Presentation Adrenal

8/8/2019 Presentation Adrenal

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Anatomy, Embryology & Physiology

Sreeja Biswas


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INTRODUCTION

ADRENALS :

y Two small yellow flattened bodies at the back ofabdomen, retroperitoneal

yAbove & in front of upper end of each kidneys

y Size varies from 3-5 cm length

4-6 mm thickness

less in width

yAverage weight is about 1.5-2.5 gms each

y Most highly perfused of all organs

(blood flow 2000 ml/kg/min)


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DEVELOPMENT

ADRENAL CORTEX :

y Celomic mesoderm(near cephalic end of mesonephros)

y Recognizable first at about 4thweek of gestation(series of

buds at root of mesenterysuprarenal ridge)

ADRENAL MEDULLA:

y Sympatho-chromaffin tissue(ectoderm)

y Recognizable first at about 5th to 6thweek of gestation


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SURGICAL RELEVANCE :

Extra-adrenal sites for cortex & medulla - usually along thepaths of migration during embryogenesis


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ANATOMY

RIGHT SUPRARENAL GLAND :

y Triangular in shape

y 2 surfaces - anterior & posterior

y

Anterior surface - forward and laterallyInferior Vena Cava mediallyRight lobe of liver laterally

y Posterior surface upper part-diaphragm

lower part-right kidney

y Base downwardy Hilum below apex, suprarenal vein emerges from anterior

border


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ANATOMY (cont.)

y LEFT SUPRARENAL GLAND :y Larger, crescentric medial & lateral borders

anterior & posterior surfacesy Medial border convex

y Lateral border concave(upper part of left kidney)y Anterior surface

upper part-peritoneum of omental bursalower part-tail of pancreas,lienal artery

y Posterior surface lateral area-left kidneymedial area-left crus of diaphragm

y Hilum lower end of anterior surface


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ANATOMY cont.

y The surfaces of the suprarenal glands are surroundedby areolar tissue containing much fat & closely

invested by a thin fibrous capsule, which is difficult toremove on account of the numerous fibrous processes& vessels entering the organ through the furrows on itsanterior surface and base


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HISTOLOGY

EXTERNAL CORTEX

INTERNAL MEDULLA

y CORTEX 3parts

(outside inwards)

Zona Glomerulosa

Zona Fasciculata

Zona Reticularis

y MEDULLA


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HISTOLOGY (cont.)

CORTEX:y 1. zona glomerulosa situated just beneath the capsule,

rounded cells - very granular & stain deeply

y 2. zona fasciculata composed of columns of cells

arranged in a radial manner intracellular finergranules & lipoid materials

y 3. zona reticularis composed of irregularly arrangedcylindrical masses of cells intracellular pigment

granules which makes this zone darker than the rest ofthe cortex


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HISTOLOGY (cont.)

MEDULLA:y Extremely vascular ,large irregular

polyhedral chromaphil cells finely

granular cytoplasm

y Large anastomosing venous sinusoidsbathing the medullary cells directly in

blood at some places where the

endothelium is deficient.

y

Loose network of supporting non-striped muscle fibers richly supplied with non-medullated nerve fibers &occasional sympathetic ganglia


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VASCULATURE, LYMPHATICS & NERVES

ARTERIAL :

y 1. superior adrenal branch of inferior phrenic

y 2. middle adrenal branch of aorta

y3. inferior adrenal branch of renal artery


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(cont.)

VENOUS : arise from medullary venous plexus

solitary drainage

emerge from the hilum

1. right adrenal (0.5cm) directly to inferior vena cava

2. left adrenal (2.0cm) to left renal vein

y

In 20% of cases right adrenal vein drains to accessoryright hepatic vein or at the confluence of a vein


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(cont.)LYMPHATICS :

to the lumbar glands

NERVES :

from celiac & renal plexus

enters through the lower & medial part ofthe capsule ends in the medulla


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PHYSIOLOGY

ADRENAL MEDULLA:y Secretes epinephrine(E), nor-epinephrine(NE)y In humans,80% of output is epinephriney Effects are same as direct symphathetic nervous

stimulationy Synthesis of catacholamines begins with tyrosine, which is

taken up by the chromaffin cells in the medulla &converted to NE/E .

y NE/E are stored in electron-dense granules along with ATP& neuropeptides.

y Release is stimulated by ACh from pregangloinicsympathetic fibers innervating the medulla and Stressfactors


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PHYSIOLOGY(cont.)

