual regulation;
3. The differential diagnosis with other pathological conditions - clinical, laboratory and instrumental
research.
To be able:
1. Collect gynecological anamnesis;
2. Diagnostic of organ damage.
Base knowledges, abilities, skills, necessary are studying themes.
To know
Mechanism of regulation of sex hormones.
Mechanism of regulation of hormone
Path. Physiology
disorders.
Synthesis of sex hormones.
Biochemistry
Gynecological and endocrinology aspects
Obstetric and Gynaecology
of pathology.
Neiroendocrinology syndromes.
Endocrinology
To be able
Discipline
Physiology
Diagnostic tests set.
Diagnostic tests set.
Assessment questions:
1. Anatomical and physiological features of the reproductive system.
2. Hormones of the reproductive system.
3. Premature male sexual development.
4. Hormone producing tumors of testis.
5. Main principles of hormone regulation with regard to the reproductive system.
6. Assess methods of reproductive status. Diagnostic methods.
7. Classification of adreno - genital syndrome.
8. Laboratory diagnostic of all forms adreno - genital syndrome.
9. Principle of treatment of other forms of adreno-genital syndrome.
10. Classification of hermaphroditism.
11. Stein-Leventhal syndrome.
12. Virilization.
13. Hormone producing tumors of ovaries.
14. Clinical signs of delayed puberty.
15. Signs of hypogonadism depends on age.
16. Clinical features of hy pergonadotropic hypogonadism in girls.
17. Clinical features of secondary hypogonadism in girls: clinical signs, diagnosis.
Self-assessment examination:
# 1.
Which of the following results would be diagnostic of this patient's condition?
A. Decreased serum ACTH
B. Decreased serum aldosterone
C. Increased serum DHEA
D. Increased serum 17-OH-progesterone
E. Increased urinary 17-ketosteroids
# 2.
If a young woman had 11-hydroxylase deficiency, which of the following presentations would be most
likely?
A. Adrenal insufficiency
B. Elevated 11-deoxycortisol
C. Hyperkalemia and hypotension
D. Increased aldosterone
E. Normal menses and hair growth
# 3.
Overproduction of androgens is evidenced by:
A. Low level of 17-KS in urine
B. Hirsutism
C. Gigantism
D. Cretinism
E. Mental retardation
# 4.
Temporary lack of pubertal development due to the following conditions, except:
A. Isolated gonadotropin deficiency
B. Malnutrition
C. Emotional stress
D. Excessive physical stress
E. Untreated endocrinopathies
# 5.
What statement is not correct relatively to the polycystic ovary syndrome?
A. Alopecia is common
B. Polycystic ovary syndrome presents with elevated androgen levels
C. Patients with polycystic ovary syndrome have amenorrhea
D. Hirsutism is common
E. Obesity is often found
# 6.
Choose the drug, which will not cause gynecomastia
A. Isoniazid
B. Cimetidine
C. Hexestrolum
D. Metformin
E. Digitoxin
# 7.
Differential diagnosis of ambiguous genitalia includes the following measures, except:
A. Bone age x ray
B. Physical examination
C. Contrast urography
D. Chromosomal evaluation
E. Stimulation or suppression tests
Case 1.
An 8 year old male child presented with fever. On routine examination it was observed that there was
bilateral cryptorchidism and presence of pubic hair corresponding to SMR stage 3. The scrotum was well
developed and the penis was small (with no prepuce) with an urethral opening at its tip. There was
generalized hyper-pigmentation and presence of acne. These findings prompted investigation for ambiguous
genitalia. Abdominal CT scan revealed presence of uterus and its adenexa and bilateral adrenal enlargement.
Karotyping revealed 46-XX genotype. The serum 17-hydroxyprogesterone (17-OHP) level was 2.8 ng/mL
(normal: 0.2-0.5 ng/mL) and urinary 17-ketosteroids was 18 mg/d (normal: 1-4 mg/d). The clinical findings
and investigations suggested the diagnosis of a female pseudohermaphrodite. What is the preliminary
diagnosis?
