Pharm 15 Diuretic Agents By Tracy-Jo

Front 1

hydrochlorothiazide is prototypical thiazide half life is

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6-12 hrs considerably longer than loop diuretics

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what is major action of thiazides

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to inhibit sodium chloride xport in early segment of DCT; produce moderate NaCl diuresis; hypokalemic met alkalosis may occur

Front 3

reduction in the xport of sodium from the lumen into tubular cell reduces intracellular sodium and promotes sodium calcium exchange at basolateral memb; resulting in reabsorption of calcium from the urine (opposite effect of loop diuretics)

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thiazides

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what is toxic side effect of thiazides

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massive sodium diuresis with hyponatremia is uncommon but dangerous early effect; chronic therapy is assoc with potassium wasting since an increased sodium load is presented to collecting tubules

Front 5

60-70% of reabsorption of sodium takes place in what area of nephron

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PCT; no drug directly acts on NaCL reabsorption in PCT

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isosmotic reabsorption of AA's, glucose and numerous cations, sodium chloride and sodium bicarb occurs here

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PCT

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bicarbonate is poorly reabsorbed thru lumen but conversion of bicarb to CO2 permits rapid reabs of CO2 which can be ______ from Co2 within the tubular cell

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regenerated

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sodium is reabsorbed in exchange for

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hydrogen ions and transported into interstitial space by the sodium pmp

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carbonic anhydrase is target for carbonic anhydrase inhibitor diuretic drugs

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acetazolamide (bicarbonate diuretic)

Front 10

most weak acid xport occurs in straight

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S2 segment distal to convuled part (uric acid xport esp imp); weak bases in S1 and S2

Front 11

TAL pumps Na, K and Cl out of the lumeninto interstitium via a

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single carrier NKCC2; also major site of Ca and Mg reabsorption

Front 12

loop diuretics target what

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the NKCC2 carrier in TAL

Front 13

pumping of K+ into the cell from both lumen & interstitium (Na/K pump) would result in high IC K+ but K+ moves down its

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concentration gradient back into lumen; this extra + charge in the lumen drives reabsorption of Ca and Mg

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what is target of thiazide diuretics

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Na Cl cotransporter in DCT; responsible for 5-8% of Na reabsorption

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what else is reabsorbed in DCT under the control of PTH

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transfer of the reabsorbed Ca back into the blood requires the Na/Ca exhanger

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where is the last tubular site of Na reabsorption

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Cortical collecting tubule (CCT) controlled by aldosterone - reabsorption of Na via channels accompanied by equiv loss of K+ and H+

Front 17

what part of nephron is primary site of acidification of the urine and of potassium excretion

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CCT

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the descending loop dilutes the

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medulla and conc the desc loop (osmotic diuretic ?)

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what are the sites of action for the potassium sparing diuretics

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aldosterone rec and sodium channels at the CCT

Front 20

reabsorption of water in the collecting tubule is under the control of

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ADH

Front 21

since most diuretics act from the luminal side the must be present in the

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urine; filtered at the glomerulus and some secreted by the weak acid carrier in PCT; exception is spironolactone, eplernone enter basolateral

Front 22

what is mechanism of action of acetazolamide

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carbonic anhydrase inhibitor in brush border and intracellular in PCT; bicarbonate diuresis (metabolic acidosis)

Front 23

what is impact of inc sodium presented to the CCT since not reabsorbed at PCT

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some Na reabsorbed in CCT and potassium is secreted - resulting in potassium wasting

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as bicarbonate depletes, sodium bicarbonate excretion slows and the diuresis is self-limiting within

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2-3 days

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inhibitory effect of acetazolamide occurs everywhere in the body including

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secretion of bicarbonate into aqueous humr in eye and into CSF by plexus is reduced which is useful for reducing IOP; in CNS acidosis of CSF results in hyperventilation can protect against altitude sickness

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what is the major application for carbonic anhydrse inhibitors

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treatment of glaucoma; topical dorzolamide, brinzolamide

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carbonic anyhdrse inhib also used to prevent acute

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altitude sickness;

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carbonic anhydrase inhib as diuretic only if

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edema accompanied by metabolic alkalosis

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Diuretic used for mountain sickness and glaucoma

