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Endocrinology > adrenal gland > Flashcards

adrenal gland Flashcards

1
Q

What are the 3 layers to the adrenal cortex? (from outside to in)

A
  • zona glomerulosa
  • zona fasiculata
  • zona reticularis
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2
Q

What type of cells are found within the adrenal medulla?

A

chromaffin cells

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3
Q

Where are glucocorticoids, mineral corticoids and androgens released from?

A
  • mineralcorticoids from zona glomerulosa
  • glucocorticoids from zona faculata
  • androgens and glucocorticoids from zona reticularis
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4
Q

State the main mineralcorticoids, glucocorticoids and androgens

A
  • mineralcorticoids: aldosterone
  • glucocorticoids: cortisol (also cortisone)
  • androgens: DHEA, androstenedione- becomes testosterone and ostrogen
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5
Q

What type of hormones are glucocorticoids, mineralcorticoids, androgens, oestrogens and progestins?

A

steroids (derived from cholesterol)

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6
Q

How do steroids exert their effects?

A

theyre lipid soluable so enter cell, bind to nuclear receptors and modulate gene transcription

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7
Q

Describe how corticosteroids regulate gene transcription

A
  • they diffuse across plasma membrane
  • bind to receptors (which have chaperone proteins attached)
  • binding dissociates chaperones
  • receptor/ ligand complex moves into nucleus
  • can dimerise with other receptors and bind to glucocoritcoid response elements
  • or bind to transcription factors
  • both regulate expression
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8
Q

How does aldosterone travel in blood?

A

mostly bound to albumin but some binds to transcortin (another carrier protein)

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9
Q

What does aldosterone do?

A

increases expression of Na/K pump in distal tubules and collecting ducts of nephron which leads to more reabsobtion of Na and so water and excretion of K+. More water in blood leads to higher blood pressure

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10
Q

What is the difference between primary and secondary hyperaldosteronism? Give some examples of each

A

primary: defect in adrenal cortex (bilateral idiopathic adrenal hyperplasia is most common, also conns syndrome)
secondary: due to overactivity of RAAS (renin producing tumour (rare), renal artery stenosis)

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11
Q

What is conns syndrome?

A

an aldosterone secreting adrenal adenoma

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12
Q

How can you distinguish between primary and secondary hyperaldosteronism?

A

primary: LOW RENIN
secondary: HIGH RENIN

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13
Q

What are signs of hyperaldosteronism?

A 
high blood pressure (esp in young)
LV hypertrophy
Stroke 
Hypernaturaemia (High Na+)
Hypokalaemia (Low K+)
also headaches, fatigue
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14
Q

How is hyperaldosteronism treated?

A

depends on type:

  • aldosterone producing adenomas removed surgically
  • spironolactone is mineralcorticoid receptor antagonist
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15
Q

How is cortisol transported in the blood?

A

bound to transcortin

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16
Q

what effects does cortisol have on the body?

A
  • increase protein breakdown
  • incease gluconeogenesis in liver
  • increase fat break down in arms and legs (redistributes to abdomen and dorso- cervical fat pad
  • supresses immune and inflammatory response (inhibits macrophages and mast cell degranulation)
  • resists stress (increases glucose supply, raise blood pressure by making vessels more sensitive to vasoconstriction)
  • inihibits insulin induced GLUT4 translocation
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17
Q

What is the name for chronic excess cortisol

A

cushing’s syndrome

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18
Q

What can cause cushings syndrome?

A
  • prescribed glucocorticoids
  • benign pituitary adenoma secreting ATCH (cushings disease)
  • excess cortisol from adrenal tumour (adrenal cushings)
  • non- pituitary- adrenal tumours producing ATCH or rarely CRH eg small cell lung cancers
19
Q

How can you differentiate between cushings disease, adrenal cushings and non pituitary- adrenal tumours producing ACTH?

A
  • adrenal tumours producing cortisol (adrenal cushings) will lead to high cortisol levels but low ACTH
  • Cushings disease will have high cortisol and ACTH but the ACTH will supress on a supression test (as it is from pituitary cells so has receptors to respond to neg feed back, but this response will be less than normal)
  • non-pituitary- adrenal tumours producing ACTH will not react to supression test so ACTH and cortisol will always be high l
20
Q

What are signs and symptoms of cushings disease?

A
  • plethoric moon shaped face
  • buffalo hump (fat on back of neck)
  • abdominal obesity
  • purple striae
  • acute weight gain
  • hyperglyaemia
  • hypertension
  • early stages sometimes present with easy bruising and bones breaking easily
21
Q

When are steroid drugs such as prednisolone used?

