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GERR Physiology > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

Describe the location and shape of adrenal glands

A
  • 2 triangular structures placed over each kidney
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2
Q

What is the adrenal gland composed of

A
  • 2 separate endocrine tissues surrounding each other
  • adrenal cortex , adrenal medulla on inside
  • derived embryologically from different tissues
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3
Q

What is the function of the adrenal cortex and adrenal medulla

A
  • Adrenal cortex: corticosteroids

- Adrenal medulla : catecholamines

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4
Q

Name the zones of the adrenal Cortex , types of hormones it secretes and what each zone secrete

A
  • zona glomerulosa : mineralcorticoids
  • zona fasiculata : glucocorticoids
  • zona reticularis : adrenal androgens
  • cortex secretes steroid lipophilic hormones that need to be transported in blood bound to plasma proteins
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5
Q

What are mineralocorticoids , give example

A
  • hormone that regulates mineral and electrolyte balance in body
  • ex: aldosterone
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6
Q

What are glucocorticoids , give example

A
  • hormone that regulates blood glucose level and protein & fat metabolism
  • ex: cortisol
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7
Q

What are adrenal androgens ,

A
  • hormones responsible for masculinization

- important in children before puberty and adult women

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8
Q

Why are adrenal androgens not important in terms of male physiology

A
  • because males already have testes that produce testosterone and responsible for masculinization
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9
Q

What is cortisol usually bound to

A
  • corticosteroid binding globulin and albumin
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10
Q

What is aldosterone usually bound to

A
  • albumin
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11
Q

what is androstenedione usually bound to

A
  • albumin
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12
Q

Where are mineralocorticoids formed from and what stimulates it’s secretion

A
  • cholesterol

- conversion of cholesterol to second step of mineralocorticoid pathway is influenced by ACTH

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13
Q

Where are the receptors of steroid hormones located

A
  • inside the cell
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14
Q

Describe the composition and function of the adrenal medulla

A
  • modified part of SNS
  • adrenal medulla has no axon accompanying postganglionic sympathetic neurons in it so it releases chemical transmitter directly into blood
  • releases adrenaline and noradrenaline
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15
Q

Why are chemical transmitters secreted in adrenal medulla called hormones

A
  • because they are released into the blood and not transported by axons
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16
Q

What stimulates cortisol secretion

A
  • physical stress ( ex: exercise )
  • emotional
  • chemical ( hypoglycaemia )
  • extreme temperature
  • diurnal rythme for cortisol secretion
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17
Q

Describe regulation of glucocorticoids secretion

A
  • stress acts on hypothalamus to release CRH , which acts on anterior pituitary to release ACTH
  • ACTH travels in blood to zona faciculata to stimulate glucocorticoids secretions ( cortisol )
  • cortisol acts as negative feedback for ACTH and CRH secretion
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18
Q

What is the diurnal rhythm for cortisol ( same as ACTH )

A
  • low levels of ACTH at night time

- and high levels before we get up in morning

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19
Q

Why are random cortisol measurements not helpful

A
  • because cortisol follows the awake sleep diurnal rhythm

- could be reversed with people who work night shifts

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20
Q

How is cortisol measured , what would you see with normal cortisol levels

A
  • in urine or saliva
  • 85% of cortisol will be bound to transcortin in blood
  • transcortin almost fully saturated
  • free cortisol levels low
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21
Q

What would you find with high cortisol levels (3)

A
  • transcortin quickly saturated
  • greatly increased free cortisol
  • Urinary free cortisol high ( UFC)
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22
Q

Actions of glucocorticoids ( in the 4 areas )

A
  • muscle : break down protein in muscle tissue to amino acids = converted to glucose
  • liver : gluconeogensis & glycogenesis ( only anabolic action )
  • Fat cells : free fatty acid mobilization through lipolysis
  • immune system : suppressed - anti-inflammatory
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23
Q

Give example conditions where glucocorticoids are given

A
  • rheumatoid arthritis : to alleviate inflammation

- helps prevent organ rejection after transplant

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24
Q

Cortisol’s role to adaptation to stress

A
  • promotes supply of glucose to tissue ( muscle & fat break down )
  • permissive hormone : affects counter-regulatory hormones which counter insulin ( glucagon , adrenaline , GTH ) AND cortisol is required for expression of adrenergic & angiotensin II receptors in CVS
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25
Q

What is a permissive hormone

A
  • hormone that needs to be present for other hormones to work optimally
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26
Q

Describe cortisol’s action on the CVS

A
  • cortisol needs to be present for expression of adrenergic and angiotensin 2 receptors
  • stop hypotension , hypovaleamia
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27
Q

