MINISTRY OF HEALTH OF UKRAINE

National Pirogov Memorial Medical University, Vinnytsya

«APPROVE»
on methodical meeting of
endocrinology department
Head of endocrinology department,
prof. of HEI Maryna VLASENKO

“_29_”_august___ 2022 y

METHODOLOGICAL RECOMMENDATIONS
FOR INDEPENDENT WORK OF STUDENTS
BY PREPARATION FOR PRACTICAL CLASSES

Scientific discipline ENDOCRINOLOGY

(part of the discipline "Internal Medicine, including
endocrinology")
Мodule № 1 Endocrinology
substantial module №1 “Diagnostic, treatment and prophylactic basis of
main endocrinology diseases”

Topic Topic №12: Cusing‘s syndrome and disease. Etiology,

pathogenesis, clinics, diagnostics, differential
diagnosis, treatment.
Obesity. Clinics, diagnostics, differential diagnosis,
treatment, prophylactics. Methabolic syndrome.
Specialty 222 Medicine
Course 4
Faculty Faculty of Foreign Citizens Training

Vinnytsya – 2022
 Authors:
Ass-prof. of HEI Anatolii PALAMARCHUK, assistant Kateryna BILIAIEVA

METHODOLOGICAL RECOМMENDATIONS
for the students of 4-th course of medical faculty for preparation to the practical
classes from endocrinology
1.Тopic №12: Cusing‘s syndrome and disease. Etiology, pathogenesis, clinics, diagnostics,
differential diagnosis, treatment. Obesity. Clinics, diagnostics, differential diagnosis,
treatment, prophylactics. Methabolic syndrome.

2. Relevance of topic: The hypothalamic area is the integrator of vegetative and endocrine
functions. It occupies the leading part in supporting of a constancy of inner medium of an organism
- a homeostasis, and also keeping periodicity of endocrine functions. The lesion of hypothalamic
area has polymorphic character, that’s why participation of experts of various medical directions is
necessary for its identifcation. The pituitary body is bound directly to a hypothalamus. Its tropic
hormones сontrol peripheric endocrine glands’ activity. The lesion of a pituitary body also is shown
by a polymorphic symptomatology. Somatic displays of a pituitary body’s pathology are various,
variable; they have catastrophic character in case of acute development, and demand precise and
resolute actions for saving patient’s life.
Age and sex play an important role in the frequency of a given type of Cushing’s syndrome.
Adrenal carcinoma is the cause in 65 % of patients younger than 15, nonpituitary ACTH secretion
predominates in males, and 75 % of patients with pituitary – dependent Cushing’s syndrome are
females.
WHO declared obesity as a global epidemy, which is a serious threat to the population’s
health in the world because of the development of concomitant diseases - arterial hypertension,
coronary heart disease, type 2 diabetes mellitus. Mortality risk increases much when BMI is more
than 30 kg/m2.
In 2016, more than 1.9 billion adults, 18 years and older, were overweight. Of these over 650
million were obese. 39% of adults aged 18 years and over were overweight in 2016, and 13% were
obese.
Therefore, obesity is an important medical-social problem now and a factor which deteriorates
the life quality of patients. It has considerable economic consequences. Obesity adversely affects
morbidity and mortality, primarily through cardiovascular complications. The death rate from many
diseases, from accidents, and from surgery, is significantly higher among the obese, increasing with
the magnitude of the obesity. Sudden death is also common.
3. Aim of lesson:
• To learn etiology, pathogenesis, diagnostic criteria and principles of the treatment of
Cushing’s disease and syndrome and hypothalamic syndrome of pubertal period.
• To get acquainted with the spreading of Obesity in Ukraine.
Student must know:
• etiology, pathogenesis, clinical presentation and diagnostic methods of obesity, indications for
surgical treatment;
• strategies and methods of management;
• international classification of obesity.
Student must be able:
• to diagnose obesity accordingly to types, to calculate BMI, to provide curative and preventive
measures;
• to determine the type of fat distribution (gynoid, android) and provide differential diagnostics
between types of obesity;
• to administer the scheme of reducing diet, drug therapy, exercise complex for obese patients.
• to realize deontological principles in diagnostics and treatment practice of obesity
• to achieve habits to establish physiological contact and to create the confdential atmosphere
between doctor and obese patient.
• to form responsibility for well-timed and complete examination of obese patient and for
acknowledgement of patient about possible methods of treatment
4. The students have to:
Students must know:
1. Anatomy and physiology of a hypothalamo – pituitary system.
2. Clinic of Cushing’s disease.
3. Features of Cushing’s disease diagnostics.
4. Principles of differential diagnostics of Cushing’s syndrome from Cush-ing’s disease.
5. The basic directions of treatment of Cushing’s disease.
6. Definition of the Cushing’s syndrome.
7. Etiology, pathogenesis of Cushing’s syndrome.
8. Clinical features of Cushing’s syndrome.
9. Aboratory and instrumental findings in patients with Cushing’s syndrome.
10. Treatment patients with Cushing’s syndrome.

4.2 Students should be able to:

1. Examine the patient with Cushing syndrome, Cushing disease,obesity.
2.Interpret data of the laboratory and instrumental methods of examination of the patient with
Cushing syndrome, Cushing disease, obesity
3.Chose treatment strategy for the patient with adrenal disorders

5. Tests and Assignments for Self-assessment.

Multiple Choice.
Choose the correct answer/statement:
1. Which of these signs can’t be present in patient with pituitary insufficiency?
a. Hypotension.
b. Hyperpigmentation.
c. Weight loss.
d. Hypogonadism.
e. Hypothyroidism.
2. The anterior pituitary does not produce such hormone as:
a. Growth hormone.
b. Thyrotropin.
c. Oxytocin
d. Prolactin.
e. Gonadotropins.
3. A patient I., 16 years old, female, complains of increased body mass, headache, irritability, quick
fatigue. A considerable weight gain has occurred when she was 14. Now body mass is 87 kg,
height is 156 cm, regular body composition. Adipose cellular disposal is equable. There are pink
stria on the hips, abdomen and breasts.
What is the provisional diagnosis?
a. Pubertal-juvenile dispituitarism
b. Alimentary constitutive obesity
c. Cushing disease
d. Neurocirculatory distonia
e. Hypoovarial obesity

4. A 36-years-old patient complains of moderate weight enlargement, breathlessness at physical

exertion. He has no disease in anamnesis. His body mass is 108 kg, height is 160 cm. Body
composition is normal, adipose cellular disposal is equable. What disease has the patient?
a. Alimentary obesity
b. Adipose-genital dystrophy
c. Cushing disease
 d. Hypothalamic obesity
e. Hypoovarial obesity

5. A 28-years-old patient complains of general weakness, which increases to the evening, dyspnea,
frequent headache, thirst. She is ill for 4 years and infuenza is supposed to be the cause. Her height
is 168 cm, body mass is 79 kg. Adipose disposal is dysplastic, prevalent on trunk, upper body. The
face is round, red. The skin is dry. There are deep-red stria on the skin of the abdomen and hips.
Pulse is 92 st/min, blood pressure is 150/90 mmHg.
What is the provisional diagnosis?
a. Cushing disease
b. Cushing syndrome
c. Alimentary obesity
d. Pubertal-juvenile dispituitarism
e. Hypothalamic obesity

