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.

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. Mesoderm……Ct capsule.

B) Medulla:
Neural crest……..sympathetic ganglion Neuroectodermal cells migrate……invade 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.

Epinephrine secretory granules Small. (Spongicytes) Same as glomerulosa but with numerous lipid droplets. have eccentric electron dense core with limiting membrane on the granules. Cells are arranged in irregular cords that anastomose together enclosing fenestrated blood capillaries in between. Cells are arranged in cords perpendicular to the surface separated by blood capillaries. 2. Inner layer of the cortex. Cells are columnar or pyramidal with dense basal nuclei and acidic slightly vacuolated cytoplasm. Secrete mineralocortecoids Same as glomerulosa but with lipofuscin pigment. 2. 3. Lies directly under the c. Cells are large polyhedral with large pale round nuclei. 2.t capsule. Cells are arranged in closely packed rounded or arched groups surrounded by blood capillaries. mitochondria with tubular cristae and few lipid droplets. Zona Fasciculata 1. 3. 3.Norepinephrine secretory granules Large. less electron dense granules and the contents fill the granules. Secrete Glucocortecoids Zona Reticularis 1. Secrete Androgens and small amount of Glucocortecoids. Largest layer of the cortex. . Shows ultra structure features of steroid secreting cells: sER. Cells are small with acidophilic cytoplasm. cytoplasm appears pale and contains numerous vacuoles. C) Cortex: Zona Glomerulosa 1.

renal injury. 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.  Increase the rate and depth of respiration by direct excitation of the respiratory centre and indirectly by increased metabolic rate they cause bronchodilatation.  Mobilize free fatty acids from adipose tissue.  . Sudden death may occur. connected to the greater splanchnic nerve which supplies the gland. and cerebrovascular accidents. the most significant of which are pheochromocytoma. congestive heart failure. so their plasma level increased.  Excite the nervous system and increase the mental activity and alertness. and ganglioneuroma.  Stimulate glycogenolysis in the liver.Action of Catecholaimnes:Secreted in emergency and their effects are :  Increase the metabolic rate leading to increased heat production.  Increase both heart rate and its force of contraction. neuroblastoma.  They also cause vasodilation of skeletal muscle blood vessels.  Cause splenic contraction  Cause vasoconstriction to the renal blood vessels which may decrease urine volume. Manifestations:  The hypertension is associated with increased risk of myocardial ischemia.  Potentiate skeletal muscle contraction and delay the onset of its fatigue.  Norepinephrine produces vasoconstriction in most organs which increases both systolic and diastolic blood pressures. Tachycardia.  Increase the visual fields.  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.

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.  Lack of sodium causes retention of potassium by the kidneys which increase aldosterone secretion. 3. Increase in basal metabolic rate. hi the distal tubules. Functions of the mineralocortocoid (Aldosterone):  On Kidney Aldosterone increase sodium reabsorption in exchange with secretion of either K+ or H+. Mineralocorticoids Aldosterone is a steroid.  The diminished sodium leads to diminished extracellular fluid volume. This enhances formation of angiotensin II which stimulates aldosterone secretion. Regulation of Aldosterone secretion: 1. It combines loosely with the plasma proteins. 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. .  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. when excessive quantities of saliva are lost and loss of sodium in the stools.      Palpitation. Effects of aldosterone on sweat glands. Aldosterone increases the reabsorption of sodium and the secretion of potassium  by the ducts to conserve body salt in hot environments . collecting tubules and collecting duct. Hyperglycemia. It is secreted from the zona glomerulosa. with resultant diminished cardiac output and renal blood flow. salivary glands and intestinal absorption. Effect of decreased sodium on aldosterone secretion:  Diminished sodium concentration directly affects the zona glomerulosa cells to enhance aldosterone secretion. It increases formation of Na* K+ATPase.

. 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. serious cardiac toxicity including weakness of heart contraction and development of arrhythmia If severe cardiac arrest in diastole occurs. o Circulatory shock may develop rapidly.4. Mild acidosis develops due to excess hydrogen ion. 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.   Effect of deficiency of mineralocorticoid:     When aldosterone is deficient. 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. o Decrease plasma volume. The effects of excess aldosterone are:  Decrease in sodium loss in the urine with increase sodium in extracellular fluid . sodium reabsorption decreases sodiumchloride ions and water are lost in the urine this leads to: o Decrease extracellular fluid volume. Potassium and hydrogen ions are increased When potassium rises to approximately double normal. Increase potassium loss in the urine:When the potassium ion concentration falls severe muscle weakness often develops. o Decrease carding output. Paralysis may occur due to failure of transmission of action potential.

