Term
|
Definition
1. proximal tubule
2. regions of the loop of henle
3. distal tubule
4. collecting tubule/duct |
|
|
Term
| What is the difference between solute diuresis and water diuresis? |
|
Definition
solute diuresis: ion driven water movement (Na typically)*main mechanism
water diuresis: water movement only (usually through water channels) "free water movement" |
|
|
Term
| What is the phenomena of "diuretic braking"? |
|
Definition
| the ability of a drug to continue to induce diuresis. Has to do with Na balance |
|
|
Term
| Where is K and how is it regulated in the kidney? |
|
Definition
**Proximal CT
80-90% K reabsorbed via diffusion and solvent drag
**TAL
K reabsorbed via diffusion (paracellular pathway largely)
Distal convoluted tubule
K secreted via conductive (channel mediated) pathway
Collecting ducts and tubules
K secreted via conductive (channel mediated) pathway
mediated by aldosterone (allows matching of intake to excretion) |
|
|
Term
| Where is Cl and how is it regulated in the kidney? |
|
Definition
**Proximal CT
Paracellular Cl reabsorption
Cl antiport with formate and oxalate
Cl crosses basolateral membrane, symport with K
Cl antiport with Na/HCO3
**Thick ascending limb
Paracellular Cl reabsorption
Cl symport with Na/K
Cl crosses basolateral membrane, symport with K
Cl channels
**Distal convoluted tubule
Cl Symport with Na
Cl channels
**Collecting duct and tubules
Cl antiport with HCO3
Cl channels |
|
|
Term
| How is Mg regulated in the kidney? |
|
Definition
**Proximal CT
20-25% reabsorbed
**Thick ascending limb
Mg reabsorbed via paracellular pathway driven by lumen positive transepithelial potential diff
Basolateral exit via Na-Mg antiporter
Basolateral exit via Mg ATPase
**Distal convoluted tubule
5% reabsorbed
**Collecting duct and tubules
5% reabsorbed |
|
|
Term
| How is Ca regulated in the kidney? |
|
Definition
**Proximal CT
70% Ca reabsorbed by passive diffusion (paracellular route)
**Thick ascending limb (25%)
Ca reabsorbed via paracellular route by positive transepithelial potential difference
Ca reabsorbed via active transcellular pathway modulated by parathyroid hormone (PTH)
**Distal convoluted tubule
Ca reabsorbed through transcellular pathway (passive influx via Ca channels on lumen membrane) followed by extrusion across the basolateral membrane via CA-APTase
passive Ca influx acros luminal membrane (Ca ATPas)
Ca crosses basolateral membrane via Na-Ca antiport |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Name the osmotic diuretics |
|
Definition
| mannitol, urea, glycerin (metabolized), isosorbide |
|
|
Term
| Name the inhibitory of Na/K/2Cl symport (Loop diuretics) |
|
Definition
Furosemide (lasix)
ethacrynic acid (edecrin)
bumetanide (bumex)
torsemide (demadex, a sulfonylurea) |
|
|
Term
| Name the inhibitors of the Na/Cl symporter (thiazides) |
|
Definition
chlorothiazide (diuril)
HCTZ (hydrodiuril) |
|
|
Term
| Name the inhibitors of the Na channels (potassium sparing agents) |
|
Definition
amiloride (midamor)
triamterene (dyrenium, maxide) |
|
|
Term
| Name the antagonists of mineralcorticoid receptors (aldosterone antagonists (another K-sparing diuretic)) |
|
Definition
spironolactone (aldactone)
eplerenone (inspra) |
|
|
Term
| Name the drugs which alter AVP (secretion or action) |
|
Definition
1. increase ADH secretion: nicotine, isoproteronol, colchicine
2. inhibit secretion: ethanol, opiate agonists (kappa), glucocorticoids, phenytoin
