Endocrine glands

1. Pathophysiology of the endocrine
system. Neuroendocrine violations.
General adaptation syndrome.
Pathology of the hypophysis and
adrenal glands.
Assistant of Professor
Fedorchenko Y.V.

2. Structure
Structure
Disorders of hormone secretion, metabolism,
transport and reception
4
Role of endocrine system in vital activity of the organis
1
Etiology and pathogenesis of endocrine disorders
2
Disorders of endocrine glands regulation
3
Disorders of the pituitary and adrenal glands
5

4. Interesting Facts about Human Hormones
•
•
•
•
Oxytocin (the 'love hormone') causes men in
relationships to stand further away from attractive
women than single men.
95% of the serotonin in the human body is located in
the gut. Serotonin deficiency in men causes impulsive,
violent behavior and alcohol abuse.
Levels of a stress hormone called cortisol — the same
ancient chemical that instructs men to fight or flight —
tend to spike about 4 to 6 weeks after men learn that
they are going to be fathers.
Administering testosterone to patients with a social
anxiety disorder has been found to increase their
willingness to face situations which are perceived as
socially threatening.

5. Interesting Facts about Human
Hormones
•
•
Cuddling (or other ‘love’ acts) helps to heal
physical wounds faster due to the release of
Oxytocin, which is proven to reduce swelling.
A single night of sleeplessness can stimulate
insulin resistance, a component in type 2
Diabetes, thus implying that sleep deprivation
can be a major factor in the origin of type 2
diabetes.

6. Role of endocrine system in vital
activity of the organism
The endocrine system
carries out regulatory
influence with the help of
hormones practically on all
functions of an organism –
metabolism , growth,
reproduction, mental activity,
adaptation, functional
activity of all organs.

9. Etiology of endocrine disorders
•
•
•
•
•
•
•
•
•
mental trauma,
necrosis,
tumour,
inflammatory process,
bacterial and viral infections,
intoxications,
local disorders of blood circulation (hemorrhage,
thrombosis),
alimentary disorders (deficiency of iodine, redundant
consumption of carbohydrates),
ionising radiation

10. There are three variants
of endocrine functions disorders:
Hyperfunction of endocrine
glands
Hypofunction of endocrine
glands
Disfunction of endocrine glands

11. 1)
In pathogenesis of endocrine there are three main
mechanisms:
Disorders of regulation of endocrine glands
– disregulatory disorders;
2) Disorders of biosynthesis of hormones and their
secretion– glandular disorders;
3) Disorders of the transport, reception and
metabolism of hormones – peripheral disorders.

12. Disorders of endocrine gland regulation
•
•
•
•
Regulation of endocrine gland activity can be carried
out with the help of four mechanisms:
- Nervous regulation : direct nervous influences on the
activity of adrenal medulla, neuroendocrine
structures of hypothalamus;
Neuroendocrine regulation: It is carried out by
neuroendocrine cells of hypothalamus, which
transform nervous impulses in specific endocrine
process.
-Endocrine regulation: some hormones influence on
synthesis of the others (influence of tropic hormons
on activity of adrenal cortex, thyroid gland)
-Non-endocrine humoral regulation is carried out by
unspecific humoral factors (by metabolites, ions.)

13. Pathological processes which are primarily
developed in hypothalamus, lead to disorders of
transhypophysar and parahypophysar regulation
of endocrine glands function.
The activity of hypothalamic centers can be
disturbed also secondarily in connection with
disorders in limbic system and upper parts of
central nervous system which are closely
connected with hypothalamus.
Big role belongs to mental trauma and other
stress influences.

14. Role of mechanisms feedback bond
in endocrine disturbances
•
•
•
The essence of negative
feedback effects is that formed
hormones oppress activity of
structures which carry out the
previous stages of regulation.
Therefore the increase of
secretion of effectory hormone
through certain parts causes
decrease of its formation and
entering in blood, and on the
contrary, the decreasing of the
hormone contents in blood
causes increase of intensity of
its formation and secretion.
In this way regulation of

15.  Negative feedback means that when
enough hormone is in the body, the
body stops producing the hormone
until it is needed again.
You eat. Glucose (sugar)
in the blood increases.
Increased glucose is detected by receptors
that notify the brain. It sends a message
to the pancreas to produce insulin.
Insulin tells muscle and liver to take up
glucose from the bloodstream and use it for energy
or store it for later. Brain reduces appetite.
Blood glucose level drops as
it is removed by the cells.
Pancreas stops making insulin.