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

Increasing renal excretion  Decreasing bone formation by 1. Important for normal contractility 2. Deficiency >> muscular fatigue 3. Lipolytic: Increasing FFA mobilization from adipose tissues increasing their plasma level and their utilization for energy  Circulatory actions: 1. Atrophy of lymphoid tissue .intestinal absorption (anti Vitamin D action) 2. Important for normal muscular contractility & vasoconstrictive effect of NE 2. basophils . Increasing RBCs 2. Excess >> muscular atrophy due to increased protein catabolism  Actions on Ca++ metabolism:  Decreasing plasma Ca++ level by 1. Decreasing Ca++ & PO4-. Inhibition of cellular replication of osteoblasts & protein synthesis  Immunosuppressive actions: 1. monocytes & lymphocytes 3. memory & intellectual functions  Muscular actions: 1. Large doses : a. ii. Decreasing eosinophils .2. Decreasing vascular permeabiliting preserving blood volume  Nervous actions: Affecting sensations & higher functions as concentration. Increasing liver & plasma proteins Increasing gluconeogenesis c. Increasing protein synthesis in the liver by Increasing mobilization of amnioacids to the liver >> elevating blood amniacid level And this leads to: i.

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.b. Rapid resolution 2. Decreased T & B cells c. Androgens 1. Decreased level of immunity  Anti-inflammatory & anti allergic actions: Decreasing inflammation by: 1. Decreasing inflammatory cells & release of mediators 4. Stabilization of lysosomes ( decreasing release of proteolytic enzymes) 5. Decreasing vascular permeability 3. Normally >> no significant effect b. 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. In females much of the growth of pubic & axillary hair due to cortical androgens 3. lipotropin & endorphin release: a. 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 males part of cortical androgens in converted into testosterone in extracortical tissue secretion is controlled by ACTH .

Exogenous ii. 1ry adrenocortical hyperplasia or neoplasia (functioning adenoma or carcinoma) 3. Ectopic production of ACTH from a non endocrine neoplasm e. Moon face (edematous appearance > it's not edema it's fat) iii.Diseases of adrenal cortex  Hyper function (hyperadrenalism) I. Increased blood glucose > adrenal diabetes > few months > beta cells burnt out > irreversible Frank diabetes mellitus.   Cushing Syndrome Hypersecretion of cortisol It may be : i. Diminished collagen fibers in the SC tissues >> large purplish striae > SC tissues torn apart ix.) . 1ry hypothalamic pituitary disorder > ↑ACTH 2. 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. memory and concentration so it may induce Euphoria .g. Endogenous 1. vi.  Manifestations : i. : lung cancer small cell carcinoma. Lack of protein deposition and in the bone & anti vitamin D activity & Ca++ lowering effect leads to osteoporosis and bone weakness x. Increase the androgenic activity >> acne + hirsutism (ya3ny excess growth of body hair) iv. It affects brain intellectual functions. 80 % of pts suffer from hypertension (minreralocorticoid effect of cortisol) v. Decreased tissue proteins except liver and plasma > muscular mass loss + weakness vii. Immunosuppression viii.

hyperalbuminemia) ii. ↑ NaCl  ↑O. Excretion of H+  Mild degree of alkalosis  2ry hyperaldosteronism i. In males :1.Stenosis . ↑Renin  ↑Aldosterone  then causes previously discussed effects III. Neoplasms ii.II. ↑ Na+ leads to ↑ Blood volume ↑COP  hypertension 3. Due to activation of renin angiotensin system by decreased renal perfusion (AS .pregnancy . In females :1.same in female + rapid development of male sexual organs + ↑sexual desire . Effects :1. It's due to 1. Muscle development (deposition of proteins) iii. Increase Na+ reabsorption  increase Cl.  Hyperaldosteronism 1ry (Conn's Syndrome) i. Deeper voice 3. Clitoris growth >> resemble penis 5. Growth of beard 2.  Adrenal virilism Excessive androgens due to :i. Congenital adrenal hyperplasia  Effects i. Masculinizing effect through out the body ii. Prepuberty :. Increase potassium excretion  hypokalemia  muscle weakness  impaired transmission of action potential  paralysis 4.P  Osmosis 2. Functioning adenoma 65 % 2. Masculine distribution of hair on the body and on the pupis (like males' hair distribution) 4. Thick skin 6. Bilateral idiopathic adrenocortical hyperplasia 30 % ii.

