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Endocrine lectures > adrenal gland disorders > Flashcards

adrenal gland disorders Flashcards

1
Q

where are the adrenal glands located?

A

above the kidneys

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2
Q

where are the hormones that regulate cortisol and androgen production produced?

A

hypothalamus and anterior pituitary

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3
Q

what regulates aldosterone?

A

renin-angiotensin system and plasma potassium

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4
Q

when is the Renin angiotensin system activated?

A

in response to low BP

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5
Q

what does renin-angiotensin system lead to?

A

production of angiotensin II

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6
Q

what is the action of cortisol upon the CNS?

A

Mood lability
Euphoria/psychosis
reduced libido

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7
Q

what is the affect of cortisol on the immune system

A

decreased capillary dilatation/permeability
decreased leucocyte migration
decreased macrophage activity
decreased inflammatory cytokine production

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8
Q

what is the action of cortisol on bone/connective tissue?

A

Accelerates osteoporosis
reduced Serum calcium
reduced collagen formation
reduced wound healing

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9
Q

what is the affect of cortisol on the metabolic system?

A

increase blood sugar
increase lipolysis
increase proteolysis

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10
Q

what is the affect of cortisol on the circulatory/renal system?

A

increased Cardiac output
increased BP
increased renal blood flow and GFR

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11
Q

what is the main principles of use of corticosteroids?

A

suppress inflammation
suppress immune system
replacement treatment

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12
Q

when are corticosteroids used?

A

allergic disease
inflammatory disease
malignant disease

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13
Q

what does addisons disease indicate?

A

cortisol/adrenal insufficiency

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14
Q

what conditions are caused by primary adrenal insufficiency?

A

addisons disease
congenital adrenal hyperplasia
adrenal TB/malignancy

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15
Q

what are the classical features of addisons disease?

A

Anorexia, weight loss
fatigue/lethargy
Dizziness and low BP
Abdominal pain, vomiting,
diarrhoea
Skin pigmentation

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16
Q

in what % of cases of addisons are autoantibodies involved?

A

70%

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17
Q

is addisons associated with other autoimmune diseases?

A

yes

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18
Q

how is addisons diagnosed?

A

low sodium
high postassium
short synthetic ACTH test
increased renin and low aldosterone
adrenal antibodies

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19
Q

how is adrenal insufficiency managed?

A

hydrocortisone as cortisol replacement (if unwell give via IV first)
fludrocortisone as aldosterone replacement
education

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20
Q

what is the treatment in adrenal crisis?

A

fluids (saline)
steroids IV/IM hydrocortisone
(50mg/6hrs)

IF IN DOUBT TREAT

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21
Q

what causes secondary adrenal insufficiency?

A

pituitary/hypothalamic disease tumours
exogenous steroid use (most common cause)

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22
Q

what are the clinical features of secondary adrenal insufficiency?

A

similar to addisons EXCEPT
-pale skin (no raised ACTH)
-aldosterone production intact

23
Q

how is secondary adrenal insufficiency treated?

A

hydrocortisone
No fludrocortisone necessary

24
Q

what is caused by excess cortisol secretion?

A

cushings disease

25
Q

what are the clinical features of cushings?

A

easy bruising
thin skin
striae
proximal myopathy

26
Q

how do we screen for cortisol excess?

A

Overnight dexamethasone suppression test
24 hour urinary free cortisol
Late night salivary cortisol

Repeat to confirm

27
Q

what is the diagnostic test for cushings syndrome?

A

low dose dexomethasone suppression test

28
Q

what are the implications of atrophy of the adrenal cortex?

A

Unable to respond to stress (illness/surgery)
Need extra doses of steroid when ill/surgical procedure
Cannot stop suddenly
Gradual withdrawal of steroid therapy if >4-6 week

29
Q

what can indicate primary aldosterone?

A

hypertension and hypokalaemia (hypokalaemia is only in around 30% of cases though)

30
Q

what is the definition of primary aldosterone?

A

autonomous over production of aldosterone independent of its regulators

31
Q

does aldosterone increase BP?

A

yes

32
Q

what is the most common type of primary aldosterone?

A

bilateral adrenal hyperplasia (60% of cases)

33
Q

how is aldosterone excess confirmed?

A

Measure plasma aldosterone and renin and express as ratio (ARR-aldosterone to renin ratio)
→ If ratio raised (assay dependent) then investigate further with saline suppression test
→ Failure of plasma aldosterone to suppress by > 50% with 2 litres of normal saline confirms PA

34
Q

how do we confirm which subtype of primary aldosterone a patient has?

A

Adrenal CT to demonstrate adenoma
→ Sometimes adrenal vein sampling to confirm adenoma is true source of aldosterone excess

35
Q

how is primary aldosterone managed surgically?

A

Unilateral laparoscopic adrenalectomy
→ Only if adrenal adenoma (and excess confirmed in adrenal vein
sampling)
→ Cure of hypokalaemia
→ Cures hypertension in 30-70% cases

generally only used in those with a clear adenoma

36
Q

how is primary aldosterone managed medically?

A

generally only used in bilateral adrenal hyperplasia
Use MR antagonists (spironolactone or eplerenone)

37
Q

what is congenital adrenal hyperplasia?

A

an inherited group of disorders characterised by a deficiency in one of the enzymes necessary for cortisol synthesis

38
Q

when is classical CAH diagnosed?

A

in infancy

39
Q

when is non classical CAH usually diagnosed?

A

in adolescence/adulthood

40
Q

what are the symptoms of non classical CAH?

A

hirsutism, menstrual disturbance and infertility due to anovulation

41
Q

what are the symptoms of classical CAH?

A

virilisation/salt wasting

42
Q

how is CAH diagnosed?

A

Basal [or stimulated] 17-OH Progesterone
increasingly supported by genetic mutation analysis

43
Q

what is the presentation of classical CAH?

A

Adrenal insufficiency
→ Often around two to three weeks
→ Poor weight gain
→ Biochemical pattern of Addison’s disease
Females
→ Genital ambiguity (virilisation)

44
Q

what is the presentation of non classical CAH (typically in females)

A

Hirsute
Acne
Oligomenorrhoea
Precocious puberty
Infertility or sub-fertility

45
Q

what is the main treatments of CAH in childhoof?

A

Timely recognition
Glucorticoid replacement
Mineralocorticoid replacement in some
Surgical correction
Achieve maximal growth potential

46
Q

what is the main treatments of CAH in adults?

A

Control androgen excess
Restore fertility
Avoid steroid over-replacement

47
Q

what are things that indicate phaeochromocytoma?

A

Labile hypertension
* Postural hypotension
* Paroxysmal sweating, headache, pallor,
tachycardia

Also none of the above!

48
Q

why is phaeochromocytoma known as the 10% tumour?

A

10% malignant
10% bilateral
10% extra adrenal
10% not associated with hypertension

49
Q

when are 50% of phaeochromocytomas diagnosed?

A

during post mortem

50
Q

what is the classic triad of symptoms in phaeochromocytoma?

A

hypertension
headache
sweating

up to 90% of cases

51
Q

what are the signs of phaeochromocytoma?

A

hypertension
pallor
brady/tachycardia
pyrexia

52
Q

how is phaeochromocytoma diagnosed?

A

through identifying the source of catecholamines
MRI scan
MIBG- meta iodobenzylguanidine

53
Q

how would a phaeochromocytoma be treated?

A

SURGICAL MANAGEMENT
preparation for surgery- Full α and β- blockade
(A before B)
Phenoxybenzamine (α-blocker)
Propranolol, atenolol or metoprolol (β-
blocker)

Endocrine lectures (32 decks)

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