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Pharm > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

CKD

A

term which encompasses all stages of chronic renal failure and ESRD.

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2
Q

for kidney disease to be deemed chronic, you’ll have to have had it for

A

~3 months

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3
Q

two types of CKD

A

structural

functional

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4
Q

structural CKD

A

blood / protein in urine

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5
Q

functional CKD

A

reduction in GFR

<60 mL/min

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6
Q

likely causes of CKD

A

long standing hyperglycemia
uncontrolled HTN
hyperlipidemia

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7
Q

prognostic factor for progression of CKD as well as CVD

A

microalbuminuria

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8
Q

K-DOQI guidelines for CKD

above 90 GFR

A

not much wrong

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9
Q

K-DOQI guidelines for CKD

between 60-90 GFR

A

stage 2 kidney disease

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10
Q

K-DOQI guidelines for CKD

between 30-60 GFR

A

Stage 3 CKD

moderate disease

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11
Q

K-DOQI guidelines for CKD

GFR 15-30

A

stage 4 CKD

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12
Q

K-DOQI guidelines for CKD

<15 GFR

A

ESRD

may need dialysis

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13
Q

RIFLE

A 
risk
insult
failure
loss
end stage renal disease

coincides with K-DOQI guidelines for CKD stages 1-5.

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14
Q

nonpharm prevention of ckd

A

smoking cessation

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15
Q

pharm prevention options: ckd

A

manage diabetes, htn, dyslipid.

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16
Q

complications r/t CKD (5)

things to watch out for

A 
anemia 
hyperparathyroid
hyperkalemia
met acidosis
malnutrition
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17
Q

preventing progression of CKD 7

A 
treat primary disease
aggressively treat proteinuria/albuminuria
aggressively treat HTN/DM
treat hyperlipidemia
smoking cessation
protein restriction
early referral to nephrologist
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18
Q

goals for ckd

A

stabilize kidney function

delay dialysis

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19
Q

anemia of CKD

A

decreased production of EPO

blood loss from dialysis

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20
Q

when do you initiate a workup for anemia in CKD?

A

33% hct women

37% hct men

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21
Q

hct goal for CKD pt

A

33-36%

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22
Q

hgb goal for anemic ckd pt

A

11-12

dont want to give more EPO than we need to bc of clot risk.

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23
Q

Procrit (erythropoietic factor) frequency

A

3x/week

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24
Q

darbepoetin frequency

A

q2 weeks

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25
Q

erythropoeitin therapies MoA

A

stems proliferation and differentiation of RBC precursors
increases hgb synthesis
releases reticulocytes from bone marrow

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26
Q

AE epo therapy

A

htn

thrombotic event

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27
Q

EPO therapy monitoring

A

H&H q2-4 wks after initiation

avoid large jumps in hct

check bp ~1x/wk and adjust anti htn prn

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28
Q

when would you inc dose by 25-50% of epo?

A

if <2% rise in hct after a few weeks.

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29
Q

when would you decrease dose of epo by 25%?

A

if >8% inc in hct after a few weeks

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30
Q

iron supplementation therapy in ckd

A

necessary to promote adequate response to epo.

not optional.

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31
Q

iron dose

A

200mg elemental iron daily in 2-3 divided doses

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32
Q

of 325mg ferrous sulfate, what % is elemental iron?

A

20%, therefor 65mg is elemental iron.

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33
Q

3 tablets of ferrous sulfate 3x a day will

A

give you ~200mg elemental iron, which is what is needed.

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34
Q

barriers to taking iron

A

constipation

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35
Q

ferrous gluconate vs sulfate

A

gluconate has only 12% elemental, sulfate has 20%.

36
Q

If GI intolerance is too much of a barrier for iron therapy,

37
Q

PO iron interacts with

A

FQs
tetracycline
antacids
dairy

38
Q

monitoring for those on iron therapy

A

ferritin
TSat

q3 months.

39
Q

IV iron AEs

A

anaphylaxis or hypotension

40
Q

for patients with anemia in CKD, we always correct with

A

iron and EPO

41
Q

when do we give IV iron?

A

when TSat is <20%

42
Q

iron maintenance therapy

43
Q

secondary hyperparathyroidism in CKD is initiated by

2

A

decreased elimination of phosphate

decreased production in the active form of vit D

44
Q

increased phos leads to

A

decreased Ca

45
Q

if Ca decreases, what hormone is released and why

A

PTH

to increase production of calcium and mobilization of calcium from bone to blood. bones are now weakened.

