1.

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). Relations: Post. : Diaphragm Medial: celiac ganglion Post. Inf.: Kidney Ant: Right Partially peritoneum IVC Liver Left Covered by peritoneum of lesser sac Pancreas 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.

Development
Origin: 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 medulla.

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 cytoplasm. 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 Large, have eccentric electron dense core with limiting membrane on the granules.

Epinephrine secretory granules Small, less electron dense granules and the contents fill the granules.

C) Cortex: Zona Glomerulosa 1. Lies directly under the c.t capsule. 2. Cells are arranged in closely packed rounded or arched groups surrounded by blood capillaries. 3. Cells are columnar or pyramidal with dense basal nuclei and acidic slightly vacuolated cytoplasm. Zona Fasciculata 1. Largest layer of the cortex. 2. Cells are arranged in cords perpendicular to the surface separated by blood capillaries. 3. Cells are large polyhedral with large pale round nuclei, cytoplasm appears pale and contains numerous vacuoles. (Spongicytes) Same as glomerulosa but with numerous lipid droplets. Secrete Glucocortecoids Zona Reticularis 1. Inner layer of the cortex. 2. Cells are arranged in irregular cords that anastomose together enclosing fenestrated blood capillaries in between. 3. Cells are small with acidophilic cytoplasm.

Shows ultra structure features of steroid secreting cells: sER, mitochondria with tubular cristae and few lipid droplets. Secrete mineralocortecoids

Same as glomerulosa but with lipofuscin pigment. Secrete Androgens and small amount of Glucocortecoids.

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 volume. Increase the rate and depth of respiration by direct excitation of the respiratory centre and indirectly by increased metabolic rate they cause bronchodilatation. 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 stress 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.

Manifestations:
The hypertension is associated with increased risk of myocardial ischemia, congestive heart failure, renal injury, and cerebrovascular accidents. Sudden death may occur. Tachycardia.

Palpitation. Hyperglycemia. Increase in basal metabolic rate.

Mineralocorticoids

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 absorption. 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. ii. iii. Inhibitions of phospholipase A2 >> inhibition of PGs & leukotriens formation Inhibition of platelet activating factor synsthesis Inhibition of mediator release from inflammatory cells

Metabolic actions:
Hyperglycemic . Catabolic lipolytic a. Hyperglycemic: 1. Increase gluconeogenesis in the liver by: i. ii. Increasing enzyme synthesis Increasing mobilization of aminoacids from extrahepatic tissues ( muscles ) >> blood >> liver 2. Decreasing glucose utilization by the cells by decreasing glucose transport 3. Hyperglycima >> worsen diabetes b. Catabolic: 1. Decreasing proteins in extrahepatic tissues by: i. ii. iii. Decreasing protein synthesis Increasing protein catabolism 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. ii. Increasing liver & plasma proteins 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 functions

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 androgens 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 cortisol) 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 Osmosis 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 Effects 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 : o Lesion in the adrenal cortex:- impaired corticosteroids ACTH deficiency Acute : adrenal crisis Chronic : Addison's disease 2ry adrenocortical insufficiency : impaired ACTH secretion May be induced by stress (increased demand), rapid withdrawal of therapy, massive adrenal destruction. Abdominal pain >> vomiting Vascular collapse - hypotension > coma > death Addison's disease: Effect of deficiency of mineralocorticoids: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

o Types

o Adrenal crisis:

1. Decreased Na+ and Cl- (excreted in urine):-

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 melanocytes 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 Description It is derived from chromaffin cells. Neuroblastoma

A highly malignant Most of the tumors arise from the adrenal medulla. tumor. most However, in a minority of cases, the tumor arises in Neuroblastoma arises in extra adrenal sites eg. sympathetic ganglia called commonly either the adrenal paragangliomas. medulla or the retroperitoneal sympathetic ganglia. Most neuroblastomas secrete catecholamines.

