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Endocrine > Adrenal Physiology and Disorders > Flashcards

Adrenal Physiology and Disorders Flashcards

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1
Q

what are the 3 layers of the adrenal cortex from outer to inner?

A

zona glomerulosa
zona fasciculata
zona reticularis

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2
Q

what is secreted by each layer of the adrenal cortex?

A

zona glomerulosa = mineralocorticoids (e.g aldosterone)
zona fasciculata = glucocorticoids (e.g cortisol)
zona reticularis = adrenal androgens (e.g testosterone)

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3
Q

what is present within the adrenal medulla and what is secreted from here?

A

chromaffin cells
medullary veins
splanchnic veins
secretes catecholamines

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4
Q

describe the HPA axis,

A

hypothalamus releases CRH which stimulates pituitary to produce ACTH which stimulates adrenal cortex to produce cortisol

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5
Q

what can have an effect on the activity of the hypothalamus in the HPA axis?

A

illness
stress
time of day
negative feedback from cortisol levels

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6
Q

how are the kidneys involved in blood pressure?

A

kidney senses reduced BP > production of renin > converts angiotensinogen to angiotensin 1 > ACE converts angiotensin 1 to angiotensin 2 > angiotensin 2 acts on adrenals to produce aldosterone which acts back on the kidneys causing water and salt retention > increased blood pressure

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7
Q

how do corticosteroids work?

A

bind intracellular receptor in either the cytoplasm or the nucleus > receptor/ligand complex binds to DNA via phosphorylation > has effects on transcription

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8
Q

what are the 6 classes of steroid receptor?

A 
glucocorticoid
mineralocorticoid
progestin
oestrogen
androgen
vitamin D
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9
Q

how does cortisol affect the cardio/renal system?

A

increased CO, BP, renal blood flow and GFR

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10
Q

give 3 main principles of using cortisol in treatment?

A

suppress inflammation
suppress immune system
replacement therapy

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11
Q

how can cortisol be administered?

A

IV
intramuscular
orally

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12
Q

name 5 disease which cortisol can be used for?

A 
asthma/anaphylaxis
rheumatoid arthritis
ulcerative colitis
crohns
malignancy
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13
Q

what are the functions of aldosterone?

A

sodium/potassium balance (K+ out, Na+ in)
BP regulation
Extracellular volume regulation

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14
Q

where are mineralocorticoid receptors present?

A

kidneys
salivary glands
gut
sweat glands

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15
Q

give an example of a classic presentation of addisons disease

A 
unwell few months
weight loss
amenorrhoea
vomiting/dairrhoea for past 48 hrs
dark skin
dehydrated
hypotensive
high K+, low Na+
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16
Q

what is the commonest cause of primary adrenal insufficiency?

A

addisons disease

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17
Q

what is addisons disease?

A

congenital autoimmune destruction of adrenal cortex

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18
Q

what are the features of addisons disease?

A 
autoantibody positive in 70%
anorexia
weight loss
fatigue/lethargy
dizziness and low BP
abdominal pain
vomiting
diarrhoea
skin pigmentation
associated with other autoimmune diseases (T1DM, autoimmune thyroid disease, pernicious anaemia)
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19
Q

name 2 other causes of primary adrenal insufficiency

A

congenital adrenal hyperplasia (CAH)

adrenal TB/malignancy

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20
Q

name 3 causes of secondary adrenal insufficiency?

A

all due to lack of excess ACTH stimulation
iatrogenic (excess steroid medication)
pituitary/hypothalamic disorders
tumours

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21
Q

what are the clinical features of secondary adrenal insufficiency?

A

similar to addisons apart from

  • skin is pale due to no increased ACTH
  • aldosterone production intact
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22
Q

how is secondary adrenal insufficiency managed?

A

hydrocortisone replacement

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23
Q

how is adrenal insufficiency diagnosed?

A 
biochemistry
short synacthen test
ACTH levels (raised)
renin/aldosterone levels
adrenal antibodies
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24
Q

what does biochemistry show in adrenal insufficiency?

