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Pharm 3, Test 3 > Diuretics > Flashcards

Diuretics Flashcards

1
Q

What is the basic urine forming unit of the kidney? AKA the workforce of the kidney

A

The nephron

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2
Q

How much CO goes to the kidney?

A

25%

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3
Q

How much overall oxygen consumption occurs from the kidney?

A

7%

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4
Q

Where does most of the filtered sodium get reabsorbed in the kidney?

A

Proximal tubule, 65% approximately

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5
Q

How much filtered sodium is reabsorbed in the loop of henle?

A

25%

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6
Q

Whats the amount of carbon dioxide in the atmosphere?

A

0.0414%

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7
Q

What is the one carbonic anhydrase inhibitor mentioned?

A

Acetazolamide

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8
Q

What is the MOA of CAI?

A

Inhibits sodium bicarb reabsorption, producing metabolic acidosis eventually
Increases bicarb in the lumen, increasing urinary pH, increases NA concentration in the urine, causing increased diuresis

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9
Q

What is the driving force for Na reabsorption throughout the entire GI/GU system?

A

Na/K ATPase

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10
Q

What are the ADEs with CIA?

A

Acetazolamide is a sulfa derivative, so it can lead to bone marrow suppression
Skin rashes
Hypersensitivity- Allergic reactions
Kidney- Precipitation of calcium phosphate creating crytalluria

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11
Q

What are the uses of CAI?

A

Open angle glaucoma
Epilepsy
Mountain sickness prophylaxis
Diuretic

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12
Q

What is the MOA of Osmotic diuretics?

A

They are fully filtered at the glomerulus, enter the lumen of the nephron (undergo very little reabsorption), thereby increasing the osmolality of the fluid.
Water follows solutes, so less water in reabsorbed

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13
Q

What is the effects of urine osmolality on renal blood flow? Why?

A

Increased renal blood flow because there is more water because fluid is pulled from extracellular spaces, increasing blood volume

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14
Q

Can you give mannitol to a patient with heart failure?

A

Bad idea

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15
Q

Where are some other places mannitol will specifically have reabsorption?

A

Brain and eye

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16
Q

What are some ADE’s to mannitol?

A

Hyponatremia- Initially

Hypernatremia- After extensive diuresis

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17
Q

What are the uses of mannitol?

A

Acute renal failure technically
Dialysis disequilibrium syndrome
Closed head injury

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18
Q

What are the specific osmotic dieuretics we discussed?

A

Mannitol, glycerin, glucose

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19
Q

What is the electrochemical driving force for BOTH Na sodium absorption and glucose reabsorption?

A

Na/K ATPase

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20
Q

What is the MOA of sodium glucose cotransporter 2 inhibitor?

A

Blocks SGLT2 in the proximal tubule, causing osmotic effect and increasing glucose in the urine, leading to increased dieuresis

21
Q

Are SGLT2 inhibitors super strong?

A

No, fairly weak

22
Q

What are some other important uses/effects of SGL2 inhibitors?

A

Helps treat DM be increasing glucose secretion, lowering HGA1C by 0.5-1%
CHF- Reduces systolic bp, reduces risk of CKD

23
Q

What are the specific SGL2 inhibitors?

A

Daoagliflozin, canagliflozin, empagliflozin, ertugliflozin

24
Q

What are the ADEs for SGL2 inhibitors?

A

Hypoglycemic- not super common ironically
Fluid/electrolyte imbalance- Not common either, but all diuretics’ theoretically have this ADE
AKI- Initial diuresis can cause reduction in bp that some patients don’t initially tolerate
Skeletal system- Increased risk of fractures

25
Q

What is the MOA for adenosine A1 receptor antagonists?

A

Inhibits Na reabsorption by blocking A1 receptor in the proximal tubule (A1 receptors cause Na reabsorption)

26
Q

What are the different A1 receptor antagonists?

A

Methylxanthines: Caffeine, theophylline, theobromine

27
Q

What is the MOA of loop dieuretics?

A

Inhibit the Na/K/2Cl symporter in the thick ascending limb of the loop of henle

28
Q

What electrolytes do loop diuretics specifically reduce reabsorption of?

A

Na, K, Cl, Ca and Mg

29
Q

What are all loop dieuretics derivatives of? With one exception

A

Sulfonamides

30
Q

What do sulfonamides do to carbonic anhydrase?

A

Inhibit it

31
Q

How do loop dieuretics affect renal blood flow?

A

Increases it because they block Na uptake in the macula densam thereby interfering with its ability to sense sodium

32
Q

How does loop diuretics affect Mg and Ca?

A

Decreases it by reducing electrochemical gradient when the Na/Cl/K is inhibited, causing Mg and Ca to just be excreted instead of being reabsorbed

33
Q

What are the other loop diuretics effects?

A

Reduced LV filling pressure

Inhibits inner ear electrolyte transport, altering ability to send APs

34
Q

Are loop diuretics highly protein bound?

A

Yes, so they do not get filtered in the glomerulus, but instead secreted by the renal proximal tubular cells

35
Q

What is the one loop dieurtic thats not mainly secreted in the urine?

A

Torosemide

36
Q

What are the ADEs of loop diuretics?

A

Fluid/electrolyte imbalance
Ototoxicity
Sulfonamide like reactions
Hyperlipidemia-Increased LDL, decreased HDL

37
Q

What is the heavily mentioned DDI with loop diuretics?

A

Aminoglycosides- The “Mycins”, leading to synergistic ototoxicity

38
Q

What is the drug mentioned that inhibits tubular secretion of many drugs, including loop diuretics?

A

Probenicid

39
Q

What are the loop diuretics to know?

A

Furosemide, bumetanide, torsemide, ethacryanic acid

40
Q

What is the MOA of thiazide and thiazide like diuretics?

A

Inhibit the Na/Cl symporter in the distal tubule

41
Q

Are thiazides highly protein bound?

A

Yep

42
Q

What are the ADEs for thiazide and thiazide like diuretics?

A 
Electrolyte imbalances
CNS-Vertigo, HA, parathesias
GI- N/V, anorexia, diarrhea, constipation
Sulfa like reaction
Sexual dysfunction
Hyperglycemia-Reduced insulin secretion
43
Q

What are thiazides used for aside from diuretics?

A

Htn-reduced morbidity and mortality

Edema

44
Q

What is the preferred thiazide and thiazide like diuretic?

A

Chlorothiazide, longer half life

45
Q

How do K sparring diuretics work?

A

Na channel inhibitors in the late distal tubule and collecting duct

46
Q

What are the provided K sparring diuretics?

A

Amiloride and Triamterene

47
Q

What are the DDI to be aware of with K sparring diuretics?

A

NSAIDS, ACE inhibitors, K Supplements

48
Q

What is the MOA of mineralocorticoid receptor antagonists?

A

Blocks MR??

49
Q

What are the ADEs for spironolactone?

A

Hyperkalemia
Endocrine effects- Ability to interact with androgen related receptors
GI- Gastric bleeding
CNS- Drowsiness, lethargy, ataxia,

Pharm 3, Test 3 (5 decks)

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