Incidence

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. "10% tumor". 10 % of cases are bilateral 10% of cases occur in extra adrenal sites, and. 10% of tumors are biologically malignant.

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

Grossly, it varies from circumscribed spherical mass confined to the adrenal medulla to a large hemorrhagic mass. Cut section is gray to brown with areas of hemorrhage. Microscopically, it is composed of polygonal cells having abundant cytoplasm and pleomorphic nuclei.

lobular, soft tumor with grayish cut surface showing areas of necrosis, hemorrhage and calcification. Microscopically, the tumor is composed of small, dark, round cells with scant cytoplasm, arranged in masses or rosettes.

Features

Diagnosis or prognosis

It is rapidly growing cancer. It spreads locally; by lymph node metastases, and by blood stream to skull, orbit, liver and bone marrow. Is based on laboratory measuring of catecholamines It is a common cause of in plasma and urine and radiographic imaging studies cancer death in patients under 15 years of age. such as CT, MRI and ultrasound. 1.Hypertension 3. Palpitation. 4. Hyperglycemia. 5. Increase in basal metabolic rate.

Adrenal Cortex Diseases: I- Increase in secretion : 1. Cushing's syndrome:

12a) b) c)
Exogenous glucocorticoids. Endogenous causes.

Primary hypothalamic pituitary diseases Primary adrenocortical hyperplasia or neoplasia (adenoma or carcinoid). 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 syndrome). 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
Causes: May be due to sudden increase in glucocorticoid requirements in patients with chronic adrenocortical insufficiency. Rapid withdrawal of steroid therapy. Massive destruction of adrenals, e.g. neonatal adrenal hemorrhage

Addisone's disease Might be due to, Autoimmune adrenalitis (in 60%70% of cases). Infections asTB and fungi. Metastatic tumors Systemic amyloidosis.

Clinical features: vomiting, abdominal pain, Sarcoidosis hypotension, coma, and vascular collapse. Death Hemochromatosis follows rapidly unless corticosteroids are replaced immediately.

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 mineralocorticoids) Preparations :Route of administration Systemically Tab, injection Orally, parenrtal Tablets only Topical Systemic acute emergency cases Inhalation Antiinflammatory effect 1 0.8 5 4 30 Sodium retaining effect 1 0.8 0.3 0.3 ZERO Notes

Drug

Hydrocortisone Cortisone Prednisolone Prednisone Fluorinated CS (Beta & dexamethasone)

Natural Prodrug Synthetic Prodrug - Catabolic, so they may induce muscle weakness. - It causes anorexia Used in bronchial asthma Used in 1ry Addison's disease Has a long duration of action It's duration of action doesn't exceed 2hs

Beclomethasone

30

Zero

Fludrocortisones Oral (once daily) Deoxycortone Parentral

10

250

Zero

50

Aldosterone

Injection

Zero

500

Therapeutic uses :2. Replacement therapy Addisonian insufficiency 1ry Addison's disease Chronic 2ry adrenal insufficiency (ACTH)

1. Anti-inflammatory and immunosuppressant Rheumatic fever Rheumatoid arthritis Acute Gout Nephrotic syndrome Asthma 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 Iatrogenic Cushing (due to wrong dose, timing, duration) Depression Gastric ulceration & delayed ulcer healing) Hyperglycemia aggravating DM

Contraindications Hypertension Heart failure History of mental disorders Peptic ulcer patients

Immunosuppressant reactivation of dormant TB. Hypothalamic pituitary adrenal suppression especially if used late in the evening.

