prepared by MD, PhD, Associate Professor, Marta R. Gerasymchuk, pathophysiology department. Ivano-Frankivsk National Medical University

1. By MD, PhD, Associate ProfessorBy MD, PhD, Associate Professor
Ivano-Frankivsk National MedicalIvano-Frankivsk National Medical
UniversityUniversity
Pathophysiology of the endocrinePathophysiology of the endocrine
system. General adaptationsystem. General adaptation
syndrome. Violation ofsyndrome. Violation of
hypophysis and adrenal glands.hypophysis and adrenal glands.

2. CONTENTCONTENT
1.1. Endocrine regulatory dysfunction.Endocrine regulatory dysfunction.
2.2. The main types of endocrine dysfunctions: hyper-,The main types of endocrine dysfunctions: hyper-,
hypo- and dysfunction. Gland disorders of endocrinehypo- and dysfunction. Gland disorders of endocrine
function.function.
3.3. Peripheral disorders of endocrine function.Peripheral disorders of endocrine function.
4.4. Panhypopituitarism: causes, mechanisms ofPanhypopituitarism: causes, mechanisms of
development, main manifestations.development, main manifestations.
5.5. Partial hypofunction of adenohypophysis.Partial hypofunction of adenohypophysis.
6.6. Hyperfunction of adenohypophysis: eosinophilic andHyperfunction of adenohypophysis: eosinophilic and
basophilic adenoma. Cushing’s disease.basophilic adenoma. Cushing’s disease.
7.7. Disorders of hypothalamo-neurohypophysealDisorders of hypothalamo-neurohypophyseal
system. Disorders of secretion of antidiureticsystem. Disorders of secretion of antidiuretic
hormone.hormone. Diabetes insipidus.Diabetes insipidus.
8.8. Describe the etiology, pathogenesis, andDescribe the etiology, pathogenesis, and
manifestations of hyperfunction and hypofunction ofmanifestations of hyperfunction and hypofunction of
the adrenal cortex.the adrenal cortex.
9.9. Characterize aCharacterize adrenal medulla hyperfunction.drenal medulla hyperfunction.
10.10. Describe SelyeDescribe Selye′′s historic general adaptations historic general adaptation
syndrome; cite its stages. How does stress reactionssyndrome; cite its stages. How does stress reactions
develop?develop?

3. Actuality of the lecture.Actuality of the lecture.
 The endocrine system is involved in all of the integrative aspects ofThe endocrine system is involved in all of the integrative aspects of
life, including growth, sex differentiation, metabolism, andlife, including growth, sex differentiation, metabolism, and
adaptation to an ever-changing environment. This chapter focusesadaptation to an ever-changing environment. This chapter focuses
on general aspects of endocrine function, organization of theon general aspects of endocrine function, organization of the
endocrine system, hormone receptors and hormone actions, andendocrine system, hormone receptors and hormone actions, and
regulation of hormone levels.regulation of hormone levels.
 The endocrine system uses chemical substances calledThe endocrine system uses chemical substances called hormoneshormones
as a means of regulating and integrating body functions. Theas a means of regulating and integrating body functions. The
endocrine system participates in the regulation of digestion, use,endocrine system participates in the regulation of digestion, use,
and storage of nutrients; growth and development; electrolyte andand storage of nutrients; growth and development; electrolyte and
water metabolism; and reproductive functions. Although thewater metabolism; and reproductive functions. Although the
endocrine system once was thought to consist solely of discreteendocrine system once was thought to consist solely of discrete
endocrine glands, it is now known that a number of other tissuesendocrine glands, it is now known that a number of other tissues
release chemical messengers that modulate body processes.release chemical messengers that modulate body processes.
 The functions of the endocrine system are closely linked with thoseThe functions of the endocrine system are closely linked with those
of the nervous system and the immune system.of the nervous system and the immune system.

4. Role of endocrine system inRole of endocrine system in vitalvital
activity of theactivity of the organismorganism
• The endocrine system relates the most important
regulatoryregulatory systemssystems. It carries out regulatory
influence with the help of hormoneshormones practically on
all functions of an organism – metabolism, growth,
reproduction, mental activity, adaptation, functional
activity of all organs.
•The endocrine system, alongThe endocrine system, along
with the nervous system, iswith the nervous system, is
responsible forresponsible for coordinating ourcoordinating our
responsesresponses..
•The endocrine system is aThe endocrine system is a
slowerslower system and the nervoussystem and the nervous
system is asystem is a fasterfaster response.response.

5. Chemical signalsChemical signals
 Chemicals found in both systems and also asChemicals found in both systems and also as
part of other signaling mechanisms bind topart of other signaling mechanisms bind to
specific receptor proteins on or in target cells.specific receptor proteins on or in target cells.
 HormonesHormones – produced by endocrine glands,– produced by endocrine glands,
travel through the blood stream to target organstravel through the blood stream to target organs
ex – insulin, estrogenex – insulin, estrogen
 Local regulatorsLocal regulators
(a) paracrine signals – act on neighboring cells, ex.(a) paracrine signals – act on neighboring cells, ex.
– cytokines, interferon, prostaglandins– cytokines, interferon, prostaglandins
(b) autocrine signals – act on secreting cells itself,(b) autocrine signals – act on secreting cells itself,
ex – cytokinesex – cytokines

7. HormonesHormones can be synthesized:can be synthesized:
• а) by epithelial cells (one’s own
glandular ephithelium);
• b) by neuroendocrine cells
(hypothalamic cells);
• c) by myoendocrine cells (muscular
fibres of heart atriums).
– Neurotransmitters – secreted by neurons
at synapses
ex- serotonin, nitric oxide (NO)
– Neurohormones – secreted by
neurosecretory cells, travel through the
blood stream to target organs or
synapses
ex- epinephrine
– Pheromones – released into the
environment; between individuals
ex – insects marking trails, mating, etc.
(a) Endocrine signaling
Response
Blood
vessel
(b) Paracrine signaling
Response
Response
Response
Response
(c) Autocrine signaling
Neuron
(d) Synaptic signaling
(e) Neuroendocrine signaling
Neurosecretory
cell
Blood
vessel

8. According to chemical nature theyAccording to chemical nature they
differentiatedifferentiate::
 аа)) steroid hormonessteroid hormones ((mineralmineral – and– and
glucocorticoidsglucocorticoids, female and male, female and male
sexual hormones);sexual hormones);
 bb)) derivativesderivatives of aminoacidsof aminoacids
((thyreoidthyreoid hormones,hormones, catecholaminescatecholamines,,
melatoninemelatonine););
 cc)) protein peptideprotein peptide hormoneshormones
((releasingreleasing-hormones,-hormones, vasopressinvasopressin,,
oxytocinoxytocin, hormones, hormones ofof
adenohypophysis,adenohypophysis,
insuline, glucagone, parathyrin,insuline, glucagone, parathyrin,
calcitonine).calcitonine).
Somatostatin