Case 2.
A mother brings her 2-week-old daughter to the emergency department because of protracted
vomiting. She states her baby has been vomiting for the last few days and was not tolerating any milk, or
water. The baby had been "very fussy" but had not been feverish. The course of her pregnancy was
uneventful and she was vaginally delivered without any complications. On examination, the baby appears ilI,
but well developed. Her blood pressure is 50/30 mm Hg, pulse is 176/min, and respiratory rate is 35/min.
Her oral mucosa look dry and she is not tearing much. Her anterior fontanelle appears sunken, and mild
tenting can be elicited in her skin. An enlarged clitoris and partial fusion of the labial folds is noted. Serum
electrolytes are significant for sodium of 123 mEq/L, chloride of 92 mEq/L, and bicarbonate of 27 mEq/L.
Which of the following is most likely diagnosis?
Case 3.
An 11 days old infant with abnormal genitalia and failure to thrive since birth was referred to
hospital. On the 3rd day the infant had blood-stained purulent discharge from the abnormal genital opening.
She was vomiting 2-3 time a day and having 4-5 loose stools/ day containing no blood or mucus. On
examination she weighed 2,5 kg was ashen grey in color, marasmic and degydrated. The pulse was of feeble
volume, the rate – 144/min. Abdomen, heart, chest, nervous system were normal. Local examination showed
increased pigmentation around the genitalic. The clitoris was enlarged to 2,5 cm. The labila majora had
horizontal folds. What is the preliminary diagnosis?
Case 4.
A 22 years old male presented with palpable painless hardness mass lesions over bilateral testes for
two weeks. He had no history of trauma or other systemic disease. General physical examination was
normal. Laboratory studies, including complete blood count, routine urinalysis, blood coagulation studies,
blood biochemistry tests, carcinoembryonic antigen (CEA), and α-fetoprotein (AFP) tests were normal.
Endocrine evaluation revealed normal thyroid function tests and values of testosterone, estradiol, folliclestimulating hormone, luteinizing hormone, cortisol, and prolactin were normal in limits. The ACTH level –
61,3 pg/mL (normal range: 9.0~52.0 pg/mL) was found to be elevated. The semen analysis showed
azoospermia. Chromosomal analysis was normal as 46,XY. The scrotal ultrasonography (US) revealed
normal size of both testes and several round to oval hypoechoic lesions, 8 mm ~ 1.7 cm in diameter, in
bilateral mediastinum testes. They were sharply delineated from the normal parenchyma and had no acoustic
attenuation or enhancement. On magnetic resonance (MR) imaging, the lesions were isointense or
hypointense on T1-weighted and hypointense on T2-weighted MR images as compared with normal
testicular parenchyma. Which of the following is most likely diagnosis?
Standards of answers to the self- assessment examination.
Theme # 9.
D.
B.
B.
A.
A.
D.
A.
Case 1. Congenital adrenal hyperplasia resulting in adreno-genital syndrome.
Case 2. Congenital adrenal hyperplasia.
Case 3. Adreno-genital syndrome. Salt-losing form of C21-hydroxylase deficiency.
Case 4. Adrenal Nodular Hyperplasia with so Called Testicular Tumor of Adreno-genital syndrome.
REFERENCES
PRINCIPAL REFERENCES
1. Lectures.
2. Endocrinology. Textbook/ Study Guide for the Practical Classes. Ed. by prof. Petro M. Bodnar: Vinnytsya: NOVA KNYHA Publishers, 2008. – 496 pp.: Art.
3. Endocrinology Studie Guide for the Practical Classes Ed. by prof. Petro M. Bodnar, academician
APS of Ukraine Sergey D. Maksymenko. Kiev, 2007, 102 p.
4. Basic & Clinical Endocrinology. Seventh edition. Edited by Francis S. Greenspan, David G. Gardner.
– Mc Grew – Hill Companies, USA, 2004. – 976 p.
