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GERR > Adrenal Glands > Flashcards

Adrenal Glands Flashcards

1
Q

What are the two layers of the adrenal gland and what hormones do they produce?

A

Adrenal cortex - corticosteroids

adrenal medulla - catecholamines

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2
Q

Where are the adrenal glands located?

A

Above each kidney

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3
Q

What are the three layers of the adrenal cortex and what hormone do they secrete?

A

Zona glomerulosa - mineralocorticoids
zona fasciculata - glucocorticoids
zona reticularis - adrenal androgens

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4
Q

What are examples of each of the hormones secreted by the layers of adrenal cortex and what is function of each?

A

mineralocorticoids regulate mineral balance e.g. aldosterone
glucocorticoids regulate blood glucose e.g. cortisol
adrenal androgens responsible for masculisation e.g. catecholamines

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5
Q

What proteins are used to transport each hormone secreted by adrenal cortex?

A

cortisol primarily corticosteroid binding globulins
aldosterone primarily albumin
androgens primarily albumin

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6
Q

What are all corticosteroids derived from?

A

steroid hormones so cholesterol

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7
Q

What is the rate limiting step in synthesis of steroid hormones from cholesterol

A
  • Conversion of cholesterol to pregnenolone using ACTH (adrenocorticotrophic hormone) enzyme
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8
Q

What enzyme is essential in aldosterone synthesis?

A

Ang II activates aldosterone synthase which is needed in aldosterone synthesis

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9
Q

Where would you usually find adrenal steroid hormone receptors and what effect do they cause?

A

usually intracellular, readily diffuse across membrane

have genomic effect (receptor complex binds to hormone response element)

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10
Q

Where would you usually find catecholamine hormone receptors and what effect would they cause?

A

Extracellular (G-protein linked)

use cAMP as 2nd messenger and activate kinase which brings about response in target cell

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11
Q

How is hormone release from adrenal medulla regulated and what hormones are released?

A
  • Electrical signal from spinal cord travels through pre-ganglionic neurone to chromaffin cells in adrenal medulla where cell body of post-ganglionic present but not axon
  • chemical messenger secreted directly into circulation
  • usually adrenaline but can secrete noradrenaline
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12
Q

What are the triggers for cortisol secretion?

A

Physical stress - trauma or injury e.g. surgery or exercise
Emotional stress - stressful live events e.g. tests
Chemical stress - hypoglycaemia
Extreme temperature changes

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13
Q

In what way is cortisol secretion triggered?

A
  • Stress stimuli causes hypothalamic neurones to release CRH (corticotrophin hormone)
  • CRH stimulates corticotropes on anterior pituitary to release ACTH
  • ACTH travels in blood to adrenal cortex where triggers zone fasciculata to increase cortisol secretion
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14
Q

What are the negative feedback loops to stop cortisol secretion?

A

Long: ACTH and CRH secretion switched off by cortisol
short: ACTH switches off CRH

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15
Q

Why would you expect different cortisol readings throughout the day?

A

Cortisol follows diurnal rhythm

ACTH and cortisol highest just before you wake up and follow until reach lowest at night

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16
Q

What protein carries cortisol?

A

transcortin

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17
Q

How are cortisol levels tested for?

A
  • test urine or saliva over 24h period

- free (unbound) cortisol will appear in high levels in urine or saliva if excess cortisol as transcortin saturated

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18
Q

What are the actions of glucocorticoids?

A

1) muscle - net loss of amino acids so can be converted to glucose
2) Liver - amino acids and glycerol converted to glucose (gluconeogenesis) + when high glucose converted to glycogen (glycogenesis)
3) Fat - lipolysis breakdown of fat into free fatty acids
4) immune system repressed

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19
Q

What are the roles of cortisol in adaption to stress?

A

1) Promotes rapid supply of glucose to tissues

2) needs to be present for other hormones to work optimally

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20
Q

Which hormones require cortisol to work?

A

1) Insulin counter-regulatory hormones = glucagon, adrenaline and growth hormone
2) expression of adrenergic and angiotensin II receptors in CV system

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21
Q

What are the effects of the regulatory hormones on glucose metabolism?

A

glucagon inc: glycogenolysis and gluconeogenesis dec: glycogen storage
Adrenaline inc: glycogenolysis and gluconeogenesis dec: glucose oxidation, glycogen storage and muscle/adipose glucose uptake
Growth Hormone inc: gluconeogenesis dec: muscle/adipose glucose uptake, glycogen storage and glucose oxidation

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22
Q

What are the effects of Insulin on glucose metabolism?

A

decrease gluconeogenesis and glycogenolysis

increase glycogen storage, glucose oxidation and muscle/adipose tissue glucose uptake

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23
Q

What are the effects of cortisol on glucose metabolism?

