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Y2 Endocrine > Adrenal Glands and Disorders > Flashcards

Adrenal Glands and Disorders Flashcards

1
Q

____ is formed in the adrenal glomerulosa

A

mineralocorticoids

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2
Q

predominant mineralocorticoid

A

aldosterone

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3
Q

____ is formed in the adrenal fasiculata

A

glucocorticoids

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4
Q

primary glucocorticoid

A

cortisol

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5
Q

____ is formed in the adrenal reticularis

A

gonadocorticoids

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6
Q

predominant gonadocorticoids

A

testosterone

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7
Q

Aldosterone promotes __ reabsoprtion and __ excretion

A

Na reabsorption and K excretion

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8
Q

aldosterone production is stimulated by the ________ apparatus in the kidney

A

juxtaglomerular

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9
Q

The production of cortisol is controlled by____

A

ACTH

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10
Q

When is cortisol highest and lowest?

A

highest first thing, lowest late at night

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11
Q

where is Na reabsorption promoted by aldosterone?

A

DCT and collecting duct

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12
Q

Main effects of cortisol on the body?

A

increased BG, anti-inflammatory effects, increased CO, BP and renal blood flow, osteoporosis, decreased wound healing

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13
Q

androgens produced by the adrenal glands

A

DHEA, testosterone

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14
Q

Produced in the adrenal medulla?

A

epinephrine (80%), norepinephrin (20%)

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15
Q

Congenital adrenal hyperplasias are inherited in a ____ manner

A

Autosommal recessive

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16
Q

Pathophysiology in congenital adrenal hyperplasia

A

deficiency of an enzyme for steroid biosynthesis usually leading to decreased cortisol, increased ACTH and increased androgens

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17
Q

most common enzyme deficiency in congenital adrenal hyperplasia

A

21a hydroxylase

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18
Q

presentation of congenital adrenal hyperplasia

A

salt wasting, simple virilising, hyperandrogenism, ambiguous genitalia (girls), poor feeding, poor weight gain, similar presentation to addisons

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19
Q

treatment for congenital adrenal hyperplasa

A

glucocorticoid replacement, possible mineralocorticoid replacement, restore fertility and achieve maximal growth

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20
Q

Conn’s syndrome is…

A

usually associated with diffuse or nodular hyperplasia of both adrenal glands causing hyperaldosteronism

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21
Q

Common cause of Conn’s syndrome

A

35% are due to benign adenomas

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22
Q

What does a Conn’s adenoma look like?

A

small bright yellow tumour of spironolactone bodies

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23
Q

common symptoms of conn’s syndrome?

A

weakness, cramps, paraesthesia, polyuria, polydipsia and sometimes increased BP; may be asymptomatic

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24
Q

What is the effect of hyperaldosteronism on electrolytes?

A

increased Na, decreased K

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25
Q

Primary investigation for conn’s syndrome?

A

plasma renin:aldosterone ratio - if raised then investigate with suppression test

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26
Q

Suppression test for conn’s syndrome?

A

failure of plasma aldosterone to suppress by 50% following 2L of saline

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27
Q

How is Conn’s syndrome managed surgically?

A

unilateral laproscopic adrenalectomy - cure of hypokalaemia; cure of hypertension if adrenal adenoma

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28
Q

How is Conn’s syndrome managed medically?

A

use of MR antagonists when bilateral adrenal hyperplasia –> spironolactone, eplerenone

29
Q

Examples of MR antagonists (K+ sparing diuretics)

A

Spironolactone, eplerenone

30
Q

What is the most common cause of Cushing’s syndrome?

A

exogenous steroid use

31
Q

Endogenous cushing’s can be ACTH dependent or ACTH independent. What is meant by ACTH dependent Cushings?

A

ACTH is secreted from a pituitary adenoma causing Cushing’s DISEASE (70%) or from an ectopic source such as SCLC or carcinoid tumours (cause adrenal hyperplasia)

32
Q

Which form of lung cancer may cause Cushing’s syndrome?

A

Small Cell Lung Cancer

33
Q

Endogenous cushing’s can be ACTH dependent or ACTH independent. What is meant by ACTH independent Cushings?

A

An adrenal adenoma or carcinoma

34
Q

What group is Cushings most common?

A

women; 20-40 years

35
Q

What are some symptoms of Cushing’s? (5)

A

increased weight, mood changes, proximal weakness, gonadal dysfunction (irregular menses, hirsutism, erectile dysfunction), acne

36
Q

What are some signs of Cushing’s? (7)

A

central obesity with moon face, buffalo neck hump, skin and muscle atrophy with bruising and abdominal straie, oesteoporosis, increased BP and blood glucose, infection prone with poor wound healing

37
Q

What is the 1st line test in Cushing’s?