5. Harrison′s Endocrinology.Editor J. Larry Jameson. Mc Grew – Hill, USA, 2006. – 563 p.
SUPPLIMENTARY REFERENCES
1. Fetal Adrenal Development. In Williams Obstetrics, 20th ed. Stamford, CT: Appleton & Lange,
1997.
2. Fetal Treatment. In Medical Genetics, ed. Lynn B. Jorde, et al. St. Louis: Mosby, 1995.
3. Hay Jr., William W., et al., eds. Current Pediatric Diagnosis and Treatment. Stamford, CT: Appleton
& Lange, 1997.
4. Richard A.A., Shawn M.M., Philip A.I., et al. Clinical and pathological features associated with the
testicular tumor of the adrenogenital syndrome. J. Urol. 2007; 177: 546-549
Prepared by MD, PhD, Associate of professor Kostitska I.O.
Adopted at the Chair Sitting №…… , …… . … . 2010 y.
MINISTRY OF HEALTH, UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY
CHAIR OF ENDOCRINOLOGY
METHODOLOGICAL PROTOCOLS BY POST-AUDITORIUM
INDIVIDUAL WORK OF ENDOCRINOLOGY
FOR FOURTH - YEAR STUDENTS
OF FACULTY OF PREPARATION OF FOREIGN CITIZENS
WITH THE SPECIALITY “MEDICINE”
Theme # 10. METABOLIC OSTEOPATHIES ASSOCIATED
WITH ENDOCRINOPATHIES.
IFNMU
2010
Actually
Osteoporosis, a condition characterized by decreased bone strength, is prevalent among postmenopausal
women but also occurs in men and women with underlying conditions or major risk factors associated with
bone demineralization. Its chief clinical manifestations are vertebral and hip fractures, although fractures can
occur at any skeletal site. Osteoporosis affects 10 million individuals in the United States, but only a small
proportion are diagnosed and treated. Endocrinous osteoporosis constitutes the largest group among the
secondary osteoporosis. This problem has been thoroughly studied in Ukraine at the Gerontology Institute
(prof. V. V. Povoroznjuk et al., 2001), under the Academy of Medical Sciences of Ukraine and
V. P. Komyssarenko Institute of Endocrinology and Metabolic Processes under the Academy of Medical
Sciences of Ukraine (prof. V. А. Oleinyk et al., 2000).
Study aim
1.
2.
3.
4.
5.
6.
To know:
Factors that influence the functional status of bone tissue;
The main risk factors for osteoporosis;
Classification of osteoporosis;
Clinical picture of osteoporosis;
Diagnostic criteria of osteoporosis;
Principles of prevention and treatment of osteoporosis.
To be able:
1. Reveal a history of risk factors of osteoporosis;
2. Diagnostic criteria of osteoporosis using X-ray, morphometric, histochemical, densitometric,
biochemical methods;
3. Appoint a permanent and preventive treatment of osteoporosis.
Base knowledges, abilities, skills, necessary are studying themes.
Discipline
Physiology
Path. Physiology
Radiology
Biochemistry
Endocrinology
To know
Calcium homeostasis in the human body
Disturbance of calcium homeostasis in
the human body
X-ray of the bones and densitometry
Biochemical markers of bone metabolism
Risk factors for osteoporosis
To be able
Identify of pathological disturbance
in the bones.
Rate data obtained
Identify risk factors of osteoporosis
in anamnesis
Assessment questions:
1. The most important first messengers for Dental Biochemistry include parathyroid hormone,
calcitonin, insulin, and glucagon.
2. Define calcium balance.
3. Anatomy and physiology of a bone tissue.
4. The function of main cells of a bone tissue – osteoclasts, osteoblasts, osteocytes.
5. Hormonal regulation of bone remodeling.
6. Classification of endocrine osteoporosis.
7. Describe the properties and mechanism of action of parathyroid hormone (PTH) including G-protein
function.