A

increase gluconeogenesis and glycogen storage

decrease muscle/adipose tissue uptake of glucose and oxidation of glucose

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24
Q

What are the causes of glucocorticoid excess (Cushing syndrome)?

A

1) hypothalamic tumour
2) anterior pituitary tumour
3) adrenal tumour
4) Ectopic tumour usually lungs
5) Iatrogenic Cushing syndrome

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25
Q

What is Cushing disease?

A

Cushing syndrome when caused by anterior pituitary tumour

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26
Q

What do primary and secondary hyper secretion mean?

A

Primary: adrenal cortex tumour so excessive cortisol secretion
Secondary: hypothalamic or anterior pituitary tumour so excessive CRH or ACTH release causing excessive cortisol release

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27
Q

What are the common symptoms of Cushing Syndrome?

A
  • Abnormal fat deposition: fat in face and abdomen very thin elsewhere
  • round face and red cheeks due to warmth
  • warm
  • Stretch marks (abdominal striae)
  • easy bruising (due to thinning of blood vessels)
  • easy to get infections as immune system suppressed
28
Q

What effects does Cushing syndrome have on metabolism?

A

Carbohydrate:
Hyperglycaemia
hypertension as cortisol bids to aldosterone receptors
Protein:
causing protein shortage, striae, easy bruising and thinning of skin

29
Q

Why can you sometimes get osteoporosis when taking glucocorticoids?

A

impacts calcium metabolism:

  • reduces calcium uptake form GI
  • increases reabsorption of calcium from bone
  • increases excretion of calcium
30
Q

What is the Cushing mnemonic?

A

C - Central obesity, Collagen fiber weakness and comedones (acne)
U - Urinary free cortisol and glucose increase
S - Striae and surpassed immunity
H - hypercortisolism, hyperglycaemia, hypertension and hypercholesterolamia
I - iatrogenic (causes)
N - noniatrogenic (causes)
G - glucose intolerance and growth retardations

31
Q

What does the RAAS system regulate?

A

Blood pressure using blood volume and systemic vascular resistance

32
Q

What are the two main stimuli of RAAS?

A

1) increased potassium concentration in ECF which directly stimulates aldosterone secretion
2) Ang II which directly stimulates adrenal cortex to secrete aldosterone

33
Q

What stimulates Ang II secretion?

A

1) dehydration
2) sodium deficiency
3) dec in blood volume (e.g. in haemorrhage)

34
Q

Why does decrease in blood volume increase Ang II secretion?

A
  • Decrease in Blood volume decreases BP which decreases renal plasma flow and in response juxtaglomerular cells of kidneys produce renin
  • Renin converts Angiotensinogen in liver to Angiotensin I
  • Angiotensin converting enzyme located in blood capillaries in lungs converts Ang I to Ang II
35
Q

How does aldosterone decrease BP?

A
  • Aldosterone works in kidneys to increase sodium and water reabsorption and in return get increased secretion of potassium and hydrogen ions
  • When sodium reabsorbed, water reabsorbed as well which increases blood volume and so blood pressure
36
Q

What does aldosterone do in the cell of distal nephron?

A
  • Receptor mainly in cytoplasm of cell
  • Causes genomic effects increasing protein production and so increases ion channels (in particular sodium channels) to:
    1) increase sodium into blood
    2) increase potassium excretion
    3) increase Blood volume
37
Q

What can be taken as a replacement for aldosterone?

A

fludrocortisone

38
Q

What can be taken as a replacement for Cortisol?

A

hydrocortisone

39
Q

In what three ways can aldosterone deficiency be fatal?

A

1) increased loss of sodium and water means dehydration and hypotension which can cause circulatory shock
2) renal retention of potassium = hyperkalaemia and so cardiac excitability and ventricular fibrillation
3) renal retention of hydrogen and cause metabolic acidosis

40
Q

What is primary hyper and hypo - aldosteronism?

A

Hyper - also called Conns syndrome, caused by adrenal tumour

Hypo - caused by adrenal insufficiency (usually enzymes needed to manufacture aldosterone)

41
Q

What is secondary hyper and hypo - aldosteronism?

A

Hyper - caused by overactivity of RAAS system usually secondary to other problems
Hypo - caused by renal insufficiency e.g. CKD so not enough renin

42
Q

What does Conns syndrome cause?

A
  • Hypertension
  • hypokalaemia
  • hypervolemia
  • metabolic alkalosis
43
Q

Pathology of primary hyperaldosteronism?

A
  • tumour secretes aldosterone
  • aldosterone increases sodium retention and increases ECF
  • increases BP
  • plasma volume expansion decreases renin
  • increase potassium loss and hydrogen loss
44
Q

What is Addisons disease?