Diabetic patients (especially fluorinated corticosteroids they intensify DM more than other drugs) Tuberculosis patients Presence of infection

Precautions :Bp - Body weight - Blood glucose Blood Potassium - Bone (back pain osteoporosis) : 5B .. <<<<<

1. Check patient regularly for : 2. Double Or Regain the dose

In case of stress (emotional, surgery ) If pt has already stopped taking the drug tell him to regain the last dose he was taking If pt is taking the drug .. he should double the dose 3. Gradual To avoid withdraw of Relapse drug And addisonian crises 4. Time of You should follow the neuronal administrati circadian rhythm on It's taken in the morning except in : Short term use ER 5. In Pregnancy

Very important :D

:D :D

3 : ( ) : 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 doses Never give live attenuated vaccines they may induce infection and death as CS suppress immunity Give killed vaccines or toxoids (active immunization)

MCQ
1. Regarding the adrenal cortex all are true EXCEPT :
a. It secretes steroid hormones b. It is mesodermal in origin c. It differentiates into zona glomerulosa , zona fasiculata and zona reticulate d. All are true 2. Regarding the right suprarenal gland all are true EXCEPT: a. It is triangular in shape b. It is related anteriorly to IVC and the pancreas c. It is related posteriorly to the diaphragm d. The IVC collects the venous blood from it 3. Regarding the left suprarenal gland all are true EXCEPT: a. It is semilunar in shape b. It is covered by the peritoneum of lesser sac c. Its upper border is related to the body of pancreas d. It is supplied by three suprarenal arteries 4. Which of the following is false regarding the arterial supply of the suprarenal gland: a. Each gland is drained by a single vein and supplied by three arteries b. The middle suprarenal artery is branched from the abdominal aorta c. The left renal vein and IVC are the main drainage of left suprarenal d. The superior part is supplied by an artery coming from the inferior phrenic artery. 5. During the intrauterine life: a. the primary cortex of the suprarenal gland develops from a mesodermal origin. a. the secondary cortex develops from the primary cortex then the primary one degenerates. b. the secondary cortex differentiates into 3 parts. c. all of the above.

6. Regarding the development of the suprarenal gland , all are true EXCPT : a. The medulla originates from the migrating sympathogonia. b. The C.T. capsule of the gland is mesodermal in origin c. Accessory medullary tissue is found in broad ligament of the uterus due to migrating neuroectodermal cells

8. Stroma is a connective tissue capsule that sends thin trabecullar septa inside the gland to support the secretory cells: a. True b. False 9. Which of the following is NOT true about chromaffin cells: a. Their cytoplasm is pale and contains large spherical nuclei, numerous mitochondria, smooth ER, prominent Golgi complex and secretory granules b. They are arranged in rounded groups or short cords away from blood capillaries and vessels c. They are the only type of cells responsible for the secretion of epinephrine and norepinephrine d. A & B e. All of the above

d. All are true

7. All of the following is true about the suprarenal medulla EXCEPT: a. Its ectodermal in origin b. Its a modified nervous tissue that acquired an endocrine activity c. Its the reddish-brown central area of the adrenal gland d. It has two types of cells chromaffin cells and sypmathetic ganglion cells that secrete chatecholamines e. None of the above

10.

The granules of the

13.

Which of the following is not a. It forms 15% of the total volume of the gland b. It lies immediately under the stroma c. Has closely packed cells surrounded by blood capillaries d. The cells in this zone are columinar or pyramidal in shape with dense basal acidophilic nuclei e. The cells in this zone have smooth ER, mitochondria with tubular cristea and filled with lipid droplets f. None of the above

chromaffin cells secreting norepinephrine are: a. Large b. Small c. Have an eccentric electrondens core within the limiting membrane of the granules d. Have a less electron-dens core filling the granules e. A & C f. B & C g. A & D 11. Secretion of catecholamines is

true Zona glomerulosa :

intiated by acetylcholine released from preganglionic sympathatic fibers in the splanchnic nerves a. True b. False 12. Which of the following is not a. Its the yellowish prepheral layer of the adrenal gland b. Its mesodermal in origin c. It secretes the steroid hormones d. Its divided into 3 zones, Zona glomerulosa, Zona fasciculata and Zona reticularis e. None of the above true about the adrenal cortex : 14.