Decreased Na+ and Cl. Increased H+ >> mild acidosis 3. massive adrenal destruction.2.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.(excreted in urine):- .impaired corticosteroids ACTH deficiency Acute : adrenal crisis Chronic : Addison's disease 2ry adrenocortical insufficiency : impaired ACTH secretion May be induced by stress (increased demand). Adults :. 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. rapid withdrawal of therapy. Abdominal pain >> vomiting Vascular collapse .difficult to diagnose (androgens have the same effects as testosterone hormone)  Hypoadrenalism :o It may be due to :        o  Lesion in the adrenal cortex:.

If it's exposed to any type of stress >> Death may occur 5. most However. : 1.g. 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. in a minority of cases. medulla or the retroperitoneal sympathetic ganglia. Hypothalamic pituitary neoplasms / infections 2. tumor.1. sympathetic ganglia called commonly either the adrenal paragangliomas. Hypothalamic pituitary suppression (long term steroid therapy). Melanin pigmentation of mucous membrane and skin (lips . metabolic functions need Glucocorticoids to be maintained) 3. Patient can't maintain normal blood glucose concentration between meals (decreased gluconeogenesis) 2.(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. . Neuroblastoma A highly malignant Most of the tumors arise from the adrenal medulla.nipples) . the tumor arises in Neuroblastoma arises in extra adrenal sites eg. Summary of Pathology Adrenal Medulla diseases Pheochromocytoma Description It is derived from chromaffin cells. Most neuroblastomas secrete catecholamines. Anemia 4.

it varies from circumscribed spherical mass confined to the adrenal medulla to a large hemorrhagic mass. Morphology Morphology: Pheochromocytoma is known as the Grossly. and by blood stream to skull.Increase in secretion : 1. Endogenous causes. with strong male predominance. the tumor is composed of small. and. Microscopically. 1. 4. 5. • 10% of tumors are biologically malignant. Cut section is gray to brown with areas of hemorrhage. sporadic. round cells with scant cytoplasm. Palpitation. hemorrhage and calcification. it is composed of polygonal cells having abundant cytoplasm and pleomorphic nuclei. dark. arranged in masses or rosettes. Ectopic production of ACTH by a non-endocrine neoplasm. Features Diagnosis or prognosis It is rapidly growing cancer. Adrenal Cortex Diseases: I. soft tumor with grayish cut surface showing areas of necrosis. It spreads locally. Increase in basal metabolic rate. familial lesions may arise in childhood.Incidence Pheochromocytomas occur sporadically (90%). "10% tumor". such as CT. by lymph node metastases. lobular. Hyperglycemia. . Microscopically. • 10 % of cases are bilateral • 10% of cases occur in extra adrenal sites. Primary hypothalamic pituitary diseases Primary adrenocortical hyperplasia or neoplasia (adenoma or carcinoid). it appears as a Grossly. or as Most of the cases are a part of multiple endocrine syndrome. female prevalence.Hypertension 3. however. liver and bone marrow. MRI and ultrasound. orbit. Most sporadic lesions occur in adulthood with slight familial cases also occur. Cushing's syndrome: 12a) b) c) Exogenous glucocorticoids. 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.

coma. e. It is characterized by increased level of plasma renin. b.g. Sarcoidosis hypotension. Primary hyperaldosteronism (Conn's syndrome): It is due to:   Aldosterone-producing adrenocortical adenoma occurs in 65% of cases (Conn's syndrome). Death Hemochromatosis follows rapidly unless corticosteroids are replaced immediately. Metastatic tumors Systemic amyloidosis. decreased renal perfusion (arteriolar nephrosclerosis. Secondary hyperaldosteronism It occurs in response to activation of the renin-angiotensin system. Autoimmune adrenalitis (in 60%70% of cases).Adrenocortical Hypofunction Adrenal Crisis Causes: May be due to sudden increase in glucocorticoid requirements in patients with chronic adrenocortical insufficiency. . • • Adrenal Verilism : Causes of excessive androgens: May be due to: Adrenocortical neoplasms (carcinoma more than adenoma). Infections asTB and fungi. Clinically. renal artery stenosis). hypoalbuminaemia and pregnancy. Rapid withdrawal of steroid therapy. and vascular collapse. II. Hyperaldosteronism: a. Clinical features: vomiting.   3. and Congenital adrenal hyperplasia. it occurs in cases of congestive heart failure. neonatal adrenal hemorrhage Addisone's disease Might be due to.2. Bilateral idiopathic adrenocortical hyperplasia (30% of cases). abdominal pain. Massive destruction of adrenals.

