4- Adrenal Booklet

8/3/2019 4- Adrenal Booklet

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1. Summaries :Anatomy of the supra renal gland

Site: Upper poles of the kidneyN.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:

LeftRightCovered by peritoneum of lessersac

Partially peritoneum

PancreasIVCSplencic vesselsLiver

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.


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Development

Origin:

Cortex: Ceolemic epithelium

Medulla: neural crest

A) Cortex:

Proliferation of Ceolemic epithelium.1ry fetal cortex.invade themedulla..proliferates again..2ry fetal cortex

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

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

MesodermCt capsule.

B) Medulla:

Neura l 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.


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Histology of supra renal glands

Each gland is composed of :

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

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

A) Stroma:

The gland is covered by a C.T capsule that sends thin trabecullar septa inside thegland. 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:

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.

L.M

Cytoplasm contains:rER, numerous mitochondria, Prominentgolgi complex, secretory granulescontacting catecholamines.

E.M


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Epinephrine secretory granulesNorepinephrine secretory granulesSmall, less electron dense granules and

the contents fill the granules.

Large, have eccentric electron dense core

with limiting membrane on the granules.

C) Cortex :

Zona Reticularis Zona Fasciculata Zona Glomerulosa1. Inner layer of thecortex.2. Cells are arranged in

irregular cords thatanastomose togetherenclosing fenestratedblood capillaries inbetween.3. Cells are small withacidophilic cytoplasm.

1. Largest layer of thecortex.2. Cells are arranged

in cords perpendicularto the surfaceseparated by bloodcapillaries.3. Cells are largepolyhedral with largepale round nuclei,cytoplasm appearspale and containsnumerous vacuoles.(Spongicytes)

1. Lies directly under the c.tcapsule.2. Cells are arranged in closely

packed rounded or arched groupssurrounded by blood capillaries.3. Cells are columnar or pyramidalwith dense basal nuclei and acidicslightly vacuolated cytoplasm.

Same as glomerulosabut with lipofuscinpigment.

Same as glomerulosabut with numerouslipid droplets.

Shows ultra structure features ofsteroid secreting cells: sER,mitochondria with tubular cristaeand few lipid droplets.

Secrete Androgensand small amount ofGlucocortecoids.

SecreteGlucocortecoids

Secrete mineralocortecoids


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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 withstress

There is a special centre in the medulla oblongata, connected to the greatersplanchnic nerve which supplies the gland.

Diseases of Adrenal MedullaEffect of Deficiency: Unlike the adrenal cortex the adrenal medulla does not appear to be essential tolife as all its vital functions are done by sympathetic nervous systemEffect 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. Suddendeath may occur.

Tachycardia.


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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 increasesformation of Na* K +ATPase.

Effects of aldosterone on sweat glands, salivary glands and intestinalabsorption.

Aldosterone increases the reabsorption of sodium and the secretion of potassiumby the ducts to conserve body salt in hot environments , when excessive quantitiesof 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 toincrease secretion of aldosterone

2. Effect of the renin-angiotensin system on aldosterone secretion:Angiotensin II is responsible for stimulating the synthesis and release ofaldosterone 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 enhancesformation of angiotensin II which stimulates aldosterone secretion.

Diminished sodium concentration causes the anterior pituitary gland to secretesome substances called the unidentified pituitary factor which affects theadrenal glands to increase aldosterone secretion.


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4. Effect of ACTH on aldosterone secretion: It has a permissive effect on aldosterone secretion and all the above regulationsof 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 osmoticpressure so osmosis of water occurs increasing extracellular fluid volume andblood volume which may lead to increase cardiac output and hypertension,

Increase potassium loss in the urine: When the potassium ion concentrationfalls severe muscle weakness often develops. Paralysis may occur due to failureof 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 leadsto 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 Ifsevere cardiac arrest in diastole occurs.

Mild acidosis develops due to excess hydrogen ion.


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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 mediatorsd. Mediators of metabolic actions >> enzymes ( cAMP dependant kinase)e. Mediators of anti-inflammatory & immunosuppressive actions >> lipocortin

lipomodulin leading to:i. Inhibitions of phospholipase A2 >> inhibition of PGs &

leukotriens formationii. Inhibition of platelet activating factor synsthesisiii. Inhibition of mediator release from inflammatory cells Metabolic actions:

Hyperglycemic . Catabolic lipolytic

a. Hyperglycemic:1. Increase gluconeogenesis in the liver by:

i. Increasing enzyme synthesisii. Increasing mobilization of aminoacids from extrahepatic tissues (

muscles ) >> blood >> liver2. Decreasing glucose utilization by the cells by decreasing glucose

transport3. Hyperglycima >> worsen diabetes

b. Catabolic:1. Decreasing proteins in extrahepatic tissues by:

i. Decreasing protein synthesisii. Increasing protein catabolismiii. Decreasing aminoacid transport to extrahepatic tissues