ADRENAL CORTEX:

Adrenal steroid

biosynthesis pathway-y 1. aldosterone

y 2. cortisol

y 3. androgens


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GLUCOCORTICOIDS

CORTISOL : major glucocorticoid

Control of cortisol secretion


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GLUCOCORTICOIDS(cont.)

CORTISOL :

Mechanism of action

y 1. cortisol binds to cytoplasmic receptor

y 2. hormone-receptor complex is transferred to thenucleus

y 3. complex binds to nuclear DNA response element

y Cortisol circulates in blood bound to transcortin, only10% of the hormone is in free form.


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GLUCOCORTICOIDS(contd.)

IMMUNOSURPPRESSIVE ACTIONS:

y Reduce lymphocyte & eosinophil countsy Increase neutrophil count

y Suppress histamine release

y Promote lymphocyte apoptosis

y Reduce prostaglandin synthesis


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MINERALOCORTICOIDS

ALDOSTERONE : major mineralocorticoid

Control of aldosterone secretion

y 1. K+ concentration in extracellular fluid

(even small increase in K+

strongly stimulates)y 2. angiostensin II level in blood

(the Renin-Angiotensin-Aldosterone-Axis)

y 3. others -

ACTH (short-term stimulation)

Na+ deficiency stimulates

Atrial natriuretic peptide(ANP), high Na+ and lowK+ concentration supress aldosterone secretion


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MINERALOCORTICOIDS(cont.)

ALDOSTERONE :

Mechanism of action

y 1. renal resorption sodium & water

y 2. renal excretion of potassium


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MINERALOCORTICOIDS(cont.)

REMOVAL OF THE ADRENALS LEADS TO DEATH

Effects of lack of ALDOSTERONE activity

salt and water wasting & K+/H+ retention

-hyponatremia

-hypovolemia

-hyperkalemia

-acidosis-decreased cardiac outputshock/death


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DISEASE STATES

ADDISONS DISEASE:

yAdrenal insufficiency

y Characterised by hypoadrenocorticism ie. both

mineralocorticoid(aldosterone) andglucocorticoid(cortisol) deficiency

y Lethal unless hormonereplacement(mineralocorticoid) treatment is

institutedy Death due to shock & electrolyte inbalances


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DISEASE STATES (cont.)

CONNS DISEASE :

y Primary hypersecretion of aldosterone

y High BP is usually the only finding due to salt & water

retentionyAssociated hypokalemia can present with muscle

fatigue

y Treatment includes spironolactone or surgical removal

of the adrenal adenoma


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CUSHINGS DISEASE :

y Causes exogenous steroidadministration(commonest)

y

Maybe due to ACTH secreting pituitaryadenoma(cushings syndrome) or ectopic ACTH/CRHsecretion from nonendocrine tumours(small cell lungcarcinoma,thymic and pancreatic carcinoma) oradrenal neoplasia.

y Characterised by hyperadrenocorticism ie. increasedlevels of both glucocorticoids & mineralocorticoids


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CUSHINGS DISEASE (cont.) :

y Typically presents with moon facies, interscapularbuffalo hump, truncal obesity but thin extremities,

hypertension, muscle fatigue, osteoporosis, glucoseintolerance etc

y Management depends on the etiology : surgical forneoplastic causes followed by post-operative radiation

therapy.Ketoconazole decreases adrenalsteroidogenesis.


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PHEOCHROMOCYTOMA:y Adrenal medullary tumour arising from the chromaffin

cells of the sympathetic nervous system.y Extra-adrenal pheochromocytomas arise from the celiac,

superior mesenteric & inferior mesenteric gangliay Epinephrine/Nor-epinephrine secretion causes episodic

tachycardia, hypertension, sweating & flushingy Dopamine secretion occurs in the familial syndromes(5%

cases autosomal dominant either alone or in associationwith MEN type Iia/b) & are not associated with

hypertensiony Treatment with alpha-adrenergic blockers

(phentolamine/phenoxybenzamine) and surgical resection


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y THANK YOU

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Presentation Adrenal