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acetazolamide

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SE of acetazolamide

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Paresthesias, alkalization of the urine (which may ppt. Ca salts), hypokalemia, acidosis, and encephalopathy in patients with hepatic impairment

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MOA of loop diuretics

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inhibits Na+/K+/2Cl- cotransport

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Site of action of loop diuretics

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Thick ascending limb

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SE of loop (furosemide) diuretics

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Hyperuricemia, hypokalemia and ototoxicity

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SE of CA inhibitor

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alkalinization of urine by these drugs may cause precipitation of calcium salts and form renal stones

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what is prototypical loop agent

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furosemide (bumentanide, torsemide are sulf

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Carb anhy inhib - acetazolamide causes increase in what ions in urine

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Na+ and HCO3-

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carbonic anhydrase inhib

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inc NaCl, NaHCO3 and K+ in urine and causes acidosis in body pH

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loop diuretics short or long acting

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short

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diluting ability of nephron is reduced with

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loop diuretics

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inhib of Na/K/Cl xporter results in loss of divalent cations

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calcium excretion is increased

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prostaglandins imp in maintaining glomerular filtration so when inhibited by NSAIDs reduces efficacy with

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loop diuretics

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major application of loop diuretic

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heart failure, ascites and particular value in pulm edema since has pulm vasodialting action

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toxicity of loop diuretics induce

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hypokalemic metabolic alkalosis; ototoxicity

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what is affect of thiazide on calcium

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reduction of xport of Na from lumen reduces intracellular Na and promotes Na/Ca exchange (Na leaves so more sodium comes into cell from interstitium and Ca goes back in as exhange) and reabsorption of Ca (opp of loop diuretic)

Front 45

Because thiazides act in the diluting egment, may reduce excretion of water and cause

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dilutional hyponatremia

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Hydrochlorothiazide is prototypical thiazide half life is

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HTN

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loop diuretic cause following electrolyte changes

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in urine: major inc NaCL, inc K+; body pH alkalosis

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thiazides cause following electrolyte changes

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in urine: inc NaCl, ? NaHCO3, inc K+; body pH alkalosis

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K+ spairing diuretics cause following electrolyte changes

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in urine: inc NaCl, dec K+; body pH acidosis

Front 50

K+sparing diuretics, spironolactone and eplerenone act as

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antagonists of aldosterone in CTs; reduce expression of genes controlling synthesis of sodium channels and Na/K ATPase; slow onset 24-72 hrs

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amiloride and triamterene (K+ sparing) act by blocking

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sodium channels in CTs (do not block excitable Na channels) duration of action 12-24 hr

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what is most common combo of diuretics

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thiazide with K+ sparing

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spironolactone and eplerenone have significant long term

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benefits with heart failure

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K+sparing diuretics should never be given with K+

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supplements

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mannitol is prototypical

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osmotic diuretic, freely filtered by glomerulus but poorly reabsorbed, remains in lumen and holds water

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major location of action for mannitol is

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PCT; water resorb also reduced in desc loop; volume of urine is inc

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with osmotic diuretic sodium excretion is inc because

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rate of urine flow is fast and sodium xporters cant respons fast enough

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mannitol can reduce volume in brain and thus

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intercranial pressure, also reduces intraocular pressure in acute glaucoma

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toxicity of mannitol

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may cause hyponatremia (from removal of water intracellularly) and Pulm edema; as water is excreted hypernatremia may follow with headache N/V

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ADH and desmopressin are

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ADH agonists: faciliates water reabsorption from CT via act of V2 rec inc adenylyl cyclase via Gs, inc cAMP and inserts aquaporins

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demeclocycline and conivaptan are ADH

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antagonists (and lithium but never used) inhib V rec inhibits distal to generation of cAMP and interferes with water channels

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ADH and desmopressin are

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useful in pituitary DI; not in nephrogenic form; reduce urine volume; use salt restr, thiazide, loop diruetics for nephro reduce blood volume

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some tumors (small cell carc of lung) can cause

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water retention and hyponatremia - syndrome of inapprop ADH secretion (SIADH)

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SIADH can be treated with

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demeclocycline and conivaptan

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large presence of ADH or desmo may cause

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HTN

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demeclocycline (like other tetracyclines) cause

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bone and teeth abnormalities

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lithium causes

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nephrogenic DI and becuz toxic is never used to treat SIADH