Aldosteronism (Darrow) - MT Flashcards
How does hyperaldosteronism lead to glucose intolerence?
Hypokalemia induced by excess aldosteronism causes a decrease in Insulin secretion.
( Insulin secretion is dependent on Beta cell intracellular potassium)
What can cause polyuria or polydipsia? ( > 3 L / day)
C-DRIPPED pneumonic
- Cortisol excess
- DI/DM
- Recovery from renal failure
- Ions like hyper Calcemia, hypo K; IV infusion (manitol)
- Parkinson’s (nocturnal nocturia)
- psychogenic polydipsia
- enzyme (ADH)
- Drugs (lithium, demeclocycline, cis-platinum)
Hypokalemi produces a defect in activation of ______ and thus, causes _______ leading to ________.
- Renal adenyl cyclase
- nephrogenic DI
- Polyuria
A patient comes in to see you during an asthma attack. She tells you she has a history of frequent attacks and uses a lot of albuterol to releive her symptoms. What lab result is in her metabolic panel do you expect to be low?
- K+ levels (hypokalemia) d/t insulin release stimulated by albuterol
* insulin drives K+ into the cells
- The distal convoluted tubules of the kidneys are sensitive to what molecule?
- The Collecting ducts of the kidneys are sensitive to what molecule?
- Aldosterone
- ADH
Conn’s disease patients don’t have edema b/c…?
No edema d/t volume expansion with production of ANP, which somewhat counteracts aldosterone effect and production.
Causes of non essential HTN include?
AMPS pneumonic
- Aldosteronism
- Myxedem and hypercalceMia
- Pheochromocytoma
- Steroid excess (cushings and CAH)
3 Causes of hyperaldosteronism (Conn syndrome) seen in 5-10% of HTN patients are?
- Adrenal Adenoma (Conn syndrome under influence ACTH)
- Unilateral or bilateral hyperplasia (super sensitive to physiological leels of Ang II)
- Genetic defect w/ overly strong effects on ACTH on aldosterone production
How would you differentiate and diagnose primary hyperadrenalism d/t:
- unilateral adenoma of the adrenal gland
- Adrenal hyperplasia
* Both require 24 hour urine collection with high urine aldosterone of >20 mcg/24 hours coniciding with low plasma renin <5 mcg/L/h to confirm primary aldosteronism
- CT scan for unilateral adenoma
- Postural stimulation test that shows a supine baseline plasma aldosterone of <20 ng/dL with significant post supine postural elevation of the aldosterone level
How would you treat a patient that has b/l adrenal hyperplasia causing non essential HTN?
With medications that are aldosterone antagonists like:
- Spironolactone: gynecomastia ADR
- Eplerenone
What type of cells do Spironolactone and eplerenone act on in the renal tubules to counteract the effects of primary hyperaldosteronism?
Principle cells
(Aldosterone antagonsists)
What are the 6 steps in the diagnostic workup of suspected primary hyperaldosteronism?
(Give lab test and diagnostic levels)
- Test renin a 8-10 AM (nml or high renin disproves hyperaldosteronism)
- if Aldosterone is low, stand up for 3 hours and look at plasma Aldosterone/Renin ratio. if A/R ratio > 30 ng/dL then probable hyperaldsteronism
- If A/R ratio increased, confirm with Na loading and 24 hour urine for aldosterone: urine aldosterone > 20 mcg/24 hours indicates primary hyperaldosteronism
- If urine aldosterone increased, do adrenal CT or adrenal vein sampling to distinguish hyperplasia from adenoma
- if unsure, do postural stimulation test (draw plasma aldosterone at 8 am after 4 hours upright). aldosterone base level of 20 ng/dL will rise if b/l hyperplasia, but will not if adenoma
- if adenoma do surgery, if hyperplasia use spironolactone or eplerenone
A patient comes in complaining of headaches. On PE you discover a 5 cm left shifted PMI from left MCL. She has developed atherosclerosis d/t her history of previously untreated DM II. She has noted that she eats a lot of licorice. How could the licorice be possibly contributing to her current condition?
- What does it inhibit?
- What does the molecule that it inhibits usually do?
- Licorice inhibits 11 beta HSD2, thus allowing cortisol to drive mineralcorticoid receptors with resultant hypertension (renin and aldosterone levels will be low)
- 11 beta HSD2 in principle cells prevent cortisol from activating the MRE by converting cortisol (active) into cortisone (incactive)
Licorice will cause what to happen to Plasma renin activity (PRA) and Plasma aldosterone concentration (PAC)?
- Decreases both of them by inducing an 11 beta HSD2 deficiency.
Types of aldosteronism include Primary, secondary, and pseudohyperaldosteronism. What are some of the causes of secondary (x3) and pseudo subtypes (x4)?
- Secondary (physiologic homeostatic response): Inc Renin, Inc Aldost
1. diuretics
2. Vomiting
3. Nasogastric suction - Pseudohyperaldosteronism: dec renin, dec aldost
1. liddle’s syndrome
2. cushings, exogenous steroids
3. CAH
4. Licorice
