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MET2 > 37 - Adrenals > Flashcards

37 - Adrenals Flashcards

1
Q

Embryological origin of the adrenals, gonads and kidneys

A

Embryonic ridge

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2
Q

What does the embryonic ridge spilt into

A

Adrenogonadal primordium
and neural crest cells
- forms foetal adrenal which has 4 zones

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3
Q

Zones of the adrenals from outermost to inner

A

Zona glomerulosa
Zona fasciculata
Zona reticularis

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4
Q

Where are the adrenals and what are they made up of

A

Above the kidney

Made up of adrenal cortex and medulla

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5
Q

Blood supply of the adrenal gland

A

Flows in from the capsule and flows centrally
Blood is exposed to cortisol produced in zona fasciculata
Blood supply into adrenal medulla has been exposed to steroids

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6
Q

Hormone from Zona glomerulosa + receptor

A

Adosterone

CYPIIB2

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7
Q

Hormone from Zona fasciculata + receptor

A

Cortisol

CYPIIBI

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8
Q

Hormone from Zona reticularis + receptor

A

Testosterone

CYPI7AI

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9
Q

What is the function of aldosterone

A

Vasoconstriction
K+ Secretion
Na+ re absorption
= Increases BV

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10
Q

Hyperaldosterism

A

Low K+
High BP
Metabolic Alkalosis
Hypernatremia

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11
Q

Where is the mineralcorticoid receptor

A

In nucleus almost everywhere

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12
Q

What does the mineralcorticoid receptor bind to

A

Cortisol and aldosterone

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13
Q

What converts cortisol to cortisone in the kidney

A

11BHS2

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14
Q

Why is cortisol converted to cortisone

A

As more cortisol in the blood

Cortisone doesn’t active the receptor and allows for aldosterone to bind too

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15
Q

What does aldosterone bind to in the kidney

A

Mineralcorticoid receptor in principle cell in distal convulated tubule

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16
Q

What does aldosterone do in the kidney DCT

A

Activate Na+/K+ ATPse
Upregulates ENaC so Na reabsorbed and K+ excreted
Cl- absorbed to maintain neutrality

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17
Q

What does aldosterone do in in the intercalated cells (A and B cells)

A

Binds to the MR receptor
Activates Na+./K+ pump
Activate H+/K+ ATPase causes loss of H+ –> acid urine and alkalotic blood

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18
Q

Conn’s Syndrome

A

Primary hyperaldosterism

  • Hypertension
  • Suppressed plasma renin activity
  • increased aldosterone secretion
  • Aldosterone producing adenoma, bilateral adrenal hyperplasia
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19
Q

How do you diagnose Conn’s syndrome

A 
Aldosterone:renin ration
Saline suppression test(to try and suppress aldosterone)
CT adrenal
Adrenal venous sampling
Metomidate PET
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20
Q

What can cause glucocorticoid remediable aldosteronism

A

Aldosterone synthase and 11 B hydroxylase can cross over and form a mutated gene
ACTH activates promotor of 11B hydroxylase and increases aldosterone

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21
Q

What is glucocorticoid remediable aldosteronism

A

Low potassium
High BP
Met alk

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22
Q

How do you treat GRA

A

Steroids

Can suppress ACTH and so suppresses aldosterone

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23
Q

What does liquorice inhibit and what does it do

A

11BHSD2

Stops activation of cortisol

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24
Q

How can cortisol cause hyperaldosterism

A

Cortisol binds to MR

Can lead to syndrome of apparent mineralocorticoid excess

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25
Q

Liddle syndrome

A

Mutation which increases ENaCs
Hypertension, hypokalaemia, metabolic acidosis
Low aldosterone

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26
Q

What does the HPA axis respond to

A

Stress

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27
Q

Where is corticotropin-releasing hormone released

A

Hypothalamus

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28
Q

Where is ACTH released and what does it bind to

A

Released from anterior pituitary
Binds to MC2R in adrenal gland
Glucocorticoids released

29
Q

Feedback loops int the HPA axis

A

Cortisol inhibits production of CRH and ACTH
ACTH inhibits CRH
ACTH inhibits its own production

30
Q

What do steroids activate

A

Hippocampus which inhibits hypothalamus

31
Q

What does the immune response activate

A

Hypothalamus to release CRH and is inhibited by glucocorticoids

32
Q

What activates and inhibits the hypothalamus

A

Activates - stress, catecholamines, ang II, ghrelin

- inhibits - Opiates, ANP and oxytocin

33
Q

What inhibit and activates ACTH

A

CRIF inhibits

Ang II and cytokines activate

34
Q

When is cortisol highest and lowest

A

Highest as you wake up

Lowest when you are asleep

35
Q

How do we respond to starvation, infection and hypotension

A

Starvation - Tissue breakdown for fuel
Infection - Immunosuppression
Hypotension - increase BP

