2. I. IntroductionI. Introduction
Adrenal GlandsAdrenal Glands
• suprarenal – they sit on top of the
kidneys
• each is composed of 2 distinct regions:
A.A. Adrenal MedullaAdrenal Medulla
- the inner region
- comprises 20% of the gland
- secretes epinephrine and
norepinephrine
- derived from ectoderm

3. B.B. AdrenalAdrenal
CortexCortex
• the outer regionthe outer region
• comprises 80% of thecomprises 80% of the
glandgland
• secretes corticosteroidssecretes corticosteroids
• derived from mesodermderived from mesoderm

4. 1) Zona Glomerulosa1) Zona Glomerulosa (outermost region)(outermost region)
- produces mineralocorticoids (aldosterone)
2) Zona Fasiculata2) Zona Fasiculata (middle region)(middle region)
- produces glucocorticoids (cortisol) as well as
estrogens and androgens
3) Zona Reticularis3) Zona Reticularis (innermost region)(innermost region)
- same function as zona fasiculata
DHEA – dehydroepiandrosteroneDHEA – dehydroepiandrosterone
• an adrenal androgen in females
• responsible for growth of pubic and axillary hair

5. CC. Pathologies Associated with Adrenal. Pathologies Associated with Adrenal
AndrogenAndrogen
HypersecretionHypersecretion
1.1.Adrenogenital SyndromeAdrenogenital Syndrome
- hypersecretion of androgens or estrogens- hypersecretion of androgens or estrogens
a)a) in the adult femalein the adult female::
- masculinization (i.e. hirsutism)- masculinization (i.e. hirsutism)
b)b) in the female embryoin the female embryo::
- female pseudohermaphroditism- female pseudohermaphroditism
c)c) in the adult malein the adult male::
- no effect- no effect
d)d) in young boysin young boys::
- precocious pseudopuberty- precocious pseudopuberty

6. II. MineralocorticoidsII. Mineralocorticoids (Aldosterone)(Aldosterone)
A.A. FunctionsFunctions
- promotes reabsorption of Na+
and
secretion of K+ from the distal portion of the
nephron
B.B. Regulation of SecretionRegulation of Secretion
1. Renin Angiotensin
- Angiotensin II stimulates aldosterone
secretion
2. Potassium
- high levels of K+
induce aldosterone
secretion

7. C.C. PathologiesPathologies
1. Hypersecretion1. Hypersecretion
a.a. primary hyperaldosteronismprimary hyperaldosteronism
- Conn’s syndrome- Conn’s syndrome
- usually due to a tumor on the gland- usually due to a tumor on the gland
- too much secretion of gland itself- too much secretion of gland itself
b.b. secondary hyperaldosteronismsecondary hyperaldosteronism
- default in renin angiotensin system- default in renin angiotensin system
- most common in atherosclerosis of- most common in atherosclerosis of
renal arteriesrenal arteries
2. Hyposecretion (defer to2. Hyposecretion (defer to

8. III. GlucocorticoidsIII. Glucocorticoids (Cortisol)(Cortisol)
A. Metabolic Effects
- overall effect: increase plasma glucose
levels, often at the expense of proteins
and fats
1. CHO Metabolism
a. gluconeogenesis
cortisol helps convert skeletal muscle
protein to CHO’s and eventually
glycogen
b. decrease glucose utilization(anti-
insulin effect)

9. 2. Protein Metabolism2. Protein Metabolism
- proteins are mobilized by cortisol to be
converted to CHO’s in a fasting
state
- lean body mass decreases
3. Fat Metabolism3. Fat Metabolism
- cortisol causes lipolysis (inhances
catecholamines)
- expectations: person will be thin, but if
excessive cortisol see unusual fat
distribution (i.e. “buffalo
hump”)
4. Increases Hunger4. Increases Hunger

10. B. Other EffectsB. Other Effects
1.1. Fetal DevelopmentFetal Development
• Cortisol aids in maturation of the
lungs, especially with the production
of surfactant
• Maturation of g.i. enzymes

11. B. Other Effects AdultsB. Other Effects Adults
1.1. StressStress
- Hans Selye: experimented by stressing
animals
- results: stress is associated with
increased levels of glucocorticoids
- explanation: glucocorticoids mobilize
a pool of amino acids to construct needed
proteins or enzymes to face the stress

12. B. Other Effects (cont.)
2. Anti-inflammatory
- during tissue damage, phospholipase A2activity
increases releasing arachadonic acid to
aid in synthesis of prostaglandins &
leukotrienes
- glucocorticoids enhance production of
macrocortin which inhibits phospholipase
A2and thus the inflammatory response
3. Immune Response
- glucocorticoids suppress the immune system
by decreasing the number of T
lymphocytes
- used frequently after organ transports

13. B. Other Effects (cont.)
4. Vasoconstriction
- Glucocorticoids necessary for
vasocontriction
effects of the catecholamines
5. Stimulates Erythropoietin
6. Increases Bone Reabsorbtion
7. Decreases REM Sleep

14. C. RegulationC. Regulation
- it’s a classic negative feedback system
- low glucocorticoid levels cause the
hypothalamus to secrete corticotropin
releasing hormone (CRH)
- CRH and low glucocorticoid levels cause the
anterior pituitary to release ACTH
- ACTH stimulates glucocorticoid production
at the adrenal cortex
* Stress and hypoglycemia can also trigger the
release of CRH

15. D.D. PathologiesPathologies
1)1) HypersecretionHypersecretion
- Cushing’s Syndrome
- caused by too much exogenogeous cortisol,
too much ACTH, an adrenal tumor, or ACTH
secreting tumor
– Symptoms
» Proteolysis
» Moon-faced and buffalo hump

16. D.D. Pathologies CONT.Pathologies CONT.
2)2) HyposecretionHyposecretion
a)a) Primary Adrenal CorticalPrimary Adrenal Cortical
InsufficiencyInsufficiency
- Addison’s Disease
- due to autoimmuno destruction of the
gland
b)b) Secondary Adrenal CorticalSecondary Adrenal Cortical
InsufficiencyInsufficiency
- due to too little ACTH

18. EICOSANOIDSEICOSANOIDS
ARACHIDONIC ACID
prostaglandinsprostaglandins
leukotriensleukotriens
thromboxanesthromboxanes
prostacyclinsprostacyclins

19. Prostaglandin Nomenclature
•3 Groups
•PGA
•PGE
•PGF
•Double BondsDouble Bonds
•Optical IsomerOptical Isomer

20. Prostaglandin Functions
• Reproduction
• Respiratory
• Nervous
• Immune
• MANY OTHERS!!