9. Lipid-solubleLipid-soluble hormones (steroidhormones (steroid
hormones)hormones) pass easilypass easily throughthrough
cell membranes, whilecell membranes, while water-water-
solublesoluble hormones (polypeptideshormones (polypeptides
and amines)and amines) do notdo not
The solubility of a hormoneThe solubility of a hormone
correlates with the location ofcorrelates with the location of
receptors inside or on thereceptors inside or on the
surface of target cellssurface of target cells
• Water-solubleWater-soluble hormones are secretedhormones are secreted
byby exocytosisexocytosis, travel freely in the, travel freely in the
bloodstreambloodstream, and bind to cell-surface, and bind to cell-surface
receptorsreceptors
• Lipid-solubleLipid-soluble hormones diffusehormones diffuse
acrossacross cell membranescell membranes, travel in the, travel in the
bloodstream bound to transportbloodstream bound to transport
proteins, and diffuse through theproteins, and diffuse through the
membrane of target cellsmembrane of target cells
Signal
receptor
TARGET
CELL
Signal receptor
Transport
protein
Water-
soluble
hormone
Fat-soluble
hormone
Gene
regulation
Cytoplasmic
response
Gene
regulation
Cytoplasmic
response
OR
Signal receptor
Water-
soluble
hormone
Fat-soluble
hormone
TARGET
CELL
NUCLEUS(a) (b)
Transport
protein
Signal
receptor
(a)
NUCLEUS
(b)

10. According to functional effectsAccording to functional effects
hormones can be:hormones can be:
 а) affectors (act directly on
organs - targets);
 b) tropic (regulate synthesis
of effecting hormones);
 c) releasing-hormones
(regulate synthesis and
secretion of tropic
hormones).

11. Multiple Effects of HormonesMultiple Effects of Hormones
 The same hormone may have differentThe same hormone may have different
effects on target cells that haveeffects on target cells that have
• Different receptors for the hormoneDifferent receptors for the hormone
• Different signal transduction pathwaysDifferent signal transduction pathways
• Different proteins for carrying out the responseDifferent proteins for carrying out the response
due to different transcription factors theydue to different transcription factors they
activateactivate
 A hormone can also have differentA hormone can also have different
effects in different specieseffects in different species

12. Glycogen
deposits
β receptor
Vessel
dilates.
Epinephrine
(a) Liver cell
Epinephrine
β receptor
Glycogen
breaks down
and glucose
is released.
(b) Skeletal muscle
blood vessel
Same receptors but different
intracellular proteins (not shown)
Epinephrine
β receptor
Different receptors
Epinephrine
α receptor
Vessel
constricts.
(c) Intestinal blood
vessel

13. Mechanisms of hormone actionMechanisms of hormone action
1. Target cells [with receptors]1. Target cells [with receptors]
 a. On cell membranea. On cell membrane
 b. Inside the cellb. Inside the cell
2. Effects on target cells2. Effects on target cells
 a. Membrane permeability or potentiala. Membrane permeability or potential
 b. Protein synthesisb. Protein synthesis
 c. Enzymesc. Enzymes
 d. Secretiond. Secretion
 e. Mitosise. Mitosis
3. Plasma membrane receptors and second-messenger systems [all3. Plasma membrane receptors and second-messenger systems [all
amino acid-based hormonesamino acid-based hormones (except thyroid hormone) &(except thyroid hormone) &
eicosanoids]eicosanoids]
 a. The cyclic AMP signaling mechanisma. The cyclic AMP signaling mechanism
4. Intracellular receptors and direct gene activation [steroid (& thyroid)4. Intracellular receptors and direct gene activation [steroid (& thyroid)
hormones]hormones]

14. Target cell specificityTarget cell specificity
1. Blood levels of hormone1. Blood levels of hormone
2. Number of hormone receptors [receptors are constantly being synthesized and broken down;2. Number of hormone receptors [receptors are constantly being synthesized and broken down;
generally, a target cell hasgenerally, a target cell has 2000-100,000 receptors for a particular hormone2000-100,000 receptors for a particular hormone]]
• a.a. Down-regulationDown-regulation: decrease in number of receptors [i.e., hormone levels are high]: decrease in number of receptors [i.e., hormone levels are high]
• b.b. Up-regulationUp-regulation: increase in number of receptors [i.e., hormone levels are low]: increase in number of receptors [i.e., hormone levels are low]
3. Affinity of hormone & receptor3. Affinity of hormone & receptor
4. Other hormones [see below, "Interaction of hormones at target cells"]4. Other hormones [see below, "Interaction of hormones at target cells"]
• Half-life, onset, and duration ofHalf-life, onset, and duration of
hormone activityhormone activity
1. The concentration of a hormone reflects its rate of release, and the rate of inactivation and1. The concentration of a hormone reflects its rate of release, and the rate of inactivation and
removal from the body.removal from the body.
2. The half-life of a hormone is the duration of time a hormone remains in the blood, and is2. The half-life of a hormone is the duration of time a hormone remains in the blood, and is
shortest for water-soluble hormones.shortest for water-soluble hormones.
3. Target organ response and duration of response vary widely among hormones.3. Target organ response and duration of response vary widely among hormones.
• Interaction of hormones at target cellsInteraction of hormones at target cells
1.1. PermissivenessPermissiveness [one hormone must be present in adequate amounts for the full exertion of[one hormone must be present in adequate amounts for the full exertion of
another hormone's effect; e.g., thyroid hormone increases the number of receptors foranother hormone's effect; e.g., thyroid hormone increases the number of receptors for
epinephrine in cells]epinephrine in cells]
2.2. SynergismSynergism [actions of several hormones are complementary and their combined effects is[actions of several hormones are complementary and their combined effects is
grater than the sum of their separate effects; e.g., follicle stimulating hormone (FSH) andgrater than the sum of their separate effects; e.g., follicle stimulating hormone (FSH) and
testosterone on spermatogenesis]testosterone on spermatogenesis]
3.3. AntagonismAntagonism [when one hormone causes the loss of another hormone's receptors; e.g.,[when one hormone causes the loss of another hormone's receptors; e.g.,
progesterone inhibits uterine responsiveness to estrogen]progesterone inhibits uterine responsiveness to estrogen]

15. Etiology of endocrine disordersEtiology of endocrine disorders
 Reasons and kinds of endocrine disorders.Reasons and kinds of endocrine disorders. Among numerousAmong numerous
ethiological factors of endocrine disorderss it is possible to selectethiological factors of endocrine disorderss it is possible to select
the following main ones:the following main ones:
 a mental trauma,a mental trauma,
 necrosis,necrosis,
 tumour,tumour,
 inflamatory process,inflamatory process,
 bacterial and viral infections,bacterial and viral infections,
 intoxications,intoxications,
 local disorders of blood circulation (hemorrhage, thrombosis),local disorders of blood circulation (hemorrhage, thrombosis),
 alimentary disorders (deficiency of iodine and cobalt in food andalimentary disorders (deficiency of iodine and cobalt in food and
drinking water, redundant consumption of carbohydrates),drinking water, redundant consumption of carbohydrates),
 ionising radiation,ionising radiation,
 inherent chromosome and gene defects.inherent chromosome and gene defects.

