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Metabolism CC > Adrenals > Flashcards

Adrenals Flashcards

1
Q

3 cortical zones

A 
Zona glomerulosa (outer)
Zona fasciculata
Zona reticularis (facing medulla)
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2
Q

Right gland shape

A

Pyramidal

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3
Q

Left gland shape

A

Crescent

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4
Q

Human adrenal gland location

A

Anterior and superior to upper part of kidney

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5
Q

What encloses the medulla

A

Myofibroblasts

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6
Q

Where do veins and lymphatic vessels leave

A

Hilum

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7
Q

Where do arteries and nerves enter the gland

A

Multiple sites

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8
Q

Vessels entering the gland form a…

A

Subcapsular capillary plexus that gives rise to fenestrated sinusoids
–> pass through gland to reach further plexus in ZR

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9
Q

What allows efficient delivery of hormones to bloodstream

A

Most cells in adrenal gland one or two cells away from vascular endothelial cell

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10
Q

Zona Glomerulosa

A

Small, narrow, polyhedral cells in round clusters
Deep staining nuclei + basophilic cytoplasm
Abundant smooth ER
Mitochondria have lamelliform (shelf-like) cristae
15% of cortex
Aldosterone production

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11
Q

Zona Fasciculata

A

Cells larger than ZG
Clear cells- paler staining properties
Laid in columns 2 cells wide, parallel to fenestrated sinusoids
Mitochondrial cristae tubulovesicular in shape
Glucocorticoid- cortisol secretion

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12
Q

Zona Reticularis

A

Smaller, compact cells
Numerous smooth ER + multiple lysosomes with brown lipofuscin pigment
Produces glucocorticoid + secreted adrenal androgens DHEA and DHEAS

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13
Q

What doe ZG secrete

A

Mineralocorticoid- Aldosterone

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14
Q

What does ZF secrete

A

Glucocorticoid- Cortisol

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15
Q

What does ZR secrete

A

Glucocorticoid + adrenal androgens DHEA and DHEAS

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16
Q

Medulla

A

Chromaffin cells
Large, large nuclei + fine cytoplasmic granules which stain brown
Catecholamine hormones packed within granules- released from symp nerve terminals stimulation
80%- adrenaline
20%- noradrenaline

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17
Q

Medulla secretes

A

80% cells adrenaline

20% cells noradrenaline

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18
Q

Steroid production

A

Cholesterol uptake
Cholesterol –> inner mitochondrial membrane
Converted to pregnenolone by cytochrome P450

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19
Q

Aldosterone release stimulated by

A

Secreted by ZG

ZG cells respond to ACTH, but angiotensin II + K extracellular conc increase are main regulators

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20
Q

Aldosterone release inhibition

A

Somatostatin
Heparin
ANP
Dopamine

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21
Q

Binding of Ang II to GPCR AT1

A

Activates downstream signalling pathways
Mostly phospholipase C activation –> Ca2+ intracellular increase
Increasing K+ depolarises ZG cell membrane, also leading to Ca2+ influx
In long term, upregulated aldosterone synthase

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22
Q

Aldosterone effects

A 
Mediated by binding to mineralocorticoid receptor in cytosol
Increases retention of sodium and water
Stimulates NaK ATPase
Inserts additional ENaC
Stimulates H+ ATPase
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23
Q

Mineralocorticoid receptor (MR) affinity

A

Equal affinity to both cortisol and aldosterone

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24
Q

Cortisol clearance

A

Cortisol inactivated into cortisone by action of 11BetaHSD-2 in kidney

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25
Q

Aldosterone binding to MR

A

Induces retention of Na+ by upregulating epithelial Na+ channels (ENaC) in distal tubules

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26
Q

Hypertension caused by hyperaldosteronism

A

Direct action of aldosterone on vasculature and CNS
Aldosterone can promote inflammation and oxidative stress
Oxidative stress upregulates MR expression in cardiac cells
–>induces cardiac remodelling + fibrosis
Aldosterone causes impaired insulin signalling –> induces swelling + stiffening of endothelial cells + counters ability to trigger vasodilation

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27
Q

Primary hyperaldosteronism causes

A

Conn’s syndrome
Aldosterone-producing adenoma
Bilateral adrenal hyperplasia

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28
Q

Conn’s syndrome

A

Hypertension
Suppressed plasma renin activity
Increased aldosterone production

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29
Q

Primary hyperaldosteronism diagnosis

A 
Aldosterone:Renin ratio
Saline suppression test
CT adrenal
Adrenal venous sampling
Metomidate PET
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30
Q

Primary hyperaldosteronism treatment

A

MR antagonists- spironolactone, eplerenone

Unilateral adrenalectomy- proven single aldosterone-secretion adenoma

31
Q

Liddle Syndrome

A

Mutation that inserts additional ENaC
–> more Na+ taken from filtrate
Stimulates Na+/K+ ATPase –> 3Na+ reabsorbed into bloodstream in exchange for 2K+, which is excreted

32
Q

Liddle Syndrome effects

A

Hypertension
Hypokalaemia
Metabolic acidosis

33
Q

Familial Aldosteronism

A

Autosomal dominant
ACTH dependent activation of aldosterone synthase
Can be reversed by treatment with glucocorticoid to inhibit ACTH from pituitary gland

34
Q

Familial Aldosteronism effects

A

Early onset, severe, refractory hypertension
Early onset haemorrhagic stroke
No hypokalaemia