.8 5 4 30 Sodium retaining effect 1 0.3 ZERO Notes Drug Hydrocortisone Cortisone Prednisolone Prednisone Fluorinated CS (Beta & dexamethasone) Natural Prodrug Synthetic Prodrug .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 . parenrtal Tablets only Topical Systemic  acute emergency cases Inhalation Antiinflammatory effect 1 0.8 0.Catabolic. injection Orally.3 0. so they may induce muscle weakness.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.

) Adverse effects  Iatrogenic Cushing (due to wrong dose. Therapeutic uses :2. 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. 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 . Hypothalamic pituitary adrenal suppression especially if used late in the evening. platelets .lymphoma  Blood diseases due to antibodies formed against blood elements (RBCs. Replacement therapy    Addisonian insufficiency 1ry Addison's disease Chronic 2ry adrenal insufficiency (↓ACTH) 1.   Diabetic patients (especially fluorinated corticosteroids they intensify DM more than other drugs) Tuberculosis patients Presence of infection  .

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 . Precautions :Bp . Check patient regularly for : 2.Bone (back pain osteoporosis) ‫نقول للمريض : زوروونى كل شهر مرة ونشوف ال‬ 5B . Double Or Regain the dose In case of stress (emotional. Gradual To avoid withdraw of  Relapse drug  And addisonian crises 4.Body weight . ‫اللى هما‬ <<<<< 1.. he should double the dose 3.. 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 ‫خليـــك دايمًا الصبح بدرى كده‬ :D :D ‫هتعمل 3 حاجات‬ : ‫ اوال‬ ‫إوزن المسألة (هل المريضة هتموت من غير الدوا‬ )‫وال أل ؟‬ : ‫ ثانيًا‬ Dose given should be as little as u can :D ‫ليييييييييييه ؟‬ Because hypothalamic pituitary in sufficiency in babies occurs only with mothers taking high doses ً : ‫ ثالثا‬ fluorinated CS ‫ابعد عن ال‬ ‫ليييييييييييه ؟؟‬ teratogenic & catabolic ‫عشان دول‬ ‫هتجيبلك عيّل عضمـــة من اآلخر‬ anti-r3r3a hormone ‫أصل هو‬ .Blood glucose Blood Potassium .

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) .

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

They are the only type of cells responsible for the secretion of epinephrine and norepinephrine d. b. prominent Golgi complex and secretory granules b. all are true EXCPT : a. Which of the following is NOT true about chromaffin cells: a. It’s ectodermal in origin b. Stroma is a connective tissue capsule that sends thin trabecullar septa inside the gland to support the secretory cells: a. It’s a modified nervous tissue that acquired an endocrine activity c. True b. smooth ER. numerous mitochondria. The C. A & B e. The medulla originates from the migrating sympathogonia. capsule of the gland is mesodermal in origin c. All are true 7. None of the above . False 9. They are arranged in rounded groups or short cords away from blood capillaries and vessels c. All of the above d. It has two types of cells chromaffin cells and sypmathetic ganglion cells that secrete chatecholamines e. It’s the reddish-brown central area of the adrenal gland d. Regarding the development of the suprarenal gland .T. Accessory medullary tissue is found in broad ligament of the uterus due to migrating neuroectodermal cells 8.6. Their cytoplasm is pale and contains large spherical nuclei. All of the following is true about the suprarenal medulla EXCEPT: a.

Secretion of catecholamines is true Zona glomerulosa : intiated by acetylcholine released from preganglionic sympathatic fibers in the splanchnic nerves a. Have a less electron-dens core filling the granules e. The cells of Zona glomerulosa are responsible for the secretion of glucocorticoids b. It’s divided into 3 zones. The cells in this zone are columinar or pyramidal in shape with dense basal acidophilic nuclei e.10. None of the above true about the adrenal cortex : 14. Zona glomerulosa. Small c. A & C f. The cells of Zona glomerulosa are responsible for the secretion of aldosterone statements is correct : . Which of the following a. None of the above chromaffin cells secreting norepinephrine are: a. It lies immediately under the stroma c. It’s the yellowish prepheral layer of the adrenal gland b. The cells in this zone have smooth ER. A & D 11. Which of the following is not a. Large b. False 12. True b. It secretes the steroid hormones d. It forms 15% of the total volume of the gland b. Have an eccentric electrondens core within the limiting membrane of the granules d. Which of the following is not a. B & C g. The granules of the 13. Has closely packed cells surrounded by blood capillaries d. mitochondria with tubular cristea and filled with lipid droplets f. It’s mesodermal in origin c. Zona fasciculata and Zona reticularis e. The cells of Zona fasciculata are responsible for the secretion of androgens c.