Which of the following a. The cells of Zona glomerulosa are responsible for the secretion of glucocorticoids b. The cells of Zona fasciculata are responsible for the secretion of androgens c. The cells of Zona glomerulosa are responsible for the secretion of aldosterone

statements is correct :

d. The cells of Zona reticularis are responsible for the secretion of adrogens e. A & B f. C & D 15. Which of the following is the a. Zona glomerulosa b. Zona fasciculata c. Zona reticularis d. Non of the above 16. Which of the following is not

17.

Which of the following is a

common feature between cells of Zona glomerulosa and that of Zona reticularis: a. They both have acidophilic cytoplasm b. They both have few lipid droplets c. They are both surrounded by fenestrated blood capillaries d. They both have mitochondria with lamellar cristea e. A & B f. A & C 18. Which of the following is not

largest layer of the cortex:

true about the cells in Zona fasciculata : a. They are arranged into cords perpendicular to the surface separated by longitudinally arranged fenestrated blood capillaries b. They are large polyhedral with large, pale round nuclei c. Unlike the cells in Zona glomerulosa they contain numerous vacuoles as well as numerous lipid droplets d. They secrete glucorticoids unlike the cells of the other zones of the adrenal cortex e. Non of the above

a common feature between cells of Zona fasciculata and that of Zona reticularis : a. They both have lipid droplets b. They both have acidophilic cytoplasm c. They both have smooth ER d. They both secrete glucocorticoids e. Non of the above

19.

Glucocorticoids are secreted a. Zona glomrulosa b. Zona fasciculata c. Zona reticularis d. Adrenal medulla

23.

The net effect of cortisol on a. Increase plasma protein synthesis b. Increase liver catabolism of protein c. Decrease amino acid level in blood d. Increase protein synthesis in muscle

from :

protein metabolism :

20.

Percentage of cortisol bound a. 80 % b. 94% c. 6 % d. 20 % 24.

to plasma protein is :

The lipolytic effect is caused a. GH b. Thyroxine c. Insulin d. Cortisol

by all except :

21.

One of the following has

different action on glucose level of blood from others : a. Growth hormone b. Insulin c. Adrenaline d. Glucocorticoids 22. All of the following are 25.

All of the following are a. Increase free fatty acids in blood b. Maintains blood volume c. Enhance Vasoconstrictive d. Increase Utilization of glucose

effects of cortisol except :

effects of glucocorticoids on protien except : a. Mobilization of amino acids from extrahepatic tissues b. Reduce protein synthesis in stomach c. Reduce protien synthesis in liver d. Increase catabolism of protein in muscle 26.

Cortisol is essential for all of a. Muscular activity b. Inflamation mechanism maintenance c. Nervous function d. Glucose level

the following except :

27.

Effect on cortisol is like 30. Feedback mechanism of a. Hypothalamus b. Pituitary gland a. Increase Ca excretion ,, and bone Ca deposition b. Increase Ca absorption and bone formation c. Increase Ca excretion and bone resorption d. Decrease Ca absorption and bone resorption 31. All of the following hormones are released simultaneously with ACTH except : a. Lipotropin b. MSH c. Endrophin d. Liponectin 32. Stress increases cortisol c. Adrenal cortex d. Both (a) and (b) cortisol acts directly on :

calcitonin and parathormone at the same time ,, which of the following statements explain this ?

28.

All of the following are

effects of cortisol on inflamation except : a. Increase stability of lysosomal membranes b. Increase permeability of capillaries c. Decrease number of inflamatory cells d. Rapid resolution of inflamation 33. 29. ACTH long term stimulation to adrenal cortex leads to increase proliferation of adrenal cortex significantly except : a. Zona reticularis b. Zona fasiculata c. Zona Glomerulosa d. None of the above

secretion through acting directly on : a. Hypothalamus b. Anterior pituitary gland c. Adrenal cortex d. All of the above Cortisol is highest in : a. Noon b. Early morning c. Evening d. Midnight

34.