36
Q

Cushings syndrome

A

Excess cortisol

37
Q

Symptoms of cushing’s syndrome

A 
Dorsal fat pad - buffalo hump
Enlarged heart - high BP
Obesity
Muscle weakness
Osteoporosis
Easy bruising 
Skin ulcers
Swollen face and abdomen
38
Q

Causes of cushings

A

iatrogenic
Corticotroph adenoma of the pituitary
Ectopic ACTH secreting neuroendocrine tumour
Bilateral adrenal hyperplasia

39
Q

How do diagnose cushings

A

Overnight dexamethasone suppression test
24 hour urine free cortisol
0.5mg dexamethasone every 6 hours for 48 hours, Cortisol day curve plus midnight sleeping cortisol

40
Q

Imaging to diagnose cushings syndrome

A

MRI pituitary, CT adrenals, Inferior petrosal sinus sampling, NM: Octreotide uptake scan

41
Q

Pituitary treatment for cushings syndrome

A

Transsphenoidal surgery

External beam radiotherapy

42
Q

Adrenal treatment for Cushing’s syndrome

A

Adrenalectomy

Metyrapone/ketoconazole/etomidate

43
Q

Addison’s disease

A

Low levels of corticosteroids

44
Q

Causes of addisons disease

A

Primary adrenal failure - autoimmune, TB

45
Q

Symptoms of addison’s disease

A

Hyperpigmentation, fatigue, weakness, anorexia, weight loss

46
Q

What is an addisonian crisis

A

Failure to respond to stress

Low BP, low glucose, low Na, high K+

47
Q

Diagnosis of addison’s disease

A

Low 9am cortisol
High ACTH
Short synacthen test (Give ACTH and see if cortisol rises)

48
Q

Management of addison’s disease

A

Replace steroids with hydrocortisone, flurocortisone

49
Q

How do treat an addisonian’s crisis

A

IV fluid resuscitation, IM hydrocortisone

50
Q

What occurs in a 21-Hydroxylase mutation

A

ACTH rises
hyperplastic adrenal glands and so androgen increases (cannot make aldosterone or cortisol as need 21H)
- Congenital adrenal hyperplasia

51
Q

Congenital adrenal hyperplasia

A

Salt losing
Adrenal insufficiency
Virilisation
Adrenal hyperplasia

52
Q

What are catecholamines

A

Amines made from tyrosine

E.g Dopamine, adrenaline, noradrenaline

53
Q

What converts adrenaline to noradrenaline

A

PNMT via cortisol

Adrenaline → Metadrenaline and NA → Normetadrenaline via COMT

54
Q

Where are chromaffin cells

A 
In Adrenal medulla 
Para-aortic sympathetic chain
Organ of zuckerkandl 
Wall of urinary bladder 
neck and mediastinal sympathetic chain
55
Q

Phaechromocytoma

A

Chromaffin cell tumour arising from within the adrenal medulla

56
Q

Paraganglioma

A

Chromaffin cell,, Extra-adrenal tumour

57
Q

both Phaechromocytoma and Paraganglioma

A

PPGL

58
Q

Input to adrenal medulla

A

Sympathetic nerves

59
Q

What is released in hypoglycaemic stress

A

Adrenaline

60
Q

What is released in hypovolemic stress

A

Noradrenaline

61
Q

A1 adrenoreceptor

A

vascular and smooth muscle contraction

62
Q

A2 adrenoreceptor

A

presynaptic, inhibitory to noradrenaline release - suppresses BP

63
Q

B1 adrenoreceptor

A

positive inotropic and chronotropic in the heart; increased renin; lipolysis

64
Q

B2 adrenoreceptor

A

bronchial, vascular, uterine smooth muscle relaxation; glycogenolysis

65
Q

B3 adrenoreceptor

A

Lipolysis, energy expenditure, eg at brown fat tissue

66
Q

D1 adrenoreceptor

A

cerebral, renal, mesenteric, coronary vasculature dilatation

67
Q

D2 adrenoreceptor

A

presynaptic inhibition of noradrenaline and prolactin release

68
Q

Catecholamine excess

A

Impending doom, hypertension, tremor, nausea, vomiting, weight loss, fatigue, dyspnea, headache, fatigue

69
Q

PPGL Case detection

A

Hyperadrenergic spells, resistant hypertension, familial syndrome

MET2 (28 decks)

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