3. potentiate ADH: clofibrate, chloroprapanide, carbamazepine
4. enhance antidiuretic effect of AVP: NSAIDs
5. impair AVP action: lithium and demeclocycline |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| Demadex: loop diuretic (a sulfonylurea) |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| midamor, Na-channel inhibitor(k-sparing agent) |
|
|
Term
|
Definition
| Dyrenium, Maxide: Na-channel inhibitor (K-sparing agent) |
|
|
Term
|
Definition
| Aldactone: mineralcorticoid antagonist (k-sparing diuretic) |
|
|
Term
|
Definition
| Inspra, mineralocoricoid (k-sparing diuretic) |
|
|
Term
| T/F the hypotonicity of the cortex interstitium plays a vital role in the ability of mammals and birds to concentrate their urine and therefore is a key adaptation necessary for living in a terrestrial environment. |
|
Definition
| False. Its the hypERtonicity of the MEDULLARY interstitium that allows the formation of concentrated urine. |
|
|
Term
| What is the glomerular filter composed of? |
|
Definition
1. capillary endothelial cells
2. basement membrane
3. urinary endothelial cells |
|
|
Term
| What does the single-nephron glomerular filtration rate depend on? |
|
Definition
1. capillary and bowman's space hydrostatic pressure (Pgc and Pt)
2. glomerular capillary and proximal tubule colloid osmotic pressure(pi)
3. ultrafiltration coefficient (Kf) |
|
|
Term
| What affects hydrostatic pressure? |
|
Definition
1. arterial blood pressure
2. arterial pressure transmitted to glomerular capillaries |
|
|
Term
| What affects osmotic pressure? |
|
Definition
1. concentration of protein in arterial blood entering the glomerulus
2. single nephron blood flow |
|
|
Term
| What areas of the nephron are considered the diluting segments, and why? |
|
Definition
| the distal convoluted tubule and the thick ascending limb, because they actively transport NaCl out of the lumen and are impermeable to H2O. |
|
|
Term
| T/F the interstitium around the distal convoluted tubule is hypotonic. |
|
Definition
|
|
Term
| What accounts for the hypertonic interstitium in the thick ascending limb? |
|
Definition
|
|
Term
| T/F approximately 50% of the Na is reabsorbed in the proximal tubule. |
|
Definition
| false. 65% is reabsorbed in the PCT |
|
|
Term
| List the general mechanisms of renal epithelial transport. |
|
Definition
1. solvent drag
2. simple diffusion
3. conductive pathway (pore)
4. passive diffusion (channel-mediated)
5. carrier-mediated/ facilitated diffusion (uniport)
6. ATP-mediated transport
7. symport/antiport (secondary active transport) |
|
|
Term
| T/F diuretics are directed toward reducing ECF volume by decreasing total body NaCl contents. |
|
Definition
|
|
Term
| What is diuretic braking? |
|
Definition
| renal compensatory mechanisms that bring Na excretion in line with Na intake. (the ability of a drug to continue to induce diuresis) |
|
|
Term
|
Definition
1. osmotic pressure
2. hydrostatic pressure/oncotic pressure
3. renal plasma (blood) flow
4. Peritubular capillaries
5. filtration barrier |
|
|
Term
| Explain the tubuloglomerular feedback (TGF) system. |
|
Definition
| serves to protect the organism from salt and volume wasting. It's mediated by the macula densa cells. |
|
|
Term
| T/F The descending limb is permeable to water, but not to ions. |
|
Definition
| True. it is permeable to water and has a low permeability to ions. |
|
|
Term
Which of the following are considered diuretic braking mechanisms?
