ADRENAL GLANDS

ANATOMY,
functions.
 Professor of endocrinology
 NUNU BERIDZE
Hypocorticism,
diagnosis and
treatment
ANATOMY AND FUNCTION OF ADRENAL
GLANDS
 Mycroscopic structura of
adrenal glands (AG)
 I AUTER LAGEST PART, so called adrenal cortex contains:
 1) ZONA GLOMERULOZA
 2) ZONA FASCIKULATA
 3)ZONA RETICULARIS

 II TE ADRENAL MEDULLA, located inside the adrenal cortex in the center of the glands

 Each of them produces cpecific hormones

HORMPNES< PRODUCED BY ADRRENAL CORTEX

 ZONA GLOMERULOSA (ZG) produces ALDOSTERON. It is deficient in enzyme 17aHydrolase and thus can not
produce CORTOSOL and ANDROGENES

 ZONA FASCUCULATA (ZF) is the sickest layer and produces androgens and cortisol,

 ZONA RETICULARIS(ZR) also produces CORTISOL and ANDROGENS



 ONLY ZONA FASCICULATA and ZONA RETICULOZA function are regulated by PITUITARY ACTH

 BECAUSE of enzymatic differencies between ZG And inner tow hormones AC functions as tow different units
 With different regulation and secretory products.
 CORTIZOL
 COrTISOL is GLUCOCORTICOID and it effects on body’s carbohydrate, fat and protein
metabolism
 Suppresses the inflammation, regulates blood pressure, increases blood sugar level,
decreases bone formation, controls the sleep –wake cycle. It is released during times
of stress to help your body to get a boost
 and better hendl an emergency situation.

 CORTIZOLE is a part of HYPOTHALAMO-PITUITARY ADRENAL AXIS and its’ secretion is

regulated by the mins of a negative feedback mode.
 ALDOSTERON plays a central role in the regulation of blood pressure and certain
electrolytes (sodium and potassium)
 SECRETION of ALDOSTERON is primarily regulated by renin-ANGIOTENZINE sytem and
 DEHYDROEPIANDROSTERON AND ANDROGEN STEROIDS

 They are WEAK MALE HORMONES.

 They are PRRECURSOR hormones and are converted in females into female
hormones (ESTROGENS)
 And in the testes into MALE HORMONES
 Estrogens and androgens for the other hand are produced in much larger
amount in ovaries and testis

 They are derivatives of CHOLESTEROL and they interact with their specific
receptors in cytoplasm and after that
 in cell nucleu. s
 CLASSIFICATION OF AC INSUFFICIENCY
PRIMARY : autoimmune.metastatic malignancies,
adrenal hemorragie, infections,
dystrophia,amiloidos, hemoxromatose, congenital
adrenal hyperplasia, skin hyperpigmentation,vitiligo,
amenorrhea, loss of axillary and pubical hear.

SECONDARY: caused by pituitary tumors, massive

exogenous corticosteroid therapy
 EFFECTS OF CORTISOL
 LIVER -stimulates gluconeogenesis itself and by stimulating hepatic response to gluconeogenic hormones
 (permissive) effect; increases the mobilization of substrates from peripheral tissues; increases hepatice
 Gluconeogenesis.
 MUSClE – inhibits glucose uptake
 ADIPOSE TISSUE – inhibits glucose uptake and stimulates lipolysis;
 CONNECTIVE TISSUE –loss of collagen
 BLOOD – decrease of lymphocyte production;
 IMMUNE SYSTEM: inhibits PROSTAGLANDINE synthesis,decreases secretion of LYMFOKINES,ANTIBODY PRODUCTION
and clearance;
 HEART: increases cardial output and peripheral vascular tone, stimulates expression of adrenergic receptors;
 RENAL function: increase of sodium and water excretion;
 CNS – by yet unknown mechanism influence on behavior;
 GONADAL FUNCTION – it in inhibits gonadotropin secretion, in women inhibits LH secretion
CLINICAL SIGNES OF PRIMARY AC INSUFFICIENCY
 Weakness, fatigue,anorexia,nausea,vomotong, low blood
pressure,hypoglycemia, decrease of sodiuma ans increase of blood
potaccium levels.

 Skin hyperpigmentation, vitiligo, may be loss of axillar and pubic hear

 Sometimes amenorrhea

 Amenorrea in several cases

 ACUTE ADRENOCORTICAL INSUFFICIENCY
 develops when patients are exposed to stress trauma, surgery, dehydration,
vomiting,diarrhea
 Clinical manifestations of acute adrenocortical crisis:
 Hypotension and even shock,fiver,dehydration, volume depletion, hypoglycemia,
tachycardia, depression, acute abdominal pain, flank, back pain,
 Abdomenal distension, rigidity, chest pain.
 Blood hormone level: low normal or decreased cortisol level and increased ACTH
 Level.
 Blood electrolites: hyponatremia and hyperkaliemiaas a result of mineralcorticoid
deficiency.
 Due ru volume depletion azotemia, increased creatinine level, metabolic acidosis
 SECONDARY ADRENOCOETICAL DEFICIENCY

 ETIOLOGY: pituitary tumors, hemorragia, as a resupt of prolonged exogenous

glucocorticoid treatment
 CLINICAL MANIFESTATIONS are the same as in chronic AC deficiency, excluding skin
darkenss bacause the absence of the increase of melanocyte stimulatin hormone.
 Symptoms are usually chronic with nonspecific manifestations
 Hyperkaliemia and hypernatremia are usually absent as well as mineralcorticois
insufficiency.
 Prominent features:lethargy,wekeness,easy fatigability anorexia, nosea,occasionally
 Vomiting, arthralgia myalgia, cignes of other diseases of pituitary
 Other laboratory data: normochromic anemia. Neutropenia,
lymphocytosis,neutropenia.
 TREATMENT
 In primary hypocorticism replacement therapy with cortisol and mineral corticoid such as cortinef.

 In secondary in secondary hypocorticism only cortisol