All of the following is true a. Exert slight masculinizing effect on female throughout life b. Some are converted to testosterone c. Controlled by ACTH d. Starts to be secreted at the beginning of puberty

38.

Catecholamines cause

about androgens except :

vasodilation to the renal blood vessels so increase urine volume a. True b. False 39. All of the following stimulate

the secretion of catecholamines except : a. Muscular exercise b. Haemorrhage c. Hyperglycemia d. Exposure to cold 40. Catecholamines have only a

35.

All of the following actions

are produced in stress due to catecholamines secretion except : a. Increase the metabolic rate b. Increase heart rate c. Vasoconstriction of skeletal muscle blood vessels d. Increase the visual field 36. All of the following are hyperglycemic hormones except a. Catecholamines b. Growth hormone c. Thyroid hormone d. Prolactin 37. All of the following are true a. Stress hormone b. Hyperglycemic c. Calorigenic d. Steriods 41.

direct effect on respiratory centre to increase the depth & rate of respiration a. True b. False All of the following are

manifestation of pheochromocytoma except a. Tachycardia b. Palpitation c. Hypotension d. Hyperglycemia

about catecholamines except :

42.

.. Is the dominant clinical

46.

Aldosterone decrease loss of a. Stools b. Sweat c. Saliva d. All of the following

manifestation of pheochromocytoma a. Hypertension b. Hypoglycemia c. Bradycardia d. Tachycardia

salt in

47. 43. All of the following are true a. Mineralocorticoid b. Na+ and K+ metabolism regulator c. Protien in nature d. Secreted by zona glomerulosa 48. 44. Aldosterone acts on . a. Cytoplasmic b. Nuclear c. Palasma membrane d. Non of the above 45. Aldosterone regulates Na+ a. Increase Na+ reabsorption b. Increase K+ secretion c. Increase formation of Na+ K+ ATPase d. All of the above 49. Receptors on kidney about aldosterone except

in potassium ion

concentration causes direct stimulation of zona glomerulosa to increase secretion of aldosterone a. Decrease b. Increase c. Non of the above All of the following stimulate a. Increase in K+ b. Increase in Na+ c. Hypovolemia d. Unidentified pituitary factor ACTH has a direct effect on a. True b. False

secretion of aldosterone except

and K+ metabolism by

aldosterone secretion

50.

All of the are effects of a. Severe muscle weakness b. Hypertension c. Acidosis d. Paralysis

54.

Hyperkalemia is one of the

conns syndrome except

manifestation of aldosterone deficiency and it may cause a. Cardiac toxicity b. Weakness of heart contraction c. Arrhythmia d. All of the following 55. Hyper function of the adrenal

51.

Primary hyperaldosteronism

occurs in response to activation of the renin angiotensin system a. True b. False 52. All of the following may occur cortex may produce all of the following diseases EXCEPT: a. Cushing syndrome b. Conns syndrome c. Addisons disease d. Virilism e. None of the above 56. Regarding Cushing disease as a result of mineralocorticoid deficiency except a. Circulatory shock b. Acidosis c. Paralysis d. Cardiac arrest 53. When aldosterone is deficient a. Decrease extracellular fluid volume b. Decrease plasma volume c. Decrease cardiac output d. Alkalosis due to functioning adenoma of the pituitary gland , the patient may develop all of the following EXCEPT: a. Osteoporosis b. Melanin pigmentation of the mucous membranes c. Euphoria d. Hypertension e. None of the above ,all of the following occur except

57.

Concerning Cushing syndrome,

60.

