Renal Agents Flashcards by Joel Glotfelty

Filter approximately 1300 mL blood per min or 700 mL plasma

Kidneys

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In the kidney, the peritubular capillary network surrounds the

Convoluted tubules

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Passes close to the glomerulus between the afferent and efferent arterioles

Distal Convoluted Tubule

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Osmotic diuretics that promote water retention in the tubular fluid

Mannitol or glucose

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Water permeability in collecting duct is controlled by

ADH

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Inhibits ADH secretion by the pituitary

Alcohol

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A carbonic anhydride inhibitor that blocks sodium bicarbonate reabsorption, resulting in decrease in NaCl reabsorption

Acetazolamide

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Acetazolamide functions on the

Proximal tubule

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Osmotic agents act on the thin descending limb to promote

Water retention

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Block the NKCC2 cotransporter

-Act on thick ascending limb

Loop diuretics (i.e. furosemide)

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Relatively impermeable to water

DCT

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Blocks the electrically neutral Na+/Cl- cotransporter NCC

Thiazides diuretics

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Reabsorption in DCT is via parathyroid hormone regulated apical Ca2 channel and a basolateral Na+/Ca2+ exchanger

Ca2+

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The site of mineralcorticoid and ADH action

Collecting tubule

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The major site of K+ secretion

Collecting tubule

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Sodium bicarbonate reabsorption by the PCT is initiated by the action of the

-Allows Na+ to enter the cell

Na+/H+ exchanger NHE3

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Inhibits carbonic anhydride and acts predominantly in the proximal tubule by blocking sodium bicarbonate reabsorption

Acetazolamide

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The bicarbonate loss from carbonic anhydride inhibitors can cause a

Hyperchloremic metabolic acidosis

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The portion of acetazolamide that can cause allergic reactions, bone marrow depression, and skin toxicity

Sulfonamide group

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Carbonic anhydride inhibitors should be avoided in patients with

Hepatic Cirrhosis

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Used to treat glaucoma, acute mountain sickness, metabolic alkalosis, and to alkalinize the urine

C.A. Inhibitors

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Raise CO2 content of tissues, which in turn stabilizes deoxyhemoglobin

-Useful for counteracting acute mountain sickness

C.A. Inhibitors

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Osmotic diuretics such as mannitol act in the

-Where the cells are freely permeable to water

PT and Descending limb of Henle’s loop

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Causes loss of water, reduced intracellular volume, and hypernatremia risk

Mannitol

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Function to increase water excretion in preference to Na+ excretion - Reduces intracranial and intraocular pressure - Promotes prompt removal of renal toxins

Osmotic Diuretics

Water expansion into the extracellular compartment causing hyponatremia -Effect of osmotic diuretic toxicity

Extracellular volume expansion

Can complicate congestive heart failure and may produce florid pulmonary edema

Extracellular Volume Expansion

Excessive use of osmotic diuretics w/out carefully monitoring serum ion composition and fluid balance can lead to

Dehydration and Hypernatremia

Loop diuretics act in the loop of Henle and block the

NKCC2 cotransporter

Loop diuretics cause an increase in the excretion of

Mg2+ and Ca2+

Furosemide, bumetanide, ethacrynic acid, and torsemide are the

Loop Diuretics

The most effective diuretics currently available

Loop diuretics

A phenoxyacetic acid derivative containing an adjacent ketone and methylene group

Ethacrynic Acid

What is the duration of effect for 1. ) Furosemide 2. ) Torsemide

1. ) 2-3 hours | 2. ) 4-6 hours

Block tubuloglomerular feedback by inhibiting salt transport into the macula densa

Loop Diuretics

Induce synthesis of renal prostaglandins by expressing COX-2

Loop Diuretics

Inhibit cyclooxygenase and can reduce prostaglandin synthesis in the kidney and interfere with loop diuretics

NSAIDs

Can both relieve pulmonary congestion and reduce LV filling pressures in CHF before a measurable increase in urinary output occurs

Furosemide and ethacrynic acid

Most important indications are acute pulmonary edema, other edematous conditions, and acute hypercalcemia

Loop Diuretics

A major adverse effect of loop diuretics is

Hypokalemic metabolic alkalosis

Can also cause impaired carbohydrate tolerance, hyperglycemia, dehydration, and hyponatremia

Loop diuretics

Both loop diuretics and thiazides can cause

Hypokalemic metabolic alkalosis

Is mostly just used for patients sensitive to sulfonamides

Ethacrynic acid

Furosemide, bumetanide, and torsemide may demonstrate cross reactivity in patients who are sensitive to other

