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Case 12: Female Reproductive System > Adrenal Insufficiency > Flashcards

Adrenal Insufficiency Flashcards

1
Q

What hormone is produced by zona glomerulosa

A

Aldosterone

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2
Q

What controls aldosterone production

A

RAAS

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3
Q

What hormone is produced by zona fasciculate

A

Cortisol

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4
Q

What hormone is produced by zona reticularis

A

Androgen precursors

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5
Q

What controls androgen precursors production

A

HPA

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6
Q

What controls cortisol production

A

HPA

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7
Q

What is the HPA axis

A

CRH then ACTH then cortisol

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8
Q

When is ACTH the highest

A

8 in the morning

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9
Q

When is ACTH the lowest

A

Midnight

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10
Q

What hormone does the adrenal medulla produce

A

Catecholamines

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11
Q

What controls catecholamines production

A

Sympathetic nervous system

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12
Q

What determines the hormone being produced

A

The enzyme in the specific zone

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13
Q

How does RAAS work

A

Low blood pressure cause renin release from juxtaglomerular apparatus of the kidney that splits angiotensinogen into angiotensin 1 and ACE in the lungs covert it to angiotensin 2 that triggers release of aldosterone.
Aldosterone cause vasoconstriction increasing blood pressure & triggers release of ADH from pituitary & cause salt retention & therefor water retention

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14
Q

What also stimulate aldosterone

A

High potassium levels
ACTH

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15
Q

Steroid hormone production pathway

A

DIAGRAM

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16
Q

What is 7 biochemical actions of cortisol

A

Increase protein catabolism
Increase hepatic glycogen synthesis
Increase hepatic gluconeogenesis
Maintain blood pressure
Initiation of diuretics
Inhibit inflammatory & immune response
Inhibits bone formation

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17
Q

What is 3 actions of cortisol in stress response

A

Increase availability of fuel substance
Act on pancreas to decrease insulin & increase glucagon to promote glucose availability
Increase of enhance catecholamines activation

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18
Q

What is 2 molecular actions of cortisol

A

Increase transcription of glucocorticoid
Inhibit inflammatory gene expression

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19
Q

What is congenital adrenal hyperplasia

A

Autosomal recessive metabolic disorder

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20
Q

What is the epidemiology of 21-hydroxylase deficiency

A

Most of CAH (90%)

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21
Q

What is the epidemiology of 11-OH deficiency

A

5-10% of CAH

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22
Q

What is the epidemiology of 17-OH deficiency

A

Less than 5% of CAH

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23
Q

What is the epidemiology 3 21-BHSD deficiency

A

Rare

24
Q

What pathophysiology does all CAH have in common

A

Decrease GC that decrease negative feedback that increase ACTH leading to adrenal hyperplasia

25
Q

What is the pathophysiology of 21-OH deficiency

A

Decreased GC
Decreased MC causing salt wasting
Increase androgens causing over virilisation in female

26
Q

What is the diagnostic precursor in 21-OH deficiency

A

Increase 17-OH progesterone

27
Q

What is the treatment of 21-OH deficiency

A

Cortisol & fludrocortisone

28
Q

What is monitoring for 21-OH deficiency

A

17-OHP
Androgens

29
Q

What is the 3 stages of severity in 21-OH deficiency

A
  1. Severe salt losing:
    Severe enzyme defect w/ potential adrenal crisis
    Hypotension, shock & hyperK
    Virilisation but males at risk
  2. Simple virilisation form:
    Mild enzyme defects w/ adequate cortisol & androgen production
    Accumulation of 17 OHP & excessive androgens
    Over virilisation of female & male
  3. Non-classical form:
    Very mild enzyme defect
    No neonatal masculinization& young female menstrual irregularity, infertility & hirsutism
30
Q

What is the pathophysiology of 3-BHSD deficiency

A

Decreased GC
Decreased MC causing salt wasting
Decrease androstenedione that decreases testosterone causing under virilisation in male
Increased DHEA over virilisation in females

