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Summaries :
Anatomy of the supra renal gland

Site: Upper poles of the kidney

N.B: Each Gland is formed of 2 parts cortex (secretes steroids) and medulla
(secretes catecholamines).


Post. : Diaphragm

Medial: celiac ganglion

Post. Inf.: Kidney


Right Left
Partially peritoneum Covered by peritoneum of lesser
IVC Pancreas
Liver Splencic vessels

Arterial supply:

For each gland:

1.Sup. suprarenal artery from inf. Phrenic artery.

2. Middle suprarenal artery from abdominal aorta.

3.Inf. suprarenal artery from renal artery.

Venous drainage:

1.Right suprarenal vein into IVC.

2. Left suprarenal vein into left renal vein.



Cortex: Ceolemic epithelium

Medulla: neural crest

A) Cortex:
Proliferation of Ceolemic epithelium.1ry fetal cortex.invade the
medulla..proliferates again..2ry fetal cortex

At end of 1st year 1ry degenerates and secondary persists

At end of 4th year 2ry proliferates into 3 zones.

MesodermCt capsule.

B) Medulla:
Neural crest..sympathetic ganglion

Neuroectodermal cells migrateinvade the 1ry cortex and give the suprarenal

Congenital anomalies:
1. Ectopic suprarenal gland

2. Accessory medullary tissues

3. Accessory cortial tissue.

4, Agenesis of the gland.

Histology of supra renal glands

Each gland is composed of:

1. Cortex: Yellow peripheral part, has the same origin as the gonads and secrete
steroid hormones.

2. Medulla: Reddish brown central layer has origin same as the sympathetic nervous
system and secrete catecholamines.

A) Stroma:

The gland is covered by a C.T capsule that sends thin trabecullar septa inside the
gland. A network of reticular fibers supports the secretory cells.

B) Medulla:

Parenchymal cells of the medulla include:

1. Chromaffin cells.

2. Sympathetic ganglion cells.

1) Chromaffin cells:

L.M 1. Arranged in rounded groups or short

cords related to blood capillaries.

2. They are large ovoid cells with large

spherical nuclei and pale basophilic


3. They contain granules that stain deep

brown with Chromaffin salts.

E.M Cytoplasm contains:

rER, numerous mitochondria, Prominent
golgi complex, secretory granules
contacting catecholamines.
Norepinephrine secretory granules Epinephrine secretory granules
Large, have eccentric electron dense core Small, less electron dense granules and
with limiting membrane on the granules. the contents fill the granules.

C) Cortex:

Zona Glomerulosa Zona Fasciculata Zona Reticularis

1. Lies directly under the c.t 1. Largest layer of the 1. Inner layer of the
capsule. cortex. cortex.
2. Cells are arranged in closely 2. Cells are arranged 2. Cells are arranged in
packed rounded or arched groups in cords perpendicular irregular cords that
surrounded by blood capillaries. to the surface anastomose together
3. Cells are columnar or pyramidal separated by blood enclosing fenestrated
with dense basal nuclei and acidic capillaries. blood capillaries in
slightly vacuolated cytoplasm. 3. Cells are large between.
polyhedral with large 3. Cells are small with
pale round nuclei, acidophilic cytoplasm.
cytoplasm appears
pale and contains
numerous vacuoles.
Shows ultra structure features of Same as glomerulosa Same as glomerulosa
steroid secreting cells: sER, but with numerous but with lipofuscin
mitochondria with tubular cristae lipid droplets. pigment.
and few lipid droplets.
Secrete mineralocortecoids Secrete Secrete Androgens
Glucocortecoids and small amount of
Action of Catecholaimnes:-
Secreted in emergency and their effects are :
Increase the metabolic rate leading to increased heat production.
Stimulate glycogenolysis in the liver,
Mobilize free fatty acids from adipose tissue, so their plasma level increased.
Increase both heart rate and its force of contraction.
Norepinephrine produces vasoconstriction in most organs which increases both
systolic and diastolic blood pressures.
Cause splenic contraction
Cause vasoconstriction to the renal blood vessels which may decrease urine
Increase the rate and depth of respiration by direct excitation of the
respiratory centre and indirectly by increased metabolic rate they cause
Potentiate skeletal muscle contraction and delay the onset of its fatigue.
They also cause vasodilation of skeletal muscle blood vessels.
Excite the nervous system and increase the mental activity and alertness.
Increase the visual fields.
Control of Secretion:
Catecholamines secretion is low in basal states but is markedly increased during
emergencies as a part of the diffuse sympathetic discharge to withstand with
There is a special centre in the medulla oblongata, connected to the greater
splanchnic nerve which supplies the gland.
Diseases of Adrenal Medulla
Effect of Deficiency:
Unlike the adrenal cortex the adrenal medulla does not appear to be essential to
life as all its vital functions are done by sympathetic nervous system
Effect of Excess:
Most adrenomedullary disorders are neoplasms, the most significant of which are
pheochromocytoma, neuroblastoma, and ganglioneuroma.

The hypertension is associated with increased risk of myocardial ischemia,
congestive heart failure, renal injury, and cerebrovascular accidents. Sudden
death may occur.
Increase in basal metabolic rate.
Aldosterone is a steroid.
It is secreted from the zona glomerulosa.
It combines loosely with the plasma proteins.
Functions of the mineralocortocoid (Aldosterone):
On Kidney
Aldosterone increase sodium reabsorption in exchange with secretion of either K+
or H+. hi the distal tubules, collecting tubules and collecting duct. It increases
formation of Na* K+ATPase.

Effects of aldosterone on sweat glands, salivary glands and intestinal

Aldosterone increases the reabsorption of sodium and the secretion of potassium
by the ducts to conserve body salt in hot environments , when excessive quantities
of saliva are lost and loss of sodium in the stools.