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2. Increasing protein synthesis in the liver by

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

And this leads to:

i. Increasing liver & plasma proteinsii. Increasing gluconeogenesis

c. Lipolytic:

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

Circulatory actions:1. Important for normal muscular contractility & vasoconstrictive effect of NE2. Decreasing vascular permeabiliting preserving blood volume

Nervous actions:

Affecting sensations & higher functions as concentration, memory & intellectualfunctions

Muscular actions:1. Important for normal contractility2. Deficiency >> muscular fatigue3. 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 RBCs2. Decreasing eosinophils , basophils , monocytes & lymphocytes3. Large doses :

a. Atrophy of lymphoid tissue


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b. Decreased T & B cellsc. Decreased level of immunity

Anti-inflammatory & anti allergic actions:

Decreasing inflammation by:

1. Rapid resolution2. Decreasing vascular permeability3. Decreasing inflammatory cells & release of mediators4. Stabilization of lysosomes ( decreasing release of proteolytic enzymes)5. Inhibition of fibrosis & adhesions

Regulation of cortisol secretion

Stimulus ( physiological stress) >> hypothalamus >> corticotrophin releasingfactor release >> anterior pituitary >> ACTH release

ACTH >> adrenocortical cells >> cortisol & androgens release ACTH>> MSH, lipotropin & endorphin release:

a. Normally >> no significant effectb. 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. Androgens1. During fetal life:

Androgens are continuously secreted from adrenal cortex + minuteamounts of female sex hormones

Part of early development of male sex organs due to childhood

release of androgens2. In females much of the growth of pubic & axillary hair due to cortical

androgens3. In males part of cortical androgens in converted into testosterone in

extracortical tissue secretion is controlled by ACTH


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Diseases of adrenal cortex

Hyper function (hyperadrenalism)I. Cushing Syndrome

Hypersecretion of cortisol It may be :i. Exogenousii. Endogenous

1. 1ry hypothalamic pituitary disorder > ACTH2. 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 (3lafekra 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 ofcortisol)

v. Increased blood glucose > adrenal diabetes > few months > beta cellsburnt out > irreversible Frank diabetes mellitus.

vi. Decreased tissue proteins except liver and plasma > muscular mass loss+ weakness

vii. Immunosuppressionviii. Diminished collagen fibers in the SC tissues >> large purplish striae > SC

tissues torn apartix. Lack of protein deposition and in the bone & anti vitamin D activity &

Ca++ lowering effect leads to osteoporosis and bone weaknessx. It affects brain intellectual functions, memory and concentration so it

may induce Euphoria ;)


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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

Osmosis2. Na+ leads to Blood volume COP hypertension3. Increase potassium excretion hypokalemia muscle weakness

impaired transmission of action potential paralysis4. 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. Neoplasmsii. Congenital adrenal hyperplasia Effectsi. Masculinizing effect through out the bodyii. In females :-

1. Growth of beard2. Deeper voice3. Masculine distribution of hair on the body and on the pupis (like

males' hair distribution)4. Clitoris growth >> resemble penis5. Thick skin

6. Muscle development (deposition of proteins)iii. In males :-

1. Prepuberty :- same in female + rapid development of male sexualorgans + sexual desire


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2. Adults :- difficult to diagnose (androgens have the same effectsas testosterone hormone)

Hypoadrenalism :-o It may be due to :- Lesion in the adrenal cortex:- impaired corticosteroids ACTH deficiency

o Types Acute : adrenal crisis Chronic : Addison's disease 2ry adrenocortical insufficiency : impaired ACTH secretion

o Adrenal crisis: May be induced by stress (increased demand), rapid withdrawal of

therapy, massive adrenal destruction. Abdominal pain >> vomiting Vascular collapse - hypotension > coma > death

o Addison's disease: Effect of deficiency of mineralocorticoids:-

1. Decreased Na+ and Cl- (excreted in urine):-o Decreased ECF volumeo Decreased plasma volumeo Decreased COPo hypotensiono Circulatory shock

2. Increased H+ >> mild acidosis3. Increased K+ >> hyperkalemia it leads to:-

o Serious cardiac toxicityo Weakness of myocardial contractiono Development of arrhythmiao Cardiac arrest in diastole Why ? >> decreased k+ out flux during

repolarization > stoppage of MP at a depolarized state >> excitedcells cardiac arrest in diastole

Effect of deficiency of glucocorticoids


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1. Patient can't maintain normal blood glucose concentration between meals(decreased gluconeogenesis)