Non of the above a common feature between cells of Zona fasciculata and that of Zona reticularis : a. A & B f. They both have acidophilic cytoplasm b. They both secrete glucocorticoids e. They are large polyhedral with large. They are arranged into cords perpendicular to the surface separated by longitudinally arranged fenestrated blood capillaries b. A & B f. They secrete glucorticoids unlike the cells of the other zones of the adrenal cortex e. They both have lipid droplets b. Which of the following is a common feature between cells of Zona glomerulosa and that of Zona reticularis: a. The cells of Zona reticularis are responsible for the secretion of adrogens e. A & C 18. pale round nuclei c. They both have acidophilic cytoplasm c. Zona fasciculata c.d. Zona glomerulosa b. Zona reticularis d. Which of the following is the a. Which of the following is not 17. They both have smooth ER d. Non of the above . They both have mitochondria with lamellar cristea e. They are both surrounded by fenestrated blood capillaries d. Non of the above 16. Unlike the cells in Zona glomerulosa they contain numerous vacuoles as well as numerous lipid droplets d. They both have few lipid droplets c. Which of the following is not largest layer of the cortex: true about the cells in Zona fasciculata : a. C & D 15.

GH b. Zona reticularis d. 80 % b. Decrease amino acid level in blood d. Adrenaline d. Zona glomrulosa b. Insulin c. Growth hormone b. Cortisol is essential for all of a. Cortisol by all except : 21. Nervous function d. Increase plasma protein synthesis b. All of the following are a. Increase Utilization of glucose effects of cortisol except : effects of glucocorticoids on protien except : a. Mobilization of amino acids from extrahepatic tissues b. Enhance Vasoconstrictive d. Adrenal medulla 23. Glucose level the following except : . Glucocorticoids 22. Percentage of cortisol bound a. The net effect of cortisol on a.19. Muscular activity b. Increase protein synthesis in muscle from : protein metabolism : 20. Inflamation mechanism maintenance c. One of the following has different action on glucose level of blood from others : a. 20 % 24. Increase liver catabolism of protein c. to plasma protein is : The lipolytic effect is caused a. Insulin d. 94% c. 6 % d. Zona fasciculata c. All of the following are 25. Increase catabolism of protein in muscle 26. Reduce protein synthesis in stomach c. Glucocorticoids are secreted a. Increase free fatty acids in blood b. Thyroxine c. Maintains blood volume c. Reduce protien synthesis in liver d.

Noon b. Increase Ca excretion and bone resorption d. Increase Ca absorption and bone formation c. Feedback mechanism of a.. Rapid resolution of inflamation 33. Anterior pituitary gland c. ACTH long term stimulation to adrenal cortex leads to increase proliferation of adrenal cortex significantly except : a. None of the above secretion through acting directly on : a. All of the following are effects of cortisol on inflamation except : a. Endrophin d. Hypothalamus b.27. Pituitary gland a. Decrease Ca absorption and bone resorption 31. Liponectin 32. Evening d. Adrenal cortex d. Increase Ca excretion . Early morning c. Lipotropin b. Decrease number of inflamatory cells d. 29. Stress increases cortisol c. Increase permeability of capillaries c. MSH c.. Adrenal cortex d. Midnight . Both (a) and (b) cortisol acts directly on : calcitonin and parathormone at the same time . which of the following statements explain this ? 28. and bone Ca deposition b. All of the following hormones are released simultaneously with ACTH except : a. Effect on cortisol is like 30. Zona reticularis b. Increase stability of lysosomal membranes b. All of the above Cortisol is highest in : a. Zona fasiculata c. Hypothalamus b. Zona Glomerulosa d.