Regulation of Aldosterone secretion:

1. Effect of potassium ion concentration on aldosterone secretion: An increase
in potassium ion concentration causes direct stimulation of zona glomerulosa to
increase secretion of aldosterone
2. Effect of the renin-angiotensin system on aldosterone secretion:
Angiotensin II is responsible for stimulating the synthesis and release of
aldosterone from the cells of the zona glomerulosa.
3. Effect of decreased sodium on aldosterone secretion:
Diminished sodium concentration directly affects the zona glomerulosa cells to
enhance aldosterone secretion.
Lack of sodium causes retention of potassium by the kidneys which increase
aldosterone secretion.
The diminished sodium leads to diminished extracellular fluid volume, with
resultant diminished cardiac output and renal blood flow. This enhances
formation of angiotensin II which stimulates aldosterone secretion.
Diminished sodium concentration causes the anterior pituitary gland to secrete
some substances called the unidentified pituitary factor which affects the
adrenal glands to increase aldosterone secretion.
4. Effect of ACTH on aldosterone secretion:
It has a permissive effect on aldosterone secretion and all the above regulations
of aldosterone secretion will occur if there is only a minimal amount of ACTH.

The effects of excess aldosterone are:

Decrease in sodium loss in the urine with increase sodium in extracellular
fluid , this also causes reabsorption of chloride causing increased osmotic
pressure so osmosis of water occurs increasing extracellular fluid volume and
blood volume which may lead to increase cardiac output and hypertension,
Increase potassium loss in the urine:When the potassium ion concentration
falls severe muscle weakness often develops. Paralysis may occur due to failure
of transmission of action potential.
Excess aldosterone causes tubular secretion of hydrogen ion instead of sodium
causing decrease in hydrogen ion concentration in extracellular fluid which leads
to mild degree of alkalosis.
Effect of deficiency of mineralocorticoid:
When aldosterone is deficient, sodium reabsorption decreases sodiumchloride
ions and water are lost in the urine this leads to:
o Decrease extracellular fluid volume.
o Decrease plasma volume.
o Decrease carding output.
o Circulatory shock may develop rapidly.
Potassium and hydrogen ions are increased
When potassium rises to approximately double normal, serious cardiac toxicity
including weakness of heart contraction and development of arrhythmia If
severe cardiac arrest in diastole occurs.
Mild acidosis develops due to excess hydrogen ion.
Adrenocortical hormones released under the control of ACTH

1. Glucocorticoids
2. Androgens
1. Glucocorticoids
Steroid hormones ( group I ) so:
a. They bound to plasma proteins ( transcortin)
b. 94% bound inactive . 6% free active
c. They bound to cytoplasmic & nuclear receptors >> transcription &
translation of mediators
d. Mediators of metabolic actions >> enzymes ( cAMP dependant kinase)
e. Mediators of anti-inflammatory & immunosuppressive actions >> lipocortin
lipomodulin leading to:
i. Inhibitions of phospholipase A2 >> inhibition of PGs &
leukotriens formation
ii. Inhibition of platelet activating factor synsthesis
iii. Inhibition of mediator release from inflammatory cells
Metabolic actions:
Hyperglycemic . Catabolic lipolytic
a. Hyperglycemic:
1. Increase gluconeogenesis in the liver by:
i. Increasing enzyme synthesis
ii. Increasing mobilization of aminoacids from extrahepatic tissues (
muscles ) >> blood >> liver
2. Decreasing glucose utilization by the cells by decreasing glucose
3. Hyperglycima >> worsen diabetes
b. Catabolic:
1. Decreasing proteins in extrahepatic tissues by:
i. Decreasing protein synthesis
ii. Increasing protein catabolism
iii. Decreasing aminoacid transport to extrahepatic tissues
2. Increasing protein synthesis in the liver by

Increasing mobilization of amnioacids to the liver >> elevating blood amniacid level

And this leads to:

i. Increasing liver & plasma proteins

ii. Increasing gluconeogenesis
c. Lipolytic:

Increasing FFA mobilization from adipose tissues increasing their plasma level and
their utilization for energy

Circulatory actions:
1. Important for normal muscular contractility & vasoconstrictive effect of NE
2. Decreasing vascular permeabiliting preserving blood volume
Nervous actions:

Affecting sensations & higher functions as concentration, memory & intellectual


Muscular actions:
1. Important for normal contractility
2. Deficiency >> muscular fatigue
3. Excess >> muscular atrophy due to increased protein catabolism
Actions on Ca++ metabolism:
Decreasing plasma Ca++ level by
1. Decreasing Ca++ & PO4-- intestinal absorption (anti Vitamin D action)
2. Increasing renal excretion
Decreasing bone formation by
1. Inhibition of cellular replication of osteoblasts & protein synthesis
Immunosuppressive actions:
1. Increasing RBCs
2. Decreasing eosinophils , basophils , monocytes & lymphocytes
3. Large doses :
a. Atrophy of lymphoid tissue
b. Decreased T & B cells
c. Decreased level of immunity
Anti-inflammatory & anti allergic actions:

Decreasing inflammation by:

1. Rapid resolution
2. Decreasing vascular permeability
3. Decreasing inflammatory cells & release of mediators
4. Stabilization of lysosomes ( decreasing release of proteolytic enzymes)
5. Inhibition of fibrosis & adhesions

Regulation of cortisol secretion

Stimulus ( physiological stress) >> hypothalamus >> corticotrophin releasing

factor release >> anterior pituitary >> ACTH release
ACTH >> adrenocortical cells >> cortisol & androgens release
ACTH>> MSH, lipotropin & endorphin release:
a. Normally >> no significant effect
b. Increased ACTH doses >> MSH & ACTH ( has MSH activity) >>
melanin pigments formation by melanocytes
High level of cortisol >> -ve feedback inhibition of CRF & ACTH release
Cotrisol level is high in early morning & is low in late morning