6. A patient D., 17 years old, complains of overweight, increased appetite, headache, weakness,
fatigue. She had frequent quinsy before. A growth of weight has begun from the age of 12 years,
especially it progressed at last year. The patient doesn’t limit herself in carbohydrates and doesn’t
follow any diet. Her mother is obese. Patient’s height is 161 cm, body mass is 88 kg. Adipose
cellular disposal is equable. Pulse is 86 st/min, blood pressure 135/85 mmHg.
What is the provisional diagnosis?
a. Alimentary obesity
b. Adipose-genital dystrophy
c. Pubertal-juvenile dispituitarism
d. Hypothalamic obesity
e. Cushing disease
7. A patient M., 16 years old, has overweight. He was born in asphyxia at premature delivery with
body mass 2600 g, length 46 cm. His weight gain has begun at the age of 10. Now his height is 169
cm, body mass is 85 kg. Female stature, gynecomastia are present. Secondary sexual charachters are
bad developed - hair growth at the face is absent, pubic hair is lean. The penis is 3,5 cm length.
What is the provisional diagnosis?
a. Adipose-genital dystrophy;
b. Pubertal-juvenile dispituitarism;
c. Alimentary obesity;
d. Hypothalamic obesity;
e. Cusing‘s disease
Answer: 1 – b. 2 – c. 3 – a. 4 – a. 5 – a. 6 – a. 7 – a.

6. Questions to be learned during the lesson:

1. Clinic of Cushing’s disease.
2. Features of Cushing’s disease diagnostics.
3. Principles of differential diagnostics of Cushing’s syndrome from Cush-ing’s disease.
4. The basic directions of treatment of Cushing’s disease.
5. Definition of the Cushing’s syndrome.
6. Etiology, pathogenesis of Cushing’s syndrome.
7. Clinical features of Cushing’s syndrome.
8. Aboratory and instrumental findings in patients with Cushing’s syndrome.
9. Treatment patients with Cushing’s syndrome.
10. Clinical features of hypothalamic syndrome of pubertal period.
11.Treatment of patients with hypothalamic syndrome of pubertal period.
12.Clinical features of hypothalamo-hypophysial obesities.
13.You should prepare for the practical class using the existing text books and lectures. Special
attention should be paid to the following:
14. Etiology and pathogenesis of obesity.
15. Clinical presentation of obesity and concomitant complications. International classifcation of
 obesity.
16. Diagnostic criteria of different forms of obesity. (Alimentary, hypothalamic,Pickwickian
syndrome, Barrakcer – Simmons’s disease, Babinsky-Frelych’s disease, Dercum’s disease,
Laurence – Moon – Biedl syndrome, Morganyi – Stuart – Morel’s syndrome, postnatal
neuroendocrine syndrome )
17.Methods of treatment of obesity.Main principles of reducing diet. Medicines for treatment of
obesity.

7.Short content of theme

Cushing's syndrome
is a constellation of signs and symptoms caused by prolonged excessive amounts of circulating
cortisol.
The source of cortisol excess can be:
- the adrenal gland (endogenous Cushing's syndrome);
- administration of supraphysiologic doses of a glucocorticoid (exogenous Cushing's syndrome).
Endogenous Cushing's syndrome can be:
1) ACTH – dependent, caused by:
- increased pituitary ACTH secretion (it has frequently been reffered to as Cushing’s disease,
implying a partucular physiologic abnormality. Patients with Cushing’s disease may have a
basophilic adenoma of the pituitary, or a chromophobe adenoma. In some cases, no histologic
abnormality is found in the pituitary despite clear evidence of ACTH overproduction.
Microadenomas, which are difficult to visualize radiographically, are often the cause);
- nonpituitary ACTH secretion by nonendocrine tumors;
2) Non – ACTH – dependent:
- caused by cortisol secretion by benign or malignant adrenal tumors;
- micronodular or macronodular dysplasia of the adrenal (the condition occurs most commonly in
children and young adults).
CUSHING DISEASE
Cushing disease (Icenko-Cushing disease) is a hypothalamo-hypophysial disorder, characterized
with increased secretion of corticotrophin and following bilateral adrenal hyperplasia with their
hyper function (hypercortisolism).
Disease often is observed in females, mostly in 20-50 years of age.
The hypercorticortisolism syndrome consists of the several diseases accompanied with hyper
secretion of steroidal hormones by the adrenal cortex.
Etiology
Etiology isn't completely defined. The predisposed factors are a craniocerebelle injuries,
concussion of the brain, encephalitises, arachnoiditises, labor and pregnancy.
In the most cases there is a basophilic hypophysial adenoma in the Icenko-Cushing disease.
Among all hypophysial adenomas, the 90% are a microadenomas and 10% - macroadenomas. Only
in some cases the hypophysial adenoma isn't diagnosed, there is only the pituitary body basophilic
cells hyperplasia, which producing corticotrophin.
Pathogenesis
On a base of the Icenko- Cussing disease is a poor neuromediatoric hypothalamic control for
corticoliberine secretion (reducing of the dofaminergic and serotoninergic activity).
As a result there is changed the circadian cycle of corticoliberine secretion and mechanism of
reverse regulation of its production. The corticoliberine production becomes constantly increased,
that causes corticotrophin by the anterior lobe of the pituitary body. This leads to adenoma or
hypophysial hyperplasia development. Corticotrophin hypersecretion causes bilateral hyperplasia of
adrenal cortex and increasing of corticosteroidal hormones secretion. So, there is developed a
hypercorticoidism, causing development of all clinic symptomatology.
Figure №19