16. Disorders of hormones
biosynthesis and their secretion:
a)
1.
1. By changes of functionally active endocrine cells
amount:
by decrease of their amount (removal of gland or
its part, damage, necrosis) that results in
endocrine hypofunction;
b) by increase of their amount (benign and
malignant tumors of glandular epithelium) leads to
endocrine hyperfunction.
2.
2. Qualitative changes in cells:
a) by disorders of biosynthesis of hormones;
b) by disorders of processes of their secretion.

17. Disorders of transport, reception and
hormones metabolism
1. Disorders of the hormones transport in
organism.
2. Disorder of metabolic inactivation of
hormones.
3. Disorders of interaction of hormones with
peripheral cells - targets.

18. All hormones
circulate in two
forms –
connected and
free. Connected
hormone is
biologically
inactive. The
activity is peculiar
only to free form
of hormone.
The disorders of hormone
transport in organism can appear
in two types of endocrine
dysfunction:
а) hypofunction – increase of
hormone binding
and decrease of its free form
content;
b) hyperfunction – decrease of
hormone binding
and increase in blood of free form
concentarion.

19. •
•
•
The blockage of hormonal receptor is the
widespread mechanism, which results to hormonal
insufficiency:
active hormone does not find receptor on a cell
because of receptor loss
conformation changes of the receptor
Usually concentration of hormone in such cases is
normal or increased.
Disorders of endocrine functions, connected with
disturbances of hormone interaction with
peripheral cells:

20. Disorder of endocrine functions, connected
with disturbances of hormones metabolism:
•
•
In case of slowing- down of hormones
inactivation their content in blood is increased,
that appears in glands hyperfunction.
And on the contrary, the accelerated
transformationof hormones in their inactive
forms is accompanied by development of
endocrine hypofunction.

22. The pituitary gland also called the hypophysis and
is located within the cranium inferior to the
brain. It sits on the hypophyseal fossa of the
sella turcica. This gland connects to the
hypothalums through infundibulum.

23. Adenohypophysis:
Different cell types produce hormones
including:
a. Growth hormone (GH)- signals growth
of the body
b. Somatotropic hormone(SH) signals
growth of the body
c. Prolactin- stimulates the breast tissue
to produce milk
d. Thyroid-Stimulating hormone-
stimulates thyroid gland to secrete
hormones that influence our metabolism.
e. Adrenocorticotropic hormone (ACTH)-
stimulates adrenal gland to signal its
hormones that help us deal with stress.
f. Melanocyte-stimulating hormone (MSH)
- stimulates melanocytes of the
epidermis to produce more melanin.
g. Follicle stimulating hormone (FSH)-
act on testes or ovaries an stimulate the
maturation of sperm and induce
secretion of sex hormones
h. Leutinizing hormone (LH)- during the
menstrual cycle it signals ovulation.

24. Hypothalamic control of hormone
secretion from the
adenohypophysis:
the hypothalamus had neurons
that produce hormones and
release them like
neurotransmitters are released.
These travel through the
hypophyseal portal system into
the anterior pituitary and stimulate
its hormone secretion.
The hypophysial portal system
involves two beds of capillaries
connected by a vein.
It allows a high level of horomone
concentration within a small
region and it is designed so that
the hormones released by the
hypothalamus travel directly to the
anterior pituitary and it in turn
release hormones into systemic
circulation.

25. Neurohypophysis: also known as
the posterior pituitary gland, it is
technically part of the brain and it
composed of neurons.
Rather than making hormones it
stores those produced by the
hypothalamus and releases them
when it receives a neural impuls.
The hormones produced by the
hypothalamus but released by the
neurohypophysis are:
a. Antidiuretic hormone (ADH)-
stimulates the collecting
tubules of the kidney to
concentrate the urine in order
to reduce water loss.
b. Oxytocin- induces
contractions of smooth
muscle of the sexual organs,
such when a mother
experiences contractions of
the uterus during labor.

26. •
•
•
Panhypopituitarity – is the decrease of formation
of all adenohypophysis hormones.
The following clinical forms of
panhypopituitarity are known:
Hypophysar cachecsia of Simonds;
Afterbearing necrosis of hypophysis – Sheehan
syndrome;
Chromophobe hypophysis adenoma

27. The clinical manifestations of
panhypopituitarity are related to deficiency of
adenohypophysis hormones and disorders of
activity of peripheral endocrine glands (thyroid
gland, cortex of adrenal, sexual glands).
The first symptoms of lesion of
adenohypophysis occur in 75 % of gland tissue
damage, and for development of complete
picture of panhypopituitarity destruction of 90
% of adenohypophysis is necessary.