2. Androgens
1. During fetal life:
Androgens are continuously secreted from adrenal cortex + minute
amounts of female sex hormones
Part of early development of male sex organs due to childhood
release of androgens
2. In females much of the growth of pubic & axillary hair due to cortical
3. In males part of cortical androgens in converted into testosterone in
extracortical tissue secretion is controlled by ACTH
Diseases of adrenal cortex

Hyper function (hyperadrenalism)

I. Cushing Syndrome
Hypersecretion of cortisol
It may be :
i. Exogenous
ii. Endogenous
1. 1ry hypothalamic pituitary disorder > ACTH
2. 1ry adrenocortical hyperplasia or neoplasia (functioning adenoma
or carcinoma)
3. Ectopic production of ACTH from a non endocrine neoplasm e.g. :
lung cancer small cell carcinoma.
Manifestations :
i. Mobilization of fat from the lower part of the body > thin legs >
deposition of fat in thoracic and abdomen >> buffalo torso shape (3la
fekra torso ya3ny human trunk )
ii. Moon face (edematous appearance > it's not edema it's fat)
iii. Increase the androgenic activity >> acne + hirsutism (ya3ny excess
growth of body hair)
iv. 80 % of pts suffer from hypertension (minreralocorticoid effect of
v. Increased blood glucose > adrenal diabetes > few months > beta cells
burnt out > irreversible Frank diabetes mellitus.
vi. Decreased tissue proteins except liver and plasma > muscular mass loss
+ weakness
vii. Immunosuppression
viii. Diminished collagen fibers in the SC tissues >> large purplish striae > SC
tissues torn apart
ix. Lack of protein deposition and in the bone & anti vitamin D activity &
Ca++ lowering effect leads to osteoporosis and bone weakness
x. It affects brain intellectual functions, memory and concentration so it
may induce Euphoria ;)
II. Hyperaldosteronism
1ry (Conn's Syndrome)
i. It's due to
1. Functioning adenoma 65 %
2. Bilateral idiopathic adrenocortical hyperplasia 30 %
ii. Effects :-
1. Increase Na+ reabsorption increase Cl- NaCl O.P
2. Na+ leads to Blood volume COP hypertension
3. Increase potassium excretion hypokalemia muscle weakness
impaired transmission of action potential paralysis
4. Excretion of H+ Mild degree of alkalosis
2ry hyperaldosteronism
i. Due to activation of renin angiotensin system by decreased renal
perfusion (AS - Stenosis - pregnancy - hyperalbuminemia)
ii. Renin Aldosterone then causes previously discussed effects
III. Adrenal virilism
Excessive androgens due to :-
i. Neoplasms
ii. Congenital adrenal hyperplasia
i. Masculinizing effect through out the body
ii. In females :-
1. Growth of beard
2. Deeper voice
3. Masculine distribution of hair on the body and on the pupis (like
males' hair distribution)
4. Clitoris growth >> resemble penis
5. Thick skin
6. Muscle development (deposition of proteins)
iii. In males :-
1. Prepuberty :- same in female + rapid development of male sexual
organs + sexual desire
2. Adults :- difficult to diagnose (androgens have the same effects
as testosterone hormone)
Hypoadrenalism :-
o It may be due to :-
Lesion in the adrenal cortex:- impaired corticosteroids
ACTH deficiency
o Types
Acute : adrenal crisis
Chronic : Addison's disease
2ry adrenocortical insufficiency : impaired ACTH secretion
o Adrenal crisis:
May be induced by stress (increased demand), rapid withdrawal of
therapy, massive adrenal destruction.
Abdominal pain >> vomiting
Vascular collapse - hypotension > coma > death
o Addison's disease:
Effect of deficiency of mineralocorticoids:-
1. Decreased Na+ and Cl- (excreted in urine):-
o Decreased ECF volume
o Decreased plasma volume
o Decreased COP
o hypotension
o Circulatory shock
2. Increased H+ >> mild acidosis
3. Increased K+ >> hyperkalemia it leads to:-
o Serious cardiac toxicity
o Weakness of myocardial contraction
o Development of arrhythmia
o Cardiac arrest in diastole Why ? >> decreased k+ out flux during
repolarization > stoppage of MP at a depolarized state >> excited
cells cardiac arrest in diastole
Effect of deficiency of glucocorticoids
1. Patient can't maintain normal blood glucose concentration between meals
(decreased gluconeogenesis)
2. Reduction of mobilization of fat and protein from the tissues >> depress
many other metabolic functions of the body >> weak muscles why?
(although there is large amounts of glucose and nutrients available,
metabolic functions need Glucocorticoids to be maintained)
3. Anemia
4. If it's exposed to any type of stress >> Death may occur
5. Melanin pigmentation of mucous membrane and skin (lips - nipples) - (most
important feature)
o Causes:-
ACTH by feedback mechanism >> MSH
MSH & ACTH >> stimulate formation of melanin by
o 2ry adrenocortical insufficiency :-
Due to hypothalamic or pituitary disorder >> ACTH
E.g. :
1. Hypothalamic pituitary neoplasms / infections
2. Hypothalamic pituitary suppression (long term steroid therapy).

Summary of Pathology
Adrenal Medulla diseases
Pheochromocytoma Neuroblastoma
Description It is derived from chromaffin cells. A highly malignant
Most of the tumors arise from the adrenal medulla. tumor.
However, in a minority of cases, the tumor arises in Neuroblastoma most
extra adrenal sites eg. sympathetic ganglia called commonly arises in
paragangliomas. either the adrenal
medulla or the
sympathetic ganglia.
Most neuroblastomas
secrete catecholamines.
Pheochromocytomas occur sporadically (90%), or as Most of the cases are
a part of multiple endocrine syndrome. sporadic; however,
Most sporadic lesions occur in adulthood with slight familial cases also occur.
female prevalence; familial lesions may arise in
childhood, with strong male predominance.