Dysplastic obesity Trophic dermal Arterial

impairments hypertension
 Encephalopathy Myopathy
Hypercorticoidi
sm
h
Secondary Symptomatic Systemical Sexual
Clinical manifestation diabetes mellitus osteoporosis function
immunodeficien
cy disorders
1. Complains during the Icenko- Cussing disease are very typic:
- change of appearance;
- obesity development;
- excessive total and muscular weakness;
- appearance of red over extensional stripes on abdominal, thoracic, femoral skin;
- dermal dryness;
- hairs shedding on head;
- hyperpilosis oh face and trunk;
- reduced libido and potency in men;
- menstrual cycle disorders in women
- pains in bones of vertebral column;
- sleep disorders, headaches;
- thirst (if the diabetes mellitus develops).
2. Results of visual examination have a great diagnostic meaning.
There are the next pathognomonic signs:
- dysplastic spreading of the subcutaneous fat with surpluses in region of brachial girdle, thorax,
abdomen, cervical vertebral column ("climacteric humpback "), face ("moon", round face) in
this upper and lower limbs stay relatively slim, buttocks- are plat;
- dryness, slenderness, marbleizes of skin, impetigo of different localization;
- a red- crimson face. In female there is hyperpilosis on face (moustaches, beard), acne and
impetigo;
- sties - a wide stripes of extension with red - violet, crimson color in axillary spaces, in region of
mammary glands, femurs, lower and lateral abdominal parts;
- petechial and ecchymoses on skin of shoulders, forearms, anterior surface of cruses;
- hairs shedding on head in women and men, surplus growth of hairs in femurs, cruses region of
females;
- reducing of excessiveness of the secondary sexual characters in men;
- gynecomastia in males;
- decreasing of tomes and straight of muscles and their atrophy.
This symptomatology diagnosed during visual examination, is caused by surplus of the
glucocorticoid hormones and their catabolic effect, that is expressed in atrophy of skin and
muscles. Hypertrichosis in women in region of face, thighs and hairs shedding on a head are
caused by the androgens surplus (adrenal genesis).
3. Condition of the cardiovascular system. Glucocorticoids surplus, hypernatremia promote a
development of arterial hypertension (BP may oscillate from 150/100 until 240/160 Hg. Pr.).
After putting of blood pressure cult there are appearing a petechial. Arterial hypertension causes
a headache, vertigo, reduced vision, the left ventricle hypertrophy. Glucocorticoids surplus and
potassium deficiency came a steroid cardiopathy development, that is showed with feeble first
sound above cardiac apex, cow systolic murmur above all auscultation points. Owing to arterial
hypertony there is auscultated the accent second sound above aorta. The excessive cardiopathy
may lead to development of variety stades of blood circulation insufficiency. ECY alterations
are characterized by decreasing of the T wave amplitude, displacement of ST interval to down
from isoline in some loads.
4. State of the respiratory organs. Patients have predisposition to immunal system activity (the
secondary immunodeficiency).
5. State of the digestive system. In patient there are often observed a gingivitis, caries, chronic
gastritis with hypersecretion, it may be appeared the "steroid" ulcers of stomach and duodenum.
In the excessive disease from it is possibly the enlargement of liver and changing of its
functional activity.
6. The urinary system state. It may be developed the urolithiasis, bursting of small concrements
during resizes. Appearance of urolithiasis is caused by hypercalciemia and calciuria (owing to
dysbalance of calcium- regulated hormones in blood and osteoporosis). Because of development
of urolithiasis and secondary immunodeficiency oftenly is appearing the chronic pyelonephritis.
7. Sexual system. In women frequently there are develop a colpitis, hypoplastic uterus,
amenorrhea. On men there are a gynecomastia, change of consistantion and volume of testicles,
prostate, development of impotency. These changes are caused by hypercorticoidism, higher
level of hydrocarbon in blood, in females - increasing of androgens level, in males - estrogens
level increasing and reducing of the testosterone producing.
8. Osteoarticulat system. The basic characteric sign of the osteoarticular system affection is a
steroid osteoporosis. First all there is alliterated the vertebral column, that manifestoes with
pains, pathologic fractures, reducing of growth. Also there are a typical pain and in offer bones
and articules.
Result of the laboratory examinations
1. Total blood count - increasing of hemoglobin, erithrocytosis, leukocytosis advantagly (owing to
the segmented neutrophils increasing), lymphopenia, eosinopenia, stab deviation to the left, a
higher ESR.
2. Analysis of the urine : reaction frequently is alkaline, glucosuria, proteinuria, leukocyturia,
triplphosphaturia.
3. Biochemical blood analysis - hypokaliemia, hypernatremia, moderative hypercholesterinemia,
increasing of the common and ionisated potassium level, activity of alkaline phosphates, alanine
and asparagin aminotransferases, increasing of beta- lipoproteid concentration, triglycerids, a
higher prothrombin index, decreasing of the common protein, hyperphosphatemia.
4. Immunal blood test: reducing of the IgM and IgG level, decreasing of phagocytic activity of
neutrophils, absolute quantity of T- lymphocytes, concentration of seric and leukocytic
interferon.
5. Results of the hormones blood level test:
- the hypothalamo-hypophysial system: increasing secretion of corticoliberine, endorphins,
corticotrophin, melanocyte - stimulating hormone, prolactin, reducing of concentration in blood
the somatotrophin, gonadotrophins;
- the hypophysial - adrenal system: increasing of level in blood the corticotrophin, hydrocarbon,
corticosteron in the morning (in 79 hours) and evening (in 22 - 24 hours), that is a distortion of
circadian cycle of secretion of corticotrophin mid hydrocarbon. Contents of aldosteron may be
higher. Increasing of the excretion (per day) with urine the 17 - OCS, 17 - CS,
dehydroepiandrosteron;
- the hypophysial - gonad system: reducing of gonadotrophins testosterone levels in blood of
men, oestradiole in women and increasing of testosterone level in females blood:
- the calcium - regulating harmonies: higher level of parathormones in blood and lower of
calcitonine;
- Functional test:
"Major test" with dexamethasone: preparation is used to 2 mg in 6 hours per two days, then
is tested the urinal excretion of the independent hydrocarbon and 17-OHP per day and
comparing results with rates before probe. In the Icenko- Cussing disease excretion of the
independent hydrocarbon and 17-OCS in urine decreases in comparing with the initial on
50% and more over (the principle of the reversal connection is retained during use of
dexamethasone with days doses - 8mg; if there was used a 2mg days doses, then the
suppression is absent). In corticosteroma (the Icenko - Cussing syndrome) depression of the
surplus secretion of hydrocarbon isn't, even if there is using the 8mg of days doses of
 dexamethasone (corticosteroma has an ability to autonomic hydrocarbon hypersecretion)
and the 17-OCS and independent hydrocarbon excretion doesn't decrease per day.
Test with adrenal stimulation with synasten-depo (ACTH) is used in two modifications. The
minor test is conducted so: in 8hours (morning) intramusculary is injected 250mg of
synancten and in 30 and 60 minutes is defined contains of hydrocarbon or 17-OCS in blood.
