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Y3 MedEd > Adrenals > Flashcards

Adrenals Flashcards

1
Q

What is made in adrenal glomerulosa

A

Mineralocorticoids

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2
Q

What is made in adrenal fasciculata

A

Glucocorticoids

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3
Q

What is made in adrenal reticularis

A

Sex steroids

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4
Q

What is made in adrenal medulla

A

Adrenaline

Noradrenaline

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5
Q

Which part of the adrenal makes mineralocorticoids

A

Mineralocorticoids

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6
Q

Which part of the adrenal makes glucocorticoids

A

Fasciculata

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7
Q

Which part of the adrenal makes sex steroids

A

Reticularis

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8
Q

Which part of the adrenal makes catecholamines

A

Medulla

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9
Q

4 causes of primary hyperaldosteronism

A 
Adrenal adenoma: Conn’s syndrome (70%)
Bilateral adrenal cortex hyperplasia (30%)
Familial hyperaldosteronism
RARE:
Aldosterone producing adrenal carcinoma
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10
Q

What is the normal population of Conns

A

young females

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11
Q

What is the normal population of bilateral hyperaldosteronism

A

older males

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12
Q

Symptoms of hypokalaemia that may be present in hyperaldosteronism (4)

A

Muscle weakness/cramps
Polyuria/nocturia
Paraesthesia
Mood disturbances/letharfy

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13
Q

Signs of hyperaldosteronism

A

HYPERTENSION (HTN)
Difficult to control with antihypertensive medications
Complications of hypertension e.g retinopathy of hypertension, headaches

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14
Q

Main 4 Ix for primary hyperaldosteronism

A 
Plasma K+ levels
Low in 20% of patients
Urine K+ - high
Plasma aldosterone - high
Plasma aldosterone:renin ratio – high
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15
Q

How to confirm primary hyperaldosteronism

A

Failure of aldo suppression post fludrocortisone salt load – confirms 1’ hyperaldosteronism

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16
Q

Mx of hyperaldosteronism by cause (2)

A

Adrenal adenoma
Adrenalectomy (laparoscopic)

Bilateral adrenal hyperplasia (or those not fit for/don’t want surgery)
Spironolactone (aldosterone inhibitor)
Eplerenone if side effects not tolerated
Monitor serum K+, creatinine and BP

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17
Q

SE of spironolactone (3)

A

gynaecomastia, impotence, muscle cramps

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18
Q

Most common cause of Cushing’s syndrome

A

steroid exposure

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19
Q

5 ways of acquiring Cushing’s syndrome endogenously

A

ACTH-dependent (80%)
Excess ACTH from pituitary adenoma (Cushing’s disease)
Ectopic ACTH e.g lung tumour, pulmonary carcinoid tumour

ACTH-independent (20%)
Benign adrenal adenoma
Bilateral adrenal hyperplasia
Adrenal carcinoma (rare)

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20
Q

Ix for Cushing’s disease (5)

A 
Serum glucose – high risk diabetes
Pregnancy test
Overnight dexamethasone suppression test
Low-dose dexamethasone suppression test
High dose
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21
Q

What is the use of the HD dexamethasone suppression test and explain

A

Differentiate between CD and CS
High dose suppresses cortisol –> pituitary adenoma
High dose doesn’t suppress cortisol –> ectopic (lung) or adrenal pathology

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22
Q

Normal population of Cushing’s syndrome (age and gender)

A

W:M = 4:1

20-40yrs

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23
Q

Mx of Cushing’s (medical 2 and surgical)

A

MEDICAL
Metyrapone/ketoconazole – inhibit cortisol synthesis
Use pre-operatively or if unfit for surgery

SURGICAL – preferred treatment
Pituitary adenoma: trans-sphenoidal resection of adenoma
Adrenal adenoma/carcinoma: surgery to remove
Ectopic ACTH: treatment directed at tumour

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24
Q

Complications of Cushing’s (4)

A

Diabetes
Osteoporosis
Hypertension
Pre-disposition to infections

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25
Q

Prognosis of Cushing’s

A

untreated, 5yr survival rate is 50%.

Depression often persists for years following successful treatment

26
Q

What is an adrenal paraganglioma

A

Extra-adrenal tumour of the adrenal medulla

27
Q

Common triad in phaeochromocytoma

A

“Palpitations
Headaches
Episodic sweating”

28
Q

3 familial syndromes that can result in phaeochromocytomas

A

“Multiple Endocrine Neoplasia 2a (MEN2a)
Von Hippel Lindau syndrome (VHL)
Neurofibromatosis type 1 (NF1)”

29
Q

Which group of patients should you consider phaeos in

A

Consider phaeos in patients with young-onset or resistant intractable hypertension

30
Q

Ix for phaeochromocytomas (5)

A

“24 hr urine collection - check for catecholamines, metanephrines + normetanephrines
Plasma free metanephrines/normetanephrines
Genetic testing

Tumour localisation:
CT > MRI
I-123 MIBG scintigraphy”

31
Q

What is primary adrenal insufficiency also known as

A

Addisons disease

32
Q

What is primary adrenal insufficiency also known as

A

Pituitary or hypothalamic disease hits decreased ACTH secretion

33
Q

Inherited causes of adrenal insufficiency (2)

A

Adrenoleukodystrophy

ACTH receptor mutation

34
Q

Iatrogenic causes of adrenal insufficiency (2)

A

Sudden cessation of long-term steroid therapy

After bilateral adrenalectomy

35
Q

Infectious causes of adrenal insufficiency (3)

A 
"TB
Meningococcal septicaemia (Waterhouse-Friderichsen Syndrome); CMV ; Histoplasmosis"
36
Q

Ways of acquiring adrenal insufficiency (6)