A. activation of symp nervous system
B. activation of RAA
C. decreased arterial BP
D. hypertrophy of renal epithelial cells
E. increased expression of renal epithelial transporters
F. alterations in ANP (atrial natriuretic peptide) |
|
Definition
| All of them are diuretic braking mechanisms |
|
|
Term
| T/F Carbonic anhydrase plays a key role in NaCl reabsorption and acid secretion. |
|
Definition
| False. CA plays a key role in NaHCO3 reabsorption and acid secretion |
|
|
Term
| What are the primary and secondary sites of action in CA inhibitors? |
|
Definition
1: PCT: inhibits NaHCO3 reabsorption
2: collecting duct: secretion of titratable acid |
|
|
Term
| What changes do CA inhibitors cause? |
|
Definition
1. 35% increase in HCO3 excretion
2. increased urinary pH
3. metabolic acidosis
4. increased delivery of Na and Cl to loop of henle
5. triggers TGF: contrict afferent arterioles, reduce RBF, reduce GFR |
|
|
Term
| What happens when CA inhibitors increase the delivery of Na and Cl to the loop of henle? |
|
Definition
| the LOH has a large reabsorptive capacity and captures most of the Cl and a portion of the Na. Thus, only a small increase in Cl excretion occurs, HCO3 being the major anion excreted along with Na and K. |
|
|
Term
| What happens to K when you increase the delivery of Na to the distal nephron? |
|
Definition
|
|
Term
| What triggers TGF? and what happens when it is triggered? |
|
Definition
| increased delivery of solutes to the macula densa. Results in constriction of the afferent arterioles, reduced renal blood flow and GFR |
|
|
Term
| What are the toxicities/adverse reaction of CA inhibitors? |
|
Definition
sulfonamide derivatives: allergies, bone marrow repression
Na and K wasting (contraindicated if deficient in these ions) |
|
|
Term
| What are actions, other than diuresis, for CA inhibitors? |
|
Definition
ocular: decrease HCO3 formation for aqueous humor
some CNS effects
net increase in peripheral tissue CO2 and decreased CO2 of expired gases |
|
|
Term
| T/F all diuretics have a net movement of Na into the urine. |
|
Definition
|
|
Term
| What are the routes of elimination for the four osmotic diuretics? |
|
Definition
1. glycerin (80% metabolic, 20% unknown)
2. isosorbide (renal excretion)
3. mannitol (80% renally excreted, 20% metabolic and bile)
4. urea (excreted renally) |
|
|
Term
| What osmotic diuretic has the highest half life? |
|
Definition
isosorbide.
mannitol has the lowest half-life. |
|
|
Term
| What are the toxicities/adverse effects of osmotic diuretics? |
|
Definition
1. Osmotic agents diffuse into ECF space and therefore increased osmolality results in increased ECF volume (edema)
2. Can cause pulmonary edema in congestive heart failure patients
3. Causes hyponatremia (LOW Na in the BLOOD): leading to headache, nausea, vomiting
4. Contraindicated in patients with periferal edema or heart failure |
|
|
Term
| What is the major site of action in osmotic diuretics? |
|
Definition
| loop of henle. (secondary in PCT) |
|
|
Term
| How do osmotic diuretics work? |
|
Definition
extract water from intracellular compartments-->expands the ECFV, decreases blood viscosity, and inhibits renin release--> increases RBF (removes NaCl and urea from medulla)**reduces medullary tonicity! (thus decreasing extraction of H2O from the DtL (diminishes passive reabsorption of NaCl in the AtL)
It also inhibits Mg reabsorption |
|
|
Term
| What electrolytes are excreted in the urine with the use of osmotic diuretics? |
|
Definition
| nearly all of them. Na (++), K, Ca, Mg (++), Cl, HCO3, and H2PO4 |
|
|
Term
| T/F Glycerin and isosorbide can be given orally, whereas mannitol and urea must be administered intravenously. |
|
Definition
|
|
Term
| What are osmotic diuretics used for? |
|
Definition
a rapid decrease in GFR (such as in acute renal failure (ARF) and in acute tubular necrosis (ATN) which accounts for most intrinsic ARF).