The laboratory investigations

one type of the following cells can show increase of number ( proliferation ) : a. Lymphocytes b. Osteoblasts c. Muscle cells d. Erythrocytes e. None of the above 58. Which of the following is not

collected from patients of Cushing disease due to hypothalamic disorder will show all of the following EXCEPT: a. Increased cortisol level in the blood b. Increased ACTH level c. Increase in the count of lymphocytes d. Increased CRF level e. None of the above 61. Regarding Cushing disease due to primary adrenal disorder, all of the following is manifested EXCEPT: a. Increased cortisol level b. Increased RBCs count c. ACTH level is normal d. The patient is hypertensive e. All are true 62. Osteoporosis is one of the

accepted to be a complication of Cushing syndrome? a. Circulatory shock b. Death due to severe infection c. Osteoporosis d. Franks diabetes e. None of the above 59. Moon-like face of Cushings

patients is due to: a. Excess secretion of glucocorticoids b. Fat mobilization from the lower limbs to the face & upper limbs c. meniralocortical effect of the cortisol d. salt and water retention e. all of the above complications of Cushing syndrome. It results from : a. The inhibitory effect of the cortisol on protein synthesis. b. The inhibitory effect of cortisol on the osteoblasts c. Anti-vitamin D action of the cortisol d. a & c e. all of the above

63.

The inhibitory effect of 67. severe muscle weakness in a. protein catabolism b. alkalosis c. hypokalemia d. hypernatremia 68. secondary hyperaldosteronism Conns syndrome is due to:

cortisol in protein synthesis in Cushing syndrome causes all the following EXCEPT: a. Muscle wasting b. Delayed wound healing c. Osteoporosis d. Anemia e. All are true 64. Conns syndrome is manifested a. hypertension b. muscle weakness c. bradycardia d. alkalosis 65. the hypertension in Conns by all the following EXCEPT:

is associated with all the following EXCEPT: a. decreased potassium level in the blood b. increased blood volume & pressure c. increased blood Sodium level d. increased the level of plasma renin e. all are true 69. meniralocorticoid deficiency is

syndrome is due to all of the following EXCEPT: a. vasoconstriction b. salt and water retention c. increased blood volume d. increase in the COP e. not mentioned 66. all the following are

manifested by all of the following EXCEPT: a. hypovolemia b. low COP c. cardiac toxicity d. alkalosis

acceptable complications of hyperaldosterone secretion EXCEPT: a. hypertension b. circulatory shock c. paralysis d. d hypokalemia & tetany

70.

which of the following is a

74.

In cushing syndrome whats a. Increase androgen secretion . b. increase lipolysis with extra deposition in the upper part of the body. c. muscle weakness. d. mental changes.

complication of Addisons disease? a. hypertension b. cardiac arrest in systole c. anemia d. tetany 71. Panhypopituitarism is

called( buffalo torso) is due to :

manifested by all of the following EXCEPT: a. adrenal virilism b. addisons manifestations c. premature senility d. myxedema e. tetany 72. Addisons disease is 76. adrenal diabetes is due to : a. increase gluconeogenesis b. anti insulin effect of cortisol. c. burn out of beta cells. d. A,b 77. conns disease is due due a. cortisol b. aldosterone c. adronegen. d. all the above manifested by all of the following EXCEPT: a. melanin pigmentation of the mucous membranes b. muscle weakness c. acidosis d. hypertension 73. all the following hormones are increase secretion of : elevated in addisons disease EXCEPT: a. ACTH b. MSH c. CRH d. Cortisol 75. acne ,histrutism is due to a. androgen b. cortisol c. aldosterone increase secretion of :

78.

which of the following are

82.