Normally and during the Icenko -Cussing disease - concentration of hydrocarbon and 17-
OCS in blood grouting in two and more over ones, during corticosteroma it doesn't. The
major test is conducted if there is absent reaction during the minor test. In 8 hours (in the
morning) to inject intramusculary 1mg of the synancten-depo and to discovery the contains
of hydrocarbon and 17-OCS in blood (in 1,4, 6, 8, 24 hours). During the Icenko-Cussing
disease rates growthing, but on corticosteroma they don't.
Results of instrumentally examinations
1. ECY: sign of kaliemia, the left ventricular cardial hypertrophy.
2. USE of suprarenal glands: diffuse or diffusonodular enlargement of suprarenal glands (more
over then 3 sm. over the altitude).
3. USE of kidneys abdominal organs: characters of chronic pyelonephritis, lined hepatosis,
lipomatosis of pancreas, concrements in kidneys.
4. Computed and magnific - resonant adrenal tomography: diffuse or diffusonodular adrenal
hyperplasia.
5. Radioimmual adrenal scanning: bilateral increasing of the iod-cholesterol absorption by
suprarenal glands.
6. Visualization of pituitary body with using of craniography, computed ad magnitic - resonant
tomography.
On craniogram there are a cranial bones and dorsum seller osteoporosis, signs of intracranial
hypertension, in 19 - 20% there is an enlargement of the dorsum seller sizes, which is owing to
hypophysial adenoma.
Using of computed and magnitic resonant tomography in 60 - 65% of patients there is a
hypophysial adenoma, who in 10% cases, locates extrasellary. MIT may be observed an
increasing intracranial pressure signs.
7. Neuroophthalmologic examination: narrowing off the visual fields (during hypophysial
adenoma presence) ; congestion phenomenon on the funds of eyes, hypertonic angiopathia.
8. Roentgenologic osteal examination: osteoporosis of bones of the axial skeleton (in 95% of
patients), of peripheries departments (in 55% of patients), aseptic necrosis of heads of the
femurs in different patients. On the excessive disease form, there are a compressive fractures of
bodies of vertebras of the thoracic and lumbar vertebral column departments.
9. Densimetry of bones discoveries an early signs of osteoporosis (look an "Osteoporosis" chapter).
Diagnosis.
There are two phases of investigation:
- confirmation of the presence or absence of Cushing’s syndrome;
- differential diagnosis of its cause.
1. Exogenous Cushing's syndrome should offer no problems in diagnosis since a history of chronic
ingestion of suprapliysiologic doses of glucocorlicoids is usually present. However,
occasionally patients deny, either deliberately or because of ignorance, that they have been
taking the glucocorticoid. In this case, the diagnosis can easily be made by obtaining a blood
sample at 8 a.m. for corlisol and ACTH, both of which are characteristically low.
Glucocorlicoids suppress ACTH secretion, causing adrenal atrophy and decreased cortisol syn-
thesis. Current radioimmunoassay techniques for measuring cortisol in plasma are very specific
and do not detect appreciable quantities of any of the synthetic glucocorticoids (prednisone,
prednisolone, dexamethasone, etc.) that the patient may be taking. Cortisol is unlikely to yield a
significant plasma level as well since the steroid has a short half-life; it disappears from blood 4
to 8 h after oral administration. If a plasma ACTH assay is not available, a plasma cortisol
determination is sufficient.
2. Single-dose dexamethasone suppression test. This is the preferred procedure for screening
patients for Cushing's syndrome. The patient ingests 1.0 mg of dexamethasone at bedtime (10 to
 12 p.m.), and a blood sample for plasma cortisol is obtained the following morning at 8 a.m. In
normal patients, the steroid suppresses plasma cortisol below 5 mkg/dl. whereas patients with
Cushing's syndrome do not respond and cortisol values of greater than 20 mkg/dl are not
unusual. This procedure is simple, convenient, and inexpensive since it does not require
hospitalization. It is also very reliable, being accurate in about 95 percent of the patients. A few
patients with Cushing's syndrome will respond to 1.0 mg of dexamethasone by suppression of
plasma cortisol. If the clinical suspicion is strong, 0.5 mg of dcxamethasone should be given and
cortisol determination should again be made. This procedure takes advantage of the fact that
while normal subjects suppress equally well with 0.5 and 1.0 mg of dexathasone, the few
patients with Cushing's syndrome who suppress with 1.0 mg will not suppress with the lower
dosage.
(There are a few clnical situations in which failure of dexamethasone suppression occurs in the
absence of Cushing's syndrome. Patients who are under acute stress, particularly those with fever
and infections, and depressed individuals may not respond to dexamelhasone. Therapy with
estrogen, and occasionally phenobarbital or phenothiazines may alter the response to
dexamethasone. To some extent, all these drugs induce the hepatic microsomal enzymes that
metabolize dexamethasone, and acceleration of the hepatic metabolism of the steroid results in
insufficient plasma levels to yield A normal response. In these conditions, and in any others in
which an abnormality in the metabolism of dexamethasone is suspected, simultaneous quantitation
of the plasma dexamethasone concentration offers extremely useful information. Compared with
individuals who exhibit no abnormalities in the metabolism of the steroid, individuals with altered
hepatic metabolism have a much lower plasma concentration. Estrogens also increase the synthesis
of corticusteroid-binding globulin (CBG) by the liver. Since plasma cortisol assays measure both
bound and free cortisol, values are high in people on estrogen medication.)
3. 48 – hour low dose dexamethasone test. The results obtained with the single-dose
dexamethasone suppression test are comparable to those of the first suppression test developed
by Liddle. In this procedure, eight 0.5-mg doses of dexamethasone at 6-h intervals are given
orally; 24-h urine samples for 17-hydroxycorticosteroids (17-OHCS) excretion are collected
before and during dexamethasone administration. In normal subjects, 17-OHCS values are
below 3 mg per 24 h on the second dexamethasone day. Patients with Cushing's syndrome fail
to suppress. Not only is this test less convenient and more expensive but it may not be accurate
if incomplete urine collections have been obtained.
4. High-dose dexamethasone suppression test. After the oral administration of a single dose of 4.0
mg of dexamethasone between 10 p.m. and midnight, the measured 8 a.m. cortisole the
following morning is less than 2 mkg/dl in normal individuals. Patients with pituitary-dependent
Cushing’s syndrome demonstrate a plasma cortisol suppression of more than 50 % compared
with the baseline values. Those wiyh adrenal tumors or nonpituitary ACTH-secreting tumors do
not respond. (This procedure is comparable to the high-dose dexamethasone suppression test
developed by Liddle(2.0 mg dexamethasone every 6 h for eight doses with three 24-h urine
sample collections for 17-OHCS, one collection before and two during dexamethasone
administration). The single-dose 4.0 mg dexamethasone suppression test is simpler, less
expensive, and more convinient.
5. RADIOLOGIC DIAGNOSIS Includes X-ray examination for a pituitary tumor, and computed
tomography which is the most popular procedure for visualizing the adrenals in patients with
Cushing's syndrome.