Morphology Morphology: Pheochromocytoma is known as the Grossly, it appears as a

lobular, soft tumor with
"10% tumor".
grayish cut surface
10 % of cases are bilateral
showing areas of
10% of cases occur in extra adrenal sites, and.
necrosis, hemorrhage
10% of tumors are biologically malignant.
and calcification.
Grossly, it varies from circumscribed spherical Microscopically, the
mass confined to the adrenal medulla to a large tumor is composed of
hemorrhagic mass. Cut section is gray to brown with small, dark, round cells
areas of hemorrhage. with scant cytoplasm,
arranged in masses or
Microscopically, it is composed of polygonal cells
having abundant cytoplasm and pleomorphic nuclei.

Features 1.Hypertension It is rapidly growing

3. Palpitation. cancer. It spreads
4. Hyperglycemia. locally; by lymph node
5. Increase in basal metabolic rate. metastases, and by
blood stream to skull,
orbit, liver and bone

Diagnosis Is based on laboratory measuring of catecholamines It is a common cause of

or in plasma and urine and radiographic imaging studies cancer death in patients
such as CT, MRI and ultrasound. under 15 years of age.
Adrenal Cortex Diseases:
I- Increase in secretion :
1. Cushing's syndrome:
1- Exogenous glucocorticoids.
2- Endogenous causes.
a) Primary hypothalamic pituitary diseases
b) Primary adrenocortical hyperplasia or neoplasia (adenoma or carcinoid).
c) Ectopic production of ACTH by a non-endocrine neoplasm.
2. Hyperaldosteronism:
a. Primary hyperaldosteronism (Conn's syndrome): It is due to:

Aldosterone-producing adrenocortical adenoma occurs in 65% of cases (Conn's

Bilateral idiopathic adrenocortical hyperplasia (30% of cases).

b. Secondary hyperaldosteronism
It occurs in response to activation of the renin-angiotensin system. It is
characterized by increased level of plasma renin.

Clinically, it occurs in cases of congestive heart failure, decreased renal

perfusion (arteriolar nephrosclerosis, renal artery stenosis), hypoalbuminaemia
and pregnancy.
3. Adrenal Verilism :
Causes of excessive androgens: May be due to:
Adrenocortical neoplasms (carcinoma more than adenoma), and
Congenital adrenal hyperplasia.

II- Adrenocortical Hypofunction

Adrenal Crisis Addisone's disease
Causes: May be due to sudden increase in Might be due to,
glucocorticoid requirements in patients with chronic Autoimmune adrenalitis (in 60%-
adrenocortical insufficiency. 70% of cases).
Rapid withdrawal of steroid therapy. Infections asTB and fungi.
Massive destruction of adrenals, e.g. neonatal Metastatic tumors
adrenal hemorrhage Systemic amyloidosis.
Clinical features: vomiting, abdominal pain, Sarcoidosis
hypotension, coma, and vascular collapse. Death
follows rapidly unless corticosteroids are replaced
Pharmacology of corticosteroids

Corticosteroids include:-
o Glucocorticoids (cortisol)
o Mineralocorticoids (aldosterone)
ACTH controls only cortisol and androgens, So :-
o In case of impaired secretion of ACTH use only glucocorticoids
o If suprarenal gland is damaged give both (glucocorticoids and
Preparations :-

Drug Route of Anti- Sodium Notes

administration inflammatory retaining
effect effect
Hydrocortisone Systemically 1 1 Natural
Cortisone Tab, injection 0.8 0.8 Prodrug
Prednisolone Orally, 5 0.3 Synthetic
Prednisone Tablets only 4 0.3 Prodrug
Fluorinated CS Topical 30 ZERO - Catabolic, so
(Beta & Systemic they may induce
dexamethasone) acute muscle
emergency weakness.
cases - It causes
Beclomethasone Inhalation 30 Zero Used in
Fludrocortisones Oral (once 10 250 Used in 1ry
daily) Addison's
Deoxycortone Parentral Zero 50 Has a long
duration of
Aldosterone Injection Zero 500 It's duration of
action doesn't
exceed 2hs
Therapeutic uses :-

1. Anti-inflammatory and 2. Replacement therapy

Rheumatic fever Addisonian insufficiency
Rheumatoid arthritis 1ry Addison's disease
Acute Gout Chronic 2ry adrenal insufficiency
Nephrotic syndrome (ACTH)
Organ transplantation
Systemic lupus erythematosis
Severe Allergic reactions
Eczema (Topically)
ICP (cerebral tumor)
Active chronic hepatitis
Anaphylactic shock
Lymphocytic leukemia - lymphoma
Blood diseases due to antibodies
formed against blood elements
(RBCs, platelets .. )
Adverse effects Contraindications
Iatrogenic Cushing (due to wrong Hypertension
dose, timing, duration) Heart failure

Depression History of mental disorders

Gastric ulceration & delayed ulcer Peptic ulcer patients


Hyperglycemia aggravating DM Diabetic patients (especially

fluorinated corticosteroids they
intensify DM more than other drugs)
Immunosuppressant reactivation Tuberculosis patients
of dormant TB. Presence of infection

Hypothalamic pituitary adrenal

suppression especially if used late in
the evening.
Precautions :-
1. Check Bp - Body weight - Blood glucose - :
patient Blood Potassium - Bone (back pain - 5B
regularly osteoporosis) ..
for : <<<<<
2. Double Or In case of stress (emotional,
Regain the surgery )
dose If pt has already stopped
taking the drug tell him to
regain the last dose he was
If pt is taking the drug .. he
should double the dose
3. Gradual To avoid Very important :D
withdraw of Relapse
drug And addisonian crises
4. Time of You should follow the neuronal
administrati circadian rhythm :D :D
on It's taken in the morning except in
Short term use
5. In 3
Pregnancy :
Dose given should be as little as u
can :D

