endo Flashcards

1
Q

aldosterone acts on nephrons to : (3)

A
  • Increase sodium reabsorption from distal tubule
  • increase potassium secretion from distal tubule
  • increase hydrogen secretion from the collecting ducts
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2
Q

what secretes renin?

A

juxtaglomerular cells

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3
Q

role of renin?

A

converts angiotensinogen into angiotensin 1

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4
Q

when is renin secreted

A

in response to low blood pressure

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5
Q

Angiotensin II affect on blood vessels?

A

causes constriction

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6
Q

3 layers of adrenal gland? & what each layer releases

A

zona glomerulosa - mineralocorticoid (aldosterone being the main one)

zona fasiculata - glucocorticoid

zona reticularis - dehydroepiandrosterone (DHEA) (androgens)

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7
Q

where is CRH released from

A

cortisol releasing hormone (CRF) released from hypothalamus

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8
Q

where is ACTH released from and stimulated by what

A

CRH stimulates anterior pituitary gland to release ACTH

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9
Q

role of ACTH

A

stimulates adrenal gland to release cortisol

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10
Q

what does medulla of adrenal gland release

A
  • noradrenaline
  • adrenaline
  • dopamine
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11
Q

what drug is the same as the active form of cortisol?

A

hydrocortisone

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12
Q

what cells make up the adrenal medulla

A

chromaffin cells

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13
Q

what is a phaechromocytoma

A

neuroendocrine tumour of the chromaffin cells

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14
Q

phaechromocytoma triad of symptoms?

A
  • pounding headache
  • palpitations
  • sweating
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15
Q

where is aldosterone released from & what does it do?

A

zona glomerulosa releases aldosterone (mineralocorticoid)

reabsorb Na+ from kidney along with water to increase blood pressure

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16
Q

management of phaechromocytoma

A
  • Alpha blocker: Phenoxybenzamine

- Propranolol

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17
Q

cause of secondary adrenal insufficiency

A

reduction in ACTH release

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18
Q

Cause of tertiary adrenal insufficiency

A

reduction in CRH

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19
Q

what is tertiary adrenal insufficiency most commonly seen following?

A

following chronic glucocorticoid steroid use

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20
Q

features of androgen deficiency seen in women?

A
  • loss of libido

- hair loss in axilla/pubic region

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21
Q

precursor of ACTH?

A

POMC = proopiomelanocortin

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22
Q

what can ACTH excess result in

A

hyperpigmentation due to melanocyte stimulation

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23
Q

where does hyperpigmentation tend to appear

A

oral mucosa & palmar creases

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24
Q

when does cortisol reach its highest level?

& lowest level?

A

8 am

lowest level @ 1am

25
Q

where is renin released from?

and in response to what?

A

released by granular cells of the juxtaglomerular apparatus in response to low blood pressure

26
Q

affects of angiotensin 2

A
  • stimulates adrenal cortex to release aldosterone
  • causes vasoconstriction
  • increases sodium reabsorption
  • stimulates release of ADH
  • increases sympathetic permissiveness
27
Q

what is aldosterone released in response to?

A
  • Angiotensin 2
  • ACTH
  • Potassium levels
28
Q

primary function of aldosterone?

A

Increase the number of epithelial sodium channels in the distal tubule; resulting in sodium & water reabsorption & potassium excretion

29
Q

worldwide most common cause of adrenal insufficiency

A

Tuberculosis

30
Q

most common cause of adrenocortical insufficiency in western world

A

autoimmune destruction of the adrenal cortex

31
Q

autoimmune process in addisons

A

autoantibodies target enzymes involved in biosynthesis of steroids e.g. Enzyme 21-hydroxylase

32
Q

Waterhouse-Friderichsen syndrome pathophysiology

A

adrenal haemorrhage secondary to meningococcal septicaemia

33
Q

abdominal symptoms of Addisons disease?

A
  • dehydration
  • n & v & abdo pain
  • weight loss
34
Q

neurological symptoms of Addisons disease?

A
  • depression
  • psychosis
  • fatigue
35
Q

weight loss
muscle wasting
postural hypotension
hyper-pigmentation

are features of what?

A

Addison’s disease

36
Q

how may a patient present with Addisonian crisis?

A
  • tachycardia
  • postural hypotension
  • oliguria
  • weak
  • confused
  • comatose
37
Q

predisposing factors for Addisonian crisis?

A
  • infection
  • sudden withdrawal of steroids
  • surgery
  • trauma
  • missed medications
38
Q

electrolyte imbalance seen in addisons?

A
  • hyponatraemia

- hyperkalaemia

39
Q

1st line screening tool for adrenal insufficiency

A

8/9am serum cortisol

40
Q

test to distinguish between primary and secondary/tertiary adrenal insufficiency?

A

Plasma ACTH level

41
Q

what does high & low ACTJ level indicate, in the context of low 9am serum cortisol?

A

High ACTH –> primary adrenal insufficiency/Addisons

Low ACTH –> secondary or tertiary adrenal insufficiency

42
Q

what does the Synacthen test involve?

A

IV administeration of 250 mcg tetracosactide, a synthetic analogue of ACTH & measure cortisol @0,30&60 minutes

43
Q

management of addisons disease? (4 components)

A

1) Glucocorticoid replacement: Hydrocortisone 15-30 mg/day
2) Mineralocorticoid replacement: Fludrocortisone (50-300 mcg/day) (adjusted to levels of exercise & metabolism)
3) Androgen replacement
4) Patient education

44
Q

what should patients with addisons disease always carry

A

Steroid card & MediAlert identification

45
Q

How is Addisonian crisis managed?

A
  • IV hydrocortisone (100mg)

- IV fluid resus

46
Q

what should be monitored in Addionian crisis?

A

cardiac, electrolyte and blood sugar

47
Q

most common cause of secondary hypertension

A

Hyperaldosteronism

48
Q

2 causes of primary aldosteronism?

A
  • Adrenal adenoma

- Idiopathic adrenal hyperplasia

49
Q

3 factors that can stimulate aldosterone release?

A
  • Angiotensin 2
  • ACTH
  • Potassium levels
50
Q

where in the kidneys does aldosterone work and what does it do?

A

Collecting ducts - increase number of sodium channels in principal cells –> Sodium reabsorption (followed by water)

51
Q

cause of type 3 familial hyperaldosteronism

A

Mutations in KCNJ5 gene

52
Q

symptoms of hypokalaemia

A
  • muscle weakness
  • paraesthesia
  • mood disturbance
53
Q

classical biochemistry finidngs in conns syndrome

A

hypokalaemic, hypertension & metabolic alkalosis

54
Q

1st and 2nd line invx for primary hyperaldosteronism

A

1st: Aldosterone renin ratio
2nd: CT adrenal glands

55
Q

gold standards test to differentiate between bilateral & unilateral adrenal hyperaldosteronism

A

adrenal vein sampling

56
Q

med management of conns

A

aldosterone antagonists: spironolactone & eplerenone

57
Q

medication if aldosterone antag are not tolerated for patients with conns

A

ENaC inhibitor - amiloride

58
Q

3 causes of secondary hyperaldosteronism & why they collectively occur

A

when kidney BP is much lower than the BP of rest of body; excessive renin is released which stimulates the adrenal gland to release aldosterone

  • renal artery stenosis
  • renal artery obstruction
  • fibromuscular dysplasia