Cusing‘s disease treatment

Cushing's disease treatment programm:
1. Pathogenic treatment.
1 -1. Irradial therapy.
1-2. Surgical treatment (transsphenoidal hypophysis corticotropinoma removal,
adrenalectomia, suprarenal destruction);
 1-3. Drug therapy.
1-3-1. Corticotropine secretion suppressing drugs.
1-3-2. Suprarenal steroid's biosynthesis blocking drugs.
2. Symptomatic treatment.
1. Pathogenic treatment.
Basic sight of pathogenic treatment is a hypothalamus-hypophysis disorders normalization.
1-1. Irradial therapy.
-therapy and proton hypophysis irradiation are used now for Kushing's disease treatment.
-therapy applies as a separate method of treatment and in combination with surgical and drug
therapy, -therapy - irradiation of hypothalamus-hypophysis region with apparatus in which Co60 is
the source of irradiation.
Irradiation conducts on static (AGAT-S), rotational (AGAT-R) and rotational-convergent
(IROKUS') vehicles. Fractional methods of irradiation are used in doses of 1,5 - 1,8 Gy 5 -6 times
at week, summary dose is 40-50 Gy.
-therapy effect appears in 5-6 months after end of the treatment course and maximal effect
appears in 12-24 months.
-therapy causes the remission onset in 60 % of patients, effect is more expressed in patients
under 40.
The advantage of -therapy is a small quantity of radial complications and rarely development
of after-radial hypopituitarism. The drawbacks of -therapy are the durance of treatment, slow
development of therapeutically effect, low efficiency in moderate and hard forms of Kushing's
disease treatment without use of other methods of treatment.
In last 10-15 years for Kushing's disease treatment the hypophysis irradiation by narrow
fascicle of heavy protons. The indications for proton irradiation of hypophysis are the light and
moderate grade of Cushing's disease.
A convergent method is used for patient's irradiation. Treatment lasts 20 min and lightly bears
by patients. Summary dose in Cushing's disease is 80-100 Gy.
Hypophysis proton irradiation has next advantages as compared with -therapy:
• High dose local hypophysis irradiation probability;
• Absence of surrounding tissues' lesion;
• Possibility of second hypophysis irradiation after 6 months and later;
• Efficiency of proton therapy in light and moderate forms of Kushing's disease is 80-100%;
• After-irradial panhypopituitarism is not typical and appears rarely.
The development of clinical improvement o full remission usually occurs in 6-8 months, last
time of remission onset is 2 years after the treatment.
It is possible to use proton therapy for Kushing's disease even if the not efficient the course
ofroentgenotherapy or -therapy was applicated.
But proton therapy has the next limitations:
• Proton therapy is used only for patients with Kushing's disease with endocel-lular adenoma
or hypophysis hyperplastic processes treatment;
• Seize of sella turcica ahs to be not more than 15 mm with it's round shape;
• Proton therapy is not recommended for patients with head traumas and intra-cranial
hypertension. Also with lack of breath, cough, increased nervous excitement.
In hypophysis adenoma with supra- and paracellular development, in it's diameter more than
15 mm with it's oval shape which are not corresponding to the section of the proton fascicles - the
method of the choice is y-therapy.
Irradial therapy could be used in combination with surgical and drug's treatment.
By E.I. Marova data (1991) in majority of the cases in moderate grade of Kushing's disease
the combination of surgical removal of one adrenal gland and irradial therapy of interbrain -
hypophysis region applies.
1-2. Surgical treatment.
7-2-7. Transsphenoidal adenomectomia.
 In bond of intensive development and application of microsurgical technique the
transsphenoidal adenomectomia is the most adequate method of Kushing's disease treatment.
Usually microadenoma's and small adenoma's of hypophysis removes transsphe-noidally.
Remission observed in 60 % of the cases and by Boggan data (1988) in 90 % of the cases. After this
operation preserves other hormones secretion, the level of corticotropin normalizes in 6-12 months.
The indications to the transsphenoidal adenomectomia are light and moderate forms of
Kushing's disease.
In case of hypophysis macroadenoma the transsphenoidal adenomectomia applies.
7-2-2. Adrenalectomia.
Adrenalectomia could be homo- or bilateral.
Homolateral adrenalectomia is not the independent method of treatment, because of after
removal of one adrenal gland the remaining gland became more active functionate under the
influence of continuing corticotropin secretion. That's why the homolateral adrenalectomia has to be
combined with hypophysis irradiation.
Combination of irradial therapy with homolateral adrenalectomia is indicated in moderate
grade of Kushing's disease in case of the absence of the separate irradial therapy effect. In this case
a homolateral adrenalectomiaare carried out in year, in symptomatics of Kushing's disease
progression even in 6 months after irradial therapy.
Bilateral adrenalectomia indicated in hard forms of Kushing's disease and in hy-
percorticoidism complications progression. The operation fulfils in 2 stages. On first stage removes
on e adrenal gland, after the close of operation wound the second adrenal gland removes with
autotransplantation of the part of adrenal gland into the roughage to decrease the dose o
substitutional therapy (2 stages).
The life substitutional gluco- and mineralcorticoide therapy is applicated to these patients.
Nelson's syndrome develops in 38 % of patients - a syndrome of hyperpigmenta-tion, third
nerve damage and enlarging sella turcica caused by development of a pituitary tumor after
adrenalectomia.
y-therapy or proton therapy applies after total adrenalectomy for Nelson's syndrome
prevention.
Drugs blocking a corticotripin secretion are used for Nelson's syndrome (Cypro-heptadin,
Bromergocryptin, Sodium valproate, irradiate therapy and surgical remove-ment ofadenoma are
used too.
1-2-3. Destruction of adrenal glands.
Destruction of adrenal glands in Kushing's disease consist in destruction of hyper-plastic
adrenal gland (apolexia) by injection of contrast substation or ethanol. Method is used only in
complex treatment (i.e. in combination with irradial and drug therapy). The efficiency in combined
therapy is 50-60 %.
1-3. Drug therapy of Cushing's disease.
1-3-1. Corticotropin secretion suppressing drugs.
These drugs are decreasing a corticotropin level and improving a Kushing's disease clinics
could be used like the addition to the basic treatment only. It is not recommended to begin treatment
from these drugs or use them before irradial therapy because of decrease of it's efficiency.
Parlodel - dophamin receptor's agonist, adenohypophysis hormone's secretion decreases. This
drug applies in Kushing's disease treatment after the irradial therapy, adrenalectomy and in
combination with steroidogenesis blockers in adrenal glands. Parcodel is specially indicated in
increased level of blood prolactin. The drug produces in 2,5 mg tablets.
The treatment begins from 0,5-1 mg daily, gradually increases to 5-7,5 mg in 10 -15 days.
Supporting daily doses of the drug is 2,5 - 5 mg, treatment lasts 6-24 months. Drug action ceases
soon after it's abolition.
Parlodel's possible undesirable actions: nausea, decreasing of blood pressure.
Peritol - antiserotonin drug, decreases corticotropin secretion by it's action on the
serotoninergic system. The specific daily dose is 8 - 24 mg. The drug could cause the sleeplessness,
raise appetite. Usually it is used like additive drug. The drug produces in 0,004 g tablets.
GABA-ergic medicines.
 GABA (y-aminobutiric acid) - a constituent of the CNS suggested as a transmitter of
inhibitary nerve impulses. GABA-ergic drugs produces the action similar to GABA action and
decrease corticotropin production.
GABA-ergic drugs has a positive action in encephalopathy and indicated for patients with
Kushing's disease after irradial therapy and in Nelson's syndrome.
Aminalon (GABA) - produces in 0,25 g tablets, applies in 3 tablets 3 times daily, treatment
course duration is 2 - 6 months.
Phenibut - a phenyl derivative of GABA, produces in 0,25 g tablets, applies in 2 tablets 3
times daily in 2 - 3 months.
7-3-2. Suprarenal steroidogenesis blockers.
Suprarenal steroidogenesis blockers devides into cortisteroid biosynthesis blockers drugs
which causes the destruction of the suprarenal cells and drugs which blocks steroids biosynthesis
only.
Chloditan - o,n - dichlorphenyldichoethane. The drug causes degeneration and atrophia of
adrenal gland's cortical secretory cells, suppresses corticosteroid secretion. The drug produces in 0,5
g tables.
Chloditan uses in combination with irradial therapy in middle glade of hypercorti-coidism
befbreor after the irradial therapy. Chloditan applies for temporary normalization of suprarenal
cortical function in patients with Cushing's disease preparation to homo- or bilateral adrenalectomy.
Besides that, chloditan applies in Cushing's syndrome in inoperable malignance. The drug applies in
2 - 4 g daily up to the suprarenal cortical function normalization than it applies as substitutive
therapy in 1 - 2 g daily in 6-12 months.
Undesirable action of chloditan: nausea, decreasing of appetite, headache, sleep-lessness.
Aminoglutatimid (Mamomit, Elipten) - corticosteroides synthesis inhibitor, mainly cortisole
inhibitor. The drug applies for the adrenalectomypredoperational preparation, also in 1 - 2 months
before irradial therapy in doses of 0,75 - 1,5 g daily in a smooth expressed middle grade cortisolism.
Suprarenal steroidogenesis blocker' treatment has to be applied under the control of liver
function and block thrombocyte contention. It is better to use hepatic protectors in steroidogenesis
blocker's treatment (Essenciale, Carsil).
2. Symptomatic hypercorticoidism treatment.
2-1. Hypotensive therapy.
For arterial hypertension treatment it is better to use Adelfan, Adelfan-Esidrex, etc. Doses of
these drugs has to be applied individually (1-3 tablets daily).
Corinfar (Niphedipine) could be used in 0,01 - 0,02 tablets 3 times daily in absence of
tachycardia.
2-2. Steroid cardiopathy and hypokaliemia treatment.
Potassium drugs, Spironolactone, anabolic steroid drugs, ryboxin, polyvitamin complexes,
phosphaden applies.
2-3. Osteoporosis treatment.
It is recommended to use calcium preparations in combination with calcitonin and vitamin 03
under the control of blood calcium, oosyn, osteoxyn, in moderate grade of osteoporosis, anabolic
steroids. Osteoporosis treatment lasts about 12-18 months.