28. Vascular disorders in hypophysis and
hypothalamus
(most frequently after bearing longtime
spasm of vessels of brain and hypophysis
owing of haemorrhage), trauma of the skull
basis, tumour of hypophysis and
hypothalamus, inflammatory
damage of hypophysis, inherent aplasia and
hypoplasia can lead to development of
panhypopituitarity.
The most frequently gonadotropic function
of hypophysis and secretion of STH is
damaged with the consequent nonsufficient
secretion of ТТH, ACTH and prolactine.

29. Pituitary cachexia (Simmond's disease)
Simmonds' disease is a syndrome
ascribed to destruction of the
hypophysis (chiefly the anterior
portion).
Clinically syndrome is characterized
by cachexia, premature senility,
atrophy of the gonads and genitalia,
with amenorrhea, atrophy of the
breasts, loss of pubic and axillary hair,
loss of libido, anorexia, hypotension
and muscular weakness,
hypoglycemia, decreased sugar
tolerance, lowered basal metabolism
and depressed specific dynamic
action of proteins, anemia,
lymphocytosis and sometimes
eosinophilia.

30. Sheehan syndrome
•
•
•
Sheehan syndrome is a condition that
happens when the pituitary gland is
damaged during childbirth. It’s caused by
excess blood loss or extremely low blood
pressure during or after labor.
Such extensive bleeding may reduce the
blood flow to the pituitary gland causing the
pituitary cells to be damaged or die
(necrosis). Thus, the production of the usual
pituitary hormones will be reduced.
During pregnancy the pituitary gland may
double in size. At this time the gland is
especially vulnerable to a severe drop in
blood pressure (sometimes called shock)
and excessive maternal bleeding may induce
the shock and the damage to the cells of
the gland. At that time the amount of
hormones produced by the pituitary may be
decreased giving rise to the symptoms
associated with hypopituitarism.

31. Partial hypopituitarity - is the disorder of
formation of separate hormones of
adenohypophysis
•
•
•
•
Hypophysar nanism (dwarfishness) - deficiency
of STH;
Secondary hypohonadism - deficiency of FSH and
LH;
Secondary hypothyrosis - deficiency of TTH;
Secondary hypocorticism - deficiency of ACTH.

32. The insufficiency of STH results in development
of hypophysar dwarfishness, or nanism and
appears by such mechanisms:
1) decrease of intensity of protein synthesis that leads
to delay and stop of growth (more than 30 % from
average) and development of bones, internal organs,
muscles.
The disorders of protein synthesis in connective tissue
results in loss of its elasticity;
2) decrease of inhibiting action of STH on an absorption
of glucose with predominance of insulinic effect and
development of hypoglycemia;
3) fallout of fat mobilizing action and tendency to
obesity.

33. Nanism

34. Nanism

35. •
•
The insufficiency of ACTH leads to secondary
partial insufficiency of adrenal cortex. The
glucocorticoid function suffers mainly.
Mineralocorticoid function practically does not vary.
Insufficiency of TTH causes secondary decrease
function of thyroid gland and development of
secondary hypothyroidism symptoms. As against in
case of primary hypofunction of thyroid gland the
introduction of TTH can restore its function.

36. Insufficiency of gonadotropic hormones results in
decrease of ability of Sertoli cells to accumulate
androgens and oppression of spermatogenesis and
ability to impregnation in men.
In case of defect of LG hormone the function of
Leidig’s cells is infringed, the formation of androgens
ceases and develops eunuchoidism with
preservation of partial ability to impregnation, as the
process of spermatozoids maturing does not stop.

37. Hyperfunction of adenohypophysis
(hyperpituitarism)
•
•
•
The main reasons of hyperpituitarism development are the
benign tumours – adenomas of endocrine cells.
Eosinophilic adenoma develops from acidophilic cells STH.
Clinically hyperproduction of STH represents by giantism (if
adenoma develops in children and young people before
closing of epiphysar cartilages) and acromegalia (in adults).
Basophilic adenoma grows from basophilic cells of
adenohypophysis which more often produce ACTH.
During this the Itsenko-Cushing disease develops.
characterized by: а) secondary hypercorticism; b) increased
pigmentation of skin.