Causes of glucocorticoids excess ( Cushing’s syndrome ) - 5 causes

A
  • tertiary : hypothalamic tumour
  • secondary : anterior pituitary tumour
  • primary : adrenal tumour
  • ectopic tumour ( outside of hypothalamus , pituitary , adrenal gland )
  • iatrogenic Cushing’s syndrome : excessive use of exogenous glucocorticoids
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28
Q

What is the difference between Cushing’s syndrome and Cushing’s disease

A
  • Cushing’s syndrome is anything that causes an excess of glucocorticoids
  • Cushing’s disease is when an anterior pituitary tumour causes excess glucocorticoids
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29
Q

What would a patient with Cushing’s disease look like

A
  • deposition of adipose tissue in face
  • warm : pink cheeks
  • deposition of fat in abdominal region & stretch marks
  • very thin limbs
  • bruising of skin : skin and walls of blood vessels begin to thin due to excess cortisol
  • cervical fat pad : fat is mobilized to centre of body
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30
Q

Effects of Cushing’s syndrome on carbohydrate metabolism

A
  • hyperglycaemia : increased blood glucose levels

- adrenal diabetes

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31
Q

What can cause flushed look on patient with Cushing’s syndrome

A
  • cortisol binds with mineralocorticoids, so excess cortisol will increase blood pressure
32
Q

Effects of Cushing’s syndrome on protein metabolism

A
  • muscle weakness
  • osteoporosis
  • delayed healing of fractures and wounds
  • cortisol reduces Ca uptake from GI tract and increases absorption of Ca from bone which is then excreted
33
Q

Cushing’s syndrome Symptom mnemonic

A

C: central obesity . collagen fibre weakness, comedones
U : urinary free cortisol and glucose
S: striae, suppressed immunity
H : hypercortisolism, hypertension, hyperglycaemia , Hypercholesterolaemia
I: iatrogenic
N: iatrogenic
G: glucose intolerance , growth retardation

34
Q

In an adult patient with diagnosed Cushing’s disease what treatment is preferred ?

a: bilateral adrenalectomy b: unilateral adrenalectomy c: resection of pituitary tumour

A

C: resection of pituitary tumour

35
Q

What is the RAAS and what does it do

A
  • renin angiotensin aldosterone system
  • regulator of blood volume and systemic vascular resistance
  • important for long term regulation of blood pressure
  • composed of renin , angiotensin I and angiotensin II
36
Q

What are the two stimulants of aldosterone

A
  • increased potassium in ECF which directly stimulates adrenal cortex
  • angiotensin II directly stimulates adrenal cortes
37
Q

What stimulates angiotensin II

A
  • dehydration
  • sodium deficiency
  • decrease in blood volume
38
Q

Why is angiotensin II stimulated by decreased blood volume

A
  • decrease BV decreases BP decreases renal blood flow
  • juxtaglomerular cells in kidney release renin
  • Renin converts angiotensinogen to Angiotensin I
  • angiotensin I converts to angiotensin II in lung
39
Q

What is the function of aldosterone

A
  • works in kidneys to increase sodium reabsorption
  • increase potassium and H + excretion in urine
  • water reabsorbed with sodium which increases blood volume and blood pressure
40
Q

What is the role of ACTH in aldosterone secretion

A
  • not a big role

- angiotensin II is the stimulant not ACTH

41
Q

Aldosterone deficiency consequences

A
  • increased loss of sodium and water in urine = dehydration , plasma depletion , hypotension
  • renal retention of potassium = hyperkalaemia = increase cardiac excitability = V fib
  • renal retentions of H+ results in acidosis
42
Q

Why is aldosterone deficiency serious

A
  • acute aldosterone deficiency can lead to death in 2 days
43
Q

What are the two forms of hypoaldosteronism and what happens each

A
  • primary : adrenal insufficiency - problem with synthesis of enzymes needed to synthesize aldosterone
  • secondary : renal sufficiency - renal failure results in no renin production
44
Q

What is Conn’s syndrome

A
  • primary hyperaldosteronism
  • due to adrenal adenoma
  • very rare condition
  • excess secretion of aldosterone results in hypertension , hyperkalemia , hypervolemia and alkalosis
45
Q

What is the difference between primary and hyperaldosteronism

A
  • renin levels in primary are low but high in secondary due to overactivity of RAAS
46
Q

What is Addison’s disease

A
  • primary adrenocortical insufficiency

- destruction of both adrenal cortices ( usually autoimmune )

47
Q

What happens if one adrenal cortex is destroyed

A
  • other adrenal cortex will hypertrophy , hyperplasia will take place
  • it will take over secretion of cortisol
48
Q