Which of the following

effect of excess secretion of aldosterone : a. hyper tension. b. severe muscle weakness. c. activation of reninangiotensin system. d. all the above. e. A,B 79. At conns syndrome muscle a. hyponatremia b. hypokalemia c. hyperkalemia d. all the above 80. secondary hypraldosteronism : a. due to pituitary adenoma. b. adrenal cortex adenoma c. activation of reninangiotensin system. d. all the above 81. which of the following is true a. It cause intense masculinizing effect . 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 weakness is due to :

produces the least sodium retention? a. b. c. d. Prednisone Prednisolone Betamethasone Deoxycortone

83. Which of the following produces the least antiinflammatory effect? a. Prednisone b. Prednisolone c. Betamethasone d. Deoxycortone 84. Which of the following corticosteroids is only injectable ? a. Prednisone b. Prednisolone c. Betamethasone d. Deoxycortone 85. Which of the following glucocorticoids is used only by inhalation? a. Beclomethasone b. Betamethasone c. Dexamethasone d. hydrocortisone

about adrenogenital syndrome:

86. the corticosteroid used to replace aldosterone in primary Addisons disease is : a. prednisone b. dexamethasone c. fludrocorisone d. cortisone 87. All the following corticosteroids are used in the treatment of secondary adrenocortical insufficiency EXCEPT: a. Hydrocortisone b. Fludrocortisone c. Prednisone d. Prednisolone e. Not mentioned 88. The pro-drug which have high anti-inflammatory effect is: a. Cortisone b. Prednisolone c. Prednisone d. Deoxycortisone 89. The glucocorticoid preparation which can be used topically for the treatment of allergy : a. Hydrocortisone b. Prednisone c. Fludrocortisone d. Betamethasone

90. The best combination for the treatment of primary Addisons is : a. Hydrocortisone + aldosterone b. Betamethasone + aldosterone c. Hydrocortisone + fludrocortisone d. Betamethasone + fludrocortisone e. None of the above 91. The best glucocorticoid preparation for the treatment of bronchial asthma is : a. Hydrocortisone b. Beclomethasone c. Prednisolone d. Cortisone e. dexamethasone 92. Which of the following glucocorticoids is never used for the treatment of active chronic hepatitis? a. Hydrocortisone b. Prednisolone c. Prednisone d. dexamethasone

93. during the treatment by glucocorticoids, the doctor should follow all of these precautions EXCEPT: a. low dose of prednisolone at the midnight b. check the patient for hypertension c. double dose during severe stress d. withdrawal should be gradual 94. the safest glucocorticoid preparation for the treatment of asthma in a pregnant woman is : a. betamethasone b. dexamethasone c. beclomethasone

d. hydrocortisone 95. the corticosteroids preparation should be avoided in diabetic patients is: a. betamethasone b. beclomethasone c. hydrocortisone d. fludrocortisone e. not mentioned 96. all the following conditions are treated by using different preparations of glucocorticoids EXCEPT: a. rheumatic fever b. TB c. SLE d. Nephrotic syndrome

Answers:
1. D 2. B 3. C 4. C 5. A 6. C 7. D 8. A 9. E 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. E A C E F B D E E B B B C A C D B C B C D D A 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. 55. 56. 57. 58. 59. 60. 61. 62. 63. 64. B D C D D B C B C A C A D D B B B C B C D D c e d a e c c e d c 65. 66. 67. 68. 69. 70. 71. 72. 73. 74. 75. 76. 77. 78. 79. 80. 81. 82. 83. 84. 85. 86. 87. 88. 89. 90. 91. 92. 93. 94. 95. 96. a b c e d c a d d B A D B E B C D C D D A C B C D C B C A C A b

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. 2. 3. 4. 5. 6. 7.

Mention the action of Catecholaimnes on Metabolism ? Mention action of catecholamines on CVS ? Mention action of catecholamines on GIT ? Mention action of catecholamines on Respiratory system ? Mention action of catecholamines on skeletal muscle ? Mention action of catecholamines on Nervous system ? 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 absorption. 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 glucocorticoids 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 secretion 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 inappropriate metabolic and systemic functions ? 32. What are the effects of excess aldosterone ? 33. Discuss secondary hyperaldosteronism ? due to

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 corticosteroids? 52. Mention adverse Effects of Corticosteroid Therapy? 53. Mention contraindications to the use of corticosteroids for antiinflammatory use.