Also used to control intraocular pressure in glaucoma patients and to reduce cerebral edema. |
|
|
Term
| T/F Loop diuretics increase the delivery of solutes to the loop of henle. |
|
Definition
| False. Loop diuretics increase the delivery of solutes OUT of the loop of henle. |
|
|
Term
the Na/K/2Cl symporter operates via:
A. facilitated diffusion
B. osmosis
C. active transport
D. secondary active transport
E. against the concentration gradient |
|
Definition
| D. secondary active transport. it uses the Na-K ATPase concentration gradient. |
|
|
Term
| Why are loop diuretics so efficacious? |
|
Definition
| Because they inhibit the Na/K/2Cl symport in the TAL. (The thick ascending limb has a great absorptive capacity, so turning them off would allow a lot to stay in the lumen. |
|
|
Term
| Name the four loop diuretics. (brand and generic) |
|
Definition
1. Furosemide (Lasix)
2. Bumetanide (Bumex)
3. Ethancrynic acid (Edecrin)
4. Torsemide (Demadex) |
|
|
Term
| What loop diuretics contain a sulfonamide moiety? |
|
Definition
| furosemide and bumetanide |
|
|
Term
| What loop diuretics contain a sulfonylurea? |
|
Definition
|
|
Term
| What loop diuretic is a phenoxyacetic acid derivative? |
|
Definition
|
|
Term
| Loop diuretics increase the urinary excretion of Na nd Cl profoundly. How do they increase the excretion of Ca and Mg? |
|
Definition
| excretion of Ca and Mg increases with abolition of the transepithelial potential difference. |
|
|
Term
| T/F Drugs with carbonic anhydrase-inhibiting activity increase the urinary excretion of HCO3 and phosphate. |
|
Definition
|
|
Term
| All inhibitors of the Na/K/2CL symporter increase the urinary excretion of K and titratable acid. why? |
|
Definition
| this effect is due in part to increased delivery of Na to the distal tubule which enhances excretion of K and H. |
|
|
Term
| explain the acute and chronic effects of loop diuretics on uric acid. |
|
Definition
| Acutely, loop diuretics increase the excretion of uric acid, whereas chroic administration of these drugs results in reduced excretion of uric acid. (chronically perhaps due to uric acid reabsorption) |
|
|
Term
| List the possible mechanisms for loop diuretics resulting in enhanced excretion of H and K. |
|
Definition
1. increased Na delivery to the distal tubule.
2. flow-dependent enhancement of ion secretion by the collecting duct
3. nonosmotic vasopressin release
4. activation of the renin-angiotensin-aldosterone axis |
|
|
Term
The Na/K/2Cl symporter:
A. produces a hypotonic medullary interstitium
B. produces a hypertonic medullary interstitium
C. block the ability of the kidney's to concentrate urine during hydropenia
D. markedly impair the kidney's ability to excrete a dilute urine during water diuresis. |
|
Definition
B. produces a hypertonic medullary interstitium
C. block the ability of the kidney's to concentrate urine during hydropenia
D. markedly impair the kidney's ability to excrete a dilute urine during water diuresis. |
|
|
Term
| What are loop diuretic effects on renal hemodynamics? |
|
Definition
| loop diuretics block TGF by inhibiting salt transport into the macula densa so that the macula densa can no longer detect NaCl concentrations in the tubular fluid. Loop diuretics do not decrease GFR by activating TGF. Loop diuretics are powerful stimulators of renin release. |
|
|
Term
| How does furosemide benefit patients with pulmonary edema, even before diuresis ensues? |
|
Definition
| furosemide acutely increases systemic venous capacitance and thereby decreases left ventricular filling pressure, thus benefiting pulmonary edema patients. |
|
|
Term
| What are the two ways that loop diuretics get to their site of action? What is there primary site of action? |
|
Definition
1. secretion by the organic acid transport system in the proximal tubule
2. bound to plasma proteins via filtration (but it is limited)
the primary site of action if is the Thick Ascending Limb. |
|
|
Term
| What is "postdiuretic Na retention"? How can it be overcome? |
|
Definition
1. As the concentration of loop diuretic in the tubular lumen declines, nephrons begin to avidly reabsorb Na, which often nullified the overall effect of the loop diuretic on total-body Na.