16. There are three variants ofThere are three variants of
endocrine functions disorders:endocrine functions disorders:
1. HyperfunctionHyperfunction of endocrine glands
2. HypofunctionHypofunction of endocrine glands
3. DisfunctionDisfunction of endocrine glands
Disfunction is characterized by
different changes of hormonal
production and production physiologic
active precursors of their biosynthesis
in the same endocrine gland or
synthesis and entering in blood of
atypical hormonal products.

17. Pathogenesis of endocrinePathogenesis of endocrine
disordersdisorders
• The mechanisms of function
disorders of an endocrine gland
can be various depending on
localization and character of
process. In pathogenesis of
endocrine disorders it is possible to
select three main mechanismsmechanisms:
1) 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.

18. DisordersDisorders of endocrine gland regulationof endocrine gland regulation
 RegulationRegulation ofof endocrine glandendocrine gland activity can be carried out with theactivity can be carried out with the
help of four mechanisms:help of four mechanisms:
1.1. NervousNervous ((impulse-mediatorsimpulse-mediators) or) or parahypophysis regulationparahypophysis regulation. With the. With the
help of direct nervous influences the activity of following structures ishelp of direct nervous influences the activity of following structures is
regulated:regulated:
 аа)) adrenal medullaadrenal medulla;;
 bb)) neuroendocrineneuroendocrine structuresstructures of hypothalamusof hypothalamus;;
 cc)) epiphysisepiphysis..
2.2. NeuroendocrineNeuroendocrine oror transhypophysartranshypophysar regulationregulation. It is carried out. It is carried out byby
neuroendocrine cells of hypothalamusneuroendocrine cells of hypothalamus,, which transformwhich transform nervousnervous
impulses in specificimpulses in specific endocrineendocrine process. Along releasing-hormones,process. Along releasing-hormones,
which regulate activity of adenohypophysis are synthesized and getwhich regulate activity of adenohypophysis are synthesized and get
secretedsecreted in the system of portal vesselsin the system of portal vessels of hypophysisof hypophysis..
3.3. Endocrine regulationEndocrine regulation. It is that some hormones influence on. It is that some hormones influence on
synthesis and other influence secretion of the others. An example ofsynthesis and other influence secretion of the others. An example of
this mechanism is the influence of adenohypophysis tropic hormonesthis mechanism is the influence of adenohypophysis tropic hormones
on activity of adrenal cortex, thyroid gland, sexual glands.on activity of adrenal cortex, thyroid gland, sexual glands.
4.4. Non-endocrine humoral regulationNon-endocrine humoral regulation is carried out by unspecificis carried out by unspecific
humoral factors, in particular by metabolites, ions.humoral factors, in particular by metabolites, ions.

19.  Pathological processes which are
primarity developed in hypothalamusprimarity developed in hypothalamus lead
to disorders of transhypophysartranshypophysar and
parahypophysarparahypophysar regulation of endocrine
glands function.
 The activity of hypothalamic centers can be
disturbed also secondarilysecondarily in connection with
disorders in limbicdisorders in limbic systemsystem (hypocampus, tonsil,
olfactory brain) and upper parts of central
nervous system which are closely connected with
hypothalamus. At that the large role belongs to
mental traumamental trauma and other stress influencesstress influences.

20.  TranshypophysarTranshypophysar regulation includesregulation includes synthesis ofsynthesis of
peptidespeptides which arewhich are moving by axonsmoving by axons and reachand reach
adenohypophysisadenohypophysis in neurosecretory cellsin neurosecretory cells
of mediobasal part of hypothalamus. Here they eitherof mediobasal part of hypothalamus. Here they either
stimulate or inhibit formation of tropic hormonesstimulate or inhibit formation of tropic hormones..
 Stimulating peptidesStimulating peptides have received the name ofhave received the name of
liberins or releasing-factorsliberins or releasing-factors, they are:, they are:
thyroliberin, gonadoliberin, somatoliberin etc.thyroliberin, gonadoliberin, somatoliberin etc.
 Inhibiting peptidesInhibiting peptides are namedare named statinsstatins ––
thyrostatin, somatostatin etc.thyrostatin, somatostatin etc.
 Their ratio among themselves is determined formationTheir ratio among themselves is determined formation
ofof appropriate tropic hormoneappropriate tropic hormone. Then formation of tropic. Then formation of tropic
hormones begins in adenohypophysis –hormones begins in adenohypophysis – somatotropicsomatotropic
(STH),(STH), gonadotropicgonadotropic (GTH) etc.(GTH) etc.
 Tropic hormonesTropic hormones act on appropriate targets andact on appropriate targets and
stimulate derivation of hormones in appropriate glands,stimulate derivation of hormones in appropriate glands,
andand STHSTH stimulatesstimulates formation offormation of somatomedinessomatomedines inin
tissues – polipeptide hormones,tissues – polipeptide hormones, through which theythrough which they
actact..

22. • By means of parahypophysarparahypophysar mechanism
secretory, vessel and trophic influence of CNS on
the function of endocrine glands is carried out.
• For adrenal medulla, Langerhans’ islets and
parathyroid glands it is a major pathway of their
regulation. In realization of the function of other
glands both pathways of regulation take place. So,
the function of thyroid gland is determined not
only by TTH, but also by sympathetic impulsation.
• The direct irritation of sympathetic nerves
increases absorption of iodine by the gland,
synthesis of thyroid hormones and their secretion.
• Denervation of ovaries causes their atrophy and
weakens response on gonadotrophic hormones.

23.  The disorders ofThe disorders of trans- andtrans- and
parahypophysarparahypophysar regulationregulation
leads to disfunction of endocrineleads to disfunction of endocrine
glands.glands.
 The disturbance of one glandThe disturbance of one gland
function is calledfunction is called monoglandularmonoglandular
process, several glands –process, several glands –
pluriglandularpluriglandular process.process.
 The disorders of the glandularThe disorders of the glandular
function can befunction can be partialpartial, when, when
production of only oneproduction of only one
hormone is disturbed, orhormone is disturbed, or totaltotal,,
when secretion of all hormoneswhen secretion of all hormones
is changed.is changed.

