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What are the Mechanisms for Na+ absorption throughout the Nephron?
- PT- NaHCO3
- LH- Na/K/2Cl Symport
- DT-NaCl
- CT- Na/K channel
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What is the location of the Strongest and most efficatious Diuretics?
in the LH, becaues it has less compensation later on.
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What are the Inhibitors of Na+ K+2Cl Co-transport?
What is the Efficacy?
Furosemide
Ethacrynic acid
- High eficacy
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What are the Inhibitors of Na-Cl Co-transport?
What is the efficacy?
Chlorothiazide, Chlorthalidone, Metolazone and Indapamide (thiazide like diuretic).
-Medium Efficacy
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Diuretics that act in the PT,LH,DT cause some degree of compensation in the CT. What is the primary Toxicity of these diuretics?
- -Hypokalcemia--> can cause Arrythmias
- -Metabolic Alkalosos
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Carbonic anhydrase inhibitor diuretic
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Acetazolamide
Does NOT cause Alkalosis
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Potassium sparing diuretics
Where is its action?
When is this used?
- Collecting Duct action
- Aldosterone antagonist :
Spironolactone, Eplerenone
Used in 2ary Aldosterone release from Heart faliure
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Inhibitors of renal epithelial Na channel
What are these used for?
Triamterene, Amiloride
Used for Ascities in Hepatic faluire
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Osmotic diuretics
Mannitol, Glycerol
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What is Furosemide?
Location?
Toxicity?
What will intravenous use cause?
What is this the DOC for?
Inhibitors of Na+ K+ 2Cl Co-transport a High ceiling loop diuretic.
- -Thick ascending loop of Henle
- -Mild alkalosis at high dose
- -rapid increase in systemic venous capacitance and decrease left ventricular filling pressure
pulmonary edema
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Furosemide
What does it increase?
What can be seen?
What is a common toxicity seen in intravenous administration?
- -Increases calcium excretion
- -Hyperglycemia and hyperuricemia can be occasionally seen with loop diuretics.
- Ototoxicity frequently
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What drug shouldnt be given with Furosemide?
Aminoglycosides, because both cause ototoxicity.
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