2. restricing dietary Na intake, or by more frequent administration of the loop diuretic. |
|
|
Term
| What makes a loop diuretic reabsorb more Mg and Ca in the thick ascending limb? |
|
Definition
| change the transmembrane potential difference |
|
|
Term
| In loop diuretics, what ions are being excreted the most? |
|
Definition
| Na, K, Ca, Mg, Cl in the thick ascending loop |
|
|
Term
| What happens when the loop diuretics block the TGF by inhibiting salt transport into the macula densa? |
|
Definition
| They can no longer detect NaCl concentrations in the tubular fluid, resulting in: increased renal blood flow, no change in GFR, and decreased filtration fraction variable. (furosemide has direct vascular effects, action causes systemic venous constriction) |
|
|
Term
| What can happen with overzealous use of a loop diuretic? |
|
Definition
| serious depletion of total-body Na. This may manifest as hyponatremia and/or ECFV depletion associated with HTN, reduced GFR, circulatory collapse, thromboembolic episodes, and in patients with liver disease, hepatic encephalopathy. Can cause ototoxicity. |
|
|
Term
| Why is ethacrynic acid not to be used unless the patient cannot tolerate the other loop diuretics? |
|
Definition
| because of the higher incidence of ototoxicity as compared to the other loop diuretics. |
|
|
Term
| toxicities and side effects of loop diuretics. |
|
Definition
too much drug results in:
hypo-
Na, K, Ca, Mg, Cl, H
hyper-
urea, glycemia
increased LDL and lower HDL
bone marrow depression, GI disturbances, photosensitivity, etc |
|
|
Term
Which of the following are loop diuretics used to treat:
A. Acute pulmonary edema
B. Chronic pulmonary edema
C. Edema of nephrotic syndrome
D. Ascites of liver cirrhosis
E. Hypercalcemia
F. Hyponatremia
G. Edema associated with chronic renal insufficiency |
|
Definition
All of them, except B.
Hypercalcemia (when combined with isotonic NS to prevent volume depletion)
Hyponatremia (when combined with hypertonic saline for life-threat) |
|
|
Term
| What give the loop diuretics their potency of action? |
|
Definition
1. changes in water movement
2. changes in ion concentration (Na, K, Cl)
3. changes in transmembrane potential difference |
|
|
Term
| What are the drug interactions in loop diuretics? |
|
Definition
1. Aminoglycosides (ototoxicity)
2. Anticoagulants (increased anticoagulant activity)
3. Digitalis glycosides (arrhythmias)
4. Lithium (increased lithium plasma levels)
5. Propranolol (increased plasma levels)
6. Sulfonylureas (hyperglycemia)
7. Cisplatin (ototoxicity)
8. NSAIDs (salicylate toxicity)
9. Probenecid (blunted diuretic response)
10. Thiazide diuretics (profound diuresis)
11. Amphotericin B (nephrotoxicity and electrolyte imbalance) |
|
|
Term
What do loop diuretics do to serum K?
A. increase
B. decrease |
|
Definition
| B. decrease (causes hyperglycemia depending on the K levels) |
|
|
Term
| What happens to Ca with chronic dosage of a Thiazide? |
|
Definition
| there is a decrease in the excretion of Ca |
|
|
Term
| Furosemide is a carbonic anhydrase inhibitor as well as a loop diuretic. Would you expect loss of HCO3? |
|
Definition
|
|
Term
| High doses of thiazides affect what transporters? What is it's effect? |
|
Definition
| Na/K and Na/Ca. Higher diuresis effect. |
|
|
Term
| Thiazides have a greater effect on what ion? |
|
Definition
|
|
Term
| T/F Patients with sulfonamide sensitivities can take thiazides. |
|
Definition
| False. thiazides are contraindicated in patients with sulfonamide sensitivity |
|
|
Term
|
Definition
Chlorothiazide (Diuril)
Hydrochlorothiazide (Hydrodiuril) |
|
|
Term
| What are the primary and secondary site of action located for thiazides? |
|
Definition
1: late distal convoluted tubule
2: PCT |
|
|
Term
| What do Thiazides inhibit? |
|
Definition
| Na/Cl symporter in the late distal convoluted tubule. |
|
|
Term
| Why do thiazides typically leave renal function alone? |
|
Definition
| Because they function past the macula densa. |
|
|
Term
| If GFR is <40mL/min, which diuretics do not work well? |