24. Role of mechanisms feedback bondRole of mechanisms feedback bond
in endocrine disturbancesin endocrine disturbances
• TheThe mechanism of feedbackmechanism of feedback bond is obligated link inbond is obligated link in selfself
regulationregulation of glandular activity. The essence of negativeof glandular activity. The essence of negative
adverse effects is that formed hormones oppress activity ofadverse effects is that formed hormones oppress activity of
structures which carry out the previous stages of regulation.structures which carry out the previous stages of regulation.
• Therefore theTherefore the increase of secretionincrease of secretion ofof
effectory hormone through certain partseffectory hormone through certain parts
causescauses decrease of its formationdecrease of its formation andand
entering in bloodentering in blood, and on the contrary, the, and on the contrary, the
decreasing of the hormone contentsdecreasing of the hormone contents inin
blood causesblood causes increase of intensity of itsincrease of intensity of its
formation and secretionformation and secretion. In this way. In this way
regulation of cortizol secretion, thyroid andregulation of cortizol secretion, thyroid and
sexual hormones is carried out.sexual hormones is carried out.
• By the principle of the mechanism ofBy the principle of the mechanism of
feedback bond inhibition of the functionfeedback bond inhibition of the function
(even atrophy) of the gland during(even atrophy) of the gland during
treatment by their or other hormones cantreatment by their or other hormones can
occur.occur.

25. Pathway Example
Stimulus
Low pH in
duodenum
S cells of duodenum
secrete secretin ( )
Endocrine
cell
Blood
vessel
PancreasTarget
cells
Response
Bicarbonate release
Negativefeedback
–
• Hormones are
assembled into
regulatory pathways
• A negative
feedback loop
inhibits a response
by reducing the
initial stimulus
• Negative
feedback regulates
many hormonal
pathways involved
in homeostasis
Negative feedback andNegative feedback and
antagonistic hormone pairsantagonistic hormone pairs
are common features of theare common features of the
endocrine systemendocrine system

26. Control of hormone releaseControl of hormone release
1. Negative feedback ["stimulatory-inhibitory"]
2. Positive feedback ["stimulatory-stimulatory"]
3. Endocrine gland stimuli: humoral stimuli, neural stimuli, hormonal stimuli

27. Disorders of hormones biosynthesisDisorders of hormones biosynthesis
and their secretionand their secretion
• Strictly glandular disorders of endocrine functions can be
conditioned:
1. By changes of functionally active endocrine cells amount :
• a) by decreasedecrease of their amount (removal of gland or its
part, damage, necrosis), that results to endocrineendocrine
hypofunctionhypofunction;
• b) by increaseincrease of their amount (benignt and malignant
tumors of glandular epithelium) that is accompanied by
features of endocrine hyperfunctionendocrine hyperfunction.
2. Qualitative changes in cells:
• a) by disorders of biosynthesis of hormones;
• b) by disorders of processes of their secretion.

28. The main possible reasons of protein-The main possible reasons of protein-
peptide hormones synthesis disorders are:peptide hormones synthesis disorders are:
• 1) disorders of transcription;
• 2) disorders of translation;
• 3) deficiency of essential aminoacids;
• 4) deficiency of ATP;
• 5) disorders of posttranslatory modification
and activation.

29. Disorders of transport, reception and
hormones metabolism
• The peripheral mechanisms determine activity of hormones
excreted into blood, development of peripheral disorders of
endocrine functions occurs due to:
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.
• All hormones is excreted from glands associate with proteins
in blood and circulate in two forms – connectedconnected and freefree.
From these two forms connected hormone is biologically
inactive. The activity is peculiar only to free form of hormone.
• The disorders of the hormone transport in an organism can
appear in two types of endocrine function disorders:
• а) hypofunctionhypofunction – increase of hormone binding and
decrease of its contents in the free form;
• b) hyperfunctionhyperfunction – decrease of hormone binding and
increase in blood of concentration of the free form.

30. DisorderDisorderss ofof endocrineendocrine functions, connectedfunctions, connected
with disturbanceswith disturbances of interaction ofof interaction of hormoneshormones
withwith peripheralperipheral cellscells
• The influence of hormones on cells -
targets is carried out through their action
on specific proteins – receptors and is
performed in three ways:
1) influences on permeability of biological
membranes;
2) stimulation or oppression of enzymes
activity;
3) influences on the genetic apparatus of a
cell.

31. This gland makes me wake up in theThis gland makes me wake up in the
morning and ready to go!morning and ready to go!
Pineal
Gland
melatonin
"The 3rd Eye""The 3rd Eye"

32. Coordination of Endocrine andCoordination of Endocrine and
Nervous Systems in VertebratesNervous Systems in Vertebrates
TheThe hypothalamushypothalamus receives information fromreceives information from
the nervous system and initiates responsesthe nervous system and initiates responses
through the endocrine systemthrough the endocrine system
Attached to the hypothalamus is theAttached to the hypothalamus is the pituitarypituitary
glandgland composed of the posterior pituitary andcomposed of the posterior pituitary and
anterior pituitaryanterior pituitary
TheThe posterior pituitaryposterior pituitary stores and secretesstores and secretes
hormones that are made in the hypothalamushormones that are made in the hypothalamus
TheThe anterior pituitaryanterior pituitary makes and releasesmakes and releases
hormones under regulation of thehormones under regulation of the
hypothalamushypothalamus

33. This glandThis gland
is called theis called the
“master gland”“master gland”
because itbecause it
secretes ninesecretes nine
hormoneshormones
many of whichmany of which
control othercontrol other
endocrineendocrine
glands byglands by
feedbackfeedback
control.control.
Pituitary GlandPituitary Gland

35. Tropic effects only:
FSH
LH
TSH
ACTH
Nontropic effects only:
Prolactin
MSH
Nontropic and tropic effects:
GH

36. Anterior
Pituitary
Posterior
pituitary Stimulates milk
ejection and uterine
contractions
Ovary and testisOxytocin
Conservation of
body water
KidneyAntidiuretic hormone
Control of reproductive
function
Ovary and testisFollicle stimulating
hormone
Control of reproductive
function
Ovary and testisLuteinizing hormone
Milk productionMammary glandProlactin
Stimulates secretion of
glucocorticoids
Adrenal gland cortexAdrenocorticotrophic
hormone
Stimulates secretion of
thyroid hormones
Thyroid glandThyroid stimulating
hormone
Promotes growth (indirectly),
control of protein, lipid and
carbohydrate metabolism
Liver, adipose tissueGrowth hormone
Major physiologic
effects
Major target organsHormone