2. Reduction of mobilization of fat and protein from the tissues >> depressmany other metab olic 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. Anemia4. If it's exposed to any type of stress >> Death may occur5. 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

melanocyteso 2ry adrenocortical insufficiency :- Due to hypothalamic or pituitary disorder >> ACTH E.g. :

1. Hypothalamic pituitary neoplasms / infections2. Hypothalamic pituitary suppression (long term steroid therapy).

Summary of Pathology

Adrenal Medulla diseases

Pheochromocytoma Neuroblastoma

Description It is derived from chromaffin cells.Most of the tumors arise from the adrenal medulla.However, in a minority of cases, the tumor arises in

extra adrenal sites eg. sympathetic ganglia calledparagangliomas.

A highly malignanttumor.Neuroblastoma most

commonly arises ineither the adrenalmedulla or theretroperitonealsympathetic ganglia.Most neuroblastomassecrete catecholamines.


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Incidence Pheochromocytomas occur sporadically (90%), or asa part of multiple endocrine syndrome.Most sporadic lesions occur in adulthood with slightfemale prevalence; familial lesions may arise in

childhood, with strong male predominance.

Most of the cases aresporadic; however,familial cases also occur.

Morphology Morphology: Pheochromocytoma is known as the"10% tumor". 10 % of cases are bilateral 10% of cases occur in extra adrenal sites, and. 10% of tumors are biologically malignant.

Grossly, it varies from circumscribed sphericalmass confined to the adrenal medulla to a large

hemorrhagic mass. Cut section is gray to brown withareas of hemorrhage.

Microscopically, it is composed of polygonal cellshaving abundant cytoplasm and pleomorphic nuclei.

Grossly, it appears as alobular, soft tumor withgrayish cut surfaceshowing areas ofnecrosis, hemorrhageand calcification.Microscopically, thetumor is composed of

small, dark, round cellswith scant cytoplasm,arranged in masses orrosettes.

Features 1.Hypertension3. Palpitation.4. Hyperglycemia.

5. Increase in basal metabolic rate.

It is rapidly growingcancer. It spreadslocally; by lymph node

metastases, and byblood stream to skull,orbit, liver and bonemarrow.

Diagnosisorprognosis

Is based on laboratory measuring of catecholaminesin plasma and urine and radiographic imaging studiessuch as CT, MRI and ultrasound.

It is a common cause ofcancer death in patientsunder 15 years of age.

Adrenal Cortex Diseases:

I-

Increase in secretion :1. Cushing's syndrome: 1- Exogenous glucocorticoids. 2- Endogenous causes. a) Primary hypothalamic pituitary diseasesb) Primary adrenocortical hyperplasia or neoplasia (adenoma or carcinoid).c) Ectopic production of ACTH by a non-endocrine neoplasm.


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2. Hyperaldosteronism:a. Primary hyperaldosteronism (Conn's syndrome): It is due to:

Aldosterone-producing adrenocortical adenoma occurs in 65% of cases (Conn'ssyndrome).

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 renalperfusion (arteriolar nephrosclerosis, renal artery stenosis), hypoalbuminaemiaand pregnancy.

3. Adrenal Verilism : Cause s of excessi ve and rogens: May be due to: Adrenocortical neoplasms (carcinoma more than adenoma), and Congenital adrenal hyperplasia.

II- Adrenocortical HypofunctionAdrenal Crisis Addisone's disease

Causes: May be due to sudden increase inglucocorticoid requirements in patients with chronicadrenocortical insufficiency.Rapid withdrawal of steroid therapy.Massive destruction of adrenals, e.g. neonataladrenal hemorrhage

Clinical features: vomiting, abdominal pain,hypotension, coma, and vascular collapse. Deathfollows rapidly unless corticosteroids are replacedimmediately.

Might be due to,

Autoimmune adrenalitis (in 60%-70% of cases).Infections as TB and fungi.Metastatic tumorsSystemic amyloidosis.

