Chronic Kidney Disease Flashcards
(86 cards)
1
Q
CKD
A
term which encompasses all stages of chronic renal failure and ESRD.
2
Q
for kidney disease to be deemed chronic, you’ll have to have had it for
A
~3 months
3
Q
two types of CKD
A
structural
functional
4
Q
structural CKD
A
blood / protein in urine
5
Q
functional CKD
A
reduction in GFR
<60 mL/min
6
Q
likely causes of CKD
A
long standing hyperglycemia
uncontrolled HTN
hyperlipidemia
7
Q
prognostic factor for progression of CKD as well as CVD
A
microalbuminuria
8
Q
K-DOQI guidelines for CKD
above 90 GFR
A
not much wrong
9
Q
K-DOQI guidelines for CKD
between 60-90 GFR
A
stage 2 kidney disease
10
Q
K-DOQI guidelines for CKD
between 30-60 GFR
A
Stage 3 CKD
moderate disease
11
Q
K-DOQI guidelines for CKD
GFR 15-30
A
stage 4 CKD
12
Q
K-DOQI guidelines for CKD
<15 GFR
A
ESRD
may need dialysis
13
Q
RIFLE
A
risk insult failure loss end stage renal disease
coincides with K-DOQI guidelines for CKD stages 1-5.
14
Q
nonpharm prevention of ckd
A
smoking cessation
15
Q
pharm prevention options: ckd
A
manage diabetes, htn, dyslipid.
16
Q
complications r/t CKD (5)
things to watch out for
A
anemia hyperparathyroid hyperkalemia met acidosis malnutrition
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
18
Q
goals for ckd
A
stabilize kidney function
delay dialysis
19
Q
anemia of CKD
A
decreased production of EPO
blood loss from dialysis
20
Q
when do you initiate a workup for anemia in CKD?
A
33% hct women
37% hct men
21
Q
hct goal for CKD pt
A
33-36%
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.
23
Q
Procrit (erythropoietic factor) frequency
A
3x/week
24
Q
darbepoetin frequency
A
q2 weeks
25
erythropoeitin therapies MoA
stems proliferation and differentiation of RBC precursors
increases hgb synthesis
releases reticulocytes from bone marrow
26
AE epo therapy
htn
| thrombotic event
27
EPO therapy monitoring
H&H q2-4 wks after initiation
avoid large jumps in hct
check bp ~1x/wk and adjust anti htn prn
28
when would you inc dose by 25-50% of epo?
if <2% rise in hct after a few weeks.
29
when would you decrease dose of epo by 25%?
if >8% inc in hct after a few weeks
30
iron supplementation therapy in ckd
necessary to promote adequate response to epo.
| not optional.
31
iron dose
200mg elemental iron daily in 2-3 divided doses
32
of 325mg ferrous sulfate, what % is elemental iron?
20%, therefor 65mg is elemental iron.
33
3 tablets of ferrous sulfate 3x a day will
give you ~200mg elemental iron, which is what is needed.
34
barriers to taking iron
constipation
35
ferrous gluconate vs sulfate
gluconate has only 12% elemental, sulfate has 20%.
36
If GI intolerance is too much of a barrier for iron therapy,
give IV
37
PO iron interacts with
FQs
tetracycline
antacids
dairy
38
monitoring for those on iron therapy
ferritin
TSat
q3 months.
39
IV iron AEs
anaphylaxis or hypotension
40
for patients with anemia in CKD, we always correct with
iron and EPO
41
when do we give IV iron?
when TSat is <20%
42
iron maintenance therapy
PO
43
secondary hyperparathyroidism in CKD is initiated by
| 2
decreased elimination of phosphate
| decreased production in the active form of vit D
44
increased phos leads to
decreased Ca
45
if Ca decreases, what hormone is released and why
PTH
| to increase production of calcium and mobilization of calcium from bone to blood. bones are now weakened.
46
PTH secretion occurs in response to
hypocalcemia
47
PTH acts primarily on
bone
kidney
gut
48
PTH and bone
stimulates bone resorption.
releases ca + PHos into ECF. Renal tubule resorbs Ca, phos gets excreted via urine
49
PTH and kidney
modulates vit D synth
50
PTH and the gut
increases ca/phos absorption
51
renal osteodystrophy
breakdown of bone r/t renal insufficiency
52
monitoring phosphorus for pt in secondary hyperPTH
ideal 2.7-5.5
monitor weekly, then every other month.
53
monitoring calcium for the renal pt with secondary hyperPTH
ideal 8.4-9.5
adjust for albumin
monitor weekly then every other month.
54
monitoring PTH for the renal pt with secondary hyperPTH
ideally 35-500, depending on CKD stage
| monitor monthly then every 3-6 months.
55
monitoring vit D for renal pt with secondary hyperPTH
greater than or equal to 30
56
non pharm therapy for secondary hyperPTH
restrict dietary phos intake
57
foods high in phos
dairy
cola
chocolate
seafood
58
pharmacologic therapy for hyperPTH
phosphate binders to correct hyperphosphatemia
vit D and calcimimetics to decrease secretion of PTH
59
phosphate binders are given to
bind phosphate in the gut, which is then eliminated in feces.
60
when does a phosphate binder need to be taken?
with meals
61
3 types of phosphate binders
aluminum containing
calcium containing
non absorbable polymers
62
when do we initiate tx for phosphate binders?
if phos is > 4.5
63
if serum Ca x PO4 product is < 55, which phosphate binder should be used
calcium containing
64
if serum Ca x PO4 product is > 55, what phosphate binder should be used?
sevelamer
lanthanum
or aluminum salt.
65
remember to adjust calcium based on
albumin
66
Vit D therapy for secondary hyperparathyroidism
inhibits PTH secretion and promotes GI Ca absorption
67
most popular vit D therapy
calcitriol
68
AE vit D therapy
hypercalcemia
69
calcimimetic agents MoA
activates Ca receptors on PTH gland, making the receptors more sensitive to calcium, thus inhibiting PTH release.
70
calcimimetic agent example
cinacalcet
71
when will we start to screen people for secondary hyperPTH?
if GFR is < 50-60.
72
hyperkalemia in CKD
diminished K excretion and redistribution of K into extracellular fluid due to met acidosis.
73
tx of hyperkalemia depends on
serum K
| EKG changes
74
therapy for hyperkalemia is initiated when
K > 6
75
calcium IV in hyperkalemia
to protect heart
76
in order to redistribute K intracellularly,
give insulin with dextrose, beta agonist, and bicarb.
77
elimination of hyper K
kayexalate
| dialysis
78
maintenance therapy for chronic hyperkalemia in ckd
sodium polystyrene (kayexalate)
79
metabolic acidosis in CKD
due to decrease in H+ ion production and thus reduced bicarb absorption. reduced bicarb absorption leads to metabolic acidosis.
80
metabolic acidosis contributes to
osteodystrophy
| muscle loss
81
therapy for metabolic acidosis in CKD
dialysis
| bicarb replacement therapy
82
3 ways to correct acidosis, summarized.
correct underlying issue
dialysis to remove it
bicarb to correct it
83
nutrition deficiency in CKD is related to (5)
inadequate intake, dialysis, blood loss, endocrine disorders, uremic toxins.
84
nutritional decline in CKD begins before
stage 4
85
vitamin malnutrition is likely in CKD, why?
water soluble vitamins are removed in dialysis
86
fat soluble vitamins in dialysis
not removed, can accumulate in dialysis pts.
