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Pharm2 S.Horvath > diuretics and electrolytes > Flashcards

diuretics and electrolytes Flashcards

1
Q

what part of the nephron do carbonic anhydrase inhibitors work on?

A

proximal tubule

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2
Q

what part of the nephron do loop diuretics work on?

A

loop of henle

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3
Q

there is a huge reabsorption of sodium and chloride back into the body at the ____ _____

A

proximal tubule

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4
Q

what is the main concentrating segment of the nephron?

A

loop of henle

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5
Q

what part of the nephron do thiazide diuretics work on?

A

distal tubule

they compete for the Na-Cl cotransporter in the DT to inhibit reabsorption.
inhibit only urinary diluting capacity

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6
Q

where is the final concentration determined?

A

collecting duct

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7
Q

where does vasopressin work?

A

collecting duct

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8
Q

the definition of chronic kidney disease is: kidney damage for _____ defined by structural or functional abnormalities with or without decreased GFR

A

> 3 months

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9
Q

the definition of chronic kidney disease in terms of GFR =?

A

<60ml/min for >30 months with or without kidney damage

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10
Q

stage 1 CKD =

A

damage with normal or increased GFR > 90ml/min

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11
Q

stage 2 CKD =

A

damage with mild dec GFR: 60-89

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12
Q

stage 3 CKD =

A

moderate dec GFR: 30-59

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13
Q

normal GFR is above ___

A

90

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14
Q

stage 4 CKD =

A

severe dec GFRP 15-29

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15
Q

kidney failure = GFR < ___

A

15

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16
Q

stage 6 CKD =

A

dialysis

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17
Q

how does the RIFLE criteria categorize acute kidney disease

A

it looks at increased CrCl from baseline or reduction in GFR from baseline

urine output criteria is based on oliguria for 6 (risk) , 12(injury), 24h (failure)

review slide 8 for Rifle criteria

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18
Q

if someone has taken something that has damaged the nephron such as NSAIDS, aminoglycosides, pcn, they have ____ renal failure

A

intrinsic

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19
Q

pre-renal failure usually is caused by

A

dehydration

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20
Q

post renal failure is usually due to

A

obstruction - like a stone

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21
Q

what are carbonic anhydrase inhibitors actually used or these days?

A

people with increased IOP and long standing COPD and their CO2 is building up. trying to correct acid base abnormalities

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22
Q

acetazolamide (diamox)
methazolamide (neptazene)
dichlorophenamine (daranide)

are all examples of

A

carbonic anhydrase inhibitors

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23
Q

whats the MOA of a carbonic anhydrase inhibitor?

A

inhibit CA which inhibits H+ secretion in the proximal tubule. bicarb and sodium are blocked from reabsorption. the effect is short lived d/t compensation at the loop of henle

explanation: we are blocking Na and Bicarb from reabsorbing, therefore Na is staying IN the urine (not being reabsorbed back into the body.), water is going to follow and we have a diuresis. it blocks enzyme carbonic anhydrase which normally breaks down hydrogen from bit from our water and our CO2 from our bicarbs. when we block that our bicarb and sodium bind up and go out together and we have water excretion. its a very round about way of getting rid of water. tolerance will develop bc when youre working just in this front part of the nephron there’s a lot of ways that the body is going to compensate later on…lose your effect of diuresis

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24
Q

which diuretic is associated with tolerance after 2-3 days

A

carbonic anhydrase inhibitors

acetazolamide (diamox)
methazolamide (neptazene)
dichlorophenamine (daranide)

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25
Q

which diuretic is associated with hypokalemic metabolic acidosis

A

carbonic anhydrase inhibitors

acetazolamide (diamox)
methazolamide (neptazene)
dichlorophenamine (daranide)

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26
Q

blurred vision and changes in taste are side effects of

A

acetazolamide (diamox)
methazolamide (neptazene)
dichlorophenamine (daranide)

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27
Q

what are 2 examples of osmotic diuretics

A

mannitol and urea

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28
Q

how do osmotic diuretics work

A

big bulky molecule, thru osmosis it pulls water into the urine.

Non-reabsorbable solute filtered freely
at the glomerulous. Uncouples sodium and
water reabsorption by increasing the osmotic
gradient in the proximal tubule. Sodium
reabsorption initially, but water is not, leading
to decreased sodium reabsorption distally

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29
Q

mannitol causes ___ of water, ____ intracellular volume, and ____ risk

A

loss of water, reduced intracellular volume, and hypernatremia risk

30
Q

T/F Urinary ph is not altered by mannitol induced osmotic diuresis

A

TRUE

31
Q

which two drugs can work together to pull fluid out of spaces such as increased ICP and ascites

A

mannitol and loop diuretics

32
Q

IV mannitol increases or decreases plasma osmolarity?

A

INCREASES

mannitol draws fluid from intracellular to extracellular spaces.

this acutely expands the intravascular fluid volume

33
Q

what might be a detrimental effect of mannitol?

A

CHF in patients with poor myocardial function

pulm edema

34
Q

mannitol used to be used for prophylaxis against ARF and differential diagnosis of acute oliguria buuuuut….