A
  • treatment of inflammatory disorders:
  • asthma
  • inflammatory bowel disease
  • rheumatoid arthirits
  • other auto immune conditions
  • supress immune response after organ transplant
22
Q

What are side effects of steroid drugs?

A
  • hypertension
  • weight gain
  • insomnia (cortisol circadian rythm)
  • headaches
  • brusing
    • achne
23
Q

What is important about someone taking steroid drugs?

A

Their dose must be reduce slowly, the course cannot be stopped abruptly.

24
Q

Why is it that those with cushings disease often have high Na+, low K+, hypertension and urea + creatinine mildly high?

A
  • mildly high urea and creatine it due to more muscle proteolysis due to more cortisol
  • high Na+ and low k+ is because cortisol has a similar structure to aldosterone so it will increase transcription of Na/k pump in the nephrons when its levels are very high
  • leads to more Na in and more K excreted, as well as increasing BP
25
Q

What is the name for chronic adrenal insufficiency?

A

addisons disease

26
Q

What is most common cause now of addisons disease?

A

autoimmune (rarer causes inc. TB, fungal infections, adrenal cancer or haemorrhage)

27
Q

What are signs and symptoms of addisons disease?

A
  • postural hypotension
  • hyperpigmentation
  • weightloss
  • anorexia
  • lethargy
  • hypoglycaemia
  • normal Na+, high k+
  • changes to body hair distribution
28
Q

Why does hyperpigmentation occur in addisons?

A
  • less cortisol
  • means more POMC being degraded into ACTH
  • ACTH breaks down into a- MSH which causes increased melanin synthesis
  • ACTH itself can also activate melanocortin receptors on melanocytes to contribute to hyperpigmentation
29
Q

Describe an addisonians crisis, why do they occur?

A
  • nausia, vomiting, pyrexia, hypotension, vascular collapse (they get realllly unwell)
  • due to severe stress, low salt, infection, trauma, cold, over exertion or abrupt steroid drug withdrawal
  • as this is when cortisol levels need to be higher but they cant be
30
Q

How is an addisonians crisis treated?

A
  • find underlying cause
  • hydrocortison/ cortisol
  • fluids
31
Q

Why is urea often high in addisons?

A
  • low blood volume= low glomerular filtration rate
32
Q

how is androgen release regulated?

A

partially by ACTH and CRH

33
Q

What happens to DHEA and what is its function?

A
  • its converted to testosterone in testis which promote puberty and pubic hair growth
  • after puberty almost all testosterone is produced by testis, so adrenal release becomes insignificant
34
Q

Where do osteogens come from before and after menopause?

A

before: ovaries, other tissues, adrenal glands
after: adrenal glands only (a precursor is made by adrenal glands, other tissues convert it)

35
Q

How is it that 80% hormone produced by chromaffin cells is adrenaline and 20% noradrenaline

A
  • 20% cells lack N- methyl transferase to convert noradrenaline to adrenaline
36
Q

Describe the pathway in adrenaline synthesis

A
  • starts with tyrosine
  • then levodopa
  • then dopamine
  • then noradrenaline
  • then adrenaline
37
Q

What type of adrenoreceptors found in heart and what in lungs?

A

B2 in lungs
B1 in heart
(1 heart, 2 lungs)

38
Q

What is Pheochromocytoma?

A

A tumour of the chromaffin cells leading to excess catecholamine release

39
Q

What are the characteristics of a pheochromocytoma?

A
  • severe hypertension
  • headaches
  • palpatations
  • deaphoesis (increase sweating)
  • anxiety
  • weightloss
  • elevated blood glucose
40
Q

What is congenital adrenal hyperplasia and what is its cause?

A
  • genetic condition leading to deficiency in 21- hydroxylase
  • leads to decreased cortisol and aldosterone production
  • but increases androgen production (same pathway a backs up and goes down differnt route)
  • so called because low cortisol= high ACTH, which stimulates adrenal glands and causes hyperplasia
41
Q

What does congenital adrenal hyperplasia present with?

A

= genital abiguity in female infants

- salt wastin crises (high rate of loss of sodium in urine as no aldosterone)

42
Q

What tests can be performed for diagnosis of adrenocortical diseases?

A
  • plasma cortisol at differnt times of day (should decrease at midnight and be highest at 8am)
  • 24hr urinary excretion of cortisol and its breakdown products
  • ACTH stimulation tests (give synthetic ACTH- synacthen and cortisol should increase)
  • dexmethasone surpression tests (dexmethasone is synthetic steroid which should decrease ACTH and cortisol)
43
Q

describe the release of ACTH throughout the day

A
  • released in pulses that follow circadian rythm
  • more pulses in early morning
  • fewest late evening

Endocrinology (7 decks)

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