46
Q

PTH secretion occurs in response to

A

hypocalcemia

47
Q

PTH acts primarily on

A

bone
kidney
gut

48
Q

PTH and bone

A

stimulates bone resorption.

releases ca + PHos into ECF. Renal tubule resorbs Ca, phos gets excreted via urine

49
Q

PTH and kidney

A

modulates vit D synth

50
Q

PTH and the gut

A

increases ca/phos absorption

51
Q

renal osteodystrophy

A

breakdown of bone r/t renal insufficiency

52
Q

monitoring phosphorus for pt in secondary hyperPTH

A

ideal 2.7-5.5

monitor weekly, then every other month.

53
Q

monitoring calcium for the renal pt with secondary hyperPTH

A

ideal 8.4-9.5
adjust for albumin
monitor weekly then every other month.

54
Q

monitoring PTH for the renal pt with secondary hyperPTH

A

ideally 35-500, depending on CKD stage

monitor monthly then every 3-6 months.

55
Q

monitoring vit D for renal pt with secondary hyperPTH

A

greater than or equal to 30

56
Q

non pharm therapy for secondary hyperPTH

A

restrict dietary phos intake

57
Q

foods high in phos

A

dairy
cola
chocolate
seafood

58
Q

pharmacologic therapy for hyperPTH

A

phosphate binders to correct hyperphosphatemia

vit D and calcimimetics to decrease secretion of PTH

59
Q

phosphate binders are given to

A

bind phosphate in the gut, which is then eliminated in feces.

60
Q

when does a phosphate binder need to be taken?

A

with meals

61
Q

3 types of phosphate binders

A

aluminum containing
calcium containing
non absorbable polymers

62
Q

when do we initiate tx for phosphate binders?

A

if phos is > 4.5

63
Q

if serum Ca x PO4 product is < 55, which phosphate binder should be used

A

calcium containing

64
Q

if serum Ca x PO4 product is > 55, what phosphate binder should be used?

A

sevelamer
lanthanum
or aluminum salt.

65
Q

remember to adjust calcium based on

66
Q

Vit D therapy for secondary hyperparathyroidism

A

inhibits PTH secretion and promotes GI Ca absorption

67
Q

most popular vit D therapy

A

calcitriol

68
Q

AE vit D therapy

A

hypercalcemia

69
Q

calcimimetic agents MoA

A

activates Ca receptors on PTH gland, making the receptors more sensitive to calcium, thus inhibiting PTH release.

70
Q

calcimimetic agent example

A

cinacalcet

71
Q

when will we start to screen people for secondary hyperPTH?

A

if GFR is < 50-60.

72
Q

hyperkalemia in CKD

A

diminished K excretion and redistribution of K into extracellular fluid due to met acidosis.

73
Q

tx of hyperkalemia depends on

A

serum K

EKG changes

74
Q

therapy for hyperkalemia is initiated when

75
Q

calcium IV in hyperkalemia

A

to protect heart

76
Q

in order to redistribute K intracellularly,

A

give insulin with dextrose, beta agonist, and bicarb.

77
Q

elimination of hyper K

A

kayexalate

dialysis

78
Q

maintenance therapy for chronic hyperkalemia in ckd

A

sodium polystyrene (kayexalate)

79
Q

metabolic acidosis in CKD

A

due to decrease in H+ ion production and thus reduced bicarb absorption. reduced bicarb absorption leads to metabolic acidosis.

80
Q

metabolic acidosis contributes to

A

osteodystrophy

muscle loss

81
Q

therapy for metabolic acidosis in CKD

A

dialysis

bicarb replacement therapy

82
Q

3 ways to correct acidosis, summarized.

A

correct underlying issue
dialysis to remove it
bicarb to correct it

83
Q

nutrition deficiency in CKD is related to (5)

A

inadequate intake, dialysis, blood loss, endocrine disorders, uremic toxins.

84
Q

nutritional decline in CKD begins before

85
Q

vitamin malnutrition is likely in CKD, why?

A

water soluble vitamins are removed in dialysis

86
Q

fat soluble vitamins in dialysis

A

not removed, can accumulate in dialysis pts.

Pharm (31 decks)

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