38. Gigantism
Growth hormone excess
occurring before puberty and
the fusion of the epiphyses of
the long bones results in
gigantism.
It occurs when the epiphyses
are not fused and high levels
of IGF stimulate
excessive skeletal growth.
Fortunately, the condition is
rare because of early
recognition and treatment of
the adenoma.

39. Growth Hormone Excess in Adults
•
•
•
•
•
When GH excess occurs in adulthood ,the condition is referred to as
acromegaly.
The most common cause of acromegaly is a somatotropic adenoma.
When the production of excessive GH occurs after the epiphyses of
the long bones have closed, as in the adult, the person cannot grow
taller, but the soft tissues continue to grow.
Enlargement of the small bones of the hands and feet and of the
membranous bones of the face and skull results in a pronounced
enlargement of the hands and feet, a broad and bulbous nose, a
protruding lower jaw, and a slanting forehead.
The teeth become splayed, causing a disturbed bite and difficulty in
chewing.
The cartilaginous structures in the larynx and respiratory tract also
become enlarged, resulting in a deepening of the voice and
tendency to develop bronchitis.
Vertebral changes often lead to kyphosis. Bone overgrowth often
leads to arthralgias and degenerative arthritis of the spine, hips,
and knees.
Virtually every organ of the body is increased in size.

40. Acromegaly

42. Actor Irwin Keyes suffered from a rare pituitary
disorder called acromegaly

43. Hyperfunction of neurohypophysis
•
•
Related to redundant production vasopressin and
oxytocin.
Their main effects:
Vasopressine (antidiuretic hormone) renders the
following influence through V1 and V2 receptors:
1) Acting on tubulus contortus distalis and collective
tubules of kidneys, strengthens reabsorption of water;
2) Causes contraction of smooth muscles of blood
vessels;
3) Strengthens glycogenolysis and gluconeogenesis in
liver;
4) Stimulates consolidation of memory traces and
mobilization of saved information (hormone of memory);

44. Hyperfunction of neurohypophysi
s
Oxytocin renders the following
functional influences:
1) Stimulates secretion of milk
(lactation) causing contraction
of myoepithelial cells of small-
sized ducts of mammary glands
;
2)Initiates and strengthens
c ontrac tions of uterus of
pregnant woman;
3 ) W o r s e n s s t o r i n g a n d
mobilization of information
(amnestic hormone).

47. Hypofunction of neurohypophysis
•
•
Insufficient production of vasopressin results to
development of diabetes insipidus.
The decreasing of water reabsorptionin kidneys results
to poliuria and decreasing of circulatting blood volume
(hypovolemia), falling of arterial pressure and hypoxia.
The decreasing of oxytocin production appears by
disorders of lactation,weakness of labor activity.

49. Disorders of adrenal gland function
1)
2)
3)
4)
The most frequently there are following
manifestations:
Hypofunction of adrenal cortex - hypocorticism;
Hyperfunction of fascicular zone -Cushing
syndrome;
Hyperfunction of glomerulose zone-
hyperaldosteronism;
Dysfunction of adrenal cortex - adrenogenital
syndrome.

50. Insufficiency of adrenal cortex
•
•
•
Primary insufficiency arises as a result of adrenals
injury, secondary is connected with the dsamage of
hypothalamus (deficiency of corticoliberin), or with
hypofunction of adenohypophysis (deficiency of
ACTH).
Insufficiency of corticosteroids can be:
-total when the operation of all hormones drops out,
-partial fallout of activity of one adrenal hormone.
Insufficiency of adrenal cortex can be:
acute and chronic.

51. Insufficiency of adrenal cortex
•
•
•
•
Acute insufficiency are:
а) state after adrenal removal;
b) hemorrhage in adrenals which arises during sepsis,
meningococci infection (syndrome Waterhouse-
Friderixan);
c) syndrome of cancellation of glucocorticoides
preparations.
The chronic insufficiency of adrenals cortex is
characterized for Adison’s disease (bronzed disease).
The most often reasons of it are:
а) tuberculose destruction of adrenals;
b) autoimmune process.

52. Primary Adrenal Cortical Insufficiency
In 1855, Thomas Addison, an
English physician, provided
the
first detailed clinical
description of primary
adrenal insufficiency,
now called Addison’s disease.
The use of this term is
reserved for primary adrenal
insufficiency in which adrenal
cortical hormones are
deficient and ACTH levels are
elevated because of lack of
feedback inhibition.