Because hypothalamic pituitary in
sufficiency in babies occurs only
with mothers taking high doses

fluorinated CS

teratogenic & catabolic

anti-r3r3a hormone
6. In children Prolonged use > same problems as
in adults
They are catabolic >> growth
retardation occur
How to avoid ?
By intermittent scheduled
Never give live attenuated
vaccines they may induce
infection and death as CS
suppress immunity
Give killed vaccines or toxoids
(active immunization)
1. Regarding the adrenal cortex all 4. Which of the following is false
are true EXCEPT : regarding the arterial supply of
the suprarenal gland:
a. It secretes steroid
hormones a. Each gland is drained by a
single vein and supplied by
b. It is mesodermal in origin
three arteries
c. It differentiates into zona
b. The middle suprarenal
glomerulosa , zona fasiculata
artery is branched from the
and zona reticulate
abdominal aorta
d. All are true
c. The left renal vein and IVC
are the main drainage of
2. Regarding the right suprarenal
left suprarenal
gland all are true EXCEPT:
d. The superior part is supplied
a. It is triangular in shape
by an artery coming from
b. It is related anteriorly to the inferior phrenic artery.
IVC and the pancreas
c. It is related posteriorly to 5. During the intrauterine life: a.
the diaphragm the primary cortex of the
d. The IVC collects the venous suprarenal gland develops from a
blood from it mesodermal origin.
a. the secondary cortex
3. Regarding the left suprarenal develops from the primary
gland all are true EXCEPT: cortex then the primary one
a. It is semilunar in shape degenerates.
b. the secondary cortex
b. It is covered by the
differentiates into 3 parts.
peritoneum of lesser sac
c. all of the above.
c. Its upper border is related
to the body of pancreas
d. It is supplied by three
suprarenal arteries
6. Regarding the development of 8. Stroma is a connective tissue
the suprarenal gland , all are capsule that sends thin
true EXCPT : trabecullar septa inside the gland
a. The medulla originates from to support the secretory cells:
the migrating
a. True
b. False
b. The C.T. capsule of the
gland is mesodermal in origin
9. Which of the following is NOT
c. Accessory medullary tissue
true about chromaffin cells:
is found in broad ligament of
a. Their cytoplasm is pale and
the uterus due to migrating
neuroectodermal cells contains large spherical
nuclei, numerous
d. All are true
mitochondria, smooth ER,