Sarcoidosis

Hemochromatosis


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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 glucocorticoidso If suprarenal gland is damaged give both (glucocorticoids and

mineralocorticoids) Preparations :-

Drug Route ofadministration

Anti-inflammatoryeffect

Sodiumretainingeffect

Notes

Hydrocortisone Systemically 1 1 NaturalCortisone Tab, injection 0.8 0.8 ProdrugPrednisolone Orally,

parenrtal5 0.3 Synthetic

Prednisone Tablets only 4 0.3 ProdrugFluorinated CS(Beta &dexamethasone)

TopicalSystemic acuteemergencycases

30 ZERO - Catabolic, sothey may inducemuscleweakness.- It causesanorexia

Beclomethasone Inhalation 30 Zero Used inbronchialasthma

Fludrocortisones Oral (oncedaily)

10 250 Used in 1ryAddison'sdisease

Deoxycortone Parentral Zero 50 Has a longduration ofaction

Aldosterone Injection Zero 500 It's duration ofaction doesn'texceed 2hs


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Therapeutic uses :-

1. Anti-inflammatory andimmunosuppressant

2. Replacement therapy

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 .. )

Addisonian insufficiency 1ry Addison's disease Chronic 2ry adrenal insufficiency

( ACTH)

Adverse effects Contraindications Iatrogenic Cushing (due to wrong

dose, timing, duration)

Hypertension

Heart failure

Depression History of mental disorders

Gastric ulceration & delayed ulcerhealing)

Peptic ulcer patients

Hyperglycemia aggravating DM Diabetic patients (especiallyfluorinated corticosteroids they

intensify DM more than other drugs) Immunosuppressant reactivationof dormant TB.

Tuberculosis patients Presence of infection

Hypothalamic pituitary adrenalsuppression especially if used late inthe evening.


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Precautions :-1. Check

patientregularly

for :

Bp - Body weight - Blood glucose -Blood Potassium - Bone (back pain -osteoporosis)

: 5 B ..


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6. In children Prolonged use > same problems asin adults

They are catabolic >> growthretardation occur

How to avoid ? By intermittent scheduleddoses

Never give live attenuatedvaccines they may induceinfection and death as CSsuppress immunity

Give killed vaccines or toxoids(active immunization)


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MCQ

1. Regarding the adrenal cortex allare true EXCEPT :

a. It secretes steroidhormones

b. It is mesodermal in originc. It differentiates into zona

glomerulosa , zona fasiculataand zona reticulate

d. All are true

2. Regarding the right suprarenalgland all are true EXCEPT:

a. It is triangular in shapeb. It is related anteriorly to

IVC and the pancreasc. It is related posteriorly to

the diaphragmd. The IVC collects the venous

blood from it

3. Regarding the left suprarenalgland all are true EXCEPT:

a. It is semilunar in shapeb. It is covered by the

peritoneum of lesser sacc. Its upper border is related

to the body of pancreasd. It is supplied by three

suprarenal arteries

4. Which of the following is falseregarding the arterial supply ofthe suprarenal gland:

a. Each gland is drained by asingle vein and supplied bythree arteries

b. The middle suprarenalartery is branched from theabdominal aorta

c. The left renal vein and IVC

are the main drainage ofleft suprarenald. The superior part is supplied

by an artery coming fromthe inferior phrenic artery.

5. During the intrauterine life: a.the primary cortex of thesuprarenal gland develops from amesodermal origin.

a. the secondary cortexdevelops from the primarycortex then the primary onedegenerates.

b. the secondary cortexdifferentiates into 3 parts.

c. all of the above.


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6. Regarding the development ofthe suprarenal gland , all aretrue EXCPT :

a. The medulla originates from

the migratingsympathogonia.

b. The C.T. capsule of thegland is mesodermal in origin

c. Accessory medullary tissueis found in broad ligament ofthe uterus due to migratingneuroectodermal cells

d. All are true

7. All of the following is true aboutthe suprarenal medulla EXCEPT:

a. Its ectodermal in origin b. Its a modified nervous

tissue that acquired anendocrine activity

c.

Its the reddish -browncentral area of the adrenalgland

d. It has two types of cellschromaffin cells andsypmathetic ganglion cellsthat secretechatecholamines

e.

None of the above

8. Stroma is a connective tissuecapsule that sends thintrabecullar septa inside the glandto support the secretory cells:

a. Trueb. False

9. Which of the following is NOT true about chromaffin cells:

a. Their cytoplasm is pale andcontains large sphericalnuclei, numerousmitochondria, smooth ER,prominent Golgi complex andsecretory granules

b. They are arranged inrounded groups or shortcords away from bloodcapillaries and vessels

c. They are the only type ofcells responsible for thesecretion of epinephrine andnorepinephrine

d. A & Be. All of the above


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10. The granules of thechromaffin cells secretingnorepinephrine are:

a. Largeb. Smallc. Have an eccentric electron-

dens core within the limitingmembrane of the granules

d. Have a less electron-denscore filling the granules

e. A & Cf. B & Cg. A & D

11. Secretion of catecholamines isintiated by acetylcholine releasedfrom preganglionic sympathaticfibers in the splanchnic nerves

