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Endocrinology > Adrenal Tutorial > Flashcards

Adrenal Tutorial Flashcards

1
Q

from top to bottom list the layers of the adrenal glands

A 
connective tissue
cortex:
zona glomerulosa
zona fasciculata 
zonareticularis =bottom of cortex
medulla
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2
Q

what controls the zona glomerulosa

A

renin-angiotensin system

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3
Q

what controls the zona fasciculata

A

ACTH

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4
Q

what controls the zona reticularis

A

ACTH

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5
Q

what controls the medulla

A

sympathetic NS control

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6
Q

what is produced by the zona glomerulosa

A

mineralocorticoid (aldosterone)

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7
Q

what is produced by the zona fasciculata

A

glucocorticoids- cortisol, cortisone, corticosterone

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8
Q

what is produced by the zona reticularis

A

sex hormones - dehydroepiandrosterone (DHEA)

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9
Q

what is produced by the medulla

A

catecholamines- adrenaline, nor-adrenaline

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10
Q

what is all steroid hormone derived from

A

cholesterol

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11
Q

what cells in the medulla make the catecholamines

A

chromaffin cells

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12
Q

what do the chromaffin cells make the catecholamines from

A

tyrosine

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13
Q

do catecholamines have a long or short half life

A

short

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14
Q

what stimulates the synthesis and release of aldosterone

A

angiotensin II

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15
Q

what does aldosterone do

A

increased NaCl retention and reabsorbtion within the kidney
due to osmosis water is also reabsorbed
blood volume and pressure in increased
causes loss of potassium in urine due to Na+ K +ATP ase

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16
Q

how else does angiotension II cause water reabsorption

A

working with ADH

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17
Q

describe the renin angiotensin cycle

A

(decreased NaCl, ECF volume, blood pressure)

increased renin + angiotensin = angiotensin 1 + ACE = angiotensin II acts on zona glomerulosa to make aldosterone

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18
Q

what is conns syndrome

A

where a tumour present in the cells of the zona glomerulosa secretes excess amounts of aldosterone

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19
Q

what is the biochem of conns

A

increased NaCl
increased H2O
decreased K+

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20
Q

what are the symptoms of conns

A

hypertension

hypokalaemia

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21
Q

does adrenal hyperplasia affect one or both adrenal glands usually

A

bilaterally

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22
Q

are adrenal hyperplasia and conns primary or secondary aldosteronism

A

primary

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23
Q

what are the symptoms of adrenal hyperplasia

A

sames as conns- hypertension and hypokalaemia

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24
Q

how do you diagnose primary aldosteronism

A

aldosterone to renin ratio
if ratio is above 750 then carry out a saline suppression test - if aldosterone doesnt drop by 50% then primary aldosteronism

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25
Q

describe a saline suppression test

A

2 litres of saline is administered to patient over the course of 4 hours, if aldosterone levels fail to decrease by 50% then will confirm primary aldosteronism

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26
Q

what is the best treatment for unilateral primary aldosteronism

A

unilateral conns

surgery best for decreasing blood pressure

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27
Q

what is the best treatment for bilateral primary aldosteronism

A

aldosterone receptor antagonist e.g. spirinolactone- reduces reabsorption of NaCl and H20

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28
Q

what are the side effects of spironolactone

A

nausea, rashes, gynaecomastia

can use eplerenone instead

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29
Q

how do angiotensin II and ACTH stimulate the adrenal glands to produce hormones

A

cause increase growth of the cells stimulating them to produce hormones

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30
Q

what are the functions of glucocorticoids (esp cortisol)

A

maintain plasma glucose levels
when stressed provide fuel from carbs, fats and proteins (increases lipolysis leading to increased plasma fatty acids. increase proteolysis causing increased plasma amino acids)
increases responsiveness of adrenoreceptors to adrenaline- prevents shock
anti inflammatory and immunosuppressive role
increased hepatic gluconeogenesis and decreased glucose uptake in all tissues expect the brain (both cause increased plasma glucose)