7. All of the following is true about prominent Golgi complex and

the suprarenal medulla EXCEPT: secretory granules

a. Its ectodermal in origin b. They are arranged in

b. Its a modified nervous rounded groups or short

tissue that acquired an cords away from blood

endocrine activity capillaries and vessels

c. Its the reddish-brown c. They are the only type of

central area of the adrenal cells responsible for the

gland secretion of epinephrine and

d. It has two types of cells norepinephrine

chromaffin cells and d. A & B

sypmathetic ganglion cells e. All of the above

that secrete
e. None of the above
10. The granules of the 13. Which of the following is not
chromaffin cells secreting true Zona glomerulosa :
norepinephrine are: a. It forms 15% of the total
a. Large volume of the gland
b. Small b. It lies immediately under
c. Have an eccentric electron- the stroma
dens core within the limiting c. Has closely packed cells
membrane of the granules surrounded by blood
d. Have a less electron-dens capillaries
core filling the granules d. The cells in this zone are
e. A & C columinar or pyramidal in
f. B & C shape with dense basal
g. A & D acidophilic nuclei
e. The cells in this zone have
11. Secretion of catecholamines is smooth ER, mitochondria
intiated by acetylcholine released with tubular cristea and
from preganglionic sympathatic filled with lipid droplets
fibers in the splanchnic nerves f. None of the above
a. True
b. False 14. Which of the following
12. Which of the following is not statements is correct :
true about the adrenal cortex : a. The cells of Zona
a. Its the yellowish prepheral glomerulosa are responsible
layer of the adrenal gland for the secretion of
b. Its mesodermal in origin glucocorticoids
c. It secretes the steroid b. The cells of Zona fasciculata
hormones are responsible for the
d. Its divided into 3 zones, secretion of androgens
Zona glomerulosa, Zona c. The cells of Zona
fasciculata and Zona glomerulosa are responsible
reticularis for the secretion of
e. None of the above aldosterone
d. The cells of Zona reticularis 17. Which of the following is a
are responsible for the common feature between cells of
secretion of adrogens Zona glomerulosa and that of
e. A & B Zona reticularis:
f. C & D a. They both have acidophilic
15. Which of the following is the b. They both have few lipid
largest layer of the cortex: droplets
a. Zona glomerulosa c. They are both surrounded
b. Zona fasciculata by fenestrated blood
c. Zona reticularis capillaries
d. Non of the above d. They both have
mitochondria with lamellar
16. Which of the following is not cristea
true about the cells in Zona e. A & B
fasciculata : f. A & C
a. They are arranged into
cords perpendicular to the 18. Which of the following is not
surface separated by a common feature between cells
longitudinally arranged of Zona fasciculata and that of
fenestrated blood capillaries Zona reticularis :
b. They are large polyhedral a. They both have lipid
with large, pale round nuclei droplets
c. Unlike the cells in Zona b. They both have acidophilic
glomerulosa they contain cytoplasm
numerous vacuoles as well as c. They both have smooth ER
numerous lipid droplets d. They both secrete
d. They secrete glucorticoids glucocorticoids
unlike the cells of the other e. Non of the above
zones of the adrenal cortex
e. Non of the above
19. Glucocorticoids are secreted 23. The net effect of cortisol on
from : protein metabolism :
a. Zona glomrulosa a. Increase plasma protein
b. Zona fasciculata synthesis
c. Zona reticularis b. Increase liver catabolism of
d. Adrenal medulla protein
c. Decrease amino acid level in
20. Percentage of cortisol bound blood
to plasma protein is : d. Increase protein synthesis
a. 80 % in muscle
b. 94% 24. The lipolytic effect is caused
c. 6 % by all except :
d. 20 % a. GH
b. Thyroxine
21. One of the following has c. Insulin
different action on glucose level d. Cortisol
of blood from others :
a. Growth hormone 25. All of the following are
b. Insulin effects of cortisol except :
c. Adrenaline a. Increase free fatty acids in
d. Glucocorticoids blood
b. Maintains blood volume
22. All of the following are c. Enhance Vasoconstrictive
effects of glucocorticoids on d. Increase Utilization of
protien except : glucose
a. Mobilization of amino acids
from extrahepatic tissues 26. Cortisol is essential for all of
b. Reduce protein synthesis in the following except :
stomach a. Muscular activity
c. Reduce protien synthesis in b. Inflamation mechanism
liver maintenance
d. Increase catabolism of c. Nervous function
protein in muscle d. Glucose level
27. Effect on cortisol is like
calcitonin and parathormone at 30. Feedback mechanism of
the same time ,, which of the cortisol acts directly on :
following statements explain this a. Hypothalamus
? b. Pituitary gland
a. Increase Ca excretion ,, and c. Adrenal cortex
bone Ca deposition d. Both (a) and (b)
b. Increase Ca absorption and
bone formation 31. All of the following hormones
c. Increase Ca excretion and are released simultaneously with
bone resorption ACTH except :
d. Decrease Ca absorption and a. Lipotropin
bone resorption b. MSH
28. All of the following are c. Endrophin
effects of cortisol on inflamation d. Liponectin
except :
a. Increase stability of 32. Stress increases cortisol
lysosomal membranes secretion through acting directly
b. Increase permeability of on :
capillaries a. Hypothalamus
c. Decrease number of b. Anterior pituitary gland
inflamatory cells c. Adrenal cortex
d. Rapid resolution of d. All of the above
33. Cortisol is highest in :
29. ACTH long term stimulation to a. Noon
adrenal cortex leads to increase b. Early morning
proliferation of adrenal cortex c. Evening
significantly except : d. Midnight
a. Zona reticularis
b. Zona fasiculata
c. Zona Glomerulosa
d. None of the above
34. All of the following is true 38. Catecholamines cause
about androgens except : vasodilation to the renal blood
a. Exert slight masculinizing vessels so increase urine volume
effect on female throughout a. True
life b. False
b. Some are converted to
testosterone 39. All of the following stimulate
c. Controlled by ACTH the secretion of catecholamines
d. Starts to be secreted at except :
the beginning of puberty a. Muscular exercise
b. Haemorrhage
35. All of the following actions c. Hyperglycemia
are produced in stress due to d. Exposure to cold
catecholamines secretion except
: 40. Catecholamines have only a
a. Increase the metabolic rate direct effect on respiratory
b. Increase heart rate centre to increase the depth &
c. Vasoconstriction of skeletal rate of respiration
muscle blood vessels a. True
d. Increase the visual field b. False
36. All of the following are
hyperglycemic hormones except 41. All of the following are
a. Catecholamines manifestation of
b. Growth hormone pheochromocytoma except
c. Thyroid hormone a. Tachycardia
d. Prolactin b. Palpitation
c. Hypotension
37. All of the following are true d. Hyperglycemia
about catecholamines except :
a. Stress hormone
b. Hyperglycemic
c. Calorigenic
d. Steriods
42. .. Is the dominant clinical 46. Aldosterone decrease loss of
manifestation of salt in
pheochromocytoma a. Stools
a. Hypertension b. Sweat
b. Hypoglycemia c. Saliva
c. Bradycardia d. All of the following
d. Tachycardia
47. in potassium ion
43. All of the following are true concentration causes direct
about aldosterone except stimulation of zona glomerulosa
a. Mineralocorticoid to increase secretion of
b. Na+ and K+ metabolism aldosterone
regulator a. Decrease
c. Protien in nature b. Increase
d. Secreted by zona c. Non of the above
48. All of the following stimulate
44. Aldosterone acts on . secretion of aldosterone except
Receptors on kidney a. Increase in K+
a. Cytoplasmic b. Increase in Na+
b. Nuclear c. Hypovolemia
c. Palasma membrane d. Unidentified pituitary
d. Non of the above factor