Catecholamines have only a 35. Palpitation c. All of the following are true a. Hyperglycemia d. True b. False All of the following are manifestation of pheochromocytoma except a.34. All of the following are hyperglycemic hormones except a. Thyroid hormone d. Hyperglycemia about catecholamines except : . Controlled by ACTH d. False 39. Increase the visual field 36. Muscular exercise b. Steriods 41. Increase the metabolic rate b. Prolactin 37. Hyperglycemic c. Haemorrhage c. Exert slight masculinizing effect on female throughout life b. direct effect on respiratory centre to increase the depth & rate of respiration a. Increase heart rate c. All of the following actions are produced in stress due to catecholamines secretion except : a. Calorigenic d. Stress hormone b. Vasoconstriction of skeletal muscle blood vessels d. Tachycardia b. Catecholamines cause about androgens except : vasodilation to the renal blood vessels so increase urine volume a. Starts to be secreted at the beginning of puberty 38. Some are converted to testosterone c. All of the following stimulate the secretion of catecholamines except : a. Catecholamines b. Exposure to cold 40. All of the following is true a. Hypotension d. Growth hormone c. True b.

Sweat c. Increase formation of Na+ K+ ATPase d. Hypertension b. Tachycardia salt in 47. a. Non of the above 45. Decrease b. Palasma membrane d. Increase K+ secretion c. Hypoglycemia c. Increase in Na+ c. All of the following are true a. Mineralocorticoid b.42. Increase c. Is the dominant clinical 46. Non of the above All of the following stimulate a. Na+ and K+ metabolism regulator c. Aldosterone regulates Na+ a. Protien in nature d. 44. Secreted by zona glomerulosa 48. Stools b. Bradycardia d. Increase in K+ b. All of the following manifestation of pheochromocytoma a. Increase Na+ reabsorption b. Aldosterone acts on ……….. ……. True b. Hypovolemia d. Unidentified pituitary factor ACTH has a direct effect on a. Nuclear c. All of the above 49. Saliva d. Cytoplasmic b. False secretion of aldosterone except and K+ metabolism by aldosterone secretion . 43. Aldosterone decrease loss of a. Receptors on kidney about aldosterone except …… in potassium ion concentration causes direct stimulation of zona glomerulosa to increase secretion of aldosterone a.

Decrease plasma volume c. Hyperkalemia is one of the conn’s syndrome except manifestation of aldosterone deficiency and it may cause a. Decrease extracellular fluid volume b. Acidosis d. Alkalosis due to functioning adenoma of the pituitary gland . Circulatory shock b. Acidosis c. Osteoporosis b. Weakness of heart contraction c. Conn’s syndrome c. Hypertension c. When aldosterone is deficient a. Hyper function of the adrenal 51. None of the above . Paralysis d.50. All of the following may occur cortex may produce all of the following diseases EXCEPT: a. False 52. Arrhythmia d. Regarding Cushing disease as a result of mineralocorticoid deficiency except a. Euphoria d. Severe muscle weakness b. None of the above 56. Cardiac toxicity b. Cushing syndrome b. Primary hyperaldosteronism occurs in response to activation of the renin – angiotensin system a. All of the are effects of a.all of the following occur except . the patient may develop all of the following EXCEPT: a. Melanin pigmentation of the mucous membranes c. Virilism e. Paralysis 54. Hypertension e. Decrease cardiac output d. Cardiac arrest 53. All of the following 55. True b. Addison’s disease d.

None of the above 61. Lymphocytes b. Increased cortisol level b. a & c e. meniralocortical effect of the cortisol d. Moon-like face of Cushing’s patients is due to: a. Which of the following is not collected from patients of Cushing disease due to hypothalamic disorder will show all of the following EXCEPT: a. Excess secretion of glucocorticoids b. The inhibitory effect of the cortisol on protein synthesis. The laboratory investigations one type of the following cells can show increase of number ( proliferation ) : a. Circulatory shock b.57. salt and water retention e. Muscle cells d. All are true 62. all of the above . Increased cortisol level in the blood b. It results from : a. Frank’s diabetes e. Osteoblasts c. Osteoporosis d. all of the above complications of Cushing syndrome. Increased RBC’s count c. The inhibitory effect of cortisol on the osteoblasts c. Concerning Cushing syndrome. Osteoporosis is one of the accepted to be a complication of Cushing syndrome? a. Increased ACTH level c. Death due to severe infection c. Increase in the count of lymphocytes d. Regarding Cushing disease due to primary adrenal disorder. Anti-vitamin D action of the cortisol d. b. The patient is hypertensive e. None of the above 58. all of the following is manifested EXCEPT: a. Increased CRF level e. None of the above 59. 60. Fat mobilization from the lower limbs to the face & upper limbs c. ACTH level is normal d. Erythrocytes e.