Differential diagnosis of the Icenko - Cussing disease with juvenile hypothalamic syndrome is
described in the "Juvenile hypothalamic syndrome" chapter.
Hypothalamic syndrome of pubertal period.
Particularities.
1. Obesity is not cushingoid (not central).
2. Striae (pink and not very large).
3. Hypertension (constant or permanent).
4. Glucose intolerance.
Treatment.
1. Hypocaloric diet .
2. Parlodel (2.5 – 5 mg for 3 – 6 month).
3. Dehydration therapy (hypothiasid 50 – 100 mg/day MgSO4 25 % solution intramuscular 10 –
15 times).
4. Nonsteroid antiinflammatory drugs (indometacine).
5. Vitamintherapy.
6. Symptomatic therapy (hypotensive therapy).
7. Phisiotherapy.

OBESITY.
Obesity is characterized by excessive accumulation of body fat.
Obesity in not a condition for which a precise definition is particularly useful. Unlike many
“real” diseases, obesity represents one arm of distribution curve of body fat or body weight, with no
sharp cut-off point. Its importance lies in the many, often serious, complications to which obese
people are subject. In these complications that warrant undertaking a treatment that is so often
unsuccessful.
Etiology.
The cause of obesity is simple – consuming more calories than are expended as energy.
However, we usually do not know why persons consume more calories than they expend.
Predisposing factors.
1. Social factors (obesity is prevalent among lower-class people than among upper-class. Other
social factors, particularly ethnic and religious are also closely linked to obesity, how these
factors lead to obesity, or its control, has not been established, but differences in life style,
dietary and exercise patterns, probably play a major role).
2. Sex (female have greater tendency to gain weight particularly at puberty and during pregnancy),
age (at middle aged people have more tendency to become obese. Anyhow, obesity is present
among all age groups).
3. Endocrine factors. (Certain diseases of endocrine glands are associated with obesity i.e.
hypothyroidism, Cushing’s disease, hypogonadism.)
4. Psychological factor.(many obese persons report that they overeat when emotionally upset, but
many nonobese persons also overeat in such conditions. Two deviant eating patterns based on
stress and emotional disturbance, however, may contribute to the obesity of a few patients.
Bulemia is the sudden, compulsive ingestion of very large amounts of food in a very short time,
usually followed by agitation, self-condemnation, and often by self-induced vomiting. The
night-eating syndrome consists of morning anorexia, evening hyperphagia, and insomnia.
Attempts at weight reduction in these 2 conditions are usually unsuccessful and may cause the
patient unnecessary distress.)
5. Genetic factors (It is widely recognized that obesity runs in families: 80 % of the offspring of 2
obese parents are obese, compared with 40 % of the children of 1 obese parent and only 10 % of
the offsprings of 2 nonobese parents.).
6. Physical activity. (Decreased physical activity in affluent societies is often sited as a major
factor in the rise obesity.)
7. Development factors.(The increased adipose tissue mass in obesity can result from either an
increase in size of fat cells (hypertrophic obesity), from an increase in the number of fat cells
(hyperplastic obesity), or from an increase in both (hypertrophic-hyperplastic obesity). Most
persons whose obesity began in adult life suffer from hypertrophic obesity. They lose weight
solely by the decrease in the size of their fat cells; the number of fat cells does not change.
Persons whose obesity began in childhood are more likely to suffer from hyperplastic obesity,
usually of the combined hypertrophic-hyperplastic type. They may have up to 5 times as many
fat cells as either persons of normal weight or those suffering from pure hypertrophic obesity.
As a result, they may be able to reach a normal body weight only by marked depletion of the
lipid content of each fat cell.)
8. Brain damage. (Brain damage, particularly to the hypothalamus, can lead to the obesity.)
Classification by Egorov.
1. Alimentary.
2. Endocrine.
3. Cerebral.
Classification due to stages of obesity.
A. According to Brock’s index (N: weight = height – 100).
I. Weight excess < 30 %.
II. Weight excess 30 – 50 %.
III. Weight excess 50 – 100 %.
IV. Weight excess > 100 %.
B. According to Kettle’s index (N: weight, kg – height, m2).
I. 27,5 – 29,9
II. 30,0 – 34,9
III. 35,0 – 39,9
IV. > 40,0

Classification of overweight in adults by BMI (WHO, 2014)

Class BMI, kg/m2 Associated disease risk

Underweight <18,5 Low
Normal 18,5–24,9 Medium
Overweight 25,0–29,9 Increased High Very high
Class I obesity 30–34,9
Class II obesity 35–39,9
Class III obesity >40 Extremely high

Classification due to deposition of fat tissue.

- upper type (abdominal);
- lower type (gluteofemoralis).