45. Aldosterone regulates Na+ 49. ACTH has a direct effect on

and K+ metabolism by aldosterone secretion
a. Increase Na+ reabsorption a. True
b. Increase K+ secretion b. False
c. Increase formation of Na+
K+ ATPase
d. All of the above
50. All of the are effects of 54. Hyperkalemia is one of the
conns syndrome except manifestation of aldosterone
a. Severe muscle weakness deficiency and it may cause
b. Hypertension a. Cardiac toxicity
c. Acidosis b. Weakness of heart
d. Paralysis contraction
c. Arrhythmia
51. Primary hyperaldosteronism d. All of the following
occurs in response to activation
of the renin angiotensin system 55. Hyper function of the adrenal
a. True cortex may produce all of the
b. False following diseases EXCEPT:
a. Cushing syndrome
52. All of the following may occur b. Conns syndrome
as a result of mineralocorticoid c. Addisons disease
deficiency except d. Virilism
a. Circulatory shock e. None of the above
b. Acidosis
c. Paralysis 56. Regarding Cushing disease
d. Cardiac arrest due to functioning adenoma of
the pituitary gland , the patient
53. When aldosterone is deficient may develop all of the following
,all of the following occur except EXCEPT:
a. Decrease extracellular fluid a. Osteoporosis
volume b. Melanin pigmentation of the
b. Decrease plasma volume mucous membranes
c. Decrease cardiac output c. Euphoria
d. Alkalosis d. Hypertension
e. None of the above
57. Concerning Cushing syndrome, 60. The laboratory investigations
one type of the following cells collected from patients of
can show increase of number ( Cushing disease due to
proliferation ) : hypothalamic disorder will show
a. Lymphocytes all of the following EXCEPT:
b. Osteoblasts a. Increased cortisol level
c. Muscle cells in the blood
d. Erythrocytes b. Increased ACTH level
e. None of the above c. Increase in the count of
58. Which of the following is not d. Increased CRF level
accepted to be a complication of e. None of the above
Cushing syndrome? 61. Regarding Cushing disease due
a. Circulatory shock to primary adrenal disorder, all
b. Death due to severe of the following is manifested
infection EXCEPT:
c. Osteoporosis a. Increased cortisol level
d. Franks diabetes b. Increased RBCs count
e. None of the above c. ACTH level is normal
d. The patient is hypertensive
59. Moon-like face of Cushings e. All are true
patients is due to:
a. Excess secretion of 62. Osteoporosis is one of the
glucocorticoids complications of Cushing
b. Fat mobilization from the syndrome. It results from :
lower limbs to the face & upper a. The inhibitory effect of the
limbs cortisol on protein synthesis.
c. meniralocortical effect of b. The inhibitory effect of
the cortisol cortisol on the osteoblasts
d. salt and water retention c. Anti-vitamin D action of the
e. all of the above cortisol
d. a & c
e. all of the above
63. The inhibitory effect of
cortisol in protein synthesis in 67. severe muscle weakness in
Cushing syndrome causes all the Conns syndrome is due to:
following EXCEPT: a. protein catabolism
a. Muscle wasting b. alkalosis
b. Delayed wound healing c. hypokalemia
c. Osteoporosis d. hypernatremia
d. Anemia
e. All are true 68. secondary hyperaldosteronism
64. Conns syndrome is manifested is associated with all the
by all the following EXCEPT: following EXCEPT:
a. hypertension a. decreased potassium level in
b. muscle weakness the blood
c. bradycardia b. increased blood volume &
d. alkalosis pressure
c. increased blood Sodium level
65. the hypertension in Conns d. increased the level of
syndrome is due to all of the plasma renin
following EXCEPT: e. all are true
a. vasoconstriction
b. salt and water retention 69. meniralocorticoid deficiency is
c. increased blood volume manifested by all of the following
d. increase in the COP EXCEPT:
e. not mentioned a. hypovolemia
b. low COP
66. all the following are c. cardiac toxicity
acceptable complications of d. alkalosis
hyperaldosterone secretion
a. hypertension
b. circulatory shock
c. paralysis
d. d hypokalemia & tetany
70. which of the following is a 74. In cushing syndrome whats
complication of Addisons called( buffalo torso) is due to :
disease? a. Increase androgen secretion
a. hypertension .
b. cardiac arrest in systole b. increase lipolysis with extra
c. anemia deposition in the upper part
d. tetany of the body.
c. muscle weakness.
71. Panhypopituitarism is d. mental changes.
manifested by all of the following
EXCEPT: 75. acne ,histrutism is due to
a. adrenal virilism increase secretion of :
b. addisons manifestations a. androgen
c. premature senility b. cortisol
d. myxedema c. aldosterone
e. tetany
72. Addisons disease is 76. adrenal diabetes is due to :
manifested by all of the following a. increase gluconeogenesis
EXCEPT: b. anti insulin effect of
a. melanin pigmentation of the cortisol.
mucous membranes c. burn out of beta cells.
b. muscle weakness d. A,b
c. acidosis
d. hypertension 77. conns disease is due due
increase secretion of :
73. all the following hormones are a. cortisol
elevated in addisons disease b. aldosterone
EXCEPT: c. adronegen.
a. ACTH d. all the above
b. MSH
c. CRH
d. Cortisol
78. which of the following are 82. Which of the following
effect of excess secretion of produces the least sodium
aldosterone : retention?
a. hyper tension. a. Prednisone
b. severe muscle weakness. b. Prednisolone
c. activation of renin- c. Betamethasone
d. Deoxycortone
angiotensin system.
d. all the above.
83. Which of the following
e. A,B produces the least anti-
79. At conns syndrome muscle inflammatory effect?
weakness is due to : a. Prednisone
a. hyponatremia b. Prednisolone
b. hypokalemia c. Betamethasone
d. Deoxycortone
c. hyperkalemia
d. all the above 84. Which of the following
corticosteroids is only injectable
80. secondary hypraldosteronism : ?
a. due to pituitary adenoma. a. Prednisone
b. adrenal cortex adenoma b. Prednisolone
c. Betamethasone
c. activation of renin-
d. Deoxycortone
angiotensin system.
d. all the above 85. Which of the following
glucocorticoids is used only by
81. which of the following is true inhalation?
about adrenogenital syndrome: a. Beclomethasone
a. It cause intense b. Betamethasone
c. Dexamethasone
masculinizing effect .
d. hydrocortisone
b. its difficult to diagnose this
syndrome in adult male
c. in prebuberty boys it lead to
rapid grow of sexual organs
d. all the above
86. the corticosteroid used to 90. The best combination for the
replace aldosterone in primary treatment of primary Addisons
Addisons disease is : is :
a. prednisone a. Hydrocortisone +
b. dexamethasone aldosterone
c. fludrocorisone b. Betamethasone +
d. cortisone aldosterone
c. Hydrocortisone +
87. All the following fludrocortisone
corticosteroids are used in the d. Betamethasone +
treatment of secondary fludrocortisone
adrenocortical insufficiency e. None of the above
a. Hydrocortisone 91. The best glucocorticoid
b. Fludrocortisone preparation for the treatment of
c. Prednisone bronchial asthma is :
d. Prednisolone a. Hydrocortisone
e. Not mentioned b. Beclomethasone
c. Prednisolone
88. The pro-drug which have high d. Cortisone
anti-inflammatory effect is: e. dexamethasone
a. Cortisone
b. Prednisolone 92. Which of the following
c. Prednisone glucocorticoids is never used for
d. Deoxycortisone the treatment of active chronic
89. The glucocorticoid preparation a. Hydrocortisone
which can be used topically for b. Prednisolone
the treatment of allergy : c. Prednisone
a. Hydrocortisone d. dexamethasone
b. Prednisone
c. Fludrocortisone
d. Betamethasone
93. during the treatment by d. hydrocortisone
glucocorticoids, the doctor should
follow all of these precautions 95. the corticosteroids
EXCEPT: preparation should be avoided in
a. low dose of prednisolone diabetic patients is:
at the midnight a. betamethasone
b. check the patient for b. beclomethasone
hypertension c. hydrocortisone
c. double dose during d. fludrocortisone
severe stress e. not mentioned
d. withdrawal should be
gradual 96. all the following conditions are
treated by using different
94. the safest glucocorticoid preparations of glucocorticoids
preparation for the treatment of EXCEPT:
asthma in a pregnant woman is : a. rheumatic fever
a. betamethasone b. TB
b. dexamethasone c. SLE
c. beclomethasone d. Nephrotic syndrome
1. D 33. B 65. a
2. B 34. D 66. b
3. C 35. C 67. c
4. C 36. D 68. e
5. A 37. D 69. d
6. C 38. B 70. c
7. D 39. C 71. a
8. A 40. B 72. d
9. E 41. C 73. d
10. E 42. A 74. B
11. A 43. C 75. A
12. C 44. A 76. D
77. B
13. E 45. D
78. E
14. F 46. D
79. B
15. B 47. B 80. C
16. D 48. B 81. D
17. E 49. B 82. C
18. E 50. C 83. D
19. B 51. B 84. D
85. A
20. B 52. C
86. C
21. B 53. D 87. B
22. C 54. D 88. C
23. A 55. c 89. D
24. C 56. e 90. C
25. D 57. d 91. B
92. C
26. B 58. a
93. A
27. C 59. e
94. C
28. B 60. c 95. A
29. C 61. c 96. b
30. D 62. e
31. D 63. d
32. A 64. c
Essay Questions
1- Enumerate the structures related to the adrenal gland.
2- Describe the vascular supply of the adrenal gland.
3- Explain the development of adrenal gland.
4- Enumerate congenital anomalies of adrenal gland.
5- Compare between the right & left adrenal glands.
6- Identify the pointed structure, and then mention
its histological structure