37. Type ofType of
AdenomaAdenoma
SecretionSecretion StainingStaining PathologyPathology
CorticotrophicCorticotrophic
adenomasadenomas
SecreteSecrete adrenocotrophicadrenocotrophic
hormone (ACTH) andhormone (ACTH) and
ProopiomelanocortinProopiomelanocortin
(POCM)(POCM)
BasophilicBasophilic Cushing’s diseaseCushing’s disease
SomatotrophicSomatotrophic
adenomasadenomas
SecreteSecrete growth hormonegrowth hormone
(GH)(GH)
AcidophilicAcidophilic AcromegalyAcromegaly
(Gigantism)(Gigantism)
ThyrotrophicThyrotrophic
adenomas (rare)adenomas (rare)
SecretSecret thyroid stimulatingthyroid stimulating
hormone (TSH)hormone (TSH)
BasophilicBasophilic OccasionallyOccasionally
hyperthyroidismhyperthyroidism
usually does not causeusually does not cause
symptomssymptoms
GonadotrophicGonadotrophic
adenomasadenomas
SecreteSecrete luteinizing hormoneluteinizing hormone
(LH), follicle stimulating(LH), follicle stimulating
hormone (FSH)hormone (FSH)
BasophilicBasophilic Usually does notUsually does not
cause symptomscause symptoms
ProlactinomasProlactinomas SecretSecret prolactinprolactin AcidophilicAcidophilic Galactorrhea,Galactorrhea,
hypogonadism,hypogonadism,
amenorrhea,amenorrhea,
infertility andinfertility and
impotenceimpotence
Null cellsNull cells
adenomasadenomas
Do not secrete hormonesDo not secrete hormones May stain positiveMay stain positive
for synaptophysinfor synaptophysin

38. Disturbances of functions of hypophysis.
Hypofunction of adenohypophysis
(hypopituitaritism)
There are panhypopituitarity and partial hypopituitarityThere are panhypopituitarity and partial hypopituitarity

40. Panhypopituitarity – is the decrease ofPanhypopituitarity – is the decrease of
formation of all adenohypophysis hormonesformation of all adenohypophysis hormones
• The following clinical forms of panhypopituitarity are known:The following clinical forms of panhypopituitarity are known:
1) Hypophysar cachecsia of SimondsSimonds;
2) Afterbearing necrosis of hypophysis – syndrome of Schegansyndrome of Schegan;
3) Chromophobe hypophysis adenomas, i.e. tumors, which grow from chromophobe cells. For
want of it the tumour squeezes and damages glandular cells of adenohypophysis.
• The clinical manifestationsclinical manifestations of panhypopituitarity are connected with
deficiency of adenohypophysis hormones and disorders of activity of
peripheral endocrine glands (thyroid gland, cortex of adrenal, sexual
glands).
• The first symptomsfirst symptoms of lesion of adenohypophysis occur in damage of 70-
75% of gland tissue, and for development of complete picture of
panhypopituitarity destruction of 90-95 % of adenohypophysis is necessary.
• Vessels disordersVessels disorders in hypophysis and hypothalamus (most frequently
afterbearing longtime spasm of vessels of brain and hypophysis owing of
haemorrhage), trauma of the skull basis, tumour of hypophysis and
hypothalamus, inflammatory damage (tuberculosis,sepsis) of hypophysis,
inherent aplasia and hypoplasia can lead to development of
panhypopituitarity.
• The most frequently gonadotropic functiongonadotropic function of hypophysis and secretion of
STH is damaged with the consequent connection of nonsufficient secretion
of ТТH, ACTH and prolactine.

41. Hypophyseal
Simond’s
cachexia

42. Causes of HypopituitarismCauses of Hypopituitarism
Tumors and mass lesions — pituitary adenomas, cysts,
metastatic cancer, and other lesions
Pituitary surgery or radiation
Infiltrative lesions and infections — hemochromatosis,
lymphocytic hypophysitis
Pituitary infarction — infarction of the pituitary gland after
substantial blood loss during childbirth (Sheehan’s
syndrome)
Pituitary apoplexy — sudden hemorrhage into the pituitary
gland
Genetic diseases — rare congenital defects of one or more
pituitary hormones
Empty sella syndrome — an enlarged sella turcica that is
not entirely filled with pituitary tissue
Hypothalamic disorders — tumors and mass lesions
(e.g., craniopharyngiomas and metastatic malignancies),
hypothalamic radiation, infiltrative lesions (e.g., sarcoidosis),
trauma, infections

43. Partial hypopituitarityPartial hypopituitarity
is the disorder of
formation of separate
hormones
of adenohypophysis
(not all). The following
variants of partial
hypopituitarity are
described:
HypophysarHypophysar
nanismnanism
1) Hypophysar nanism
(dwarfishnessdwarfishness) - deficiency of STHSTH;
2) Secondary hypohonadism -
deficiency of FSH and LHFSH and LH;
3) Secondary hypothyrosisSecondary hypothyrosis -
deficiency of TTHTTH;
4) Secondary hypocorticismSecondary hypocorticism -
deficiency of ACTHACTH.

44. • The insufficiency of STHThe insufficiency of STH results to
development of hypophysar dwarfishness,
or nanism and appears by such disorders:
• 1) decrease of intensity of protein synthesisdecrease 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 STHdecrease of inhibiting action of STH on an
absorption of glucose with predominance of
insulinic effect and development of hypoglycemia;
• 3) fallout of fat mobilizingfallout of fat mobilizing action and tendency to
obesity.

45. By producing too much of one or more hormonesBy producing too much of one or more hormones
• Adrenocorticotropic hormoneAdrenocorticotropic hormone::
– causes weight gain (particularly in the body’s trunk, notcauses weight gain (particularly in the body’s trunk, not
the legs or arms)the legs or arms)
– high blood pressurehigh blood pressure
– high blood sugarhigh blood sugar
– brittle bonesbrittle bones
– emotional changesemotional changes
– stretch marks on the skinstretch marks on the skin
– easy bruising.easy bruising.
The insufficiency of ACTH leads to secondary partialThe insufficiency of ACTH leads to secondary partial
insufficiency of adrenal cortex.insufficiency of adrenal cortex.
The glucocorticoid function suffers mainly.The glucocorticoid function suffers mainly.
Mineralocorticoid function practically does not varyMineralocorticoid function practically does not vary

46.  Insufficiency of TTHInsufficiency of TTH
causes secondarycauses secondary
decrease function ofdecrease function of
thyroid gland andthyroid gland and
development ofdevelopment of
secondary hypothyrosissecondary hypothyrosis
symptoms. As against insymptoms. As against in
case of primarycase of primary
hypofunction of thyroidhypofunction of thyroid
gland the introduction ofgland the introduction of
TTH can restore itsTTH can restore its
function.function.