A

there is no benefit giving mannitol before giving contrast dye and we use labs diagnostiacally.

35
Q

what are 2 indications for mannitol?

A

increased ICP and IOP

36
Q

T/F Evidence exists to show that mannitol is nephroprotective

A

FALSE. no true evidence exists

37
Q

T/F Mannitol is no better than plain saline pre-radiocontrast dye

A

TRUE

except in renal transplant surgery- less incidence of ARF

38
Q

How is mannitol used to diagnose acute oliguria

A

well first of all emily says is not really used for this anymore bc we have labs..

BUT

UO is increased when the cause of acute oliguria is decreased intravascular fluid volume

if glomerular or renal tubular function is severely compromised, mannitol will not increase urine output.

39
Q

T/F mannitol requires an intact BBB because you need the gradient to create an osmotic difference

A

TRUE

40
Q

what does mannitol do to CSF volume?

A

decreases by decreasing the rate of CSF formation

41
Q

urea has concerning side effects such as

A

venous thrombosis and tissue necrosis

42
Q

T/f Increased BUN after admin of urea is a sign of acute renal failure

A

FALSE

43
Q

which class is the biggest offender of electrolyte abnormalities

A

loop diuretics

44
Q

loop diuretics cause

\_\_\_natremia
\_\_\_\_\_kalemia
\_\_\_\_calcium 
\_\_\_\_mg
metabolic\_\_\_\_
A 
hypoNA
hypoK
hypoCa
hypoMg
metabolic alkalosis (think K is dec)

normally Na K Cl are reabsorbed and brought back into the blood and then passively along with these there is movement
of ca and mg. when we block this co-transporter(“simport”) we are keeping sodium in the urine… and thats where we get our diuresis is the water following the sodium… but we are also now losing K Cl, and then secondarily Ca and Mg

45
Q

T/F with loop diuretics, peripheral vasodilation precedes the onset of diuresis

A

TRUE.

also get renal vasodilation and inc RBF

46
Q

T/F Lasix does not dec ICP by changing cerebral blood flow or plasma osmolarity.

A

TRUE.

ICP is decreased by systemic diuresis, decreasing CSF production, and improving cellular water transport.

47
Q

T/F the combination of lasix and mannitol is more effective in decreasing ICP than either drug alone.

A

TRUE

48
Q

loop diuretics + amino glycoside or cephalosporin =

A

nephrotoxicity

49
Q

T/F Thiazide Diuretics inhibit urinary diluting and concentrating capacity

A

FALSE.

inhibit only urinary diluting capacity, not concentrating capacity.

50
Q

what acid base abnormality do TZD’s cause

A

hypokalemic metabolic alkalosis

51
Q

T/F If a patient takes TZD’s they may have prolonged weakness

A

TRUE

because they potentiate non-depolarizing nmb.

52
Q

T/F patient taking TZD’s have an increased likelihood of developing dig tox

A

true - d/t hypoK

53
Q

T/F TZD’s increase the elimination of uric acid

A

FALSE - decrease

so you get hyperuricemia

54
Q

where do potassium sparing diuretics work

A

collecting duct

55
Q

potassium sparing diuretics - amiloride & triamterene- MOA

A

inhibit Na reabsorption induced by aldosterone

inhibit active counter transport of Na and K in the collecting duct

56
Q

potassium sparing diuretics -spironolactone and eplerenone- MOA

A

compete for aldosterone receptor sites in the DT to block Na reabsorption and K secretion

57
Q

which two drugs are used in combination for refractory edematous states such as CHF and cirrhosis of the liver

A

K sparing (spironolactone) + lasix

58
Q

what is the principle side effect of K-sparing diuretics

A

hyperkalemia.

59
Q

T/F Unlike thiazides, K-sparing diuretics do not produce hyperuricemia or hyperglycemia

A

TRUE

60
Q

what should you give for hyperkalemia

A

IV calcium

gluconate preferred

61
Q

how does kayexalate work

A

binds potassium in the colon exchange for sodium

62
Q

patiromer and sodium zirconium cyclosilicate work how?

A

oral GI potassium binder to increase fetal excretion

63
Q

Na replacement: no more than __mEq in the first 24h, no more than ___ in the first 48

A

12, 18

64
Q

VAPTANS - vasopression receptors should never be used for

A

HYPOvolemic HYPOnatremic

only for euvolemic and hypervolemic hyponatremia

65
Q

vaptans - vasopressin receptor blockers should only be used for

A

euvolemic and hypervolemia hyponatremia

66
Q

hyperca —-> _____parathyroidism

A

hyper

67
Q

hypoca —-> ____parathyroidism

A

hypo

68
Q

thiazides effect on ca

A

hold on

69
Q

calcium levels are dependent on

A

albumin

70
Q

tx of hypercalcemia

A

fluids, loop diuretics, IV biphosphonates

71
Q

how do biphosphonates work

A

inhibit osteoclasts, inhibit bone breakdown. forces the body to take calcium and resubmit it into the bone structure…. but complications include kidneyy damage, hypocalcemia, atypical fx, burn a hole in your esophagus…

72
Q

when is a study statistically significant

A

p < 0.05

Pharm2 S.Horvath (13 decks)

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