35
Q

Syndrome of Mineralocorticoid Excess

A

Cortisol inactivated into cortisone by 11BetaHSD2 in kidney so aldosterone allowed to bind to MR
This doesn’t happen in conditions of Cortisol excess or where enzyme has been affected
–> eating excess liquorice can inactivate 11BetaHSD2

36
Q

Mineralocorticoid excess effects

A

Low K+
Metabolic alkalosis
Low plasma renin
Low aldosterone

37
Q

ACTH

A 
Produced by anterior pituitary
Binds to MC2R (melanocortin-2 receptor)
Increases cholesterol import into cell
Increases cholesterol trafficking into mitochondria
Increases adrenal blood flow
ZF growth
38
Q

ACTH and Cortisol secretion

A

Circadian rhythm
Begins at 4am, peaks at 7am,
Daily ACTH higher in males
Stress increases amplitude

39
Q

Glucocorticoid production

A

Under HPA axis control
Activation of parvocellular neurones of paraventricular nucleus synthesise + secrete CRH and AVP into hypophyseal circulation
CRH binding to CRH receptor leads to ACTH release in systemic circulation
ACTH binds to MC2R in ZF
Activates cAMP downstream signalling pathways
Adrenal blood flow increases + ZF layer hypertrophies
ZF secretes glucocorticoid- CORTISOL

40
Q

Glucocorticoid effect

A

Modify glucose metabolism

Stimulate gluconeogenesis + antagonise insulin

41
Q

Glucocorticoids + Stress starvation

A

Causes Tissue breakdown for fuel

42
Q

Glucocorticoids + stress infection

A

Causes immunosuppression

43
Q

Glucocorticoids + Stress hypotension

A

Increases BP

44
Q

Cortisol in CV system

A

Increases transcription receptors for angiotensin II, epinephrine and norepinephrine
–> maintain BP

45
Q

Cushing’s syndrome Signs

A 
Moon face
Buffalo hump
Easy bruising
Purple Striae- obesity
Ulcers
High BP
Osteoporosis + muscle weakness
46
Q

Cushings syndrome- what is it

A

Excess cortisol

47
Q

Cushings syndrome causes

A 
Iatrogenic
Corticotroph adenoma of pituitary
Ectopic ACTH secreting neuroendocrine tumour
Cortisol secreting adrenal adenoma
Bilateral adrenal hyperplasia
48
Q

Cushings syndrome Diagnosis

A

Overnight dexamethasone suppression test
24 hour urine free cortisol
Cortisol day curve plus midnight sleeping cortisol

49
Q

Cushings Imaging

A

MRI Pituitary

CT adrenals

50
Q

Cushings treatment- pituitary

A

Transsphenoidal surgery

External beam radiotherapy

51
Q

Cushings treatment- adrenal

A

Adrenalectomy

Metyrapone

52
Q

Addisons disease

A

Primary adrenal failure- autoimmune, tuberculosis

Low cortisol

53
Q

Addisons symptoms

A

Faitgue, weakness, myalgia
Anorexia, weight loss
Hyperpigmentation

54
Q

Addisonian crisis

A

Failure to respond to stress
Low BP
Low Glucose
Low Na, High K

55
Q

Addisons diagnosis

A

Low 9am cortisol
High ACTH
Short Synacthen test

56
Q

Addisons management

A

Replacement steroid- hydrocortisone, fludrocortisone

Addisonian crisis- IV fluid resuscitation, IM hydrocortisone

57
Q

21 Hydroxylase deficiency

A

can leas to congenital adrenal hyperplasia
Salt losing
Adrenal insufficiency

58
Q

Catecholamines

A 
Adrenaline
Noradrenaline
Dopamine
Release stimulated by ACh release from preganglionic Symp Nerves
BUT basal secretion without neural imput
59
Q

Chromaffin cells

A

Adrenal medulla
Wall of urinary bladder
Neck + mediastinal symp. chain

60
Q

Phaeochromocytoma

A

Chromaffin cell tumour

Arising from within adrenal medulla

61
Q

Paraganglioma

A

Chromaffin cell tumours

Extra-adrenal tumours

62
Q

Catecholamine release

A

Haemorrhage- noradrenaline

Hypoglycaemia- adrenaline

63
Q

Fight or flight response

A

60 fold increase in catecholamine secretion

64
Q

Alpha 1 adrenoreceptor

A

Vascular and smooth muscle contraction

65
Q

Alpha 2 adrenoreceptor

A

Presynaptic
Inhibitory to noradrenaline release
Suppresses BP

66
Q

Beta 1 adrenoreceptor

A

Positive inotropic and chronotropic in the heart
Increased renin
Lipolysis

67
Q

Beta 2 adrenoreceptor

A

Bronchial, vascular, uterine smooth muscle relaxation

Glycogenolysis

68
Q

Beta 3 adrenoreceptor

A

Lipolysis
Energy expenditure
e.g. at brown fat tissue

69
Q

D1 adrenoreceptor

A

Cerebral, renal, mesenteric, coronary vasculature dilatation

70
Q

D2 adrenoreceptor

A

Presynaptic inhibition of noradrenaline and prolactin release

71
Q

Catecholamine excess

A 
Dyspnea
Headache
Hypertension
Palpitation
Nausea
Tremor
Hyperglycaemia
72
Q

PPGL tumour treatment

A

Pre-operative alpha and beta blockade - need both

Avoid opiates

73
Q

PPGL Tumour treatment- beta blockers

A

Don’t treat with only this, as will cause vasoconstriction in an already hypertensive state

Metabolism CC (29 decks)

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