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31
Q

what are the signs of cortisol excess

A 
muscle wasting 
central obesity 
cardiac output and blood flow increased (hypertension) 
plethoric 'moon' face (due to fat redistribution)
conjunctival oedema
cataracts 
easy bruising 
skin infections 
poor wound healing 
buffalo hump 
proximal myopathy, proximal muscle wasting (increased proteolysis)
thin skin 
purpura 
red/ purple striae 
back pain (muscle weakness and central obesity)
polydipsia and polyuria
bone pain
euphoria
severe depression
psychosis 
insomnia
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32
Q

what effect does ecess cortisol have on the immune system

A

decreased macrophage and cytokine activity

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33
Q

how does cortisol excess affect bone

A

reduced osteoblast activity and decreased calcium absorption- bone pain, kyphosis, osteoporosis

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34
Q

how does excess cortisol effect the skin

A

decreased collagen formation

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35
Q

describe the regulation of cortisol

A

(stress illness / diurnal rhythm) hypothalamus secretes corticotrophin releasing hormone- ant pituitary - ACTH - adrenals - cortisol (neg feeback on ant pituitary and hypothalamus)

36
Q

what are the types of cushings

A

ACTH dependent or independent

37
Q

what is the most common cause of cushings

A

ACTH dependent due to adenoma in the pituitary gland that produces ACTH

38
Q

what are the types of ACTH dependent cushings

A

adenoma in pituitary gland that produces ACTH

Ectopic cancers that secrete ACTH - lung, thymus, pancreas

39
Q

what other symptoms might a pituitary tumour produce

A

headaches and visual field impairment

40
Q

what are the types of ACTH independent cushings

A

adrenal adenoma (most common)
adrenal carcinoma
nodular hyperplasia

41
Q

in ACTH independent cushings is ACTH high or low

A

low

42
Q

why is there oversection of sex hormones in cushings

A

as the zona reticularis is also stimulated by ACTH

43
Q

what is seen in hypersecretion of DHEA

A

women: acne, amenorrhea, frontal balding, facial hair growth
men: lack of libido and impotence

44
Q

what is the definitive test for cushings

A

low dose dexamethasone test

45
Q

what is dexamethasone

A

very potent glucocorticoid

46
Q

what result in a LLDT would show no cushings

A

<50 nmol/litre

47
Q

what result in a LLDT would show cushings

A

> 100 nmol/litre suspicious of cushings

48
Q

what can determine between pituitary, adrenal and ectopic cushings

A

high dose dexamethasone test

49
Q

how does a HDDT distinguish in cushings

A

pituitary- suppressed by 50%

adrenal and ectopic -not supressed

50
Q

what are the ACTH levels like in pituitary, adrenal and ectopic cushings

A

pituitary- <300
adrenal- <1
ectopic- >300

51
Q

what does untreated cushing lead to

A

death due to complications from hypertension, diabetes mellitus, cardiovascular disease

52
Q

what is the medical therapy for cushings

A

metyrapone- a 11beta- hydroxylase blocker that stops the synthesis of cortisol

ketoconazole works in same way and is synergistic with metyrapone

53
Q

why do you need to reduce cortisol levels before surgery

A

as immune response still impaired

54
Q

how are anterior pituitary tumour usually removed

A

trans-sphenoidal removal

55
Q

what ca be done if surgery doesnt help cushings (pituitary)