a. Trueb. False

12. Which of the following is nottrue about the adrenal cortex :

a. Its the yellowish prepherallayer of the adrenal gland

b. Its mesodermal in origin c. It secretes the steroid

hormonesd. Its divided into 3 zones,

Zona glomerulosa, Zonafasciculata and Zonareticularis

e. None of the above

13. Which of the following is nottrue Zona glomerulosa :

a. It forms 15% of the totalvolume of the gland

b. It lies immediately underthe stroma

c. Has closely packed cellssurrounded by bloodcapillaries

d. The cells in this zone arecoluminar or pyramidal inshape with dense basalacidophilic nuclei

e. The cells in this zone havesmooth ER, mitochondriawith tubular cristea andfilled with lipid droplets

f. None of the above

14. Which of the followingstatements is correct :

a. The cells of Zonaglomerulosa are responsiblefor the secretion ofglucocorticoids

b. The cells of Zona fasciculataare responsible for thesecretion of androgens

c. The cells of Zonaglomerulosa are responsiblefor the secretion ofaldosterone


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d. The cells of Zona reticularisare responsible for thesecretion of adrogens

e. A & Bf. C & D

15. Which of the following is thelargest layer of the cortex:

a. Zona glomerulosab. Zona fasciculatac. Zona reticularisd. Non of the above

16. Which of the following is nottrue about the cells in Zonafasciculata :

a. They are arranged intocords perpendicular to thesurface separated bylongitudinally arrangedfenestrated blood capillaries

b. They are large polyhedralwith large, pale round nuclei

c. Unlike the cells in Zonaglomerulosa they containnumerous vacuoles as well asnumerous lipid droplets

d. They secrete glucorticoidsunlike the cells of the otherzones of the adrenal cortex

e. Non of the above

17. Which of the following is acommon feature between cells ofZona glomerulosa and that ofZona reticularis:

a. They both have acidophiliccytoplasm

b. They both have few lipiddroplets

c. They are both surroundedby fenestrated bloodcapillaries

d. They both havemitochondria with lamellarcristea

e. A & Bf. A & C

18. Which of the following is nota common feature between cellsof Zona fasciculata and that ofZona reticularis :

a. They both have lipiddroplets

b. They both have acidophiliccytoplasm

c. They both have smooth ERd. They both secrete

glucocorticoidse. Non of the above


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19. Glucocorticoids are secretedfrom :

a. Zona glomrulosab. Zona fasciculatac. Zona reticularisd. Adrenal medulla

20. Percentage of cortisol boundto plasma protein is :

a. 80 %b. 94%c. 6 %d. 20 %

21. One of the following hasdifferent action on glucose levelof blood from others :

a. Growth hormoneb. Insulinc. Adrenalined. Glucocorticoids

22. All of the following areeffects of glucocorticoids onprotien except :

a. Mobilization of amino acidsfrom extrahepatic tissues

b. Reduce protein synthesis instomach

c. Reduce protien synthesis inliver

d. Increase catabolism ofprotein in muscle

23. The net effect of cortisol onprotein metabolism :

a. Increase plasma proteinsynthesis

b. Increase liver catabolism ofprotein

c. Decrease amino acid level inblood

d. Increase protein synthesisin muscle

24. The lipolytic effect is causedby all except :

a. GHb. Thyroxinec. Insulind. Cortisol

25. All of the following areeffects of cortisol except :

a. Increase free fatty acids inblood

b. Maintains blood volumec. Enhance Vasoconstrictived. Increase Utilization of

glucose

26. Cortisol is essential for all ofthe following except :

a. Muscular activityb. Inflamation mechanism

maintenancec. Nervous functiond. Glucose level


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27. Effect on cortisol is likecalcitonin and parathormone atthe same time ,, which of thefollowing statements explain this?

a. Increase Ca excretion ,, andbone Ca deposition

b. Increase Ca absorption andbone formation

c. Increase Ca excretion andbone resorption

d. Decrease Ca absorption andbone resorption

28. All of the following areeffects of cortisol on inflamationexcept :

a. Increase stability oflysosomal membranes

b. Increase permeability ofcapillaries

c. Decrease number ofinflamatory cells

d. Rapid resolution ofinflamation

29. ACTH long term stimulation toadrenal cortex leads to increaseproliferation of adrenal cortexsignificantly except :

a. Zona reticularisb. Zona fasiculatac. Zona Glomerulosad. None of the above

30. Feedback mechanism ofcortisol acts directly on :

a. Hypothalamusb. Pituitary glandc. Adrenal cortexd. Both (a) and (b)

