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