A

radiotherapy

56
Q

what is the surgical treatment for adrenal cushings

A

bilateral adrenalectomy

57
Q

what cells make up the medulla of the adrenal glands

A

chromaffin cells

58
Q

what controls the release of catecholamines from the medulla

A

sympathetic nervous system

59
Q

what is the effect of adrenaline

A

increases rate and strength of heart, vasoconstrictor effect on peripheral vessels- increases blood pressure

vasodilation of the skeletal muscle- delivers more oxygen and glucose

60
Q

adrenaline acts on B1 receptors on the …. to have the effect of…

A

heart

increased force and rate

61
Q

adrenaline acts on alpha 1 receptors on …. to have the effect of…

A

blood vessels

vasoconstriction

62
Q

adrenaline acts on B2 receptors on …. to have the effect of…

A

skeletal muscle

vasodilation

63
Q

adrenaline acts on alpha 2 receptors on the …. to have the effect of…

A

islet beta cells

decreased insulin secretion

64
Q

how does adrenaline affect metabolism and via what receptors

A

alpha and beta 1

increases gluconeogenesis and glycogenolysis

65
Q

what are the symptoms of hypersecretion of adrenaline

A

classic triad: HPX, sweating, headaches

arrhythmias 
tachycardia/ bradycardia 
pallor 
excessive flushing 
postural hypertension
anxiety 
polydipsia
polyuria
constipation 
paralytic ileus of the bowel
66
Q

what is a phaeochromocytoma

A

rare catecholamine secreting tumour that arises from sympathetic paraganglia cells

67
Q

what are paraganglia cells

A

collections of adrenaline secreting chromaffin cells

68
Q

where are phaeochromocytoma found

A

medulla of adrenals or sympathic chain

69
Q

what are paragangliomas

A

phaeochromocytomas found at the oartic bifurcation

70
Q

what is the 10% tumour

A 
10% extra adrenal 
10% malignant 
10% bilateral 
10% in children 
10% hereditary syndrome
71
Q

what hereditary conditions are associated with phaeochromocytoma

A

MEN 2 (usually bilateral in this condition)

72
Q

what tumours do you get in MEN 2

A

thyroid, parathyroid, neuro endocrine (phaeochromocytoma)

73
Q

what can be used diagnose phaeochromocytoma

A

24hr urinary catecholamines and metabolites

CT/MRI

131 iodine MIBG (labelled with beta and gamma particles)

74
Q

what is the treatment for phaeochromocytoma

A

complete alpha and beta blockade (atenolol, phenoxybenzamine) before surgery to prevent arrhythmias and CV complications

if malignant then chemo + 131 iodine MIBG

75
Q

what can cause adrenal hypofunction

A

primary- addisons disease (automimme attack on adrenal glands)

secondary- pituitary problem, lack of ACTH

iatrogenic- steroids might cause adrenal glands to atrophy

76
Q

how does an addisonian crisis present

A

high potassium, low sodium, dehydration, low glucose, abdo pain. weakness, vomiting

77
Q

what is the treatment for an addisonian crisis

A

immediate
glucose
IV fluids
steroid replacement

78
Q

what can help distinguish primary and secondary addisons

A

increased skin pigmentation- caused by ACTH being converted to melatonin, cant be a secondary (pituitary) cause

79
Q

in addisons what causes the low sodium and high potassium

A

lack of aldosterone

80
Q

in addisons what causes the low glucose

A

lack of glucocorticoids

81
Q

what antibodies in addisons disease

A

anti-adrenal antibodies

82
Q

what can determine whether the adrenal glands are working or not

A

synACTHen test- measure cortisol produced by adrenals in response to synthetic ACTH, should be more than 500 at 30 mins

83
Q

what is congenital adrenal hyperplasia

A

where adrenal glands lack the enzymes needed for making steroids

  • can present as acute salt loss crisis or ambiguous genitalia in early childhood, or in hirsutism in late childhood/adulthood
  • treatment is steroids
84
Q

what is the hormone replacement given for adrenal insufficiency

A

hydrocortisone - replaces glucocorticoids

fludrocortisone- given to replace aldosterone (no required in all cases)

85
Q

what are the sick day rules for adrenal insufficiency and patient education points

A

if have period of illness then always double your dosage

dont suddenyl stop as this causes adrenal crisis even when well

carry identification that you are on steroids

86
Q

what would postural hypotension raise concerns of

A

adrenal insufficiency

Endocrinology (46 decks)

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