Hypothalamic-Pituitary Relationships and Biofeedback Pt.2 Flashcards
What do these layers secrete? Zona glomerulosa Zona fasciculata Zona reticularis Chromaffin cells (in medulla)
- Mineralocorticoid (aldosterone)
- glucocorticoid (cortisol and androgens/DHEA - precursor)
- glucocorticoid (cortisol and androgens/DHEA - precursor)
- Catecholamines (epinephrine and norepinephrine
Draw the HPA axis
Ok
What triggers cortisol secretion?
Stress (physical, emotional and metabolic stress)
What are the actions of cortisol?
Immunosuppression
Gluconeogenesis
Protein catabolism
Lipolysis
Describe the diurnal pattern secretion of cortisol
High in early morning and low in late evening
What is the major controller of aldosterone secretion from the adrenal cortex?
Low blood pressure
Draw the pathway/schematic of aldosterone release when when BP is low
Ok
Cushing’s syndrome
Cause
Clinical
- hypercortisolism
- obese, moon face, buffalo hump, easy bruising, hirsutism, purple striae, acne, virilization, diabetes, immunosuppression
What is the dexamethasone suppression test and how is it related to dxing Cushing’s syndrome?
Dexamethasone is an analog of cortisol. There should be negative feedback of cortisol on ACTH. In Cushing’s, this does not happen
Low dose vs high dose dexamethasone suppression test
Low dose does not specify source of ACTH overproduction
How can you distinguish the ACTH overproduction source during a high dose dexamethasone test?
Some suppression of ACTH - pituitary tumor
No response at all - ectopic tumor
What are the effects of excess glucocorticoids?
Increase overall metabolism (bone, muscle), fat deposition on viscera, salt and water retention, HTN, and immunosuppression
What can cause Cushing’s syndrome?
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)
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
Ok
*Describe the process in which aldosterone modulates salt homeostasis
Binds a cytoplasmic receptor > transcription > translation > proteins modulate Na+ and K+ channels
What is ACTH’s relationship with hyperpigmentation?
ACTH is derived from Pro-opiomelanocortin (POMC). Excess ACTH can be cleaved further into MSH and stimulate the melanocytes to produce melanin.
*What is cosyntropin stimulation test?
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.
IF there is low cortisol, how do you determine if AI is primary or secondary/tertiary using ACTH?
If high, that means the adrenal gland is not responding to ACTH stimulation = primary
If low/normal, the problem is higher up (secondary/tertiary)
If there is low cortisol, how do you determine if AI is primary or secondary/tertiary using Aldosterone?
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)
Addison’s disease:
Waterhouse-freidrichsen syndrome
Adrenal insufficiency due to autoimmune/hemorrhage/infection/metastasis aka whatever damage to adrenal gland
-due to adrenal gland damage by N. meningitidis infection
How do you treat adrenal insufficiency?
Replace the hormones the adrenal gland is not making. Replace with corticosteroids or fludrocortisone
Primary vs secondary hyperaldosteronism:
Primary: Adrenal cortex itself is making too much aldosterone, high PCA (Conn’s syndrome)
Secondary: Excess renin from kidney = increased aldosterone synthesis (high PRA)
Hypoaldosteronism:
Can be due to destruction of the adrenal cortex, defects in aldosterone synthesis or inadequate stimulation of aldosterone secretion
What is the role of enzyme 11B-HSD2?
Block cortisol from stimulating the aldosterone receptors in the body
What is the effect of adrenal enzyme deficiency?
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
Pheochromocytoma:
Adrenal tumors that secrete catecholamines. Causes HTN, headaches, palpitations and sweating
Elevated levels of catecholamines and byproducts in the bloo
Hormones produced by the adrenal medulla:
Epinephrine and norepinephrine
What regulates the synthesis of catecholamines? How does this happen?
CRH-ACTH-cortisol axis (activated during sympathetic response)
Cortisol upregulates PNMT enzyme > make the catecholamines
What is the NT used to release catecholamines from the adrenal medulla?
Acetylcholine
Draw the pathway for synthesis of catecholamines:
OK
Draw the degradation process of catecholamines
Ok
Draw the pathway of aldosterone and cortisol synthesis
Ok
