Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Case 12: Female Reproductive System > Adrenal Insufficiency > Flashcards

Adrenal Insufficiency Flashcards

1
Q

What hormone is produced by zona glomerulosa

A

Aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What controls aldosterone production

A

RAAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What hormone is produced by zona fasciculate

A

Cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What hormone is produced by zona reticularis

A

Androgen precursors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What controls androgen precursors production

A

HPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What controls cortisol production

A

HPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the HPA axis

A

CRH then ACTH then cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

When is ACTH the highest

A

8 in the morning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When is ACTH the lowest

A

Midnight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What hormone does the adrenal medulla produce

A

Catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What controls catecholamines production

A

Sympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What determines the hormone being produced

A

The enzyme in the specific zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What also stimulate aldosterone

A

High potassium levels
ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Steroid hormone production pathway

A

DIAGRAM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is 2 molecular actions of cortisol

A

Increase transcription of glucocorticoid
Inhibit inflammatory gene expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is congenital adrenal hyperplasia

A

Autosomal recessive metabolic disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the epidemiology of 21-hydroxylase deficiency

A

Most of CAH (90%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the epidemiology of 11-OH deficiency

A

5-10% of CAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the epidemiology of 17-OH deficiency

A

Less than 5% of CAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the epidemiology 3 21-BHSD deficiency

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
What is the pathophysiology of 21-OH deficiency
Decreased GC Decreased MC causing **salt wasting** Increase androgens causing over virilisation in female
26
What is the diagnostic precursor in 21-OH deficiency
Increase 17-OH progesterone
27
What is the treatment of 21-OH deficiency
Cortisol & fludrocortisone
28
What is monitoring for 21-OH deficiency
17-OHP Androgens
29
What is the 3 stages of severity in 21-OH deficiency
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
What is the pathophysiology of 3-BHSD deficiency
Decreased GC Decreased MC causing **salt wasting** Decrease androstenedione that decreases testosterone causing under virilisation in male Increased DHEA over virilisation in females
31
What is the diagnosis used for 3- BHSD deficiency
Increase pregnenolone, 17a-hydroxypregnenlone, DHEA & renin
32
What is the pathophysiology of 11-OH deficiency
Decreased GC Decreased aldosterone but increased deoxycorticosterone leading to hypertension & hypoK Increase androgens causing over virilisation in females
33
What is the diagnostic precursor in 11-OH deficiency
Increase 11-deoxycortisol & 1-OH progesterone
34
What is the pathophysiology of 17-OH deficiency
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
What is Addison disease
Impaired capacity of cortisol & aldosterone secretion
36
What is Addison disease
Primary adrenal hypofunction
37
What is 7 causes of Addison disease
Autoimmune Adrenal haemorrhage Meningococcal septicaemia Infection Neoplastic infiltration Amyloidosis Adrenoleukodystrophy
38
What is secondary adrenal hypofunction
Rapid withdrawal of prolonged steroid therapy Lack of ACTH causing a cortisol deficiency & intact aldosterone
39
What is 9 clinical features of Addison disease
Orthostatic hypotension Dehydration Hypoglycaemia Pigmentation (excess ACTH) Fatigue Muscle weakness Weight loss Anorexia Addisonian crisis
40
What is Addisonian crisis
Hypotension, shock & abdominal pain
41
What is the biochemical feature of aldosterone & cortisol deficiency
**Aldosterone deficiency** Na & water loss in urine HypoNa & hyperK Metabolic acidosis **Cortisol deficiency:** Hypoglycaemia
42
What is the 3 imaging investigation of adrenal insufficiency
CT adrenal or pituitary MRI of pituitary CXR
43
What is the 3 auto-Ab investigation of adrenal insufficiency
Anti-adrenal Anti-thyroid Anti-Islet cell
44
What is the blood test for investigation of adrenal insufficiency
Cortisol, ACTH & aldosterone
45
What is the blood results of primary adrenal insufficiency
Decrease aldosterone, cortisol & increase ACTH
46
What is the blood results of secondary adrenal insufficiency
Decreased ACTH & cortisol
47
What is a stimulation test
Evaluating the ability of adrenal to respond to stimulation of ACTH
48
What is primary adrenal insufficiency response to stimulation test
Unable tor respond
49
What is secondary adrenal insufficiency response to stimulation test
Respond after longer period of stimulation
50
What is the short ACTH stimulation test
One dose of synacthen measuring cortisol before & 30 minutes after
51
What is the long ACTH stimulation test
Synacthen for 3 days Measuring before, 1,2,4,8 & 24 hrs after last dosage
52
What is the interpretation of short ACTH stimulation test
Normal: cortisol increase more than 550 Subnormal response: primary or secondary adrenal insufficiency
53
What is the interpretation of long ACTH stimulation test
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
What is the insulin tolerance test
Induce hypoglycaemia to stimulate ACTH in stress response
55
What is the insulin tolerance test interpretation
Normal: increase to more than 550 Subnormal: primary or secondary adrenal insufficiency
56
What is the metyraprone stimulation test
Inhibits 11B-OH & reduce cortisol concentration that reduce negative feedback on HPA that increase ACTH & 11-DOC
57
What is the metyraprone stimulation test interpretation
Normal: ACTH & 11-DOH increase Subnormal: 11 DOC decrease due to primary or secondary adrenal insufficiency

Case 12: Female Reproductive System (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions