Glossary of 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.
*[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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