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9 - Kidney and HTN


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Name two differences between hypertension of known cause and essential hypertension.
1.Cause is known
2.Age of onset is earlier
3.Typically more dramatic
Renal artery stenosis causes a decrease in three measures of blood flow in the kidney - what are they?
3.Hydrostatic pressure in the kidney
What is the major cause of hypertension in renal artery stenosis?
Decreased GFR results in less NaCl being filtered. This is detected by the macula densa which then triggers a release of renin. This raises the circulating concentration of angiotensin II which raises blood pressure via several mechanisms.
Why do most patients with renal artery stenosis NOT suffer from renal failure?
The pathogenic increase in angiotensin II causes a constriction of the efferent arterioles...this raises GFR to a minimally acceptable level.
Is the hypertension caused by renal artery stenosis treated with ACE inhibitors? Why or why not?
No - the constrictive effect of angiotensin II on the efferent arterioles maintains a minimal GFR to prevent renal failure. ACE inhibitors would prevent this.
What is the essential defect in glucocorticoid remediable aldosteronism? How does this disorder cause hypertension?
ACTH inappropriately stimulates the release of aldosterone. Aldosterone stimulates Na+ reabsorption, thus increasing ECV and blood pressure.
How is glucocorticoid remediable aldosteronism treated?
Patients are administered cortisol which exerts negative feedback on the release of ACTH from the anterior pituitary.
What lab values might be strange in patients with glucocorticoid remediable hypertension?
*high circulating aldosterone
What is the essential defect in apparent mineralocorticoid excess?
The enzyme that normally converts cortisol to cortisone in the kidney is inactivated. As a result, mineralocorticoid receptors are inappropriately stimulated by cortisol, thus simulating the action of aldosterone.
How is apparent mineralocorticoid excess treated?
Patients are administered spirolactone, a specific blocker of mineralocorticoid receptors in the kidney. Inhibition of this receptor prevents up-regulation of ENaC.
Describe the lab profile of a patient with apparent mineralocorticoid excess.
*low aldosterone
*[cortisol] remains ~normal
What is the essential defect in Liddle's syndrome?
A mutation in the gene coding for ENaC causes an increase in the number and activity of this channel, leading to increased Na+ reabsorption and K+ secretion.
How is Liddle's Syndrome treated?
Amiloride, a specific blocker of ENaC
What is the anti-hypertensive that acts at the PCT and inhibits carbonic anhydrase? What is the effect of this action?
*decreases the activity of the Na+/H+ antiporter
What is the mode of action of Lasix? What is one possible side effect of this medication?
It acts at the ascending loop of Henle where it inhibits the K+/Na+/2Cl-. Hypokalemia is possible.
Thiazide is known to inhibit the activity of a Na+/Cl- transporter. Which segment of the nephron is primarily affected?
The distal convoluted tubule.
Where does amiloride act?
ENaC channels in the DCT and collecting ducts.

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