A

overnight dexamethasone suppression test - or low dose dexamethasone suppression test if unable to. Repeat to confirm

38
Q

What is the treatment of Cushings which is iatrogenic?

A

withdraw/lower steroid dose where possible over 4-6 weeks (not instantly). Be aware that will not be able to respond to stress appropriately due to ACTH suppression

39
Q

What is Nelson’s syndrome?

A

When ACTH is produced in high levels (pituitary adenoma), there is increased skin pigmentation due to it being produced as POMC which also codes for melanin.

40
Q

Management of Cushings disease?

A

remove adenoma, bilateral adrenalectomy if no obvious source

41
Q

What is the prognosis like for Cushing’s disease?

A

untreated has high vascular mortality; treated is good, but myopathy, obesity, menstrual irregularity, increased BP and osteoporosis often remain

42
Q

What happens in acute adrenocortical insufficiency?

A

either rapid withdrawl of steroid treatment or crisis in patients who have chronic insufficiency but do not up medication on ‘sick’ days.

43
Q

Other cause of Addisonian crisis

A

Massive adrenal haemorrhage

44
Q

Where might a massive adrenal haemorrhage occur?

A

newborn, anticoagulation, DIC, septicaemia

45
Q

What is Waterhouse-Fridericksen syndrome?

A

bilateral haemorrhage within the adrenal glands due to meningococcal septicaemia

46
Q

How is an addisonian crisis managed?

A

Check bloods: FBC, U&Es, cortisol and ACTH, ECG, Hydrocortisone 100mg IV stat, IV fluid bolus to support BP, Monitor glucose

47
Q

Symptoms of addisonian crisis

A

shock - increased HR, vasoconstriction, postural hypotension, oliguria, weak, confused, comatose

48
Q

3 common causes of Addisons disease

A

Autoimmune, Infections, metastatic malignancy

49
Q

Common autoimmune cause of Addisons disease

A

21hydroxylase adrenal autoantibodies (70%)

50
Q

Common infections causing Addisons disease

A

TB (commonest worldwide), HIV (Kaposi’s sarcoma), Fungal

51
Q

Common malignancies causing Addisons disease

A

lung and breast cancers

52
Q

When do symptoms of addisons disease start to occur?

A

when 90% of the gland is destroyed

53
Q

How do patients with addisons present?

A

insidious onset with vague symptoms - weakness, fatigue, anorexia, N&V, weight loss, diarrhoea, low BP

54
Q

What autoimmune diseases is Addisons associated with? (3)

A

T1DM, thyroid disease, pernicious anaemia

55
Q

Skin colour is likely to be affected in addisons disease - TRUE/FALSE

A

TRUE - increased production of ACTH to try and stimulate production of cortisol and aldosterone

56
Q

When might addisonian crisis occur?

A

due to stress i.e. infection, trauma, surgery; forgetting medication

57
Q

Test to diagnose Addisons disease?

A
  1. Short syntacthen stimulation test: plasma cortisol is measured before and 30mins after tetracosatide 250ug IM 2. test for autoantibodies and TB/malignancy when confirmed
58
Q

How is the glucocorticoid deficiency managed in Addisons disease?

A

hydrocortisone as cortisol replacement (IV if unwell), 15-30mg.day divided into doses to mimic circadian rhythm and not after 6pm to allow sleep

59
Q

How is mineralocorticoid deficiency managed in Addisons disease?

A

fludrocortion adjusted as necessary - monitor BP and K carefully when adjusting

60
Q

What education is important for Addisons disease?

A

Wear identification; sick day rules (double the dose, IM if necessary), cannot stop suddenly

61
Q

What is a phaeochromocytoma?

A

an adrenal medullary tumour derived from the chromaffin cells which secretes catecholamines

62
Q

Presentation of phaeochromocytoma

A

labile hypertension, postural hypotension, paroxysmal sweating, headache, pallor, tachycardia, palpitations, breathlessness, constipation, anxiety, fear, weight lsos, flushing

63
Q

Classic triad of phaeochromocytoma (90%)

A

hypertension, headache, sweating

64
Q

Complications of phaeochromocytoma

A

caridac failure, infarction, arrhythmias, CVA, paralytic ileus

65
Q

Diagnosis of phaeochromocytoma

A

urinary catecholamines and metabolites; hyperglycaemia, low, mild hypercalcaemia

66
Q

Imaging done in phaeochromocytoma

A

MRI, MIBG, PET scan

67
Q

Treatment of phaeochromocytoma

A

full a and b blockade - a (phenoxybenzamine) before b (atenolol)

68
Q

10% tumour

A

phaeochromocytoma

69
Q

the 10% rules of phaeochromocytoma

A

10% extra-adrenal, 10% bilateral, 10% biologically malignant, 10% not associated with hypertension, 25% familial

Y2 Endocrine (4 decks)

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