31. All of the following hormonesare released simultaneously withACTH except :

a. Lipotropinb. MSHc. Endrophind. Liponectin

32. Stress increases cortisolsecretion through acting directlyon :

a. Hypothalamusb. Anterior pituitary glandc. Adrenal cortexd. All of the above

33. Cortisol is highest in :a. Noonb. Early morningc. Eveningd. Midnight


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34. All of the following is trueabout androgens except :

a. Exert slight masculinizingeffect on female throughoutlife

b. Some are converted totestosterone

c. Controlled by ACTHd. Starts to be secreted at

the beginning of puberty

35. All of the following actionsare produced in stress due tocatecholamines secretion except:

a. Increase the metabolic rateb. Increase heart ratec. Vasoconstriction of skeletal

muscle blood vesselsd. Increase the visual field

36. All of the following arehyperglycemic hormones except

a. Catecholaminesb. Growth hormonec. Thyroid hormoned. Prolactin

37. All of the following are true

about catecholamines except :a. Stress hormoneb. Hyperglycemicc. Calorigenicd. Steriods

38. Catecholamines causevasodilation to the renal bloodvessels so increase urine volume

a. Trueb. False

39. All of the following stimulatethe secretion of catecholaminesexcept :

a. Muscular exerciseb. Haemorrhagec. Hyperglycemiad. Exposure to cold

40. Catecholamines have only adirect effect on respiratorycentre to increase the depth &rate of respiration

a. Trueb. False

41. All of the following aremanifestation ofpheochromocytoma except

a. Tachycardiab. Palpitationc. Hypotensiond. Hyperglycemia


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42. .. Is the dominant clinicalmanifestation ofpheochromocytoma

a. Hypertensionb. Hypoglycemiac. Bradycardiad. Tachycardia

43. All of the following are trueabout aldosterone except

a. Mineralocorticoidb. Na+ and K+ metabolism

regulatorc. Protien in natured. Secreted by zona

glomerulosa

44. Aldosterone acts on .Receptors on kidney

a. Cytoplasmicb. Nuclearc. Palasma membraned. Non of the above

45. Aldosterone regulates Na+and K+ metabolism by

a. Increase Na+ reabsorptionb. Increase K+ secretionc. Increase formation of Na+

K+ ATPased. All of the above

46. Aldosterone decrease loss ofsalt in

a. Stoolsb. Sweatc. Salivad. All of the following

47. in potassium ionconcentration causes directstimulation of zona glomerulosato increase secretion ofaldosterone

a. Decreaseb. Increasec. Non of the above

48. All of the following stimulatesecretion of aldosterone except

a. Increase in K+b. Increase in Na+c. Hypovolemiad. Unidentified pituitary

factor

49. ACTH has a direct effect onaldosterone secretion

a. Trueb. False


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50. All of the are effects ofconns syndrome except

a. Severe muscle weaknessb. Hypertensionc. Acidosisd. Paralysis

51. Primary hyperaldosteronismoccurs in response to activationof the renin angiotensin system

a. Trueb. False

52. All of the following may occuras a result of mineralocorticoiddeficiency except

a. Circulatory shockb. Acidosisc. Paralysisd. Cardiac arrest

53. When aldosterone is deficient,all of the following occur except

a. Decrease extracellular fluidvolume

b. Decrease plasma volumec. Decrease cardiac outputd. Alkalosis

54. Hyperkalemia is one of themanifestation of aldosteronedeficiency and it may cause

a. Cardiac toxicityb. Weakness of heart

contractionc. Arrhythmiad. All of the following

55. Hyper function of the adrenalcortex may produce all of thefollowing diseases EXCEPT:

a. Cushing syndromeb. Conns syndrome c. Addisons disease d. Virilisme. None of the above

56. Regarding Cushing diseasedue to functioning adenoma ofthe pituitary gland , the patientmay develop all of the followingEXCEPT:

a. Osteoporosisb. Melanin pigmentation of the

mucous membranesc. Euphoriad. Hypertensione. None of the above


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57. Concerning Cushing syndrome,one type of the following cellscan show increase of number (proliferation ) :

a. Lymphocytesb. Osteoblastsc. Muscle cellsd. Erythrocytese. None of the above

58. Which of the following is notaccepted to be a complication ofCushing syndrome?

a. Circulatory shockb. Death due to severe

infectionc. Osteoporosisd. Franks diabetes e. None of the above

59. Moon- like face of Cushingspatients is due to:a. Excess secretion ofglucocorticoids

b. Fat mobilization from thelower limbs to the face & upperlimbsc. meniralocortical effect ofthe cortisold. salt and water retentione. all of the above

60. The laboratory investigationscollected from patients ofCushing disease due tohypothalamic disorder will showall of the following EXCEPT:

a. Increased cortisol levelin the blood

b. Increased ACTH levelc. Increase in the count of

lymphocytesd. Increased CRF levele. None of the above

61. Regarding Cushing disease dueto primary adrenal disorder, allof the following is manifestedEXCEPT:

a. Increased cortisol levelb. Increased RBCs count c. ACTH level is normald. The patient is hypertensivee. All are true