47.  Insufficiency of gonadotropic hormonesInsufficiency of gonadotropic hormones
results inresults in decrease of ability of Sertoli cellsdecrease of ability of Sertoli cells
toto accumulate androgensaccumulate androgens andand oppression ofoppression of
spermatogenesisspermatogenesis andand ability to impregnationability to impregnation
in menin men..
 In case ofIn case of defect of LGdefect of LG ((LuteinizingLuteinizing))
hormone the function ofhormone the function of Leidig’s cells isLeidig’s cells is
infringedinfringed, the formation of androgens ceases, the formation of androgens ceases
and develops eunuchoidism withand develops eunuchoidism with
preservation of partial ability topreservation of partial ability to
impregnation, as the process ofimpregnation, as the process of
spermatozoids maturing does not stop.spermatozoids maturing does not stop.

48. Hyperfunction ofHyperfunction of
adenohypophysisadenohypophysis
(hyperpituitarism)(hyperpituitarism)
 The main reasons ofThe main reasons of
hyperpituitarism development arehyperpituitarism development are
the benign tumours – adenomas of endocrine cells.the benign tumours – adenomas of endocrine cells.
 There areThere are twotwo groups of adenomasgroups of adenomas..
 1.1. Eosinophilic adenomaEosinophilic adenoma, develops from acidophilic cells, develops from acidophilic cells
of adenohypophysis forming STH. Clinicallyof adenohypophysis forming STH. Clinically
hyperproduction of STH appears byhyperproduction of STH appears by giantismgiantism ((if adenomaif adenoma
develops in childrendevelops in children and young people before closing ofand young people before closing of
epiphysar cartilages) andepiphysar cartilages) and acromegaliaacromegalia ((in adultin adult). Giantism). Giantism
is characterized by the proportional increase of all bodyis characterized by the proportional increase of all body
components.components.

49. GigantismGigantism

50. Jane Bunford 2.41mJane Bunford 2.41m
Zeng Jinlian 249 smZeng Jinlian 249 smYao Defen 2.34Yao Defen 2.34

51. • By producing too much of one or more
hormones
• Growth hormone: causes
ACROMEGALY
– a syndrome that includes:
• excessive growth of soft tissues
and bones
• high blood sugar
• high blood pressure
• heart disease
• sleep apnea
• excess snoring
• carpal tunnel syndrome
• pain symptoms (including
headache).
• Acromegaly appears by increased
growth of hands, legs, chin, nose, tongue,
liver, kyphoscoliosis. Besides
that increased metabolic activity of STH
-hyperglycemia, insulin resistanse, even
to development of metahypophysar
diabetes, fatty infiltration of liver develop.

55. BITEMPORAL
HEMIANOPSIA

56. Usually the bitemporal hemianopsia isUsually the bitemporal hemianopsia is
NOT perfectly symmeetrical. Why?NOT perfectly symmeetrical. Why?
Because pituitary tumors are under noBecause pituitary tumors are under no
law to grow perfectly midline.law to grow perfectly midline.

58. • 2. Basophilic adenomaBasophilic adenoma, grows
from basophilic cells of
adenohypophysis which more often
produce ACTH. During this the
Itsenko-CushingItsenko-Cushing disease
develops. It is characterized by:
• а) secondary hypercorticism;
• b) strengthened pigmentation of
skin.
• There are tumors which produce
other hormones of
adenohypophysis less often: TTH,
gonadotropic hormones, prolactin,
MSH.
• The increased level of ACTH during
this disease is combined with
increase of level of other products
of proopiomelanocortin. BASOPHILIC ADENOMA OF HYPOPHYSISBASOPHILIC ADENOMA OF HYPOPHYSIS

60. Hyperfunction of neurohypophysisHyperfunction of neurohypophysis
• Leads to redundant production vasopressin andLeads to redundant production vasopressin and
oxytocin. Their main effects:oxytocin. Their main effects:
• VasopressineVasopressine (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);
5) Endogenic analgetic (depresses pain).

62. • OxytocinOxytocin 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 contractions of uterus of
pregnant woman;
3) Worsens storing and mobilization of information
(amnestic hormone).
• Redundant secretion of vasopressin arises in
tumors of different tissues forming vasopressin,
and also in disorders of hypothalamic endocrine
function regulation. Its main manifestation is
hypervolemia leading to development of constant
arterial hypertension.

63. GG
AA
LL
AA
CC
TT
OO
RR
RR
HH
EE
AA

64. Hypofunction ofHypofunction of
neurohypophysisneurohypophysis
 Insufficient production of vasopressin results toInsufficient production of vasopressin results to
development ofdevelopment of diabetes insipidusdiabetes insipidus..
There are two pathogenetic variants:There are two pathogenetic variants:
 central (neurogenic)central (neurogenic) during which will a little quantity ofduring which will a little quantity of
vasopressine, is formed andvasopressine, is formed and
 nephrogenicnephrogenic duringduring which the sensitivity of epithelialwhich the sensitivity of epithelial
cells receptors of distal nephron parts and collectivecells receptors of distal nephron parts and collective
tubules to vasopressin action (absence or a little quantitytubules to vasopressin action (absence or a little quantity
receptors) is reduced.receptors) is reduced.
 TheThe decreasing of water reabsorptiondecreasing of water reabsorption in kidneys resultsin kidneys results
toto poliuriapoliuria and decreasing of circulatting blood volumeand decreasing of circulatting blood volume
((hypovolemiahypovolemia),), falling of arterial pressurefalling of arterial pressure andand hypoxiahypoxia..
 TheThe decreasing of oxytocindecreasing of oxytocin production appears byproduction appears by
disorders of lactation, weakness of labor activitydisorders of lactation, weakness of labor activity..

66. Adrenal cortex
- secretes several classes of steroid hormones (glucocorticoids and
mineralocorticoids)
- with three concentric zones of cells that differ in the major steroid
hormones they secrete.
Adrenal medulla
- source of the catecholamines epinephrine and norepinephrine.
- chromaffin cell is the principle cell type.
- The medulla is richly innervated by preganglionic sympathetic fibers
and is, in essence, an extension of the sympathetic nervous system.

68. Effects of
mineralocorticoids:
Effects of
glucocorticoids:
1. Retention of sodium
ions and water by
kidneys
2. Increased blood
volume and blood
pressure
2. Possible suppression of
immune system
1. Proteins and fats broken down
and converted to glucose, leading
to increased blood glucose
Adrenal
gland
Kidney
Adrenal cortex
Adrenal cortex
Glucocorticoids –
glucose from noncarb
sources, such as
muscles
Mineralocorticoids
(aldosterone) –
induces kidneys to
reabsorb water and
salts
Both of these deal with
long-term stress