53. •
•
•
•
•
Addison’s disease, like type 1 diabetes
mellitus, is a chronic metabolic disorder
that requires lifetime hormone
replacement therapy.
Manifestations of adrenal insufficiency
usually do not become apparent until
approximately 90% of the gland has been
destroyed.
These manifestations are related primarily
to mineralocorticoid deficiency,
glucocorticoid deficiency, and
hyperpigmentation resulting from elevated
ACTH levels.
Mineralocorticoid deficiency causes
increased urinary losses of sodium,
chloride, and water, along with decreased
excretion of potassium.
Because of a lack of glucocorticoids, the
person with Addison’s disease has poor
tolerance to stress. This deficiency causes
hypoglycemia, lethargy, weakness, fever,

55. І. Manifestation, connected with the falling of
mineralocorticoids functions of adrenal cortex:
1) dehydration develops owing to loss of sodium
ions (decreases rearbsortion) with the loss of water
(poliuria);
2) arterial hypotension is stipulated by
decrease of circulating blood volume;
3) hemoconcentration is connected with liquid loss,
results to disorders of microcirculation and hypoxia;
4) decreasing of kidney blood circulation is
stipulated
by increase of arterial pressure with disturbances
of glomerular filtration and
development of intoxication (nitrogenemia);

56. Manifestation, connected with the falling of
mineralocorticoids functions of adrenal cortex
5) hyperpotassemia is stipulated by decrease of
channels
secretion of potassium ions and their output from
the
damaged cells.
6) distal channels acidosis.
It is connected with disorders of acidogenesis in
distal
nephron channels;
7) gastro-intestinal disorders
(nausea,vomiting, diarrhea).
Loss of sodium (osmotic diarrhea) and intoxication
have significant meaning.

57. ІІ. Manifestations stipulated by disorders
of glucocorticoid function of adrenals:
1) hypoglycemia which results to starvation;
2) arterial hypotension (permissive reaction on
catecholamines);
3) decrease reaction of fat tissue on lipotropic
stimules;
4) decrease resistance of an organism on
action of different pathogenic factors;
5) decrease of ability to remove water during
water load (water poisoning);
6) muscular weakness and fast tiredness;
7) emotional disorders (depression);
8) delay of growth and development of children
;

58. Increase of adrenals cortex function
Hyperaldosteronism
•
•
Arises during
hyperfunction of
glomerular zone of
adrenals cortex, which
produce
mineralcorticoides.
There are primary and
secondary
hyperaldosteronism.

60. •
•
•
•
Primary hyperaldosteronism (Conn syndrome) arises in adenoma of
zone glomerular, which secretes high quantity of aldosterone.
Main manifestations :
1) arterial hypertension. It is connected with increase of sodium
contents in blood and in wall of blood vessels, after what the
sensitivity of their smooth muscles to action of pressore factors,
particularly catecholamines increases.
2) hypopotassiumaemia (result of hypersecretion of potassium ions in
canaliculas of kidneys).
3) ungas alcalosis. It is connected with amplification of acidogenesis in
distall nephron canaliculas;

62. Secondary hyperaldosteronism
is a result of renin-angiotensin
system activation.
This state appears by:
a) arterial hypertension;
b) edemas;
c) hypopotassiumaemia;
d) ungas alcalosis.

63. Increase of adrenals cortex function
•
•
Cushing’s disease :
basophil adenoma of anterior hypophysis part.
Cushing’s syndrome:
а) tumoral – adenoma of zona fasticulata of adrenal
cortex;
b) ectopic production of АCТH by some malignant
tumors (pulmonar cancer);
c) iatrogenic – introduction of glucocorticoides with
the medical purpose.

64. •
•
•
•
Altered fat metabolism causes a
peculiar deposition of fat
characterized by a protruding abdomen;
There is muscle weakness, and the
extremities are thin because of protein
breakdown and muscle wasting.
Purple striae, or stretch marks, from
stretching of the catabolically
weakened skin and subcutaneous
tissues are distributed over the breast,
thighs, and abdomen.
Osteoporosis may develop because of
destruction of bone proteins and
alterations in calcium metabolism.

65. Glucocorticoid hypercorticism appears by:
1) arterial hypertension;
2) hyperglycaemia – metasteroid diabetes
mellitus;
3) obesity;
4) development of infectious diseases without
signs of
inflammation;
5) gastric hypersecretion and formation of ulcers
in stomach
and duodenum;
6) osteoporosis;
7) muscular weakness;
8) slow of wounds healing.

67. (a) Photo prior to onset of Cushing syndrome. (b)
Symptoms resulting from the excessive
glucocorticoid secretion in Cushing syndrome
include buffalo hump and moon face.