8. Review the composition of bone, and know what bone mineral is?
9. What are the two main functions of parathyroid hormone in kidney?
10. Describe the metabolic activation of vitamin D.
11. What are the actions of vitamin D?
12. What is osteomalacia? Hyperparathyroidism? Pseudohypoparathyroidism?
13. What is osteoporosis?
14. Describe physiological ways to establish and maintain maximum bone density.
15. What foods are good sources of dietary calcium?
16. Make a scheme of development of osteoporosis in case of the main endocrine diseases.
17. Clinics of osteoporosis.
18. Diagnostics and differential diagnostics of osteoporosis.
19. Prophylaxis and treatment of osteoporosis.
Self-assessment examination:
# 1.
Which of the following patients is most likely to be a candidate for bone mineral density screening?
A. A 65-year-old, thin, white woman who smokes and is 15 years postmenopausal
B. A 40-year-old white woman who exercises daily and still menstruates
C. A healthy 75-year-old white man who is sedentary
D. A 60-year-old overweight African American woman
E. A 35-year-old asthmatic woman who took prednisone 40 mg/d for a 2-week course 1 week ago
#2.
During which of the following periods in a woman’s life is the most bone mass accumulated?
A. Ages 15 to 25
B. Ages 25 to 35
C. Ages 35 to 45
D. Ages 45 to 55
# 3.
A 60 years old woman presents with the results of her DEXA scan. She has a T score of −1.5 SD at
the hip and −2.5 at the spine. Which of the following is the most accurate interpretation of these results?
A. She has osteoporosis at the spine and osteopenia at the hip
B. She has osteoporosis in both areas
C. This is a normal examination
D. She has osteoporosis of the hip and osteopenia at the spine
E. You need to know the Z score
# 4.
You see a 70-year-old woman in your office for a routine checkup, and you order a DEXA scan for
bone mineral density screening. The T score returns as −2.5 standard deviations SD in the spine and −2.6 in
the hip. Which of the following statements is most accurate?
A. This patient has osteopenia
B. Estrogen replacement therapy should be started with an anticipated rebuilding of bone mass to nearnormal within 1 year
C. Swimming will help build bone mass
D. Bisphosphonates would reduce the risk of hip fracture by 50%
# 5.
Which one of the listed signs or symptoms is more characteristic of hypocalcemia than of
hypercalcemia?
A. Calcium stones in the urine
B. Metastatic calcification
C. Peptic ulcers
D. Psychiatric changes
E. Tetany
# 6.
A 62-year-old asymptomatic woman is noted to have multiple myeloma and an elevated calcium level,
but no bone lesions or end-organ damage. Which of the following therapies is useful for immediate
treatment of the hypercalcemia?
A. Bisphosphonates
B. Erythropoietin
C. Dexamethasone plus thalidomide
D. Interferon-a
E. Observe without treatment since she is asymptomatic
Case 1.
A 75 years old white woman presents to the emergency room with right wrist pain after a fall at home.
She tripped and fell while preparing dinner, and she says that she tried to stop her fall with her outstretched
right hand. She heard a “snap” and felt immediate pain. Her medical history is remarkable only for three
normal pregnancies, menopause at age 50 years, and hypertension that is well controlled with diuretics. She
has a 50-pack per year history of smoking. Her weight is 85 kg and her height is 174 cm. Her examination is
remarkable for normal vital signs; a swollen, deformed right distal forearm and wrist, with limited mobility
because of pain; and good radial pulses and capillary refill in the right fingernail beds. An X-ray confirms a
fracture of the right radial head, and the radiologist notes osteopenia.
1. What risk factor for fracture is this woman likely to have?
2. What are the causes of this condition?
3. What can her physician offer her to prevent future fractures?
Standards of answers to the self- assessment examination.
Theme # 10.
1.
2.
3.
4.
5.
6.
A.
A.
A.
D.
E.
A.
Case 1.
1. Risk factor for fracture: Osteoporosis.
2. Causes of this condition: Decreased bone strength as a consequence of demineralization and
increased bone turnover as a result of decreased levels of sex steroids (estrogen and testosterone),
medications, other hormonal conditions, or diseases of decreased calcium absorption.