A 
Autoimmune
Infections
Infiltration
Infarction
Inherited
Iatrogenic
37
Q

What can cause infiltrative adrenal insufficiency (5)

A

metastasis (mainly from lung, breast, melanoma); Lymphomas; Amyloidosis

38
Q

Which cancers metastasise to adrenals commonly

A

Which cancers metastasise to adrenals commonly

39
Q

Signs of Addisons (4)

A

Increased pigmentation
Postural hypotension
Loss of body hair in women (androgen deficiency)
Associated autoimmune condition (e.g. vitiligo)

40
Q

Symptoms of Addisons (7)

A 
"Symptoms: VAGUE and NON-SPECIFIC
Fatigue
Weakness
Myalgia
Weight loss (+anorexia)
Diarrhoea and Vomiting 
Abdominal pain
Depression "
41
Q

Pathophysiology behind acute Addisonian crisis (4 ways)

A

“Defective production of aldosterone causes increases water and salt loss, leading to hyponatraemia and hypovolaemia. Hyperkalaemia also occurs leading irregular heart rhythm which can lead to cardiac arrest.
Defective production of cortisol leads to liver function decreasing and so hypoglycaemia leading to seizures, convulsions and loss of consciousness.
Lack of cortisol leads to nausea and vomiting and diarrhoea and cramps leading to hypovolaemia which is exacerbated by the lack of aldosterone causing hypotension leading to shock, coma, organ failure and death.”

42
Q

Sign of acute adrenal insufficiency (4)

A

Vomiting, diarrhoea, low blood pressure and

precipitated by stress

43
Q

Ix for adrenal insufficiency (5)

A 
Confirm diagnosis:
9am serum cortisol
<100nmol/L
Short SynACTHen test
Serum cortisol <550 nmol/L at 30 mins

Long SynACTHen test
Autoantibodies
Abdo CT/MRI

44
Q

Ix for acute Addisonian crisis (7 but 4 main ones)

A 
"FBC
U+Es
High urea
Low sodium
High potassium
CRP/ESR
Low glucose
Blood cultures 
Urinalysis
Culture + sensitivity"
45
Q

Mx of acute Addisonian crisis (3)

A

Rapid IV fluid rehydration
50ml 50% dextrose
IV 200mg hydrocortisone bolus
100mg 6hrly hydrocortisone till BP stable
Treat precipitating cause e.g Abx for infection
MONITOR

46
Q

Mx of Addisons disease (2)

A

Replace:
GCs with hydrocortisone (TDS)  increase dose in times of acute illness/stress
MCs with fludrocortisone

47
Q

Changes to the ECG in moderate and severe 2 hypokalaemia

A

Moderate
Flattened T wave

Severe
ST depression
U wave

48
Q

Changes to the ECG in moderate 2 and severe 2 hyperkalaemia

A

Moderate
Peaked T wave
ST depression

Severe
Widened QRS
Loss of P wave

49
Q

Causes of systemic potassium release (2)

A

rhabdomyolysis, metabolic acidosis (e.g DKA)

50
Q

Clinical features of hyperkalaemia (2)

A

Muscle weakness

ECG changes  life-threatening arrhythmia

51
Q

Mx of hyperkalaemia (5)

A

Management – 10 10 10 50 50

10ml 10% calcium gluconate
10U Actrapid
50ml 50% glucose
Nebulised salbutamol
12-lead ECG (continuous)
52
Q

Causes of hypokalaemia (4)

A

GI loss – vomiting, diarrhoea
Redistribution of K+ into cells – insulin, B-agonists, metabolic alkalosis
Renal loss – hyperaldosteronism, excess cortisol, natriuresis
Decreased K+ intake – anorexia nervosa

53
Q

Clinical features of hypokalaemia (3)

A

Muscle weakness & spasm
Cardiac arrhythmia
Polyuria and polydipsia (nephrogenic DI)

54
Q

Mx of hypokalaemia (3)

A 
Management – always correct magnesium
K+ 3.0-3.5 mmol/L
Oral potassium chloride (SandoK)
Recheck in 48 hours
K+ <3.0 mmol/L
IV potassium chloride
Max infusion rate 10 mmol/hr (peripheral irritant)
55
Q

3 main features of PCOS

A 
Clinical features of hyperandrogenism
Hirsutism
Acne
Oligo/amenorrhoea
Polycystic ovaries on USS
56
Q

Associations of PCOS (5)

A 
Obesity
Insulin resistance
Type 2 DM
Infertility
Endometrial cancer
57
Q

Aetiology of PCOS

A

Hyperinsulinaemia: increased ovarian androgen synthesis and reduced hepatic sex hormone binding globulin synthesis

Leads to an increase in free androgens (which gives rise to the symptoms)

58
Q

Signs of PCOS (3)

A

High BMI
Hirsutism
Acanthosis nigricans

59
Q

Symptoms of PCOS (3)

A 
Menstrual irregularities
Acne
Male-pattern hair loss
Weight gain
Infertility
60
Q

Blood test results for PCOS (6)

A

High LH
High LH:FSH ratio
High testosterone, androstenedione and DHEA-S
Low sex hormone binding globulin

61
Q

Ix for PCOS

A

Bloods looking at sex hormones

Transvaginal USS

62
Q

Ways of acquiring hyperkalaemia (5)

A 
Renal disease – HTN, DM
Low RAAS activity – ACE-Is, ARBs, aldosterone antagonists, adrenal failure
Systemic K+ release - rhabdomyolysis, metabolic acidosis (e.g DKA)
Damage to the DCT - type 4 renal tubular acidosis, NSAID toxicity
Spurious sample (recheck)

Y3 MedEd (34 decks)

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