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Renal MS2 > Diuretics > Flashcards

Diuretics Flashcards

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

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?

A

Furosemide and ethacrynic acid

25
Q

What is loop diuretic half life dependent upon

A

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
Q

MOA of loop diuretics

A

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
Q

What are some other effects of loop diuretics?

A

Induce synthesis of renal PG
Increase RBF
Some are weak inhibitors of carbonic anhydrase

28
Q

Toxicity and side effects of loop diuretics

A

Hyponatremia, reduced GFR, thrombohemolytic episodes

Hypokalemia metabolic alkalosis (d/t increased H+ and K+ secretion)

29
Q

What are some other undesirable side effects of loop diuretics?

A

Dose-related hearing loss (ototoxicity) - particularly in renal failure
Hypomagnesemia
Allergic rxn
Dehydration

30
Q

Contraindications for loop diuretics?

A

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
Q

Clinical indications for loop diuretics

A

Acute pulmonary edema, HTN, heart failure
Mild hyperkalemia
Acute renal failure (enhances renal flow and K+ secretion)
Anion overdose (Br, Fl, I)
Hypercalcemia

32
Q

MOA of thiazide diuretics

A

Inhibits NCC cotransporter in DCT

Enhances Ca absorption in PCT and can unmask hypercalcemia in hyperparathyroidism, carcinoma, sarcoidosis

33
Q

Longest acting thiazide?

A

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
Q

Side effects of thiazide diuretics

A

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
Q

Clinical indications for thiazide diuretics

A

HTN and HF
Nephrolithiasis (hypercalciuria)
Diabetes insipidus

36
Q

Mechanism for HCTZ in nephrogenic DI

A

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
Q

Contraindications for thiazide diuretics

A

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
Q

Prototype for mineralocorticoid receptor K+ sparing diuretic

A

Spironolactone

39
Q

Prototype for Na+ channel inhibitor K+ sparing diuretic

A

amiloride

40
Q

Pharmacokinetics of spironolactone and eplerenone (MR antagonist)

A

Given orally and need several days for effects

Eplerenone has greater sensitivity for MR than spironolactone

41
Q

Pharmacokinetics of amiloride and triamterene

A

Oral
Triamterene is metabolized extensively by the liver and has a shorter half life
Amiloride is not metabolized by liver

42
Q

Pharmacodynamics of spironolactone and eplerenone

A

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
Q

MOA of amiloride and triamterene

A

Directly blocks ENaC in apical membrane of CCT –> reduces Na reabsorption and K+ secretion

44
Q

Clinical indications for K+ sparing diuretics

A

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
Q

Contraindications for K+ sparing diuretics

A

Chronic renal insufficiency
Concomitant use with B-blockers, NSAIDs, ACEi, ARBs
Liver disease
Strong inhibitors of CYP3A4

46
Q

Toxicity for K+ sparing diuretics

A

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
Q

MOA of mannitol

A

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
Q

Clinical indications for mannitol?

A

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
Q

Contraindications for mannitol

A

Anuria
Severe dehydration
Severe pulmonary edema or congestion

50
Q

Toxicity for mannitol

A

Expansion of extracellular V and hyponatremia prior to diuresis
Dehydration, hyperkalemia, hypernatremia

51
Q

What are ADH agonists used for

A

Pituitary DI, polyuria, polydipsia, hypernatremia, nocturnal enuresis

52
Q

What is an ADH antagonist and what is it used for

A

Conivaptan
Heart failure, SIADH

Toxicity – can cause hypernatremia, nephrogenic DI

53
Q

When would you use loop agents and thiazide diuretics together?

A

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
Q

What 3 edematous states are treated with diuretics

A 
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
Q

4 nonedematous states that are treated with diuretics

A

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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