69. Actions of CortisolActions of Cortisol
Major InfluenceMajor Influence Effect on BodyEffect on Body
Glucose metabolismGlucose metabolism
Stimulates gluconeogenesisStimulates gluconeogenesis
Decreases glucose use by the tissuesDecreases glucose use by the tissues
Protein metabolismProtein metabolism
Increases breakdown of proteinsIncreases breakdown of proteins
Increases plasma protein levelsIncreases plasma protein levels
Fat metabolismFat metabolism
Increases mobilization of fatty acidsIncreases mobilization of fatty acids
Increases use of fatty acidsIncreases use of fatty acids
Anti-inflammatory actionAnti-inflammatory action
(pharmacologic levels)(pharmacologic levels)
Stabilizes lysosomal membranes of the inflammatory cells, preventingStabilizes lysosomal membranes of the inflammatory cells, preventing
the release of inflammatory mediatorsthe release of inflammatory mediators
Decreases capillary permeability to prevent inflammatory edemaDecreases capillary permeability to prevent inflammatory edema
Depresses phagocytosis by white blood cells to reduce the release ofDepresses phagocytosis by white blood cells to reduce the release of
inflammatory mediatorsinflammatory mediators
Suppresses the immune responseSuppresses the immune response
• Causes atrophy of lymphoid tissueCauses atrophy of lymphoid tissue
• Decreases eosinophilsDecreases eosinophils
• Decreases antibody formationDecreases antibody formation
• Decreases the development of cell-mediated immunityDecreases the development of cell-mediated immunity
Reduces feverReduces fever
Inhibits fibroblast activityInhibits fibroblast activity
Psychic effectPsychic effect May contribute to emotional instabilityMay contribute to emotional instability
Permissive effectPermissive effect
Facilitates the response of the tissues to humoral and neural influences,Facilitates the response of the tissues to humoral and neural influences,
such as that of the catecholamines, during trauma and extreme stresssuch as that of the catecholamines, during trauma and extreme stress

70. Disorders of adrenal gland functionDisorders of adrenal gland function
 The most frequently there are followingThe most frequently there are following
manifestations:manifestations:
1)1) HypofunctionHypofunction of adrenal cortex - hypocorticismof adrenal cortex - hypocorticism
Addison diseaseAddison disease ;;
2)2) HyperfunctionHyperfunction of fascicular zone - syndrome ofof fascicular zone - syndrome of
Itsenko-CushingItsenko-Cushing –– Hypersecretion of cortisolHypersecretion of cortisol;;
3)3) HyperfunctionHyperfunction of glomerulose zone –of glomerulose zone –
hyperaldosteronism –hyperaldosteronism – Hyperfunction of adrenalHyperfunction of adrenal
cortex resulting in excess secretion of aldosteronecortex resulting in excess secretion of aldosterone;;
4)4) DysfunctionDysfunction of adrenal cortex - adrenogenitalof adrenal cortex - adrenogenital
syndromesyndrome

71. Insufficiency of adrenal cortex
• According to etiology there are primary and secondary
kinds of adrenal cortex insufficiency.
• Primary insufficiencyPrimary insufficiency arises as a result of adrenals injury,
• secondarysecondary is connected with the defeat of hypotalamus
(deficiency of corticoliberin), or with hypofunction of
adenohypophysis (deficiency of ACTH).
• Insufficiency of corticosteroids can be totaltotal when the
operation of all hormones drops out, and partialpartial fallout of
activity of one adrenal hormone.
• Insufficiency of adrenal cortex can be acuteacute and chronicchronic.
• Examples ofExamples of acute insufficiencyacute insufficiency areare:
а) state after removal of adrenals;
b) hemorrhage in adrenals which arises during sepsis,
meningococci infection (syndrome Waterhouse-Friderixan);
c) syndrome of cancellation of glucocorticoides preparations.
• Fast falling of the adrenals function causes development of
collaps and the patients can die during the first day.

72. • TheThe chronic insufficiencychronic insufficiency ofof
adrenals cortex is characterized foradrenals cortex is characterized for
Adison’s diseaseAdison’s disease (bronzed disease).(bronzed disease).
• The most often reasons of it are:The most often reasons of it are:
а) tuberculose destruction of adrenals;
b) autoimmune process.
Tuberculose of
adrenal gland.
Adison’s
disease

74. Skin hyperpigmentation at case of Adison’s disease

76. ІІ. Manifestation, connected with the falling of. Manifestation, connected with the falling of
mineralocorticoids functions of adrenal cortex:mineralocorticoids functions of adrenal cortex:
• 1) dehydration develops owing to loss of sodium ionsloss of sodium ions (decreases
rearbsortion) with the loss of water (poliuria);
• 2) arterial hypotension is stipulated by decrease of circulating
blood volume;
• 3) hemoconcentration (condensation of blood) is connected with
liquid loss, results to disorders of microcirculation and hypoxiadisorders of microcirculation and hypoxia;
• 4) decreasing of kidney blood circulation is stipulated by
increase of arterial pressure with disturbances of glomerulardisturbances of glomerular
filtrationfiltration and development of intoxicationintoxication (nitrogenemia);
• 5) hyperpotassiumemia is stipulated by decrease of canalesdecrease of canales
secretion of potassium ionssecretion of potassium ions and their output from the damaged
cells. It causes disorders of function of arousing tissues;
• 6) distal canales acidosis. It is connected with disorders ofdisorders of
acidogenesisacidogenesis in distal nephron canales;
• 7) gastro-intestinal disorders (nausea, vomiting, diarrhea). Loss
of sodium (osmotic diarrhea) and intoxication have significant
meaning. This disorders without appropriate correction result to
death.

77. ІІІІ. Manifestations stipulated by disorders of. Manifestations stipulated by disorders of
glucocorticoid function of adrenals. To suchglucocorticoid function of adrenals. To such
manifestations concern:manifestations concern:
• 1) hypoglycemia which results to starvation;
• 2) arterial hypotension (permissive reaction on catecholamines);
• 3) decrease reaction of fat tissue on lipotrophic 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;
• 9) sensor disorders - loss of ability to distinguish separate shades
gustatory osmotic acoustical sensations;
• 10) distress-syndrome of a newborn (hyalinic membranosis). It is
stipulated by disorders of surfactant formation in lungs owing to
what lungs are not straightened after birth of a child.

78. Increase of adrenals cortex functionIncrease of adrenals cortex function
• HyperaldosteronismHyperaldosteronism.. Arises during hyperfunction of glomerular zone of
adrenals cortex, which produce mineralcorticoides.
There are primaryprimary and secondary hyperaldosteronismsecondary hyperaldosteronism.
• Primary hyperaldosteronismPrimary hyperaldosteronism (Conn syndromeConn syndrome) arises in adenoma of zone
glomerular, which secretes high quantity of aldosteron. Main manifestations of
this disease:
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). It causes disorders of arousing organs and tissues
(disorders of heart activity, miostenia, pareses);
3) ungas alcalosis. It is connected with amplification of acidogenesis in distall
nephron canaliculas;
4) polyuria arises as a consequence sensitivity of kineys canales epithelium loss
to action of vasopressin. It explains absence of volume increase of circulatting
blood and edema.
• Secondary hyperaldosteronismSecondary hyperaldosteronism is a result of renin-angiotensin system
activation. This state appears by:
a) arterial hypertension;
b) edemas;
c) hypopotassiumaemia;
d) ungas alcalosis.