Classifcation of Obesity (Dedov I.I., Melnichenko G.A., Fadeev V.V., 2000)

Primary obesity
I. Alimentary constitutive obesity
1. Android (upper type, abdominal, visceral):
a) with components of metabolic syndrome;
b) with developed symptoms of metabolic syndrome.

2. Gynoid (lower type, gluteal thigh).

3. With marked disorder of nutritional behavior:

a) night eating syndrome;

b) seasonal affective alternations;
c) with hyperphagic reaction to stress.

4. With Pickwick’s syndrome.

5. With sleep apnea syndrome.
6. Combined.

Secondary (symptomatic) obesity

I. With determined genetic defect.
II. Cerebral
1. Tumor, trauma of brain.
 2. Systemic lesions of brain, infectious diseases.
3. Hormone-inactive tumors of hypophysis, “empty” ephippium syndrome.
4. In mental diseases.
III. Endocrine
1. Hypothalamic-pituitary (hypothalamic).
2. Hypothyroid.
3. Hypoovarial.
4. Hypercorticoid.

Diseases and syndromes, accompanied with obesity

Metabolic diseases Type 2 diabetes mellitus, impaired glucose tolerance, hyperinsulinemia,

and syndromes dyslipidemia (increased level of triglycerides and low density lipoprotein
cholesterol, decreasing level of high-density lipoprotein cholesterol),
cholecystolithiasis, hyperuricemia, steatohepatitis.
Cardio-vascular Arterial hypertension, coronary heart disease, left ventricle hypertrophy,
diseases and cardiac failure, venous insuffciency
syndromes
Neoplasm Increased risk for development of neoplasm, hormone-dependent and
hormone-independent tumors
Impaired blood Hyperfbrinogenemia
clotting
Respiratory system Apnea (the stop of breathing) while sleeping, Pickwickian syndrome
diseases
Musculoskeletal Arthrosis and other degenerative diseases of joints
system disorders
Genital system Dysmenorrhea, fertility failure, loss of libido
disorders Clinical manifestations.
Obese people come to the doctor not only complain about their fitness but also with complications
(cardiovascular, pulmonary, orthopedic and others).
Clinical particularities of hypothalamic obesity.
1. Fast gain weight (20 – 30 kg during 1 – 2 years).
2. More frequent dysplastic localization of the fat.
3. The presence of the striae.
4. Symptoms associated with increased intracranial pressure and neurologic picture (somnolence,
raised appetite and others).
5. Signs of hypothalamic dysfunction (palpitation, hyperhydrosis, hypertension).

Differential diagnosis
have to be made between different types of obesity.
Alimentary obesity.
1. Genetic (family) factor.
2. Eating habits (ingestion of large amounts of food).
3. Slow progressing.
Pickwickian syndrome. It can occur in the massively obese persons. Pressure on the thorax from the
encompassing sheath of the fatty tissue combined with pressure on the diaphragm from below by
large intra-abdominal accumulations may lead to reducing of the respiratory capacity,
hypoventilation, retention of CO2 leading to decreased effects of CO2 as respiratory stimulant and
resultant hypoxia and somnolence.
Hypothalamic-pituitary disorders.
Barrakcer – Simmons’s disease (progressing lipodystrophia).
1. More frequent is in young women.
2. Atrophy of the subcutaneous adipose tissue in the region of face neck, thorax; increased
quantity of adipose tissue in the lower part of body, thighs, legs (“riding-breeches” type).
3. Duration of the disease, as a rule, without any changes in nervous and endocrine system and
patients have only cosmetic defect.
Dercum’s disease (generalized painful lipomatosis).
1. More frequent is in women in menopause.
2. There is localized, painful nodes (knots) in the subcutaneous adipose tissue. These nodes are
painful, itch, the skin over nodes is red.
3. Patient can have normal weight or be obese.
4. Person has nervous changes (CNS asthenia, neuroses) and endocrine disturbances (decreasing of
function of sexual glands).
Babinsky-Frelych’s disease (adipose-genital dystrophy).
1. More frequent is observed in boys.
2. Characterized by obesity (dysplastic type) and hypogenitalism (development of primary and
secondary sexual signs is stopped: small sizes of scrotum, penis, may be criptorchism).
3. There is often lack in growth.
Endocrine pathology.
Laurence – Moon – Biedl syndrome.
1. Obesity, hypogenitalism like in patients with Babinsky-Frelych’s disease.
2. Decreased mental activity or debility.
3. Pigmental retinitis.
4. Bones or inner organs abnormalities (polydactylia, syndactylia and others)
Morganyi – Stuart – Morel’s syndrome.
1. More frequent in young women or in climacteric female.
2. Adipose tissue localized in the region of chin, abdomen (like apron) mammary glands
(mastoptosis), skin is flabby, striae are absent.
3. Hirsutism is present (beard, moustache).
4. Hypertension.
5. Diabetes mellitus.
6. Increased thickness of lamina interna of frontal bone.
Postnatal neuroendocrine syndrome (PNES).
1. Increasing of the weight during 3 – 12 months after abortion or labor (Kettle’s index usually is
more than 30).
2. Subcutaneous adipose tissue is localized like in patients with Cushing’s syndrome.
3. Striae are present.
4. There is moderate hirsutism, tendency to hypertension and hyperglycemia.

Differential diagnosis of alimentary constitutive and hypothalamic-pituitary obesity

Complains Forms of obesity

Alimentary constitutive Hypothalamic-pituitary
1 2 3
Pain in cardiac area + +/-
Palpitation + -
Breathlessness + +
General weakness + -
Thirst - +
Sexual disorders +/- +
Pain in right subcostal area + -
Pain in abdomen + +/-
Mouth dryness + +/-
Pain in joints + +
Headache +/- +
Vertigo + +
Irritability - +
Memory impairment +/- +
Oedema at legs + +
Striae - +

Comment: “+” – the sign is present; “-” – the sign is absent; “+/-” – the sign may be.