3. Preventive measures: Several medications are available to increase bone density, which may
decrease the risk of future fractures. Also, her physician would want to work with her to prevent
future falls by limiting unnecessary medications that may cause instability, making changes in the
home environment, and evaluating her gait, visual acuity, and peripheral sensory system. The patient
should be advised to quit smoking.
REFERENCES
PRINCIPAL REFERENCES
1. Lectures.
2. Endocrinology. Textbook/ Study Guide for the Practical Classes. Ed. by prof. Petro M. Bodnar: Vinnytsya: NOVA KNYHA Publishers, 2008. – 496 pp.: Art.
3. Endocrinology Studie Guide for the Practical Classes Ed. by prof. Petro M. Bodnar, academician APS of
Ukraine Sergey D. Maksymenko. Kiev, 2007, 102 p.
4. Basic & Clinical Endocrinology. Seventh edition. Edited by Francis S. Greenspan, David G. Gardner. –
Mc Grew – Hill Companies, USA, 2004. – 976 p.
5. Harrison′s Endocrinology.Editor J. Larry Jameson. Mc Grew – Hill, USA, 2006. – 563 p.
SUPPLIMENTARY REFERENCES
1. Diagnosis and treatment of osteoporosis. Bloomington (MN): Institute for Clinical Systems
Improvement (ICSI); 2008 Sep. 67 p.
2. Heaney R.P. Advances in therapy for osteoporosis. Clin. Med. Res. Apr. 2003;1(2):93-99.
3. Wasnich R.D., Bagger Y.Z., Hosking D.J., et al. Changes in bone density and turnover after
alendronate or estrogen withdrawal. Menopause. Nov-Dec 2004;11((6 Pt 1)):622-630.
Prepared by MD, PhD, Associate of professor Kostitska I.O.
Adopted at the Chair Sitting №…… , …… . … . 2010 y.
MINISTRY OF HEALTH, UKRAINE
IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY
CHAIR OF ENDOCRINOLOGY
METHODOLOGICAL PROTOCOLS BY POST-AUDITORIUM
INDIVIDUAL WORK OF ENDOCRINOLOGY
FOR FOURTH - YEAR STUDENTS
OF FACULTY OF PREPARATION OF FOREIGN CITIZENS
WITH THE SPECIALITY “MEDICINE”
Theme # 11.
IFNMU
2010
Actually
Study aim
To know:
To be able:
Base knowledges, abilities, skills, necessary are studying themes.
Discipline
To know
Path. Physiology
Internal medicine
Pharmacology
Assessment questions:
Self-assessment examination:
# 1.
Standards of answers to the self- assessment examination.
Theme # 11.
B.
C.
B.
D.
A.
D.
B.
D.
C.
A.
D.
C.
B.
A.
B.
REFERENCES
PRINCIPAL REFERENCES
Lectures.
To be able
Endocrinology. Textbook/ Study Guide for the Practical Classes. Ed. by prof. Petro M. Bodnar: Vinnytsya: NOVA KNYHA Publishers, 2008. – 496 pp.: Art.
Endocrinology Studie Guide for the Practical Classes Ed. by prof. Petro M. Bodnar, academician APS of
Ukraine Sergey D. Maksymenko. Kiev, 2007, 102 p.
Basic & Clinical Endocrinology. Seventh edition. Edited by Francis S. Greenspan, David G. Gardner. –
Mc Grew – Hill Companies, USA, 2004. – 976 p.
Oxford handbook of endocrinology and diabetes. Edited by Helen E. Turner, John A.H. Wass. Oxford,
University press. 2006. – 1005 p.
Harrison′s Endocrinology.Editor J. Larry Jameson. Mc Grew – Hill, USA, 2006. – 563 p.
International Textbook of Diabetes Mellitus Edited by R.A. Defronzo, E. Ferrannini, H. Keen, P.
Zimmet. John Wiley & Sons, Ltd. England, 2004. – vol. 1 – 1100 p., vol. 2 – 1913 p.
SUPPLIMENTARY REFERENCES:
Prepared by MD, PhD, Associate of professor Kostitska I.O.
Adopted at the Chair Sitting №…… , …… . … . 2010 y.