hypernatremia 68. cardiac toxicity d. the hypertension in Conn’s by all the following EXCEPT: is associated with all the following EXCEPT: a. salt and water retention c. d hypokalemia & tetany . meniralocorticoid deficiency is syndrome is due to all of the following EXCEPT: a. alkalosis acceptable complications of hyperaldosterone secretion EXCEPT: a. All are true 64. muscle weakness c. circulatory shock c. alkalosis 65. protein catabolism b. hypertension b. increased blood volume & pressure c. hypovolemia b. hypertension b. bradycardia d. increased the level of plasma renin e. vasoconstriction b. Osteoporosis d. Anemia e. Muscle wasting b. hypokalemia d. increased blood Sodium level d.63. paralysis d. increase in the COP e. The inhibitory effect of 67. all the following are manifested by all of the following EXCEPT: a. all are true 69. secondary hyperaldosteronism Conn’s syndrome is due to: cortisol in protein synthesis in Cushing syndrome causes all the following EXCEPT: a. increased blood volume d. severe muscle weakness in a. not mentioned 66. Conn’s syndrome is manifested a. decreased potassium level in the blood b. Delayed wound healing c. low COP c. alkalosis c.

conns disease is due due a. Addison’s disease is 76. Cortisol 75. muscle weakness c. c. anemia d. muscle weakness. Panhypopituitarism is called( buffalo torso) is due to : manifested by all of the following EXCEPT: a. CRH d. cortisol c. d. tetany 72. aldosterone c.b 77. adrenal virilism b. cardiac arrest in systole c. which of the following is a 74. acne . increase lipolysis with extra deposition in the upper part of the body. hypertension 73.histrutism is due to a. addison’s manifestations c. In cushing syndrome whats a. ACTH b. MSH c. acidosis d. increase gluconeogenesis b. b. adrenal diabetes is due to : a. myxedema e. Increase androgen secretion . c. A. burn out of beta cells. adronegen. anti insulin effect of cortisol. cortisol b. tetany 71. androgen b. mental changes. melanin pigmentation of the mucous membranes b. d. all the above manifested by all of the following EXCEPT: a.70. aldosterone increase secretion of : . all the following hormones are increase secretion of : elevated in addison’s disease EXCEPT: a. d. hypertension b. premature senility d. complication of Addison’s disease? a.

due to pituitary adenoma. Beclomethasone b. hyper tension.78. severe muscle weakness. b. Prednisone b. all the above 80. Betamethasone d. Dexamethasone d. b. all the above. Deoxycortone 85. d. all the above weakness is due to : produces the least sodium retention? a. d. Prednisolone c. hyponatremia b. Which of the following corticosteroids is only injectable ? a. c. b. activation of reninangiotensin system. hypokalemia c. Which of the following produces the least antiinflammatory effect? a. Prednisone b. activation of reninangiotensin system. Deoxycortone 84. hydrocortisone about adrenogenital syndrome: . all the above 81. It cause intense masculinizing effect . hyperkalemia d. which of the following is true a.B 79. secondary hypraldosteronism : a. Which of the following effect of excess secretion of aldosterone : a. Betamethasone d. b. its difficult to diagnose this syndrome in adult male c. adrenal cortex adenoma c. At conns syndrome muscle a. Prednisone Prednisolone Betamethasone Deoxycortone 83. Betamethasone c. Prednisolone c. Which of the following glucocorticoids is used only by inhalation? a. d. in prebuberty boys it lead to rapid grow of sexual organs d. which of the following are 82. c. e. A.

dexamethasone c. The best combination for the treatment of primary Addison’s is : a. Beclomethasone c. Hydrocortisone b. Which of the following glucocorticoids is never used for the treatment of active chronic hepatitis? a. Hydrocortisone b. The glucocorticoid preparation which can be used topically for the treatment of allergy : a. Prednisone d. Prednisolone e. Fludrocortisone d. Prednisone d. The pro-drug which have high anti-inflammatory effect is: a. Prednisolone c. the corticosteroid used to replace aldosterone in primary Addison’s disease is : a. prednisone b. Hydrocortisone b. Deoxycortisone 89. Betamethasone + fludrocortisone e. None of the above 91. Betamethasone 90. Hydrocortisone + fludrocortisone d. Prednisone d. Not mentioned 88. cortisone 87. Cortisone e. Cortisone b. Hydrocortisone + aldosterone b. Fludrocortisone c. All the following corticosteroids are used in the treatment of secondary adrenocortical insufficiency EXCEPT: a. Betamethasone + aldosterone c. Prednisone c. dexamethasone .86. Prednisolone d. dexamethasone 92. Hydrocortisone b. Prednisolone c. The best glucocorticoid preparation for the treatment of bronchial asthma is : a. fludrocorisone d.