|
Definition
|
|
Term
| What adverse effects may occur from thiazides? |
|
Definition
ECF depletion, HTN,
hypo- Na**, K, Cl in the blood
hypokalemia leads to hyperglycemia
increase LDL cholesterol |
|
|
Term
| What are the contraindications for thiazides? |
|
Definition
sulfonamide sensitivities
it decreases the effects of anticoagulants, uricosuric agents (gout), sulfonylureas in insulin
increases the effects of anesthetics, cardiac glycosides, loop diuretics (less reabsorption of ions) |
|
|
Term
| What are the drug-drug interactions in thiazides? |
|
Definition
NSAIDs and methenamines inhibit the action of thiazides
QUINIDINE leads to severe K depletion (torsades de pointes) |
|
|
Term
| What happens when you mix a thiazide with quinidine? |
|
Definition
| severe K depletion leads to ventricular tachycardia and enhances quinidine actions. The risk of drug-induced torsades de pointes is increased by concomitant hypokalemia |
|
|
Term
The Na-Cl symporter is inhibited by a number of diuretics, but not by:
A. HCTZ
B. Furosemide
C. Acetazolamide
D. Amiloride derivatives
E. all, except A |
|
Definition
| E. furosemide, acetazolamide, and amiloride derivatives do not inhibit the Na-Cl symporter |
|
|
Term
| What symporter is expressed predominanly in the kidney and is localized to the apical membrane of the DCT epithelial cells? |
|
Definition
|
|
Term
| What regulates the expression of the Na-Cl symporter? |
|
Definition
| It is regulated by aldosterone. |
|
|
Term
| Why are thiazides only moderately efficacious? |
|
Definition
| because approx 90% of the filtered Na load is reabsorbed before reaching the DCT. (Some thiazide diuretics are also weak inhibitors of CA, an effect that increases HCO3 and PO4 excretion and probably accounts for their weak proximal tubular effects. |
|
|
Term
| What is similar between loop diuretics and thiazides? |
|
Definition
loops: Na/K/2Cl
thiazides: Na/Cl (allows the same excretion of K) |
|
|
Term
| T/F Acute administration of thiazides increases the excretion of uric acid. |
|
Definition
|
|
Term
| What ion do loop diuretics excrete, but thiazides do not? |
|
Definition
| Ca (thiazides increase Ca reabsorption in the DCT) inhibition of the Na-Cl symporter in the luminal membrane decreases intracellular Na levels, causing increased Ca basolateral exit via an enhanced Na/Ca exchanger. |
|
|
Term
| why do drugs such as probenacid attenuate the diuretic response of thiazides? |
|
Definition
| sulfonamides are organic acids and therefore are secreted into the proximal tubule by the organic acid secretory pathway. Drugs such as probenacid can attenuate the diuretic response to thiazides by competing for transport into the proximal tubule. |
|
|
Term
| T/F Thiazides should not be combined with other diuretics. |
|
Definition
| False. thiazides have additive or synergistic effects when combined with other classes of antihypertensive agents. |
|
|
Term
| Thiazides decrease the excretion of what ion? |
|
Definition
| Ca. thiazides can be employed to treat Ca nephrolithiasis and may be useful for the treatment of osteoporosis |
|
|
Term
| What are the Na Channel Blockers? |
|
Definition
| Amiloride (Midamor) and triamterene (dyrenium, maxide) |
|
|
Term
| How do Na channel blockers get into the nephron? |
|
Definition
| They are secreted via the organic BASE secretory system in the proximal tubule. |
|
|
Term
| Where is the primary site of action in Na channel blockers? |
|
Definition
| the principle cells of the late distal tubule and collecting duct. |
|
|
Term
| A lumen-negative transepithelial potential difference would drive K which direction? |
|
Definition
| the transepithelial voltage provides an important driving force for the secretion of K into the lumen via K channels. |
|
|
Term
| Intercalated cells in the late distal CT and collecting duct are useful for what and regulated by what? |
|
Definition
| Furosemide (loop) and CA inhibitors are the regulators of the intercalated cells. They are incharge of acid-base balance. |
|
|
Term
| What is the MOA of Na channel blockers? |