31
Q

What is the diagnosis used for 3- BHSD deficiency

A

Increase pregnenolone, 17a-hydroxypregnenlone, DHEA & renin

32
Q

What is the pathophysiology of 11-OH deficiency

A

Decreased GC
Decreased aldosterone but increased deoxycorticosterone leading to hypertension & hypoK
Increase androgens causing over virilisation in females

33
Q

What is the diagnostic precursor in 11-OH deficiency

A

Increase 11-deoxycortisol & 1-OH progesterone

34
Q

What is the pathophysiology of 17-OH deficiency

A

Decreased GC
Decreased cortisol but increased corticosterone
Increased MC precursors leading to low renin hypertension w/ hypoK & metabolic acidosis
Decrease androgens causing under virilisation in males & delayed puberty in females

35
Q

What is Addison disease

A

Impaired capacity of cortisol & aldosterone secretion

36
Q

What is Addison disease

A

Primary adrenal hypofunction

37
Q

What is 7 causes of Addison disease

A

Autoimmune
Adrenal haemorrhage
Meningococcal septicaemia
Infection
Neoplastic infiltration
Amyloidosis
Adrenoleukodystrophy

38
Q

What is secondary adrenal hypofunction

A

Rapid withdrawal of prolonged steroid therapy
Lack of ACTH causing a cortisol deficiency & intact aldosterone

39
Q

What is 9 clinical features of Addison disease

A

Orthostatic hypotension
Dehydration
Hypoglycaemia
Pigmentation (excess ACTH)
Fatigue
Muscle weakness
Weight loss
Anorexia
Addisonian crisis

40
Q

What is Addisonian crisis

A

Hypotension, shock & abdominal pain

41
Q

What is the biochemical feature of aldosterone & cortisol deficiency

A

Aldosterone deficiency
Na & water loss in urine
HypoNa & hyperK
Metabolic acidosis
Cortisol deficiency:
Hypoglycaemia

42
Q

What is the 3 imaging investigation of adrenal insufficiency

A

CT adrenal or pituitary
MRI of pituitary
CXR

43
Q

What is the 3 auto-Ab investigation of adrenal insufficiency

A

Anti-adrenal
Anti-thyroid
Anti-Islet cell

44
Q

What is the blood test for investigation of adrenal insufficiency

A

Cortisol, ACTH & aldosterone

45
Q

What is the blood results of primary adrenal insufficiency

A

Decrease aldosterone, cortisol & increase ACTH

46
Q

What is the blood results of secondary adrenal insufficiency

A

Decreased ACTH & cortisol

47
Q

What is a stimulation test

A

Evaluating the ability of adrenal to respond to stimulation of ACTH

48
Q

What is primary adrenal insufficiency response to stimulation test

A

Unable tor respond

49
Q

What is secondary adrenal insufficiency response to stimulation test

A

Respond after longer period of stimulation

50
Q

What is the short ACTH stimulation test

A

One dose of synacthen measuring cortisol before & 30 minutes after

51
Q

What is the long ACTH stimulation test

A

Synacthen for 3 days
Measuring before, 1,2,4,8 & 24 hrs after last dosage

52
Q

What is the interpretation of short ACTH stimulation test

A

Normal: cortisol increase more than 550
Subnormal response: primary or secondary adrenal insufficiency

53
Q

What is the interpretation of long ACTH stimulation test

A

Normal: rising cortisol levels peak at 4-8 hrs
Primary adrenal insufficiency: no/poor response
Secondary: slowly developing response with a peak at 24 hrs

54
Q

What is the insulin tolerance test

A

Induce hypoglycaemia to stimulate ACTH in stress response

55
Q

What is the insulin tolerance test interpretation

A

Normal: increase to more than 550
Subnormal: primary or secondary adrenal insufficiency

56
Q

What is the metyraprone stimulation test

A

Inhibits 11B-OH & reduce cortisol concentration that reduce negative feedback on HPA that increase ACTH & 11-DOC

57
Q

What is the metyraprone stimulation test interpretation

A

Normal: ACTH & 11-DOH increase
Subnormal: 11 DOC decrease due to primary or secondary adrenal insufficiency

Case 12: Female Reproductive System (10 decks)

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