The adrenal gland Flashcards

1
Q

Vasculature of adrenal glands, veins and arteries

A

Right adrenal gland drains into IVC. Left drains into renal vein. Both have many arteries but only one vein.

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2
Q

Adrenal medulla

A

Chromaffin cells secrete catecholamines - eg adrenaline, epinenphrine

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3
Q

Adrenal cortex

A

Secretes corticostreroids - eg aldosterone, cortisol , little bit of sex steroids

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4
Q

Layers of adrenal cortex outer to inner

A

Zona glomerulosa
Zona fasciculata
Zona reticularis

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5
Q

what are steroids

A

molecules coming from cholesterol

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6
Q

Aldosterone pathway

A

Cholesterol -
(3hydroxysteroid dehydrogenase) progesterone - (21hydroxylase) 11-deoxycorticosterone - (11) corticosterone - (18) aldosterone

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7
Q

Cortisol pathway

A

Cholesterol - (3hydroxysteroid dehydrodgenase) progesterone - (17hydroxylase) 17 - OH progesterone - (21) 11-deoxycortisol - (11) cortisol

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8
Q

Aldosterone method of action

A

To maintain blood pressure
Stiumlates Na+ reabsorption in distal convoluted tubule and cortical collecting duct in kidney (and sweat glands, gastric glands, colon)
Stimulates K+ and H+ secretion in distal convoluted tubule and cortical collecting duct.

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9
Q

Regulation of aldesterone

A

Juxtaglomerular apparatus detects low blood pressure, make renin (usually inhibited by high BP).
Renin converts angiotensinogen to angiotensin 1 converted by angiotensin converting enzyme ACE to angiotensin 2
Causes vasoconstriction but most importantly stimulates aldesterone production from Zona glomerulosa of adrenal cortex.

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10
Q

Physiological effects of cortisol

A
peripheral protein catabolism
hepatic gluconeogenesis
increased blood glucose concentration
fat metabolism
enhanced effect of glucagon and catecholamines
increase BP
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11
Q

Addisons’s disease - Primary adrenal failure. Summary is

A

Autoimmune destruction of adrenal cortex. Tuberculosis organisms eats it.
Cortisol and aldesterone deficiency, salt loss, low BP eventual death

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12
Q

Addison’s disease symptoms

A
Darkening of skin - hyperpigmentation
Severe fatigue
Unintentional weight loss
Low BP
Vomiting
Diarrhoea
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13
Q

Why do addison’s patients have hyperpigmentation?

A

POMC, pro-opio-melanocortin is a large precursor protein which is cleaved to form ACTH and MSH and endorphins.
Adrenal failure, no cortisol leads to no inhibition of ACTH production, more produced, more MSH as a byproduct.

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14
Q

Treatment of Addison’s disease

A

Rehydrate with normal saline

Dextrose to prevent hypoglycemia

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15
Q

Cushing’s syndrome symptoms

A
Lose protein in muscles, weak - myopathy
thin skin
centripetal obesity 
Mental changes - depression
High blood pressure
Diabetes
Osteoporosis
Stretch marks.
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16
Q

Cushing’s syndrome causes

A
too much cortisol
Taking steroids orally
pituitary dependent cuhsing's disease
ectopic ACTH (lung cancer)
adrenal adenoma or carcinoma
17
Q

Precursor for Adrenaline and Noradrenaline synthesis

A

Tyrosine

18
Q

Storage of catecholamines, binding of Adrenaline and Noradrenaline in blood

A

stored in cytoplasmic granules and released in response to ACh from preganglionic sympathetic neurones. Adrenaline and Noradrenaline bind to albumin

19
Q

Degradation of adrenaline and noradrenaline

A

monoamine oxidase and catechol-O-methyl transferase

20
Q

Static blood tests

A

test in morning - many hormones secreted according to circadian rhythm
only a snapshot hormone release is pulsatile, may have just missed a pulse.

21
Q

Dynamic blood tests

A

suppression test - too much hormone

stimulation test - too little hormone

22
Q

Troubleshooting test results

A

Have conditions changed?
Look at pre-test probability
Logistics of test - wrong patient?
Repeat test