|
Definition
| the drug physically blocks epithelial Na channels in the luminal membrane of principle cells in the late distal tubule and collecting duct. |
|
|
Term
| Na channel blockers only mildly increase the excretion rates of Na and Cl. Why? |
|
Definition
| because by the time you get to the distal tubule, there is only approx 2% of filtered load left. |
|
|
Term
| Blocking the Na channel hyperpolarizes the luminal membrane resulting in what? |
|
Definition
| it decreases the excretion rates of K, H, Ca, and Mg. |
|
|
Term
| Chronic administration of Na channel inhibitors does what to uric acid? |
|
Definition
| decreases uric acid secretion. |
|
|
Term
| T/F There are numerous effects in the renal hemodynamics of Na channel blockers. |
|
Definition
| False. Na channel blockers have little effect in GFR, RBF, FF, and TGF |
|
|
Term
| What happens when you administer high concentrations of Amiloride? |
|
Definition
| amiloride blocks the Na/H and Na/Ca antiporters and inhibits the Na channels and K-ATPase activity. |
|
|
Term
| What is the most dangerous side effect of Na channel inhibitors? |
|
Definition
|
|
Term
| Adverse effects of Na channel blockers. |
|
Definition
Hyperkalemia
NSAIDs can increase hyperkalemia
triamterene (reduces glucose tolerance in hyperglycemic patients) |
|
|
Term
| What is the therapeutic use for Na channel blockers? |
|
Definition
Co-therapy for potassium imbalance.
Off-sets the loss of K from other diuretics. |
|
|
Term
| Name the Mineralocorticoid receptor antagonists. |
|
Definition
Spironolactone (aldactone)
Eplerenone (Inspra) |
|
|
Term
Urine Na content in response to osmotic diuretics, CA inhibitors, loop diuretics, and thiazides.
A. increase
B. decrease
C. no change
D. no idea |
|
Definition
| a. increase urine Na concentration |
|
|
Term
TGF regulation by loop diuretics
A. increase
B. decrease
C. no change
D. no idea |
|
Definition
| B. decrease/ inhibit Na/K/2Cl symporter, so the macula densa cells can't sense the change in ion content. |
|
|
Term
Name that drug class.
Furosemide
bumetanide
ethacrynic acid
torsemide |
|
Definition
| Loops! Na/K/2Cl symporters |
|
|
Term
What diuretics are heavily bound to plasma proteins?
A. CA inhibitors
B. Osmotics
C. Loop diuretics
D. Thiazides
E. K-Sparing Diuretics |
|
Definition
|
|
Term
Filtered / secreted / other (explain)
A. CA inhibitors
B. Osmotics
C. Loops
D. Thiazides
E. Na Channel inhibitor
F. Mineralocorticoids |
|
Definition
A. filtered in through glomerulus
B. Filtered in through glomerulus
C. Secreted- organic acid transport PCT
D. Secreted- organic acid transport PCT
E. Secreted- organic base transport PCT
F. blood network (lipophilic steroid!) they don't require access to the tubular lumen to work. |
|
|
Term
| What diuretic has an increased potential for ototoxicity than all the other drugs? (brand/generic) |
|
Definition
| loops in general...specifically, ethacrynic acid (Edecrin) |
|
|
Term
| What two drugs do not require access to the tubular lumen to work? |
|
Definition
| spironolactone and eplerenone. |
|
|
Term
| T/F The higher the levels of endogenous aldosterone, the greater are the effects of mineralocorticoid receptor antagonists on urinary excretion. |
|
Definition
|
|
Term
| Which diuretics have little effect on renal hemodynamics? |
|
Definition
| Na channel inhibitors and mineralocorticoid receptor antagonists (k-sparing diuretics) |
|
|
Term
| Why does Spironolactone have such weird side effects? |
|
Definition
| it has some affinity towards progesterone and androgen receptors |
|
|
Term
| T/F spironolactone has a short half life. |
|
Definition
| T and F... non-active metabolite (1.6hrs) an active metabolite (16.5hrs) |
|
|
Term
| Whats the difference between Spironolactone and eplerenone? |
|
Definition
spiro: non-selective, dirtier drug, with female-like side effects, and has an active metabolite. Salicylates decrease efficacy.
Eplerenone: selective, no active metabolite, indirectly increases TSH levels. |
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