When is renin released?
What does renin do?
What acts as negative feedback for renin?
Renin is released when there is a decrease in blood pressure (IE hemorrhage, dehydration, sodium deplation)
Renin converts angiotensinogen into angiotensin I
Angiotensin II negatively feedbacks to renin
What two roles does angiotensin II have?
What activates angiotensin II?
- Vasoconstricts vascular smooth muscle
- Stimulates the adrenal gland to release aldosterone
Angiotensin Converting Enzyme (ACE)
What does aldosterone do?
Where does it act?
Aldosterone upregulates apical sodium channels and basolateral Na/K pumps to conserve sodium and excrete hydrogen and potassium
Collecting duct of the nephron
What are four classes of drugs that affect the RAAS pathway?
Give a drug for each class
- Direct Renin inhibitors
- ACE inhibitors
- Lisinopril, Captopril, Enalapril
- Angiotensin Receptor Blockers
- Mineralocorticoid Receptor Antagonist
What is the etiology behind primary hyperaldosteronism?
What symptoms/clinical signs are seen?
The adrenal gland overproduces aldosterone, due to some sort of overgrowth (cancer, hyperplasia, etc)
- Hypertension younger than 30
- Hypertension greater than 160/100
- Hypertension with hypokalemia
- Resistant hypertension
What are the initial tests for primary hyperaldosteronism?
What are the confirmatory tests?
- Plasma Aldosterone Concentration >15ng/dL
- Plasma Renin Activity <1.0 ng/mL/h
- PAC:PRA >20
- Imaging of Adrenal glands
- Bilateral renal vein sampling
What can cause primary hyperaldosteronism?
What can cause secondary hyperaldosteronism?
- adrenocortical adenoma
- zona glomerulosa bilateral hyperplasia
- Renal Ischemia
- Chronic Diuretic/Laxative Use
- Renal failure
- Heart failure
What should be done if a unilateral mass is found on the adrenals of a patient with hyperaldosteronism?
What should be done if both adrenals are found to be overproducing aldosteronism?
Medical management (IE spironolactone, eplerenone)
What are two genetic disorders that might produce similar symptoms as primary hyperaldosteronism?
What causes the pathology?
11-Beta hydroxysteroid dehydrogenase type 2
- Lack of 11B-HSD2 causes a build-up of cortisol
- Cortisol can activate the mineralocorticoid receptor
- mutations in the ENaC channel cause it to be constitutively active
- potassium waste