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Physiology - Endocrine > Adrenal Hormones > Flashcards

Adrenal Hormones Flashcards

1
Q

Where are the corticosteroids synthesised?

A

Cortex

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2
Q

where are the adrenal glands located

A

Loosely embedded above kidney

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3
Q

Where are the the catecholamines synthesised

A

Medulla

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4
Q

What is produced in each section of the cortex

A

zona glomerulosa - mineralocortioids
zona fasiculata- glucocorticoids
zona reticularis - adrenal androgens

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5
Q

What is the binding make up of cortisol

A

85% bound to corticosteroid - binding globulin
10% albumin
5% unbound

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6
Q

What is aldosterone bound to

A

60% bound to primary albumin

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7
Q

Role of glucocorticoids

A

Regulation of cortisol secretion

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8
Q

Stimulus of glucorticoids

A

Primary stimulus

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9
Q

Where is cortisol measured

A

Urine

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10
Q

what will normal coritsol show as

A

Transcortin almost fully saturated

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11
Q

What will high cortisol look like in the urine

A

Free cortisol - high

urinary free cortisol high

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12
Q

Actions of glucocorticoids

A

Muscle - net loss of amino acids
Fat cells - lipolysis + glucose sparing effects
Immune system and inflammation will be supressed
Liver - gluconeogenesis + glycogenesis

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13
Q

What does cortisol directly do?

A

Directly promotes rapid supply of glucose to tissue

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14
Q

How is cortisol a permissive hormone

A

Affects the other counter-regulatory hormones

required for expression of adrenergic and angiotensin II receptors in CVS

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15
Q

What does an XS of glucocorticoid cause

A

Hypothalamic tumour
ant pituary tumour (60-70%) cases - cushings disease
adrenal tumour
ectopic tumour
latrogenic cushings syndrome - exogenous glucocorticoids

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16
Q

What are the effects of glucocorticoids on carbohydrate metabolism?

A

Hyperglycaemia- increase in blood glucose levels (twice normal size)
“adrenal diabetes”

17
Q

What are the effects of glucocorticoids on protein metabolism?

A 
Protein shortage- muscle weakness
Stretch lines 
easy bruising 
thinning of skin  - inhibition of collagen 
osteoporosis - pathological fratures 
delayed healing 
suppression of immune system
18
Q

Features of CUSHINGs disease

A

Central obesity, Collagen fibre weakness, Comedones (acne)
Urinary free cortisol and glucose increase
Striae, Supressed immunity
Hypercortisolism, Hypertension Hyperglycaemia, Hypercholesterolaemia
Iatrogenic (admin of corticosteroids
Noniatrogenic (Neoplasms)
Glucose intolerance, Growth retardation

19
Q

Role of mineralocorticoids

A

regulation of aldosterone secretion

20
Q

What is the principle stimulus for secretion of aldosterone

A

Angiotensin II - principle stimulus for secretion of aldosterone

21
Q

What is the action of aldosterone

A

Increase in Na+/H20 absorption
increase in K+/H+ secretion
increase in blood volume/BP

22
Q

What does a deficiency in aldosterone lead to?

A
  • Increase loss of Na/H20 in urine- dehrydration, plasma depletion + hypotension
  • Increased renal retention of K+ and hyperkalaemia, caridac availabilty and can cause ventricular fibrilation
  • Renal retention of H+ producing a metabolic acidosis
23
Q

Cause of primary hyperaldosteronism

A

Adrenal adenoma

24
Q

Cause of secondary hyperaldosteronism

A

Overactivity of renin-angiotensin system

25
Q

What is primary adrenocortical insufficiency also known as? and why does is comes about

A

Addisons disease

destruction of both adrenal cortices

26
Q

what are features of lack of glucocorticoids

A 
Hypoglycaemia 
reduction of fat and protein metabolism 
loss of weight 
poor excersize tolerance 
poor stress tolerance
27
Q

Features of a lack of mineralocorticoids

A

Decrease in Na+. increase K+ and H+
hypovolaemia
decrease in cardiac output: circulatory collapse- shock - DEATH

28
Q

When would secondary adrenocortical insufficiency occur?

A

Lack of adrenocortical insufficiency

29
Q

What are features of secondary adrenocortical insufficiency?

A

Pit/hypothalamic abonormalities results in insufficient ACTH
sudden withdrawal of glucocorticoids drugs
failure to increase glucocorticoids during stress

30
Q

Features of adrenal stimulation

A

Exerts its effects in all cells
delay in the beginning
prolonged effects
only generalised

31
Q

What are the features of sympathetic activation

A

some organs tissue have no innervation
immediate effects
rapid decay when activation stops
localised effects

32
Q

Features of the metabolism of catecholamines

A

Reuptake by extraneuronal sites
Metabolised by monoamine oxidase or catechol- ) methyl transferase
Conjungation with glucuronide in the liver
Direct filtration into urine

33
Q

What is the mode of action catecholamine

A

Adrenergic receptors

peripheral effects depend upon type of ration of receptors in target tissue

Physiology - Endocrine (3 decks)

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