62. Osteoporosis is one of thecomplications of Cushingsyndrome. It results from :

a. The inhibitory effect of thecortisol on protein synthesis.

b. The inhibitory effect ofcortisol on the osteoblasts

c. Anti-vitamin D action of thecortisol

d. a & ce. all of the above


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63. The inhibitory effect ofcortisol in protein synthesis inCushing syndrome causes all thefollowing EXCEPT:

a. Muscle wastingb. Delayed wound healingc. Osteoporosisd. Anemiae. All are true

64. Conns syndrome is manifestedby all the following EXCEPT:

a. hypertensionb. muscle weaknessc. bradycardiad. alkalosis

65. the hypertension in Connssyndrome is due to all of thefollowing EXCEPT:

a. vasoconstrictionb. salt and water retentionc. increased blood volumed. increase in the COPe. not mentioned

66. all the following areacceptable complications ofhyperaldosterone secretionEXCEPT:

a. hypertensionb. circulatory shockc. paralysisd. d hypokalemia & tetany

67. severe muscle weakness inConns syndrome is due to:

a. protein catabolismb. alkalosisc. hypokalemiad. hypernatremia

68. secondary hyperaldosteronismis associated with all thefollowing EXCEPT:

a. decreased potassium level inthe blood

b. increased blood volume &pressure

c. increased blood Sodium leveld. increased the level of

plasma renine. all are true

69. meniralocorticoid deficiency ismanifested by all of the followingEXCEPT:

a. hypovolemiab. low COPc. cardiac toxicityd. alkalosis


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70. which of the following is acomplication of Addisonsdisease?

a. hypertensionb. cardiac arrest in systolec. anemiad. tetany

71. Panhypopituitarism ismanifested by all of the followingEXCEPT:

a. adrenal virilismb. addisons manifestations c. premature senilityd. myxedemae. tetany

72. Addisons disease ismanifested by all of the followingEXCEPT:

a. melanin pigmentation of themucous membranes

b. muscle weaknessc. acidosisd. hypertension

73. all the following hormones areelevated in addisons diseaseEXCEPT:

a. ACTHb. MSHc. CRHd. Cortisol

74. In cushing syndrome whatscalled( buffalo torso) is due to :

a. Increase androgen secretion.

b. increase lipolysis with extradeposition in the upper partof the body.

c. muscle weakness.d. mental changes.

75. acne ,histrutism is due toincrease secretion of :

a. androgenb. cortisolc. aldosterone

76. adrenal diabetes is due to :a. increase gluconeogenesisb. anti insulin effect of

cortisol.c. burn out of beta cells.d. A,b

77. conns disease is due dueincrease secretion of :

a. cortisolb. aldosteronec. adronegen.d. all the above


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78. which of the following areeffect of excess secretion ofaldosterone :

a. hyper tension.b. severe muscle weakness.c. activation of renin-

angiotensin system.d. all the above.e. A,B

79. At conns syndrome muscleweakness is due to :

a. hyponatremiab. hypokalemiac. hyperkalemiad. all the above

80. secondary hypraldosteronism :a. due to pituitary adenoma.b. adrenal cortex adenomac. activation of renin-

angiotensin system.d. all the above

81. which of the following is trueabout adrenogenital syndrome:

a. It cause intensemasculinizing effect .

b. its difficult to diagnose thissyndrome in adult male

c. in prebuberty boys it lead torapid grow of sexual organs

d. all the above

82. Which of the followingproduces the least sodiumretention?

a. Prednisoneb. Prednisolonec. Betamethasoned. Deoxycortone

83. Which of the followingproduces the least anti-inflammatory effect?

a. Prednisoneb. Prednisolone

c. Betamethasoned. Deoxycortone

84. Which of the followingcorticosteroids is only injectable?

a. Prednisoneb. Prednisolonec. Betamethasone

d. Deoxycortone

85. Which of the followingglucocorticoids is used only byinhalation?

a. Beclomethasoneb. Betamethasonec. Dexamethasoned. hydrocortisone


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86. the corticosteroid used toreplace aldosterone in primaryAddisons disease is :

a. prednisone

b.

dexamethasonec. fludrocorisoned. cortisone

87. All the followingcorticosteroids are used in thetreatment of secondaryadrenocortical insufficiencyEXCEPT:

a.

