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23 Cards in this Set

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Types of channels involved at different sites in the nephron?
PCT: Na-H exchange, co-transport glc.

Loop of Henle (thick Asc. Limb): Na-K-2Cl co-transport. NH3 can substitute for K.

DCT: Na-Cl co-transporter

Collecting Tubule: Na channels
PCT: Acetazolamide
A carbonic anhydrase inhibitor; disabling breakdown of carbonic acid. So, in the lumen, less bicarbonate + H is converted to carbonic acid, therefore less H is excreted and less Na is reabsorbed, resulting in Loss of Na and carbonic acid in bicarbonate in urine. Similarly, within the cell, less HzO and COz is converted to carbonic acid. The end result is urine alkylinization, Na, K and HCO3 loss with Cl- retention.
Acetazolamide: pharmacokinetics
Rapid GI absorption, 80% excreted unchanged, pk level within 2 hrs. After few days, causes mild hypercholoremic acidosis (due to Cl- retention) and diuretic action is terminated even with continued administration.
Acetazolamide: uses
Useful in edematous pt with metabolic alkalosis (helps with water loss and HCO3 loss), Urinary alkalization (to get rid of acidic drugs), Glaucoma (decrease aq humor production), Acute Moutain Sickness (decrease CSF production, pulmonary edema and decreases pH.)
Acetazolamide: contraindications, toxicities
Contraindicated in pts with hepatic cirrhosis (NH4 accumulation)

Toxicities: hyperchloremic metabolic acidosis, renal stones, potassium loss, hypersensitivity rxn.
PCT& Descending loop of Henle: Mannitol
An osmotic diuretic, a metabolically inert hexose sugar. Urine flow is increased resulting in increased excretion of Na, K, Cl, bicarb, Ca, Mg.

Therapeutic effect: increase urine volume (prev. or trt Acute Renal failure

Reduce intracranial and intraocular pressure

Toxicity: Dehydration, hypernatremia, extracellular vol expansion
Loop of Henle: Furosemide (Lasix), Bumetanide, Ethacrynic Acid
Inhibit Cl- transport resulting in Na excretion in urine. Effect of agents not additive. No effect on pH or HCO3. Increase urine composition of: Na, K, Cl, Ca and Mg.

These are the most potent diuretic agents available.
Loop diuretic pharmacokinetics
Protein bound drug

Ethacrynic acid: Excreted by kidney (60%) and liver (30%).

Furosemide: kidney (60%) feces (30%)

May be given IV or PO. Effects seen 30-60 min PO or 5 min after IV.

Effectiveness depends on amt of drug that reaches the lumen.
Loop diuretic Therapeutic effects
Short acting, NOT intended for use as a single agent therapy for HTN.

Reserved for pts with impaired renal fxn, refractory edema, acute pulmonary edema or hypertensive crisis. Also used in hypercalcemia and acute anion overdose.

Tox due to effect on ECF composition.
Loop Diuretics: Drug Interraction
Aminoglycosidase antibiotics, cephaloridine, lithium displace drug from plasma protein.
DCT: Thiazides and Thiazide-like agents
This includes all the –thiazide drugs.

Unlike acetazolamide (a CAI), thiazides are effective at both extremes of acid-base balance. It competes for the Cl site on the Na-Cl co-transporter. Drug actions are additive to ethacrynic acid or furosemide.
What other drugs, though not benzothia-diazines have similar diuretic action as thiazides?
Chlorthalidone, quinethazone, indapamide, metolazone
Effects of Thiazides on Urine composition?
pH increased, Na, K , Cl, HCO3 and Uric acid increased. CALCIUM decreased due to increased reabsorption of Ca in DCT.
Thiazide Pharmacokinetics?
Absorbed from GI and effective in 1- hrs with peak at 4-6 hours. Drug BINDS plasma proteins. THESE AGENTS CROSS PLACENTA.

Dose related effects: Hypokalemia, Hyperuricemia, Hyperglycemia, Hyperlipidemia, hypercalcemia
Therapeutic uses of Thiazides
IN NORMAL RENAL FUNCTION, preferred initial diuretic (ineffective in pts with impaired renal fxn). First line in essential hypertension ( lowers TPR). When used at lose dose, adverse effects of K loss, insulin resistance and lipid elevation can be avoided.
List the Therapeutic uses of Thiazides
Intial and chronic HTN therapy

Initial therapy: CHF

Edematous disorders, Idopathic hypercalciuria, Nephrogenic diabetic insipidus.
Thiazide toxicity
Hypokalemia, pancreatitis, cholecystitis, hyperlipidemia, hypercalcemia, hyerpuricemia, hyperglycemia, SEXUAL DYSFUNCTION (upto 25% males)
Collecting tubule: K-sparing Diuretics, 2 classes
SPIRONOLACTONE, an adosterone antagonist.

Triamterene, Amiloride, NOT spec inhibitors of aldosterone.

These drugs inhibit Na reabsorption at a small fraction, hence resulting in low K excretion.

NOT POTENT, and not used alone. Used with thiazides or loop diuretics to reduce K loss, minimize alkalosis and produce additive effect.
Used in CONJUCTION with ACE-i. resulted in 30 % reduction in mortality possibly due to decrease in freq of ventricular arrhythmias, and lower incidence of hypokalemia (RALES trial, in NY class III or IV Heart Failure pts).

Also active at extra-renal sites: sweat, salivary glands, large intestines. Needs a 1000:1 ratio to have its inhibitory effects on Aldosterone.
Endocrine side effects of Spironolactone?
Gynecomastia, breast pain, menstrual irregularities, impotence and decreased libido.
K-sparing Collecting Tubule: Triamterene and Amiloride
Triamterene and Amiloride act on aldosterone independent site to block the Na channel, resulting in prevention of lumen-negative transepithelial voltage that drives K secretion.
IRREVERSIBLY inhibits the transbasolateral potential difference in CD.


Tox: Crystaluria, cast formation, stones, acute renal failure.
Hyperkalemia, azotemia, glc intolerance in diabetics.
Ats at the luminal surface and REVERSIBLY inhibits the development of potential difference.

Useful in pts with polyruia and polydipsia due to lithium induced nephrogenic diabetes insipidus.

Tox: hyperkalemia