Hypothalamic-Pituitary Relationships and Biofeedback Pt.2

Question 1

What do these layers secrete? 
Zona glomerulosa 
Zona fasciculata
Zona reticularis
Chromaffin cells (in medulla)

Answer 1

• Mineralocorticoid (aldosterone)
• glucocorticoid (cortisol and androgens/DHEA - precursor)
• glucocorticoid (cortisol and androgens/DHEA - precursor)
• Catecholamines (epinephrine and norepinephrine

Question 2

Draw the HPA axis

Answer 2

Ok

Question 3

What triggers cortisol secretion?

Answer 3

Stress (physical, emotional and metabolic stress)

Question 4

What are the actions of cortisol?

Answer 4

Immunosuppression
Gluconeogenesis
Protein catabolism
Lipolysis

Question 5

Describe the diurnal pattern secretion of cortisol

Answer 5

High in early morning and low in late evening

Question 6

What is the major controller of aldosterone secretion from the adrenal cortex?

Answer 6

Low blood pressure

Question 7

Draw the pathway/schematic of aldosterone release when when BP is low

Answer 7

Ok

Question 8

Cushing’s syndrome
Cause
Clinical

Answer 8

• hypercortisolism
• obese, moon face, buffalo hump, easy bruising, hirsutism, purple striae, acne, virilization, diabetes, immunosuppression

Question 9

What is the dexamethasone suppression test and how is it related to dxing Cushing’s syndrome?

Answer 9

Dexamethasone is an analog of cortisol. There should be negative feedback of cortisol on ACTH. In Cushing’s, this does not happen

Question 10

Low dose vs high dose dexamethasone suppression test

Answer 10

Low dose does not specify source of ACTH overproduction

Question 11

How can you distinguish the ACTH overproduction source during a high dose dexamethasone test?

Answer 11

Some suppression of ACTH - pituitary tumor

No response at all - ectopic tumor

Question 12

What are the effects of excess glucocorticoids?

Answer 12

Increase overall metabolism (bone, muscle), fat deposition on viscera, salt and water retention, HTN, and immunosuppression

Question 13

What can cause Cushing’s syndrome?

Answer 13

Exogenous source of glucocorticoid (latrogenic)
Could be ACTH dependent (increased cortisol due to ACTH stimulation) or ACTH independent (increased cortisol due to some other reason - like an adenoma)

Question 14

Draw these different manifestations of cushings and its effect on CRH, ACTH and cortisol levels:
Problem at level of adrenal cortex
Problem at level of Pituitary
Ectopic ACTH source
Exogenous cortisol mimic

Answer 14

Ok

Question 15

*Describe the process in which aldosterone modulates salt homeostasis

Answer 15

Binds a cytoplasmic receptor > transcription > translation > proteins modulate Na+ and K+ channels

Question 16

What is ACTH’s relationship with hyperpigmentation?

Answer 16

ACTH is derived from Pro-opiomelanocortin (POMC). Excess ACTH can be cleaved further into MSH and stimulate the melanocytes to produce melanin.

Question 17

*What is cosyntropin stimulation test?

Answer 17

Used to detect adrenal gland insufficiency. Measure cortisol levels in the morning. If cortisol is too low, measure ACTH to see where the insufficiency stems from.

Question 18

IF there is low cortisol, how do you determine if AI is primary or secondary/tertiary using ACTH?

Answer 18

If high, that means the adrenal gland is not responding to ACTH stimulation = primary
If low/normal, the problem is higher up (secondary/tertiary)

Question 19

If there is low cortisol, how do you determine if AI is primary or secondary/tertiary using Aldosterone?

Answer 19

If aldosterone is also low = the adrenal gland itself is not working (can’t make either cortisol or aldosterone)
If aldosterone is fine = the problem is higher up (adrenal gland can make aldosterone but not cortisol, something wrong with the cortisol pathway)

Question 20

Addison’s disease:

Waterhouse-freidrichsen syndrome

Answer 20

Adrenal insufficiency due to autoimmune/hemorrhage/infection/metastasis aka whatever damage to adrenal gland
-due to adrenal gland damage by N. meningitidis infection

Question 21

How do you treat adrenal insufficiency?

Answer 21

Replace the hormones the adrenal gland is not making. Replace with corticosteroids or fludrocortisone

Question 22

Primary vs secondary hyperaldosteronism:

Answer 22

Primary: Adrenal cortex itself is making too much aldosterone, high PCA (Conn’s syndrome)
Secondary: Excess renin from kidney = increased aldosterone synthesis (high PRA)

Question 23

Hypoaldosteronism:

Answer 23

Can be due to destruction of the adrenal cortex, defects in aldosterone synthesis or inadequate stimulation of aldosterone secretion

Question 24

What is the role of enzyme 11B-HSD2?

Answer 24

Block cortisol from stimulating the aldosterone receptors in the body

Question 25

What is the effect of adrenal enzyme deficiency?

Answer 25

So adrenal gland is not making any cortisol due to enzyme deficiency. Nothing stops ACTH from being produced. ACTH keeps poking it to make more and causes adrenal hyperplasia

Question 26

Pheochromocytoma:

Answer 26

Adrenal tumors that secrete catecholamines. Causes HTN, headaches, palpitations and sweating Elevated levels of catecholamines and byproducts in the bloo

Question 27

Hormones produced by the adrenal medulla:

Answer 27

Epinephrine and norepinephrine

Question 28

What regulates the synthesis of catecholamines? How does this happen?

Answer 28

CRH-ACTH-cortisol axis (activated during sympathetic response) Cortisol upregulates PNMT enzyme > make the catecholamines

Question 29

What is the NT used to release catecholamines from the adrenal medulla?

Answer 29

Acetylcholine

Question 30

Draw the pathway for synthesis of catecholamines:

Answer 30

OK

Question 31

Draw the degradation process of catecholamines

Answer 31

Ok

Question 32

Draw the pathway of aldosterone and cortisol synthesis

Answer 32

Ok