A
  • Primary adrenocortical insufficiency

- Both adrenal cortices must be destroyed

45
Q

What causes Addisons disease?

A

autoantibodies attach adrenal cortices or can get destruction due to haemorrhage

46
Q

What is Addisonian crisis and what can happen?

A

rapid drop in corticoids usually due to haemorrhage
causes:
- Fatigue
- Dehydration
- vascular collapse
- renal shut down so decline in sodium and increase in potassium

47
Q

What are clinical implications of Addisons disease?

A

Drop in glucocorticoids:

  • hypoglycaemia
  • reduction in fat and protein metabolism
  • weight loss
  • poor exercise tolerance
  • poor stress tolerance

Drop in mineralocorticoids:

  • less sodium and water and more potassium and hydrogen
  • hypovolaemia
  • decline in CO causing circulatory shock
48
Q

What can cause secondary adrenocortical insufficiency?

A

1) pituitary/hypothalamic abnormality resting in insufficient ACTH
2) withdrawal of glucocorticoid drugs
3) failure to increase glucocorticoids during stress

49
Q

Symptoms of Addisons disease?

A
  • Hypoglycaemia
  • postural hypotension
  • weight loss
  • GI disturbances
  • Weakness
  • Changes in distribution of body hair
  • Bronze pigmentation of skin especially in palmar creases, nails and gums
50
Q

Why is there increased bronze pigmentation?

A
  • Adrenal failure means decrease in adrenal hormones
  • increase in ACTH in response
  • ACTH increase alpha-MSH
  • which stimulates melanocytes
51
Q

What neurotransmitter are used in the sympathetic and parasympathetic pre and post ganglionic nerves?

A

Sympathetic and parasympathetic pre-ganglionic = AcH released which binds to nicotinic receptors
Post-ganglionic sympathetic releases noradrenaline
parasympathetic releases AcH

52
Q

What are the actions of the sympathetic nervous system?

A
  • Dilate pupils
  • inhibits salivation
  • relaxes bronchi
  • increase HR
  • inhibits digestive activity
  • stimulate glucose release from liver
  • secretes adrenaline and noradrenaline from kidney
  • relaxes bladder
  • contracts rectum
53
Q

What are the actions of the parasympathetic nervous system?

A
  • constricts pupils
  • stimulates salivation
  • inhibits heart
  • constricts bronchi
  • stimulates digestive activity
  • stimulates gallbladder
  • contracts bladder
  • relaxes rectum
54
Q

What is the intracellular actions of catecholamines?

A
  • receptors found on outside of cell
  • G-protein linked
  • cAMP secondary messenger
  • non-genomic effect
55
Q

How are catecholamines released from chromaffin cells?

A
  • ACh binds to nicotinic receptor on chromaffin cell

- cell is depolarised which triggers release of adrenaline/noradrenaline via granules

56
Q

How are catecholamines signalled to be released?

A
  • hypothalamus sends an electrical signal via sympathetic nervous system
  • Adrenal medulla (chromaffin cells) receive signal and secrete catecholamines
57
Q

Which adrenergic receptors do noradrenaline and adrenaline have higher affinity for?

A 
adrenaline = Beta 
noradrenaline = Alpha
58
Q

How are catecholamines inactivated?

A

1) reuptake by extra-neuronal sites
2) metabolised by monoamine oxidase or catechol-O-methyltransferase
3) conjugated with glucoronide in liver
4) direct filtration into urine

59
Q

Where are adrenaline or noradrenaline more effective?

A

adrenaline better at cardiac stimulation and increasing metabolism
noradrenaline better at constriction of blood vessels

60
Q

Where would you primarily find each alpha receptor and where would you find each beta receptor?

A 
Alpha 1 = vascular 
Alpha 2 = presynaptic 
Beta 1 = heart
Beta 2 = smooth muscle
Beta 3 = fat
61
Q

What is the mechanism of action of adrenergic receptors?

A

Beta 1 and 2 increase cAMP
Alpha 2 usually inhibits cAMP
alpha one increases Inositol trisphosphate and diacylglycerol

62
Q

What is the name of the catecholamine secreting tumour?

A

Pheochromocytoma

63
Q

What are the symptoms of a catecholamine secreting tumour?

A
  • Hypertension
  • Sweating
  • Headaches
  • palpitations
  • chest pains
  • glucose intolerance
  • increased metabolic rate
  • anxiety
64
Q

What endocrine disorders can cause hypertension?

A

increased catecholamines, aldosterone and cortisol

increased thyroid hormone can also cause increased systolic but not diastolic

65
Q

Why will hypothalamus or anterior pituitary problems have a large impact on cortisol but not aldosterone?

A

Cortisol has only one way in which it can be synthesised whereas aldosterone is also synthesised though Ang II

GERR (49 decks)

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