Sulfonamides

Diuretics of the thiazides class block the electrically neutral

NCC transporter

NCC is the gene mutated in

Gitelman’s syndrome

Enhance Ca2+ reabsorption

Thiazides

Include hydrochlorothiazide, indapamide, chlorthalidone, and metolazone

Thiazides

Some members of the thiazides retain significant

CA inhibitor activity

Thiazides can be inhibited by

NSAIDS

Similar to CA inhibitors, thiazides has unsubstituted

Sulfonamide group

Thiazides that is less lipid soluble and must be given in relatively large doses -Slowly absorbed and has longer duration of action

HCTZ

Indicated for hypertension, heart failure, nephrolithiasis, and nephrogenic DI

Thiazides

In nephrogenic DI, reduce plasma volume to lower GFR which enhances proximal tubule reabsorption of NaCl and water -Causes decreased delivery of fluid to the diluting segments

Thiazides

Can cause hypokalemic metabolic alkalosis and hyperuricemia

Thiazides

Also cause impaired carbohydrate tolerance, hyperlipidemia, hyponatremia, and allergic reactions

Thiazides

Cause a 5-15% increase in serum cholesterol and increase LDLs

Thiazides

An important adverse effect of thiazides. Due to a combination of hypokalemic-induced elevation of ADH, reduction in diluting capacity of kidney, and increased thirst

Hyponatremia

Where we see 2-5% of NaCl reabsorption -Determines the final Na+ concentration in the Urine

Late Distal Tubule and Collecting Duct

The late distal tubule and collecting duct is the site of action for

Aldosterone

Major site of K+ secretion and acidification of urine

Late distal tubule and collecting duct

Major sites of Na+, K+, and H2O (ADH-sensitive) transport

Principal cells

Diuretics that increase Na+ delivery to the late distal tubule and collecting duct will therefore increase secretion of

K+ and H+

Primary sites of proton secretion

Late distal tubule and collecting duct intercalated cells

Increases expression and delivery of apical membrane channels and the basolateral Na+/K+ ATPase

Aldosterone

Competitive antagonists of the aldosterone receptor -“Potassium-sparing Diuretics”

Spironolactone and Eplerenone

More selective and has less side effects

Eplerenone

Block the ENaC Na+ channel in the apical cells of the collecting tubule

Triamterene and amiloride

Also can be inhibited by NSAIDs

Triamterene and Spironolactone

Promoted by hyperkalemia and high levels of AN-II

Aldosterone release

Has high levels in cirrhosis w/ ascites, renalvascular hypertension, adrenal tumors, and cardiac or nephrotic edema

Aldosterone

Most useful in states of mineralocorticoid excess, due either to primary hypersecretion or to secondary aldosteronism

Potassium sparing diuretics

Can be used to treat hypertension in Liddle’s Syndrome

Triamterene and amiloride

Can cause hyperkalemia

Potassium-sparing diuretics

The risk of this complication is greatly increased in the presence of renal disease or other drugs that reduce renin

Hyperkalemia from aldosterone

By inhibiting H+ secretion in parallel with K+ secretion, the K+-sparing diuretics can cause

Hyperchloremic metabolic acidosis

Synthetic steroids may cause endocrine abnormalities by effects on other steroid receptors. One of these effects is

Gynecomastia

These endocrine abnormalities can be avoided by using

Eplerenone

Patients with renal insufficiency are especially vulnerable and should rarely be treated with

Aldosterone antagonists

Patients with liver disease may have impaired metabolism of

Triamterene and spironolactone

Strong CYP3A4 inhibitors (ketoconazole and itraconazole) can markedly increase blood levels of

Eplerenone

Secreted by the posterior pituitary whenever the cardiovascular system is challenged by hypovolemia and/or hypotension

ADH

Increases the permeability of principal cells to water by binding to V2 receptors, thus increasing the number of water channels (AQP2) on apical surface

ADH

The cell that responds to ADH is the same cell that responds to aldosterone. This is the

Principal Cell

ADH receptor antagonists

Vaptans

Used to treat euvolemic hyponatremia

Vaptans

A non-selective antagonist at V1a and V2 receptors

Conivaptan

Oral agents selectively active against the V2 receptor

Lixivaptan and tolvaptan

Both appear to reduce the formation of cAMP in response to ADH and also interfere w/ cAMP in collecting tubule cells

Li+ and Demeclocyline

Are indicated to treat SIADH

ADH antagonists

If serum Na+ is not monitored closely, ADH antagonists can cause severe hypernatremia and

Nephrogenic DI

If Li+ is being used for an effective disorder, than we can treat the nephrogenic DI with

Thiazides diuretic or amiloride