What are the causes of Addison’s disease

A
  • usually autoimmune disorder

- can be haemorrhage , TB , malignancy

49
Q

What is the acute drop of adrenocorticol hormones called

A
  • addisonian’s crisis / acute adrenal crisis
50
Q

What are the results of a lack of adrenal androgens

A
  • changes in mood
  • loss of libido
  • effects females not males
51
Q

What is secondary adrenocorticol insufficiency what can cause it ( 2 causes )

A
  • abnormality in pituitary or hypothalamus that results in insufficient ACTH
  • sudden withdrawal of glucocorticoid drugs or failure to increase glucocorticoids levels during stress
52
Q

How does Addison’s disease present

A
  • bronze hyperpigmentation of skin
  • changes in body hair distribution
  • weakness
  • weight loss
  • GI disturbances
  • hypoglycaemia
  • postural hypotension
  • brown buccal pigmentation
53
Q

How does addisonian’s disease present

A
  • profound fatigue
  • dehydration
  • vascular collapse = decrease BP
  • renal shut down
  • decrease serum NA
  • increase serum K
54
Q

What combination of biochemical disturbances is the classical finding in a patient with untreated Addison’s disease

A
  • Hyponatraemia , hyperkalaemia , hypoglycaemia
55
Q

What causes hyperpigmentation in Addison’s disease

A
  • adrenal failure = adrenal hormone levels decrease = reduced negative feedback = ACTH levels increase = melanocytes stimulation = increase in MSH
56
Q

What neurotransmitters are located at preganglionic nerves of parasympathetic

A
  • ACH ( acetylcholine)
57
Q

What neurotransmitters are located at post ganglionic nerves of sympathetic

A
  • noradrenaline
58
Q

Compare the effects of catecholamines and SNS

A
  • exerts effect in all cells vs some organs / tissue having no innervation
  • delayed in beginning vs immediate effects
  • prolonged effects vs rapid decay
  • only generalized effects vs localized effects
59
Q

What secretes catecholamines

A
  • chromaffin cells in adrenaline medulla

- catecholamines derived from amino acid tyrosine

60
Q

What are the 3 catecholamines

A
  • Dopamine
  • Adrenaline
  • Noradrenaline
61
Q

What catecholamines does the adrenal medulla produce the most

A
  • adrenaline
62
Q

What stimulates catecholamines secretion and what are the results

A
  • ACH binding to chromaffin cell and depolarizing it

- chromaffin granules fuse with plasma membrane and exocytoze into blood

63
Q

Actions of adrenaline and noradrenaline ( fight or flight )

A
  • increase heart rate
  • increase BP
  • bronchioles dilation
  • increase blood glucose
  • decrease digestive activity
64
Q

What triggers adrenaline and noradrenaline secretion and give examples

A
  • stress

- ex: illness , exercise, hypoxia , cold

65
Q

Describe the metabolism of Catecholamines

A
  • inactivated rapidly ( many ways they can be inactivated)

- ex: reuptaked by cells, filtered into urine , metabolized by monoamine oxidase

66
Q

MOA of catecholamines and their two type of receptors

A
  • adrenergic receptor mediated
  • noradrenaline binds with more affinity to alpha adrenergic receptors
  • adrenaline binds with more affinity to beta adrenergic recptors
  • effects depend on type and number of receptors in target tissue
67
Q

Where are the alpha adrenergic receptors located

A
  • alpha 1 : vascular

- alpha 2 : presynaptic

68
Q

Where are the beta adrenergic receptors located

A
  • beta 1 : heart
  • beta 2 : smooth muscle
  • beta 3 : fat
69
Q

Which adrenergic receptor only binds to adrenaline

A
  • beta 2
70
Q

What has a greater physiological action in terms of cardiac stimulation

A
  • adrenaline ( beta 1 )
71
Q

What has a greater physiological action in terms of constriction of blood vessels

A
  • noradrenaline ( alpha 1 )
72
Q

What has a greater physiological action in terms of increasing metabolism

A
  • adrenaline ( beta 3 )
73
Q

Mechanism of adrenergic receptor signal transduction (for each receptor type )

A
  • beta 1 & 2 : increases cAMP
  • alpha 1 : increases IP3 by phospholipase C pathway
  • alpha 2 : decrease cAMP
74
Q

Describe Adrenomedullary dysfunction

A
  • only one disorder can cause this : catecholamine secreting tumour ( pheochromocytoma )
  • very rare
75
Q

Symptoms of Pheochromocytoma

A
  • hypertension
  • headache
  • sweating
  • palpitations
  • chest pain
  • anxiety
  • glucose intolerance
  • increased metabolic rate
76
Q

What endocrine disorders cause hypertension ( 4 )

A
  • increased aldosterone , cortisol
  • increased thyroid hormone results in increased SBP
  • pheochromocytoma
77
Q

In what cell types do pheochromocytomas originate

A
  • chromaffin cells

GERR Physiology (18 decks)

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