not mentioned 96. the safest glucocorticoid preparation for the treatment of asthma in a pregnant woman is : a. during the treatment by glucocorticoids. TB c. SLE d. all the following conditions are treated by using different preparations of glucocorticoids EXCEPT: a. beclomethasone d. betamethasone b. hydrocortisone d. rheumatic fever b. the doctor should follow all of these precautions EXCEPT: a. low dose of prednisolone at the midnight b. dexamethasone c. hydrocortisone 95.93. beclomethasone c. check the patient for hypertension c. betamethasone b. withdrawal should be gradual 94. the corticosteroids preparation should be avoided in diabetic patients is: a. Nephrotic syndrome . fludrocortisone e. double dose during severe stress d.

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

6. 9.Enumerate the structures related to the adrenal gland.Identify the pointed structure then mention its LM picture. and then mention its histological structure 7. 3. 4.Explain the development of adrenal gland. 8.Enumerate congenital anomalies of adrenal gland. 2. .Identify the pointed structure.Discuss the histological features of cells in the suprarenal medulla.Compare between catecholamines’ secreting cells. 5.Describe the vascular supply of the adrenal gland.Identify the pointed structure then mention its function ? 5.Compare between the right & left adrenal glands.Essay Questions 1.

Mention abnormalities of secretions of this hormone ? 9. 7.site of secretion and blood form of mineralocorticoids ? 10.Compare between the 3 layers of adrenal cortex.6. Effects of aldosterone on sweat glands. Mention chemical structure . 1. on Kidney 12. Mention effect of potassium ion concentration on aldosterone secretion ? . 6. 5. 13. 2.Identify the pointed structure then mention its LM picture. 7. 4. 3. Enumerate 4 mechanisms of regulation of Aldosterone secretion ? 14. salivary glands and intestinal absorption. Mention functions of the mineralocortocoids (Aldosterone)? 11. 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.

carbohydrates b. What are the effects of excess aldosterone ? 33. Mention manifestations of Cushing syndrome caused by hormones other than glucocorticoids ?? 31.Immunity h. Mention effect of ACTH on aldosterone secretion? 18. Define crtisol 21. Discuss pituitary as a regulator of cortisol secretion 27. Mention effect of the renin-angiotensin system on aldosterone secretion ? 16. Mention the other manifestations of Cushing syndrome inappropriate metabolic and systemic functions ? 32. Mention the effects of excess aldosterone ? 19.Vitamin D 23.Blood cells g. List the functions of adrenal androgens 30. Mention effects of mineralocorticoid deficiency ? 20.fat d. Give an aacount on the Effect of cortisol on : a. Give a short account on the effect of physiological stress on ACTH secretion 28. Mention effect of decreased sodium on aldosterone secretion? 17.15. Enumerate regulators of cortisol secretion 26. Explian the diffrence between the mechanisms of action of glucocorticoids 22.CVS e. Enumerate the allergic and anti inflammatory effects of cortisol 25.protiens c. Mention the anti inflammatory effects of cortisol 24. Discuss secondary hyperaldosteronism ? due to .Calcium metabolism i.Skeletal muscles f. Mention the circadian rhythm of glucocorticoid secretion 29.Bone formation j.

Discuss the prognosis of the neuroblastoma. Mention anti-inflammatory and immunosuppressant effect of corticosteroids? 52. Discuss the morphology of the neuroplastoma? 42. Give a short account on secondary hyperaldosteronism 48. Mention effects of glucocorticoid deficiency? 38. 43. . What are causes of excessive androgens? 35. Mention adverse Effects of Corticosteroid Therapy? 53.34. Mention replacement therapeutic uses of corticosteroids? 51. Mention contraindications to the use of corticosteroids for antiinflammatory use. Mention the manifestations deposited by adrenal virilism syndrome 47. Mention effect of deficiency of mineralocorticoid? 37. Mention the possible etiology of cortisol hypersecretion 44. Mention some preparation and administration of corticosteroids 49. Discuss the morphology of the pheochromocytoma? 40. Write an account on the clinical diagnosis of this disease? 41. Discuss the manifestations of cortisol hypersecretion 45. Mention the causes of melanin deposition? 39. Compare between Relative potency of corticosteroids 50. Explain the effects of excess aldosterone in conn’s syndrome 46. Mention manifestations of adrenogenital syndrome ? 36.