A

decreased Na+
increased K+
hypoglycaemia

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25
describe the short synacthen test
measure plasma cortisol before and 30 mins after ACTH injection normal = before >250nmol/L, after >550nmol/L
26
what causes skin pigmentation in adrenal insufficiency?
raised ACTH levels
27
describe renin/aldosterone levels in adrenal insufficiency
decreased aldosterone | increased renin
28
how is adrenal insufficiency managed?
``` hydrocortisone and cortisol replacement - IV first if unwell - 15-30mg daily - try to mimic diurinal rhythm fludrocortisone as aldosterone replacement education ```
29
what are the sick day rules for adrenal insufficiency?
double dose if at home and unwell 100mg IV followed by 50mg every 6 hours cannot stop suddenly
30
what are the common presenting features of cushings?
``` central weight gain acne amenorrhoea hypertension severe osteoporosis proximal muscle weakness/myopathy easy bruising facial plethora striae proximal myopathy proximal muscle wasting ```
31
what are the 2 groups of causes of cushings?
``` ACTH dependant - pituitary adenoma - ectopic ACTH - ectopic CRH ACTH independent - adrenal adenoma - adrenal carcinoma - nodular hyperplasia ```
32
how is cushings disease diagnosed?
overnight dexamethasone suppression test (mainly) 24hr urinary free cortisol late night salivary cortisol
33
what is the commonest cause of cushings syndrome?
iatrogenic - due to prolonged high dose therapy - asthma, RA, IBD, transplant - can be oral or inhaled steroids
34
how does steroid therapy affect the adrenal glands?
long term use can cause chronic suppression of pituitary ACTH production via negative feedback pituitary and adrenal atrophy
35
what are the implications of the effects of long term steroids on the adrenals?
unable to respond to stress need extra dose when ill/surgical procedure cannot stop steroids suddenly gradual withdrawal of steroid therapy if taking over 4-6 weeks
36
name 2 endocrine causes of hypertension?
primary aldosteronism | congenital adrenal hyperplasia (CAH)
37
when would you suspect an endocrine cause of hypertension instead of an idiopathic case?
young resistant hypertension high clinical suspicion
38
what is primary aldosteronism?
autonomous production of aldosterone independent of its regulators (angiotensin 2 and potassium)
39
what are the 5 functions of aldosterone?
``` increases sympathetic outflow sodium retention cytokines and ROS synthesis increases cardiac collagen altered endothelial function - increased pressure response ```
40
what are the clinical features of primary aldosteronism?
significant hypertension hypokalaemia alkalosis
41
what are the 3 subtypes of primary aldosteronism?
``` bilateral adrenal hyperplasia (most common) adrenal adenoma (conns syndrome) rare causes (genetic, unilateral hyperplasia) ```
42
how is primary aldosteronism diagnosed?
ARR-aldosterone to renin ratio - if raised, inveastigate further with saline suppression test - if plasma aldosterone doesn't suppress by 50% with 2L of saline = diagnosis of PA
43
how can you confirm the subtype of PA?
adrenal CT to demonstrate adenoma | can sometimes do adrenal vein sampling to confirm adenoma is true source of aldosterone excess
44
how is PA managed surgically?
unilateral laparoscopic adrenalectomy - only if adrenal adenoma - cures hypokalaemia and hypertension in most
45
how is PA managed pharmacologically?
if bilateral adrenal hyperplasia - use MR antagonists - spironolactone - eplerenone
46
what is congenital adrenal hyperplasia (CAH)?
rare group of autosomal recessive disorders with enzyme defects in the steroid production pathway
47
what is the most common form of CAH?
21 alpha hydroxylase deficiency
48
what are the 2 variants of 21 alpha hydroxylase deficiency?
``` classical - salt wasting - simple virilising non-classical - hyperandrogenaemia ```
49
how is 21 alpha hydroxylase deficiency diagnosed?
basal 17-OH progesterone | genetic mutation analysis
50
how does classical CAH present?
``` males - adrenal insufficiency - poor weight gain - biochemical pattern females - genital ambiguity ```
51
how does non-classical CAH present?
``` hirsute acne oligomenorrhoea precocious puberty infertility (or sub-fertility) ```
52
how is CAH managed in children?
``` quick recognition glucocorticoid replacement mineralocorticoid replacement in some surgical correction achieve max growth potential ```
53
how is CAH managed in adults?
control androgen excess restore fertility avoid steroid over-replacement
54
what is a phaeochromocytoma?
neuroendocrine tumour of the adrenal medulla originating from the chromaffin cells
55
what scan is used for phaeochromocytoma?
MRI
56
list 6 clues which could indicate a phaeochromocytoma?
``` labile hypertension postural hypotension paroxysmal sweating heachache pallor tachycardia can have none of the above ```
57
what is an extra-adrenal phaeochromocytoma known as?
paraganglioma
58
list 17 presenting symptoms of phaeochromocytoma
``` hypertension postural hypotension headache sweating palpitations breathlessness constipation anxiety fear weight loss flushing incidental finding on imaging pallor family history bradycardia tachycardia pyrexia ```
59
list 5 biochemical features of phaeochromocytoma?
``` hyperglycaemia low potassium high haematocrit mild hypercalcaemia lactic acidosis ```
60
how is phaeochromocytoma diagnosed?
``` catecholamines and metabolites in the urine can be first clue find source - MRI - MIBG - PET scan ```
61
how is a phaeochromocytoma managed?
full alpha and beta blockade (alpha and beta blockers) fluids/blood replacement careful anaesthetic assessment surgery (laprascopy, excision, de-bulking) chemotherapy if malignant
62
what is included in the follow up from phaeochromocytoma?
long term monitoring etc genetic testing family testing and investing
63
what 2 conditions is phaeochromocytoma associated with?
MEN2 | Von-hippel- lindau syndrome
64
what are the metabolic effects of cortisol?
increased lipolysis increased proteolysis increased blood glucose
65
how does cortisol affect the immune response?
dampens the immune response
66
how does cortisol affect bone/connective tissue?
accelerates osteoporosis - reduced serum calcium, collagen formation and wound healing
67
how does cortisol affect the CNS?
mood lability, euphoria/psychosis, reduced libido

Endocrine (45 decks)

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