68. A woman with Cushins Disease

69. Adrenogenital syndrome
•
•
Adrenogenital syndrome, describes a
congenital disorder caused by an
autosomal recessive trait in which a
deficiency exists in any of the enzymes
necessary for the synthesis of cortisol.
The condition is seldom diagnosed in
males at birth unless they have
enlarged genitalia or lose salt and
manifest adrenal crisis.
In female infants, an increase in
androgens is responsible for creating
the virilization syndrome of
ambiguous genitalia, with an enlarged
clitoris, fused labia, and urogenital
sinus.

71. Adrenogenital syndrome
There are three variants of adrogenital syndrome.
І. Disorders of early stages of synthesis
І. Disorders of early stages of synthesis – deficiency of
glucocorticoides, mineralcorticoides and androgens
hyperproduction. Manifestations: signs of insufficiency of gluco
- and mineralocorticoidal functions , features of early sexual
maturing in males, virilization in women (appearance of man's
sexual features).
ІІ. Disorders of intermediate stages
ІІ. Disorders of intermediate stages – deficiency of
glucocorticoides, surplus of androgens, formation of
mineralocorticoides is not infringed (classical androgenic
syndrome). Manifestations are the same, as in the first case,
only without signs of insufficiency of mineralocorticoidal
function.
ІІІ. Disorders at final stages of cortirol synthesis
ІІІ. Disorders at final stages of cortirol synthesis – deficiency of
glucocorticoides, hyperproduction of androgens and
mineralocorticoide. Features of hyperaldosteronism are
connected with manifestations of classical androgenital
syndrome.

72. Adrenogenital Syndrome

73. Disorders of adrenal medulla function
Hypofunction of adrenal medulla happens seldom
because of the fact that these functions can be accepted
by other chromaphine cell.
Hyperfunction of adrenal medulla arises during tumors of
chromaphine cells – pheochromocytome.
Appears by arterial hypertension, tachycardia,
extrasystole, flatering of atriums, hyperglycaemia,
hyperlipidaemia, hyperthermia.
Development of moderately expressed diabetus,
thyreotoxicosis is possible. In time of paroxizm vertigo,
headache, hallucinations, increased excitability of the
nervous system, cramps appear.

74. •
•
•
Pheochromocytoma is catecholamine-
secreting tumor that may precipitate
life-threatening hypertension. The
tumor is malignant in 10% of cases but
may be cured completely by surgical
removal.
The predominant clinical
manifestation of pheochromocytoma
is hypertension.
The characteristic presentation with a
hypertensive episode is one of abrupt,
precipitous elevation in blood
pressure, associated with tachycardia,
palpitations, headache, sweating,
tremor, and a sense of apprehension.
The hypertension is associated with
an increased risk of myocardial
ischemia, heart failure, renal injury,
and stroke (cerebrovascular accident).

76. Pheochromocytoma

77. In the early 1930s, the world-renowned endocrinologist Hans Selye was
the first to describe a group of specific anatomic changes that occurred
in rats that were exposed to a variety of different experimental stimuli.
Selye noted a triad of adrenal enlargement, thymic atrophy, and gastric
ulcer appeared in rats he was using for his studies.
He assumed that the hypothalamic-pituitary-adrenal (HPA) axis played a
pivotal role in the development of this response
He labeled the response the general adaptation syndrome (GAS).

80. Literature
•
•
•
•
•
•
•
General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin –
Vinnytsia: Nova Knuha Publishers – 2011. – p.286–287, 322–333.
Handbook of general and Clinical Pathophysiology / Edited by
prof.A.V.Kubyshkin. – CSMU. – 2005. – p.142–144.
Pathophysiology / Edited by prof. Zaporozan. – OSMU. – 2005. –
p.125–133, 145–153.
Essentials of Pathophysiology: Concepts of Altered Health States
(Lippincott Williams Wilkins), Trade paperback (2003) / Carol Mattson Porth,
Kathryn J. Gaspard.
Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine
Publishing. – 2010. – p.484-493, 506-512.
General and clinical pathophysiology. Workbook for medical students and
practitioners / Gozhenko A.I., Makulkin R.F., Gurcalova I.P. [at al.] // Odessa. –
2001.– P.248–254.
Gozhenko A.I. General and clinical pathophysiology/ Study guide for medical
students and practitioners / A.I. Gozhenko, I.P. Gurcalova // Odessa. – 2003.–
P.303–317.