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31 Cards in this Set
- Front
- Back
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Diuretics
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For each diuretic tell me;
Names What segment? MoA? Effects on electrolyte/ water Indication SEs |
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Carbonic anhydrase
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Acetazolamide
Proximal tubule -- blocks formation of HCO3 in tubular brush cells → (-) HCO3-Na+ cotransport ↑ HCO3- excretion Metabolic Alkalosis SE: ↑ uptake of Cl- (instead of HCO3-)→ Hypercholremic metabolic acidosis |
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Osmotic Diuretics
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Mannitol
Proximal tubule -- non-reabsorable solute → ↑ in the lumen → ↓ water reabsorption ↓ water retention HTN Medical emergencies - Cerebral edema Hypovolemia Hypokalemia (↑ urinary flow) |
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Loop Diuretics
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Furosemide (“-semide”)
TAL -- (-)Na/K/2Cl → ↓ Na/water reabsorption, ↓ K+ reabsorption, ↓ corticopapillary gradient HTN w/ CHF, Edematous states Hypovolemia Hypokalemia (↑ urine flow, ↑ Na+ delivery to distal → ↑ K+ secretion) Metabolic alkalosis (↓ Na/Cl → ↑ reabsorption of HCO3-) |
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Thiazide
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Hydrochlorothiazide (HCTZ)
Early distal -- (-)Na/Cl → ↓ Na/Water reabsorption 1st line for HTN Hypovolemia Hypokalemia (↑ urine flow, ↑ Na+ delivery to distal → ↑ K+ secretion) Metabolic alkalosis (↓ NaCl → ↑ reabsorption of HCO3-) |
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K+ Sparing Direct ENaC inhibitor
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Amiolride, Triampterene
Collecting Duct -- (-)ENaC → ↓ Na/water reabsorption Hyperaldosteronism Hyperkalemia |
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K+ Sparing Aldosterone Antagonists
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Sprinolactone
Collecting Duct -- Aldosterone antagonist → ↓ aldosterone effects → 1. ↓ ENaC → ↓ Na/water reabsorption 2. ↓ Na/K ATPase → ↓ K+ secretion 3. ↓ H ATPase → ↓ H+ secretion/ NEW HCO3- reabsorption Hypovolemia Hyperkalemia Metabolic Acidosis |
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Which is the most potent diuretic?
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Loop
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Which is the 2nd most potent diuretic?
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thiazide
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Why do NSAIDs interfere w/ Diuretic action?
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(-) PG → ↓ afferent vasodilation → ↓ GFR → ↓ Na+ filtered (diueretic effects useless)
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How do Loop and thiazides lead to hypokalemia?
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1. ↑ DT Flow (↑ Water) → ↑ Na+ delivery to principal cells in collecting duct
2. ↓ ECF → +Na intake → RAAS → ↑ Aldosterone 3. ↑ Luminal anion |
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Why is thiazide diuretic the most likely to cause hyponatremia and therefore low blood V?
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blocks both diluting segments, TAL & distal tubule
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Antihypertensives
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Treatment strategy for secondary HTN? Describe for each one
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Remove secondary cause
Pheochromocytoma → remove adrenal tumor 2o hyperaldosteronism → Fix RAS, stop glucocorticoid use Chronic Kidney Disease (glomerular disorders) → Dialysis Renal artery disease (RAS, FMD) → surgical repair |
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What is treatment strategy for primary HTN? When?
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Anti-hypertensive drugs when >140
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For the Following Anti-hypertensives:
Class? What is the MoA? How does it ↓ BP? SE? |
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Parazosin (-zosin)
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a1 antagonist → ↓ TPR (vasodilation)→ nausea, vomiting, lightheadedness but excercise tolerant
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Clonidine
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a2 agonist → ↓ NE from central → ↓ TPR (vasodilation) → dry mouth, Na/water retention overtime
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Methyldopa
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a2 agonist → ↓ NE from central → ↓ TPR (vasodilation) → dry mouth, Na/water retention overtime
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Propanolol (-olol)
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B-blocker → ↓ contractility, ↓ HR (↓ CO) → pulmonary problems (asthma) and exercise intolerant; CI for heart failure
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Lisinopril (-opril)
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ACE-I → ↓ RAAS→ ↓ Na/water retention (↓ preload → ↓ CO & TPR) → 2o Hypoalodsteronism (hyperkalemia)
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Lorsartan (-sartan)
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AT2 Receptor blocker (ARB) → ↓ RAAS → ↓ Na/Water retention (↓ preload → ↓ CO & TPR) → 2o Hypoaldosteronism (hyperkalemia)
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Direct Renin inhibitor
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↓ RAAS → ↓ Na/Water retention (↓ preload → ↓ CO & TPR) → CI w/ ACE-I & ARB b/c too much ↓ Aldosterone
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Diltiazem
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CCB → both vasculature (↓ TPR) & Heart (↓ contractility, ↓ HR = ↓ CO) → CI for HF, post mi, pregnancy
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Verapamil
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CCB → only heart (↓ contractility, ↓ HR = ↓ CO) → CI: HF, post-mi, pregnancy
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Amlodipine
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CCB → only vasculature (↓ TPR) → CI: HF, post-mi, pregnancy
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Nifedipine
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CCB → only vasculature (↓ TPR) → CI: HF, post-mi, pregnancy
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What are the Vasodilators?
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(5)
Minoxidil Diazoxide Hydralazine Nitroprusside Fenoldopam |
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MoA of Vasodilators?
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↑ NO
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SE of Vasodilators?
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Lupus!, reflex tachycardia
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