Apparent Mineralocorticoid Excess ESR [034]

Question 1

Answer 1

Question 2

inherent specificity of MR to mineralocorticoids ?

Answer 2

MR has no inherent specificity for mineralocorticoids

Question 3

The MR has a higher/lower affinity than the GR

Answer 3

Higher

Question 4

How do “Mineralocorticoid selective tissues” respond to aldosterone rather than cortisol?

Answer 4

Question 5

Causes of Apparent Mineralocorticoid Excess (AME) syndrome ?

Answer 5

Question 6

Clinical presentation of Apparent Mineralocorticoid Excess (AME) syndrome ?

Answer 6

Question 7

Why might 11Beta HSD type 2 fail?

Answer 7

Question 8

Known mutations in 11B HSD are autosomal recessive ;
What is the significance of this?

Answer 8

Question 9

Inhibitiors of 11B HSD - type 2 ?

Answer 9

Question 10

If 11B HSD type 2 is fully active, why might cortisol still gain inappropriate access to MR?

Answer 10

1- High Cortisol:

(e.g., Cushing’s disease & glucocorticoid resistance)

2- Exceeds capacity of enzyme

Question 11

Clinical Symptoms of AME ?

Answer 11

• Anti-natriuresis

• Increased fluid reabsorption

• Hypervolemic hypertension

• Kaliuresis  hypokalemia

• Muscle & cardiac weakness & fatigue

Question 12

Consequences of failure of placental 11B HSD ?

Answer 12

• Increased passage of cortisol to fetus

• Stimulates premature differentiation of fetal tissues (but need cortisol at term)

• Prevents further growth of tissues

• Culminates in IUGR

** Barker hypothesis:
Increased risk of serious adult disease ; obesity, diabetes and coronary heart disease

Question 13

Dominant 11βHSD type in Liver, lung, fat, gonad, brain & pituitary ?

Answer 13

is mostly OF Type 1

Question 14

Overexpression of 11B HSD Type 1 especially in fat cells, can lead to :

Answer 14

symptoms of Metabolic syndrome & apparent glucocorticoid excess

Question 15

Answer 15

Question 16

Explain