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- *Maintains fluid volume within narrow limits
- *Maintains acid-base balance and electrolyte blanace in the body.
- *Removes body of nitrogen wastes
- *Blood vessels
- *Afferent and efferent arterioles
- *Pertibular capillaries
- *Coiled renal tubule- Proximal, Loop of Henle, and distal.
THE PROCESS OF HOW KIDNEYS CARRY OUT THEIR FUNCTION-
- 1. Glomular filtration-
- High BP in glomerulus forces out water, ions, small molecules. Absorbed by cells of Bowman's capsule.
- 2. Tubular reabsorption-
- Substances pass from tubule back into blood, involves active and passive processes.
- 3. Tubular secretion- substances pass from blood into tubule, involves mainly active processes.
- *Ascending loop of Henle
- *Early distal tubule
- *Collecting tubules and ducts
- Reasorbs 60-70% of tubular fluid- water and sodium into renal tubule cell, then water and sodium then travel from cell back into BV's.
- -Sodium with sugars, amino acids, ions
- -Sodium with potassium and chloride
- -Carbonic anhyrase system- sodium is exchanged for hydrogen.
- 1. Ascending limb of the loop of Henle-
- Na, k, and cl cotransport system-absorbed back into blood.
- 2. Early distal tubule-
- active transport of cl, na, and water follow -all absorbed back into the blood
- 3. Late distal tubule-
- Aldosterone dependent na, k, exchange system-na is reabsorbed back into the blood and k is secreted into the renal tubule and excreted.
- *BP detected by juxtaglomerular cells
- *renin releases
- *renin stimulates production of angiotensin 1
- *angiotensin 1 is converted by ACE to angiotensin 2
- *effects of angiotensin 2- direct vasoconstriction, stimulates thirst, affects CNS tostimulate sympathetic activity.
- *Vasopressin (ADH) on the renal tubules
- *Increases reabsoprtion of water from the collecting duct:conserves body water and concentrates urine.
- *Stimuli for release of ADH
- 1. Increasing plasma osmolarity monitored by osmorecptors in hypothalmus
- 2. Volume depletion
- 3. Stress, exercise
- 4. ADH causes luminal cell membranes to become permeable to water
- Diabetes insipidus- inability to make a concentrated urine.
- *Edema due to heart failure
- *Nephrotic syndrome
DIURETIC DRUG PHARMACOKINETICS-
- *aLL AFFECT ELECTROLYTES
- *lIVER IS PRIMARY SITE OF METABOLISM
- *cAUTION WITH USING IN RENAL IMPAIRED
- *CAUTION W ITH HEPATIC DYSFUNCTION
- *METALAZONE AND BUMETANIDE AND SPIRANOLACTONE HAVE SOME EXCRETION IN FECES AND BILE
- (PLASMA HALF LIVES RANGE FROM 30-60 MIN FOR LASIX TO 30-50 HOURS FOR CHLORTHALADONE
TYPES OF DIURETICS
- 1. Loop
- 2. Thiazides
- 3. Osmotic
- 4. Carbonic anhydrase inhibitors
- 5. Postassium-sparing
- *Aldosterone antagonists
- *Nonaldosterone antagonists
- *Lasix, Edecrin, Bumetanide (Bumex)
- *MOA- blocks 1 na, 1 k, and 2 cl-cotransport system in thick ascending limb of loop of Henle
- *Most powerful of all diuretics!!!!!
- *Effects on diuresis- 25% of filtrate excreted, increased excretion of water, na, k, cl, ca, decreased excretion of uric acid
- *Effect on Hemodynamics- vasodilation in kidney increases renal blood flow.
- *SE- decreased blood volume- dehydration,shock, circulatory collapse, thrombi, and emboli.
- -Electrolyte changes (lead to alkolosis and arrythmias)
- -Ototoxicity- HIGH with Edecrin
- -RARE se- nausea, allergic reaction d/t sulfa component, deafness.
- *PO effect- 1 hour
- *IV effect- 30 min
- *Drug interactions- aminoglycosides, warfarin, clofibrate, cephaloridine
- -Edema d/t HF
- -Nephrotic syndrome
- -Pulmonary probems- edema
- -Hypercalcemic crisis
- -Renal failure
- *HCTZ, chlorthalidone (Hygroton)
- *MOA- decreases na and cl reabsoprtion at early distal tubule
- *effects on diuresis- 5-8%of filtrate excreted, increased excretion of water, decreased uric acid excretion, decreased excretion of CA!, extrarenal effects- hyperflycemia, vasodilation.
- *Drug interaction increase effect of BP medications!
- *po effect in 4-6 ours
- 1. Fluid and ELECTROLYTE IMBALNACES- decreased k, increased uric acid, hyperglycemia, increased calcium absorption, alkalosis.
- 2. Hyperlipidemia
- 3. Extrarenal s/e
- 4. Male impotence
- 5. Hypersensitivity reactions- skin rashes, blood dyscrasia, pancreatitis, acute pulmonary edema.
- 1. HTN
- 2. Edema d/t HF
- 3. nephrotic syndrome
- 4. ascities
- 5. diabetes insipidous
- 5. Hypocalcemia
- 6. Osteoporosis
- *Spironalaction, triamterene, amiloride
- *MOA- inhibition of na, k, exchange systemsi nt he distal tubule and collecting duct (only spironolactone is competitive antagonist of aldosterone)
- *effects on diuresis 2-3% of filtered load excreted, increased water and na excretion, decreased k and h excretion.
- *S/E- electroly imbalances, increased k
- *Indications- adjunct use with other diuretics to: decrease k loss in HTN, edema, hyperaldosteronism.
CARBONIC ANHYDRASE INHIBITORS-
- *Acetazolamide (Diamox)
- *MOA- inhibition of carbonic anhydrase in the proximal tubule, so that na is excreted and h is saved in the body
- *Effect on diuresis- na, k and hco3 are excreted, less cl is excreted, urine becomes alkaline.
- *S/E- k loss, acidosis, drowsiness, paresthesias, hypersensitivity, teratogenicity
- *Indications- adjunct use with other diuretics- esp when alkalosis is present, grand mal epilepsy, glaucoma, mountain sickness.
- *Mannitol (osmitrol)
- *MOA- works throughout renal tubule, provides nonabsorbable particles that exert osmotic pressure in side renal tubuel
- *Effect on diuresis- greatly increases water and solute excretion, incrreases excretion of na, k , cl, hco3, ca, mag
- *Hemodynmaic effect- increases osmolality of plasma
- *S/E- h/a, n/v, acidosis, increased edema- contraindicated in CHF
- *used to prevent renal shutdown in burn and trauma pts and brain,eye and CV surgery.
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