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Pharm II > diuretics > Flashcards

diuretics Flashcards

1
Q

Carbonic Anhydrase Inhibitors MOA

A

Inhibit formation of H+ and bicarb from H20 and CO2 via inhibition of CA and decrease resorption of NaHCO3

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2
Q

MOA of Loop diuretics

A
  • Inhibit NaCl reabsorp TALOH
  • Inhibit Na/K/2Cl transporter (lots of solutes in tubule; increase diuretic effect)renal prostaglandin prod via COX2 incr renal blood flow & inhibits Na reabsorption in the loop

Effects on blood flow thru vascular beds: relieve pul congestion prior to diuretic effect

*NOT shown to mortality

can cause you to loose magnesium and Ca

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3
Q

DTC

A

under the influence of parathyroid hormone

independent of Na
but if Na/Cl transport is blocked more Ca will be reabsorbeD?

18:mins

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4
Q

Early collecting tubule Na is reabsorbed under the presence of

A

aldosterone

Na and K is exchanged (not co transport) but you will see more K loss

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5
Q

ADH works where

A

collecting tubule

seen with decrease in serum Na

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6
Q

adenosine inhibitors

A

increase renal blood flow

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7
Q

Prostaglandins enhance the effect of what diuretics? how?

A

Role of 5 PG synthesized and with receptors in kidney poorly understood

PGE2 reduces Na reabsorption in TAL of Henle’s loop and ADH-mediated water transport in collecting tubule – enhance loop diuretics

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8
Q

if someone is on a loop diuretic what happens with protoglandins

A

increase production of prostaglandin (will be decreased under the presence of a Nonsteroidal anti-Inflammatory drug like indomethacin)

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9
Q

Made in distal tubule
Blunts sodium reabsorption
Vascular effects - decreases afferent tone and increases efferent tone leading to a increase in GFR

A

Natriuretic Peptides

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10
Q

MC: Acetazolamide (PO, ER, IV)

MC: Methazolamide (PO)

A

Carbonic Anhydrase Inhibitors(least important)

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11
Q

Carbonic Anhydrase Inhibitors MOA for glaucoma

A

Ciliary body secretes bicarbonate from blood into aqueous humor
Reduce formation of aqueous humor, thereby lowering IO pressure

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12
Q

Carbonic Anhydrase Inhibitors MOA for HTN

A

Works in PT

  • increase excretion of HCO3, Na, K
  • Decrease in H2O reabsorption- (increase rine vol & more alkaline)
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13
Q

all diuretics are eliminated

A

through the kidney

some like methazolamide is also metabolize din the liver

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14
Q

what are the main indications for carbonic anhydrase inhibitors

A

glaucoma
altitude sickness

used to be used to high BP
metabolic acidosis

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15
Q

why do we see hyperglycemia with carbonic anhydrase inhibitors

A

low potassium results in low absorption of glucose

also see reduced release of glucose

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16
Q

CNS symptoms with carbonic anhydrase inhibitors

A
  • CNS (ie. drowsiness, malaise, HA, confusion, depression,irritable, nervous, excitement, dizzy) paresthesias: numbness, tingling of tongue, lips, anus) decrease electrolyte
    o w/ high doses
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17
Q

what allergy do we worry about with carbonic anhydrase inhibitors

A
  • Hypersensitivity (sulfas)
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18
Q

hematological concerns with carbonic anhydrase inhibitors

A
  • Hematologic: anemia, leukopenia, thrombocytopenia (RARE)
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19
Q

this diabetic medication has diuretic properties.

A

SGLT2 - block Na & Glucose reabsorption.

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20
Q

increase prostaglandin production seen with can have what effect on edema

A

relieve edema even before you see diuretic effect

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21
Q

MOA of loop diuretics

A

Inhibit NaCl reabsorp Thick ascending loop of henley
Inhibit Na/K/2Cl transporter (lots of solutes in tubule; increase diuretic effect)

renal prostaglandin prod via COX2 increase renal blood flow & inhibits Na reabsorption in the loop

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22
Q

ADE of loop diuretics

A
  • Hypo-K, metabolic alkalosis
  • Hypo-Mg (check K and Mg)
  • Increases UA levels (gout)
  • Orthostatic hypotension
  • Ca loss
    Otic effects: Tinnitus, hearing impairment/loss
  • Hyperglycemia, glycosuria
  • Hypersensitivity (sulfas)
  • Electrolyte sx’s
  • GI: N/V/D, anorexia, constipation
  • Nervous, dizzy, lightheadedness, HA, paresthesias
  • Hematologic: anemia, leukopenia, thrombocytopenia (rare)
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23
Q

DI with loop diuretics

A
  • Digoxin-hypoK ír isk of toxicity
  • Other diuretics: additive HoTN agents
  • K+ loss drugs (amphloterocmin, corticosteroids)
  • Erythro/AG Auditory tox
  • Indomethacin –> dec. efficacy of loop diuretics
  • Cholestyramine, colestipol ( absorption -bind to everything)
  • Hypotension: additive effects
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24
Q

very significant DI seen with loop and thiazide seen with Indomethacin as a result of

