Physiology-Aldosterone & Catecholamines Flashcards
5 mechanisms for regulating fluid and electrolyte balance
1) ADH 2) Thirst 3) RAAS 4) ANP 5) Na Appetite
Regulation of aldosterone secretion
RAAS, serum K+ and to a lesser degree ACTH
What does aldosterone do at the distal nephron?
Excretion of K+ and H+. Reabsorption of Na+
How does the body deal with an increased sodium load?
Osmoreceptors in macula densa decrease aldosterone release and inhibit RAAS -> Na secretion & K reabsorption -> K uptake in cells to prevent hyperkalemia -> normal Na level restored -> RAAS starts again -> Na reabsorption & K secretion begins
What are the functional components of the juxtaglomerular apparatus?
Baroreceptors, chemosensor and neuroendocrine transducer. Granular cells secrete renin, macula densa cells do the sensing.
Principle drivers for renin output
1) Low sodium 2) Low volume 3) Low pressure 4) Hyperkalemia
Strongest vasoactive compound
ATII
How does hyperkalemia affect the adrenal cortex?
It acts directly on the zona glomerulosa to stimulate aldosterone secretion
How do ACTH and ATII affect synthesis of cortisol and aldosterone?
ACTH has a greater effect on cortisol synthesis when it binds the zona fasciculata. ATII has a greater effect on aldosterone synthesis when it binds the zona glomerulosa.
What happens if you have too much aldosterone?
Hypernatremia, hypertension and hypokalemia
A patient presents with hypertension, weakness, polyuria and metabolic alkalosis. She is fluid overloaded and you determine she has primary hyperaldosteronism. What is likely causing her condition?
Adrenal tumor secreting aldosterone on its own or renin suppression causing hypernatremia and hypokalemia.
A patient presents with low blood pressing, edematous legs and hypokalemia. He is low on blood volume and you determine he has secondary hyperaldosteronism. What is likely causing his condition?
Adrenal hyperplasia driven by RAAS due to ascites and fluid leaving the vasculature, making the JG cells sense low blood volume. Renal artery stenosis can also cause this.
How does congenital adrenal hyperplasia in a genetic female occur?
The enzyme deficiency in 21-hydroxylase causes cholesterol intermediate shunting towards androgens instead of making aldosterone & cortisol. The hypothalamus continues to sense deficiency in cortisol so CRH is continually released, the adrenal gland grows and more androgens are produced. Too much androgen in a developing female causes masculinization of the genitalia.
What do chromaffin cells do?
Synthesize, store and secrete NE and EPI.
Integrated response for alpha and beta adrenergic stimulation during fight or flight response.
Alphas always win (example of insulin secretion being inhibited by alpha stimulation be activation by beta stimulation)
Name some symptoms that occur during or following paroxysms in people with pheochromocytomas.
Headache, sweating, palpitations, impending death feeling, tremor, exhaustion, nausea, chest/abdominal pain or visual disturbances.
Symptoms between paroxysms in people with pheochromocytomas.
Sweating, cold hands/feet, weight loss and constipation
Why do most people with pheochromocytomas die?
MI, stroke, arrhythmia, shock, renal failure, aortic dissection. This is all from severe fight or flight stimulation.
How do you treat someone with a pheochromocytoma?
1) Surgery. Alpha blockers to decrease BP, beta blockers to decrease HR, contractility and renin production, Ca-channel blockers to decrease HR and contractility and catecholamine synthesis inhibitors.
A cell responding to a hormone has an immediate increase in intracellular concentrations of cAMP and Ca2+. The hormone is A) Progesterone B) Cortisol C) Aldosterone D) Testosterone E) Epinephrine
E. EPI is the only one not a steroid and acts on cell surface receptors. It is also the only one that causes an immediate change.
Sectioning of the pituitary stalk will result in?
Polyuria, polydipsia and hyperprolactinemia
A rapid expansion of the intra-vascular volume by an infusion of 2L isotonic saline will normally be compensated by?
Decrease in AT II production
Cirrhosis of the liver results in ascites and decreases the effective blood volume (from intravascular fluid leakage). Appropriate compensatory responses to correct this condition include?
Increased sodium reabsorption by the nephron
A substance isolated in the blood has the following characteristics: small, lipid soluble, binds to receptors located in the nucleus and increases blood volume when administered over time. The isolate substance is most likely?
Aldosterone
