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Renal MS2 > Diuretics > Flashcards

Diuretics Flashcards

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1
Q

What initiates the reabsorption of NaHCO3 in the PCT?

A

Na/H exchanger (NHE3) in the luminal membrane of proximal tubule epithelial cell

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2
Q

Where is CA located and what does it do?

A

Membrane bound and cytoplasmic

Catalyzes formation of H2CO3 from H+ and HCO3 and breakdown of H2CO3 into H20 and CO2 (so it can cross the membrane)

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3
Q

Where is the Na/K ATPase located and what does it do?

A

All portion of nephron

Maintains high levels of intracellular K and low levels of intracellular Na

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4
Q

Describe the path of ion absorption in the TAL

A

NKCC2 transporter absorbs Na, K, 2 Cl- –> creates + potential in cell which results in K+ back diffusion into lumen –> + potential in lumen drives divalent cations like Mg and Ca paracellularly into interstitium/blood

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5
Q

What is being absorbed in DCT

A

10% total NaCl via NCC
Ca2+ passive absorption by Ca channels
Thiazide diuretics act here

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6
Q

What is the major channel in the CCT and how much of NaCl absorption?

A

ENaC

2-5% of NaCl

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7
Q

What enhances K+ excretion at CCT?

A

Increased Na+ delivery

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8
Q

MOA of aldosterone

A

Increases expression of ENaC and basolateral Na/K ATPase leading to increase in Na reabsorption and K secretion –> water retention, increase in blood V and BP

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9
Q

What is being excreted in CCT

A

K exits lumen passively down concentration gradient

H+ is being secreted by its own ATPase

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10
Q

MOA of ADH

A

Controls expression of AQP2 water channels that insert into apical membrane – no reabsorption of water without ADH

Levels are regulated by serum osmolality and volume status – and alcohol

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11
Q

What is absorbed in the PCT?

A

100% glucose and AA
85% of NaHCO3
65% Na, K, H20

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12
Q

Which 2 drug agents increase urinary NaCl the most

A

Loop agents + thiazides > loop agents

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13
Q

Which class of drugs increases urinary NaHCO3

A

Carbonic anhydrase inhibitors

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14
Q

Which drug class increases urinary K+ the most

A

Loop agents + thiazides

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15
Q

Which 2 classes decrease body pH?

A

Carbonic anhydrase inhibitors and K+ sparing agents

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16
Q

Which classes increase body pH?

A

Loop agents, thiazides and loop agents + thiazides

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17
Q

Pharmacokinetics of carbonic anhydrase inhibitors?

A

They have high oral bioavailability and do not undergo hepatic metabolism!
They are secreted into the proximal tubule

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18
Q

How do CA inhibitors affect urine and body pH?

A

They increase urine pH and decrease body pH

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19
Q

What results from CA inhibition??

A

Decreased H+ formation inside cell
Decreased NHE3 activity
Increased Na and HCO3 in lumen
Increased diuresis

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20
Q

What happens after use of CA inhibitors over several days?

A

Efficacy decreases since HCO3 depletion causes enhanced NaCl reabsorption in other parts of nephron

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21
Q

Side effects/toxicity of CA inhibitor use?

A

Metabolic acidosis and bicarbonaturia
Renal stones since urine more alkaline
Potassium wasting (hypokalemia) since more Na+ delivery
Drowsiness and paresthesias

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22
Q

Contraindications for CA inhibitor use

A

Cirrhosis - decrease in NH4+ excretion leading to hyperammonemia and hepatic encephalopathy
Hyperchloremic acidosis or severe COPD - worsening of metabolic/resp acidosis

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23
Q

Clinical use for CA inhibitors

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A

Rarely used as diuretics
Glaucoma (most common indication for CAi)
Urinary alkalinization to excrete weak acids
Metabolic alkalosis (d/t excessive diuretic use in severe HF)
Acute mountain sickness
Adjuvants in epilepsy

24
Q

Prototype loop diuretics?