A

prostaglandin production is inhibited by indomethacin

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25
Q

thiazide that has been studied the most

A
  • Chlorthalidone**
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26
Q

Thiazide MOA

A

distal tubule co-transpoter sodium and chloride
- Inhibit NaCl resorpt (DCT)

increase prostaglandin too

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27
Q

chlorthalidone 1/2 life

A

40 hrs because 90% are bound to RBC

28
Q

HYDROCHLOROTHIAZIDE 1/2 life

A

5.6-9 hrs

do not use if blood pressure is uncontrolled because very short half life

29
Q

DOC: uncomplicated HTN

A

Thiazide Diuretic

30
Q

DI with thiazide

A

all the same as loop diuretics in addition

Same as Loops

  • Lithium thiazides lithium levels Li toxicity
  • Ca2+ salts hyper-Ca from renal tubular reabsorption of Ca

Thiazides + loops used for severe renal dysfunction - Check K w/i 1st/2nd wk of tx

31
Q

MOA of potassium sparing diuretics

A

Inhibit Na resorption in distal tubule

  • Amil/Tria: inhibits Na flux thru ion channels of principal cell
  • Spiron/epler: aldosterone antagonist
  • Depends on prostaglandin production
32
Q

K-sparing diuretics that act on Channels

A
  • Tramterene

- Amiloride

33
Q

K-sparing diuretics that Block Aldosterone

A

Block Aldosterone

  • Spironolactone
  • Eplerenone (more specific)
34
Q

K-sparing diuretics Combo + HCTZ

A

Dyazide

  • Maxzide
  • Moduretic
  • Aldactazide
35
Q

used in the presence of -Oliguric renal failure (prevent anuria)

A
  • Osmotic diuretics
  • Mannitol (IV

Oliguric renal failure (prevent anuria)

  • Decrease ICP prior to/during neurosurgery
  • Decrease IOP acute angle-closure glaucoma
36
Q

MOA of mannitol

A

Prevents normal resorpt of H20 via osmotic force (PCT, descending)

(large sugar molecule)

37
Q
  • ConivaptAN (po)
  • TolvaptAN (IV)

drug class

A

ADH ANTagonist

AVP V1A &V2 antagonist - diuretic

38
Q
  • ConivaptAN (po)
  • TolvaptAN (IV)

indications

A
  • HTN, Ortho HoTN, hypoK, constipation, diarrhea, HA
39
Q

-TolvaptAN warning

A

select liver damage

short term only

40
Q

Demeclocycline
-Lithium

are both what types of drugs and what are their indications

A

Other ADH ANTagonists used to treat SIADH

41
Q
  • ConivaptAN (po)
  • TolvaptAN (IV)

ADE

A
  • Nephrogenic DI severe hypernatremia
42
Q

dose adj in loop diuretics with renal failure

A

based on osmolairc volume

43
Q

poor blood pressure control might be an issued with thiazides why?

A

short 1/2 life?

44
Q

neprolithiasis might be useful to us

A

THIAZIDE

45
Q

methazolamide drug class and where it acts

A

CAI

PCT

46
Q

ADE of CAI

A

sulfa hypersensitivity
HYPERGLYCEMIA
metbaolic acidosis
drowsiness paresthesia

47
Q

name all CAI

A 
acetazolamide 
methalzolamide
dorzolamide 
brinzolamide 
dichlorhenamide
48
Q

dosage of acetazolamide

A

250mg 1-4x a day for glaucoma

250 mg -1g qd for altitude sickness

49
Q

three major loop diuretics

A

furosemide
bumetanide
torsemide

50
Q

inidcations for loop

A

Edema due to congestive heart failure, acute pulmonary edema, nephrotic syndrome, and hepatic cirrhosis
HF – used for control of fluid overload, not shown to reduce mortality, used for symptomatic relief
Hypertension – in patients with reduced renal function where thiazide diuretics may not be effective

51
Q

Hypokalemic metabolic alkalosis
Mg+ loss (check K+ and Mg+)
Ca+ loss - may be compensated by reabsorption in distal tubule if dehydrated and

and increase Vit-D dependent reabsorption in gut

Increased uric acid levels - gout

are all sxs

A

loop diuretics

52
Q

how would you treat HTN in a pt wiht reduced renal function

A

loop

53
Q

NSAIDS can affect the function of what two diuretics

A

loop and thiazide

through PG

54
Q

Cholestyramine can decrease absorption of

A

furosemide

55
Q

increases urine volume

A

Diuretic

56
Q

increases sodium excretion

A

naturuietic

57
Q

increases solute free water excretion

A

aquaretic

58
Q

high altitude sikness occurs over

A

> 9000 ft –> pulm edema

59
Q

why due you have to be careful with salt and thiazides

A

more salt consumed the more K you will lose

60
Q

which diuretics do you use in HF

A

fluid volume mngmt with thiazides but usually loop because renal function isn’t great

61
Q

which diuretic would you primarily use for HTN

A

thiazides
CrCl>30
and not CKD 4 or 5

62
Q

kidney disease what diuretic would you use

A

rentention of Na and water use thiazide or loop

63
Q

what diuretic would you use with hepatic cirrohsis

A

low albumin causes activation of RAAS
spironalactone can be very effective

loop alone may be inefective

64
Q

calcium kidney stones what diuretic would you use

A

thiazides (increases reabsorption)

65
Q

hypercalcemia

A

loop blocks Ca reabsopriton

66
Q

diabetes insipidus

A

thiazides reduce plasma volume

reduce plasma volume and GFR leads to greater Na water reabsorption and less fluid present in collecting tubule

Pharm II (16 decks)

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