Treatment.
If permanent weight loss could be achieved exclusively with behavioral reductions in food intake and
increases in energy expenditure, medications for obesity would not be needed. Weight loss is difficult
for most patients, and the patient's desire to restrict food and energy intake is counteracted by adaptive
biological responses to weight loss. The fall in energy expenditure (out of proportion to reduction in
body mass) and increase in appetite that are observed after weight loss are associated with changes in a
range of hormones . Some of these changes represent adaptive responses to weight loss and result in
altered physiology that promotes weight regain. Other changes reflect improvements in dysfunctional
hormonal systems that occur as a patient moves from being obese to being closer to a healthy weight.
The basis of weight reduction in all treatment regimens is to establish a caloric deficit by
reducing intake below output.
Diet.
The simplest way to reduce caloric intake is with a low-calorie diet. Optimal long-term
effects are achieved with a balanced diet containing readily available foods. For most people, the
best reducing diet consists of their usual foods in amounts limited with the aid of standard tables of
food values. Such a diet gives the best chance of long-term maintenance of the weight loss,
although it is the most difficult diet to follow during weight reduction. Consequently, many people
turn to novel or even bizarre diets, of which there are many. The effectiveness of these diets, if any,
results, in large part, from monotony - nearly everyone will tire of almost any food if that is all they
get to eat. Consequently, when they stop the diet and return to their usual fare, the incentives to
overeat are increased. Fasting has had considerable vogue as a treatment for obesity, but it is now
rarely used. Most patients promptly regain most of the weight they lose. Since fasting is not without
complications, it should be carried out in a hospital.
Several recommendations. Patient has to:
1) eat 4 – 5 times a day, only in a direct time, not to eat between basic meal receptions;
2) eat only one portion;
3) limit a free liquid to 1,0 – 1,2 l/day;
4) not to eat with the aim of decreasing depression, not to eat “for a company”;
5) the total daily energy intake should be between 1600 – 800 Kcal.
Physical activity.
It is frequently recommended in weight reduction regimens and its usefulness has probably been
underestimated even by its proponents. Since caloric expenditure in most forms of physical activity
is directly proportional to body weight, with the same amount of activity obese persons expend
more calories than do those of normal weight.
Physical activity has to be: 1) regular; 2) bring only positive emotions; 3) it is better to work in a
group of the patients.
Medications.

Advantages and Disadvantages Associated with Weight Loss Medications

Drug Advantages Disadvantages

Phentermine Inexpensive ($) Side effect profile

Drug Advantages Disadvantages

Greater weight lossa No long-term datab

Topiramate/phentermine Robust weight lossa Expensive ($$$)

Long-term datab Teratogen

Lorcaserin Side effect profile Expensive ($$$)

Long-term datab

Orlistat, prescription Nonsystemic Less weight lossa

Long term datab Side effect profile

Orlistat, over-the-counter Inexpensive ($) Less weight lossa

Side effect profile

Natrexone/bupropion Greater weight lossa Side effect profile

Food addiction Mid-level price range ($$)

Long-term datab

Liraglutide Side effect profile Expensive ($$$)

Long-term datab Injectable

a

Less weight loss = 2–3%; greater weight loss = >3–5%; robust weight loss = >5%.
b

Long term is 1–2 years.

We have to use medications in patients with endocrine and cerebral pathology: anti-
inflammatory drugs (to treat encephalitis, arachnoiditis), bromcreptin, peritol (to treat hypothalamic
and pituitary disorders) and others.
Physiotherapy. Massage, automassage, circulating shower-massage are very effective in the
treatment of the patients.
Surgery. Radical surgical treatment may offer some hope to persons with morbid obesity (100
% overweight) in whom all others treatments have failed.

8. The procedure for conducting a practical lesson; brief guidelines for work
students in class
Students’ group is divided into 2 sub-groups, that work near the patients’ bed: ask the patients on
organs and systems, take anamnesis of the disease , anamnesis of life, make objective exam with the
teacher’s presence. In the class-room they discuss the patients, learn data of laboratory and
instrumental exam. of these patients.
1.To group the symptoms into the syndromes.
2.To find out the leading syndrome and make differential diagnosis.
3.To formulate the diagnosis.
4.To make a plan of treatment.

9. Skills to be acquired during the lesson:

-To know the clinical picture of Cushing’s disease.
-Features of Cushing’s disease diagnostics.
-Principles of differential diagnostics of Cushing’s syndrome from Cush-ing’s disease.
-The basic directions of treatment of Cushing’s disease.
-Definition of the Cushing’s syndrome.
-Etiology, pathogenesis of Cushing’s syndrome.
-Clinical features of Cushing’s syndrome.
-Aboratory and instrumental findings in patients with Cushing’s syndrome.
-Treatment patients with Cushing’s syndrome.
-Clinical features of hypothalamic syndrome of pubertal period.
-Treatment of patients with hypothalamic syndrome of pubertal period.
-Clinical features of hypothalamo-hypophysial obesities.
-Etiology and pathogenesis of obesity.
-Clinical presentation of obesity and concomitant complications. International classifcation of
obesity.

10.Real-life situations to be solved:

As a part of a general check-up obesity and hypogonadism was found in a 16-year-old male.
The patient has no complaints. What is your diagnosis?
Answer: Babinsky-Frelych’s disease (adipose-genital dystrophy).

A 34-year-old man S. complains of headache, increased sweating, periodical palpitation,

elevation of blood pressure, severe weight gain (30 kg in 2 years), sexual failure. There are no
relatives with overweight in his family. The patient considers himself to be ill for 2 years. He
connects his disease with having infuenza.
Physical examination. The height is 165 cm, body mass is 130 kg, adipose cellular disposal is
equable. There are numerous pink thin stria on the hips and abdomen, the skin is highly wet. The left
heart border is displaced to 2 cm laterally. Cardiac sounds are dull, there is an accent of the second
heart sound above the aorta, blood pressure is 190/100 mmHg on the left arm and 160/90mmHg –
on the right arm.
Lungs are without pathology. Abdomen is enlarged because of adipose tissue, painless. Liver is
near the border rib’s arc. Secondary sexual characters are retained. Thyroid gland is not enlarged.
What is the clinical diagnosis?
Answer: hypothalamic obesity, class III.

A 30-years-old woman Z. complains of permanent headache, hard weakness, weight gain,

menstrual disorders, hypertrichosis. She is ill for 2 years, but didn’t consult a doctor. At physical
examination height is 160 cm, body mass 90 kg, adipose cellular disposal is not equable, prevalent
at face, neck, chest, abdomen. The skin is dry, pale, has vide red stria on the chest, abdomen, hips,
hypertrichosis. Blood pressure is 180/100 mmHg. Fasting glucose blood level - 7 mmol/L; urinary
17-OHCS, 17-HCS levels are increased. Glucosuria is absent. At the X-ray of the skull osteoporosis
of the Turkish saddle wall is revealed.What is the clinical diagnosis?
Answer: Cushing disease, obesity, class II.

11. References
11.1. Main literature
1. Endocrinology. Textbook/Study Guide for the Practical Classes. Ed. By Petro M. Bodnar: -
Vinnytsya: Nova Knyha Publishers, 2017.-328 p.
2. Basіc & Clіnіcal Endocrіnology. Seventh edіtіon. Edіted by Francіs S. Greenspan, Davіd G.
Gardner. – Mc Grew – Hіll Companіes, USA, 2004. – 976p.
3. Harrison‘s Endocrinology. Edited J.Larry Jameson. Mc Grew – Hill, USA,2006. – 563p.
4. Endocrinology. 6th edition by Mac Hadley, Jon E. Levine Benjamin Cummings.2006. –
608p.
5. Oxford Handbook of Endocrinology and Diabetes. Edited by Helen E. Turner, John A. H.
Wass. Oxford, University press,2006. – 1005p.
6. Caroline M. Apovian, Louis J. Aronne, et al. The Journal of Clinical Endocrinology &
Metabolism, Volume 100, Issue 2, 1 February 2015, Pages 342–362