Study These Flashcards
A

Furosemide and ethacrynic acid

25
What is loop diuretic half life dependent upon
Kidney function since it has to be secreted by proximal tubule into luminal side (do not coadminster weak acids with it because there might be competition)
26
MOA of loop diuretics
Inhibit NKCC2 in TAL -- Na, K, Cl, Mg and Ca are affected | Increase K+ excretion since more Na delivered to DCT/CCT (total body pH increases)
27
What are some other effects of loop diuretics?
Induce synthesis of renal PG Increase RBF Some are weak inhibitors of carbonic anhydrase
28
Toxicity and side effects of loop diuretics
Hyponatremia, reduced GFR, thrombohemolytic episodes | Hypokalemia metabolic alkalosis (d/t increased H+ and K+ secretion)
29
What are some other undesirable side effects of loop diuretics?
Dose-related hearing loss (ototoxicity) - particularly in renal failure Hypomagnesemia Allergic rxn Dehydration
30
Contraindications for loop diuretics?
Torsemide, bumetanide, furosemide are sulfa drugs (allergies) Hepatic cirrhosis, borderline renal failure, HF Postmenopausal osteopenic women (hypocalcemic effects) Drugs interations (aminoglycosides for ototoxicity, lithium, digoxin)
31
Clinical indications for loop diuretics
Acute pulmonary edema, HTN, heart failure Mild hyperkalemia Acute renal failure (enhances renal flow and K+ secretion) Anion overdose (Br, Fl, I) Hypercalcemia
32
MOA of thiazide diuretics
Inhibits NCC cotransporter in DCT | Enhances Ca absorption in PCT and can unmask hypercalcemia in hyperparathyroidism, carcinoma, sarcoidosis
33
Longest acting thiazide?
Chlorthalidone (47 hours) Not very lipid soluble and must be gvein in large doses Secreted in PCT (competes with uric acid which may elevate serum uric acid levels)
34
Side effects of thiazide diuretics
Hypokalemic metabolic alkalosis and hyperuricemia Impaired carb tolerance (may cause hyperglycemia because interferes with release of insulin and tissue use of glucose -- can fix this by correcting hypokalemia) Hyperlipidemia - increase in total serum cholesterol and LDL Hyponatremia Hypercalcemia Weakness, fatigability, paresthesias, allergic rxns, impotence
35
Clinical indications for thiazide diuretics
HTN and HF Nephrolithiasis (hypercalciuria) Diabetes insipidus
36
Mechanism for HCTZ in nephrogenic DI
HCTZ inhibits NCC in DCT --> increases diuresis and decreases ECV --> less volume filtered at glomerulus (decreased GFR) --> increased Na/H20 reabsorption at PT --> decreased urine output
37
Contraindications for thiazide diuretics
May diminish effects of anticoagulants, gout meds, insulin Use in caution with diabetics Efficacy may be reduced when taking NSAIDs or COX-2 inhibitors
38
Prototype for mineralocorticoid receptor K+ sparing diuretic
Spironolactone
39
Prototype for Na+ channel inhibitor K+ sparing diuretic
amiloride
40
Pharmacokinetics of spironolactone and eplerenone (MR antagonist)
Given orally and need several days for effects | Eplerenone has greater sensitivity for MR than spironolactone
41
Pharmacokinetics of amiloride and triamterene
Oral Triamterene is metabolized extensively by the liver and has a shorter half life Amiloride is not metabolized by liver
42
Pharmacodynamics of spironolactone and eplerenone
Compete with aldosterone binding of MR (nuclear hormone receptor) which affects ENaC and Na/K ATPase in late distal tubule and CCT --> reduces Na reabsorption and K secretion IT IS THE ONLY DIURETIC THAT DOES NOT NEED ACCESS TO TUBULAR LUMEN FOR DIURESIS
43
MOA of amiloride and triamterene
Directly blocks ENaC in apical membrane of CCT --> reduces Na reabsorption and K+ secretion
44
Clinical indications for K+ sparing diuretics
States of mineralocorticoid excess or hyperaldosteronism (primary or secondary) Can add these to thiazides/loop diuretics to blunt secondary hyperaldosteronism effect MR antagonists for heart failure
45
Contraindications for K+ sparing diuretics
Chronic renal insufficiency Concomitant use with B-blockers, NSAIDs, ACEi, ARBs Liver disease Strong inhibitors of CYP3A4
46
Toxicity for K+ sparing diuretics
Varying degrees of hyperkalemia - risk increased more by renal disease or agents that reduce renin/AT II activity Metabolic acidosis Gynecomastia, impotence, BPH Kidney stones
47
MOA of mannitol
Can only be given parenterally and it increases the osmotic pressure of filtrate, which inhibits reabsorption of water and electrolytes, increasing urinary output (essentially opposes ADH in CCT) Increase in urine flow rate decreases reabsorption of Na --> eventually get excessive water loss and HYPERnatremia (increased conc)
48
Clinical indications for mannitol?
Increase or maintain urine V - to prevent anuria in cases of large pigment delivery to kidney d/t hemolysis or rhabdomyolysis or to remove toxins Reduction of intracranial and intraocular pressure
49
Contraindications for mannitol
Anuria Severe dehydration Severe pulmonary edema or congestion
50
Toxicity for mannitol
Expansion of extracellular V and hyponatremia prior to diuresis Dehydration, hyperkalemia, hypernatremia
51
What are ADH agonists used for
Pituitary DI, polyuria, polydipsia, hypernatremia, nocturnal enuresis
52
What is an ADH antagonist and what is it used for
Conivaptan Heart failure, SIADH Toxicity -- can cause hypernatremia, nephrogenic DI
53
When would you use loop agents and thiazide diuretics together?
If patients fail or become refractory to usual dose of loop diuretics It is more than an additive effect Combo can block Na excretion from PCT, ascending loop AND DCT!! Routine outpatient management is not recommended
54
What 3 edematous states are treated with diuretics
``` Heart failure (decreased CO - sensed hypoperfusion to kidneys -- increased retention of Na/H20) Kidney disease (mild cases or SLE/DM; hyperkalemia that is indication of early stage renal failure) Hepatic cirrhosis (edema and ascites) ```
55
4 nonedematous states that are treated with diuretics
HTN (Thiazide + vasodilator since they cause sig Na/H20 retention) Nephrolithiasis (Thiazide increases Ca reabsorption in DCT) Hypercalcemia (Loop diuretics with saline) DI (thiazide can reduce polyuria and polydipsia in both types)

Renal MS2 (3 decks)

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