79. • There are two clinical forms of
hypercorticism with
hyperproduction of
glucocorticoides:
1. Cushing’s diseaseCushing’s disease – basophil
adenoma of anterior
hypophysis part.
2. Cushing’s syndromeCushing’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 in an organism
with the medical purpose.

82. MOON
FACIES
BUFFALO
HUMP
STRIAE

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

87. • Adrenogenital syndromeAdrenogenital syndrome results from the
hereditary stipulated blockade of cortisole
synthesis and amplified formation of androgens
from general intermediate products.
• Depending on the level of blockade of cortisole
synthesis there are three variants of adrogenital
syndrome.
• І. Disorders of early stages of synthesis –
deficiency of glucocorticoides, mineralcorticoides
and androgens hyperproduction. Manifestations:
signs of insufficiency of gluco- and
mineralocorticoidal functions of adrenal cortex
features of early sexual maturing in males,
virilization in women (appearance of man's sexual
features).
• 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
– deficiency of glucocorticoides, hyperproduction of
androgens and mineralocorticoide. Features of
hyperaldosteronism are connected with
manifestations of classical androgenital syndrome.
AdrenogenitalAdrenogenital
syndromesyndrome

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

89. HYPOADRENALISMHYPOADRENALISM
Caused by any anatomic or metabolic lesion of the adrenalCaused by any anatomic or metabolic lesion of the adrenal
cortex that impairs output of the cortical steroids.cortex that impairs output of the cortical steroids.
Primary Acute Adrenal InsufficiencyPrimary Acute Adrenal Insufficiency
-- Waterhouse Friderichsen SyndromeWaterhouse Friderichsen Syndrome
due to overwhelming septicemic infection caused bydue to overwhelming septicemic infection caused by
meningococci, but occasionally other virulentmeningococci, but occasionally other virulent
organism such as gonococci,pneumococi andorganism such as gonococci,pneumococi and
staphylococci.staphylococci.
morphology: massive bilateral adrenal hemorrhagemorphology: massive bilateral adrenal hemorrhage

90. ADRENAL MEDULLAADRENAL MEDULLA
PHEOCHROMOCYTOMA:PHEOCHROMOCYTOMA:
- associated with catecholamine-
Induced hypertension.
- occassionally, this tumor produces other
biogenic steroids or peptides associated with
Cushing’s Syndrome.
-morphology: - ave . weight of 100 gms
- Zellballen appearance

91.  This large adrenal neoplasmThis large adrenal neoplasm
has been sectioned in half.has been sectioned in half.
Note the grey-tan color of theNote the grey-tan color of the
tumor compared to the yellowtumor compared to the yellow
cortex stretched around it andcortex stretched around it and
a small remnant of remaininga small remnant of remaining
adrenal at the lower right.adrenal at the lower right.
This patient had episodicThis patient had episodic
hypertension. This is a tumorhypertension. This is a tumor
arising in the adrenal medullaarising in the adrenal medulla
- a- a pheochromocytomapheochromocytoma..
T
N

93.  Cardiovascular:Cardiovascular: Coronary arteryCoronary artery
disease, hypertension, stroke, arrhythmia.disease, hypertension, stroke, arrhythmia.
 Muscles:Muscles: Tension headaches, backacheTension headaches, backache
 Connective tissues:Connective tissues: Rheumatoid arthritisRheumatoid arthritis
 Pulmonary:Pulmonary: Asthma.Asthma.
 Immune:Immune: Immunosuppression, deficiency,Immunosuppression, deficiency,
autoimmunityautoimmunity
 Gastrointestinal:Gastrointestinal: Ulcer, irritable bowelUlcer, irritable bowel
syndrome, diarrhea, nausea and vomiting,syndrome, diarrhea, nausea and vomiting,
ulcerative colitisulcerative colitis
 Integumetary:Integumetary: Eczema, neurodermatitis,Eczema, neurodermatitis,
acneacne
 Endocrine:Endocrine: Diabetes mellitus, amenorrheaDiabetes mellitus, amenorrhea
 Central nervous:Central nervous: Fatigue and lethargy, type AFatigue and lethargy, type A
behavior, overeating, depression, insomnia.behavior, overeating, depression, insomnia.

95. Literature:Literature:
1.1. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin –General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin –
Vinnytsia: Nova Knuha Publishers – 2011. – P.Vinnytsia: Nova Knuha Publishers – 2011. – P. 588588––612612..
2.2. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P.Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P.
Gurcalova // Study guide for medical students and practitioners. Edited byGurcalova // Study guide for medical students and practitioners. Edited by
prof.Zaporozan, OSMU. – Odessa. – 2005.– P. 271–282.prof.Zaporozan, OSMU. – Odessa. – 2005.– P. 271–282.
3.3. Essentials of Pathophysiology: Concepts of Altered Health States (LippincottEssentials of Pathophysiology: Concepts of Altered Health States (Lippincott
Williams & Wilkins), Trade paperback. – 2003Williams & Wilkins), Trade paperback. – 2003 // Carol Mattson Porth, Kathryn J.Carol Mattson Porth, Kathryn J.
Gaspard. – Chapter 30, 31. – P. 529–545.Gaspard. – Chapter 30, 31. – P. 529–545.
4.4. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicineSymeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine
Publishing. – 2010. – P. 484–493, 506–512.Publishing. – 2010. – P. 484–493, 506–512.
5.5. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme.Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme.
Stuttgart. New York. – 2000. – P. 256–271.Stuttgart. New York. – 2000. – P. 256–271.
6.6. Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3thCorwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th
edition. Copyright Вedition. Copyright В.. – Lippincott Williams & Wilkins – 2008. –– Lippincott Williams & Wilkins – 2008. – Chapter 9. – P.Chapter 9. – P.
245– 249, 251–255, 260–264, 267–274, 277–279.245– 249, 251–255, 260–264, 267–274, 277–279.
7.7. Robbins and Cotran Pathologic Basis of Disease 8th edition./ Kumar, Abbas,Robbins and Cotran Pathologic Basis of Disease 8th edition./ Kumar, Abbas,
Fauto. – 2007. – ChapterFauto. – 2007. – Chapter 2020. – P.. – P. 751–757, 789–801751–757, 789–801..
8.8. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L.Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L.
Banasik // Elsevier Inc, 4th edition. – 2010. – P. 904–914, 920–926, 931–936.Banasik // Elsevier Inc, 4th edition. – 2010. – P. 904–914, 920–926, 931–936.
9.9. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, GlennPathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn
Matfin. – New York, Milwaukee. – 2009. – P. 1008–1030.Matfin. – New York, Milwaukee. – 2009. – P. 1008–1030.