Hydrocortisoneb. Fludrocortisonec. Prednisoned. Prednisolonee. Not mentioned

88. The pro-drug which have highanti-inflammatory effect is:

a. Cortisoneb. Prednisolonec. Prednisoned. Deoxycortisone

89. The glucocorticoid preparationwhich can be used topically forthe treatment of allergy :

a. Hydrocortisoneb. Prednisonec. Fludrocortisoned. Betamethasone

90. The best combination for thetreatment of primary Addisonsis :

a. Hydrocortisone +

aldosterone b. Betamethasone +aldosterone

c. Hydrocortisone +fludrocortisone

d. Betamethasone +fludrocortisone

e. None of the above

91.

The best glucocorticoidpreparation for the treatment ofbronchial asthma is :

a. Hydrocortisoneb. Beclomethasonec. Prednisoloned. Cortisonee. dexamethasone

92. Which of the followingglucocorticoids is never used forthe treatment of active chronichepatitis?

a. Hydrocortisoneb. Prednisolonec. Prednisoned. dexamethasone


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93. during the treatment byglucocorticoids, the doctor shouldfollow all of these precautionsEXCEPT:

a.

low dose of prednisoloneat the midnightb. check the patient for

hypertensionc. double dose during

severe stressd. withdrawal should be

gradual

94.

the safest glucocorticoidpreparation for the treatment ofasthma in a pregnant woman is :

a. betamethasoneb. dexamethasonec. beclomethasone

d. hydrocortisone

95. the corticosteroidspreparation should be avoided in

diabetic patients is:a. betamethasoneb. beclomethasonec. hydrocortisoned. fludrocortisonee. not mentioned

96. all the following conditions aretreated by using different

preparations of glucocorticoidsEXCEPT:a. rheumatic feverb. TBc. SLEd. Nephrotic syndrome


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Answers:

1. D2. B

3. C4. C5. A6. C7. D8. A9. E10. E

11. A12. C13. E14. F15. B16. D17. E18. E

19. B20. B21. B22. C23. A24. C25. D26. B

27. C28. B29. C30. D31. D32. A

33. B34. D

35. C36. D37. D38. B39. C40. B41. C42. A

43. C44. A45. D46. D47. B48. B49. B50. C

51. B52. C53. D54. D55. c56. e57. d58. a

59. e60. c61. c62. e63. d64. c

65. a66. b

67. c68. e69. d70. c71. a72. d73. d74. B

75. A76. D77. B78. E79. B80. C81. D82. C83. D

84. D85. A86. C87. B88. C89. D90. C91. B92. C

93.

A94. C95. A96. b


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Essay Questions1- 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 thesuprarenal medulla.

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

5- Identify the pointed structure then mention itsLM picture.


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

7- Compare between the 3 layers of adrenal cortex.

1. Mention the action of Catecholaimnes on Metabolism ?2. Mention action of catecholamines on CVS ?3. Mention action of catecholamines on GIT ?4. Mention action of catecholamines on Respiratory system ?5. Mention action of catecholamines on skeletal muscle ?6. Mention action of catecholamines on Nervous system ?7. Mention Control of Secretion of catecholamines ?8. Mention abnormalities of secretions of this hormone ?9. Mention chemical structure ,site of secretion and blood form of

mineralocorticoids ?10. Mention functions of the mineralocortocoids (Aldosterone)?11. on Kidney12. 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 ?


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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 crtisol21. Explian the diffrence between the mechanisms of action of

glucocorticoids22. Give an aacount on the Effect of cortisol on :

a- carbohydratesb- protiensc- fatd- CVSe- Skeletal musclesf- Blood cellsg- Immunityh- Calcium metabolismi- Bone formation

j- Vitamin D23. Mention the anti inflammatory effects of cortisol24. Enumerate the allergic and anti inflammatory effects of cortisol25. Enumerate regulators of cortisol secretion26. Discuss pituitary as a regulator of cortisol secretion27. Give a short account on the effect of physiological stress on ACTH

secretion28. Mention the circadian rhythm of glucocorticoid secretion29. List the functions of adrenal androgens

30. Mention manifestations of Cushing syndrome caused by hormones otherthan glucocorticoids ??

31. Mention the other manifestations of Cushing syndrome due toinappropriate metabolic and systemic functions ?

32. What are the effects of excess aldosterone ?33. Discuss secondary hyperaldosteronism ?


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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 hypersecretion44. Discuss the manifestations of cortisol hypersecretion45. Explain the effects of excess aldosterone in conn s syndrome

46. Mention the manifestations deposited by adrenal virilism syndrome47. Give a short account on secondary hyperaldosteronism

48. Mention some preparation and administration of corticosteroids49. Compare between Relative potency of corticosteroids50. 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 anti-

inflammatory use.

4- Adrenal Booklet

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