7- Discuss the histological features of cells in the

suprarenal medulla.
8- Compare between catecholamines secreting cells.
9- Identify the pointed structure then mention its function ?

5- Identify the pointed structure then mention its

LM picture.
6- Identify the pointed structure then mention its LM picture.

7- Compare between the 3 layers of adrenal cortex.

1. Mention the action of Catecholaimnes on Metabolism ?

2. Mention action of catecholamines on CVS ?
3. Mention action of catecholamines on GIT ?
4. Mention action of catecholamines on Respiratory system ?
5. Mention action of catecholamines on skeletal muscle ?
6. Mention action of catecholamines on Nervous system ?
7. Mention Control of Secretion of catecholamines ?
8. Mention abnormalities of secretions of this hormone ?
9. Mention chemical structure ,site of secretion and blood form of
mineralocorticoids ?
10. Mention functions of the mineralocortocoids (Aldosterone)?
11. on Kidney
12. Effects of aldosterone on sweat glands, salivary glands and intestinal
13. Enumerate 4 mechanisms of regulation of Aldosterone secretion ?
14. Mention effect of potassium ion concentration on aldosterone secretion ?
15. Mention effect of the renin-angiotensin system on aldosterone secretion
16. Mention effect of decreased sodium on aldosterone secretion?
17. Mention effect of ACTH on aldosterone secretion?
18. Mention the effects of excess aldosterone ?
19. Mention effects of mineralocorticoid deficiency ?
20. Define crtisol
21. Explian the diffrence between the mechanisms of action of
22. Give an aacount on the Effect of cortisol on :
a- carbohydrates
b- protiens
c- fat
d- CVS
e- Skeletal muscles
f- Blood cells
g- Immunity
h- Calcium metabolism
i- Bone formation
j- Vitamin D
23. Mention the anti inflammatory effects of cortisol
24. Enumerate the allergic and anti inflammatory effects of cortisol
25. Enumerate regulators of cortisol secretion
26. Discuss pituitary as a regulator of cortisol secretion
27. Give a short account on the effect of physiological stress on ACTH
28. Mention the circadian rhythm of glucocorticoid secretion
29. List the functions of adrenal androgens
30. Mention manifestations of Cushing syndrome caused by hormones other
than glucocorticoids ??
31. Mention the other manifestations of Cushing syndrome due to
inappropriate metabolic and systemic functions ?
32. What are the effects of excess aldosterone ?
33. Discuss secondary hyperaldosteronism ?
34. What are causes of excessive androgens?
35. Mention manifestations of adrenogenital syndrome ?
36. Mention effect of deficiency of mineralocorticoid?
37. Mention effects of glucocorticoid deficiency?
38. Mention the causes of melanin deposition?
39. Discuss the morphology of the pheochromocytoma?
40. Write an account on the clinical diagnosis of this disease?
41. Discuss the morphology of the neuroplastoma?
42. Discuss the prognosis of the neuroblastoma.
43. Mention the possible etiology of cortisol hypersecretion
44. Discuss the manifestations of cortisol hypersecretion
45. Explain the effects of excess aldosterone in conns syndrome
46. Mention the manifestations deposited by adrenal virilism syndrome
47. Give a short account on secondary hyperaldosteronism

48. Mention some preparation and administration of corticosteroids

49. Compare between Relative potency of corticosteroids
50. Mention replacement therapeutic uses of corticosteroids?
51. Mention anti-inflammatory and immunosuppressant effect of
52. Mention adverse Effects of Corticosteroid Therapy?
53. Mention contraindications to the use of corticosteroids for anti-
inflammatory use.