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Clinical Pharmacology 2 > Chronic kidney disease > Flashcards

Chronic kidney disease Flashcards

1
Q

progressive loss of function over time, reduced GFR and/or kidney damage
present for > 3 mo
progressive loss of nephrons (proteinuria, glomerular capillary HTN)

A

CKD

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2
Q

albinuria, urine sediment abnormalities, electorlyte abnormalities, structural abnormalities, kidney transplant

A

CKD

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3
Q

common causes of CKD –

A

glomerular disease (diabetes, autoimmune, nephropathy) or vascular (atheroslcerosis, HTN, vasculitis)

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4
Q

kidney damage with normal or high GFR >/= 90

A

G1

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5
Q

kidne ydamage with mildly decreased GFR 60-89

A

G2

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6
Q

mildly to moderately decreased GFR 45-59

A

G3a

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7
Q

moderately to severely decreased GFR, 30-44

A

G3b

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8
Q

severely decreased GFR 15-29

A

G4

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9
Q

kidney failure <15

A

G5

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10
Q

what staging is used in CKD?

A

CGA
Cause
Glomerular filtration rate
Albiuminuria category

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11
Q

normal to mildly increased albuminuria <30

A

A1

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12
Q

moderately increased albuminuria 30-300

A

A2

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13
Q

severely increased/nephrotic range proteinuria, >300

A

A3

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14
Q

What can you use to assess renal function?

A
  • Cr
  • CrCl
  • eGFR
  • CrCl vs eGFR (estimation)
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15
Q

what equation is used

A

cockcroft-gault equation

(140-age) * IBW/ 72*SrCr

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16
Q

What low albumin may result in low protein binding therefore increasing

A

free drug

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17
Q

If drugs are eliminated by the kidney then they have

A

decreased elimination in CKD

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18
Q

loop diuretics can

A

manage fluid overload and reduce edema
–> furosemide (40), bumetanide (1), torsemide (20)

increasing excretion of Na/K/Ca

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19
Q

What are ADRs of loop diuretics

A

hypovolemia
hypokalemia
hypocalcemia
nephrotoxic

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20
Q

What do you monitor in loop diuretic use with CKD patients?

A

serum electrolytes
renal function (BUN, Cr, GFR)
weight, fluid input, urine output

use lowest effective dose
avoid excessive use in advanced CKD stages

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21
Q

urgent dialysis is indicated in patients with

A

AEIOU
acidosis (<7.1)
electrolyte (severe hyperkalemia)
intoxication (drugs)
overload of fluids (pulmonary edema unfunctional with diuretics)
uremic symptoms (encephalopahty, elevated BUN)

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22
Q

types of dialysis

A

hemodialysis (MC)
peritoneal dialysis (CAPD, CCPD)
continous renal replacement therapy

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23
Q

phosphate binders may lower absorption of other meds like

A

digoxin, warfarin, quinolones, tetracyclines

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24
Q

where can hyperkalemia come from

A

renal insufficiency (missed dialysis, disease), diet (salt subsitutes), drugs
Digoxin
Succinylcholine
Potassium supplementation
Drugs affecting excretion: NSAIDs, cyclosporine, ACEI, K+ sparing, trimethoprim

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25
Non pharm hyperkalemia treatment
prevention -- diet, avoid k-sparing diuretics, avoid ACEI and ARB
26
what are medications to lower hyperkalemia?
calcium gluconate (stabilizes myocardial membrane) insulin and glucose (drives potassium into cells with Na/K/ATPase pump) sodium bicarbonate (alkalinizes blood) beta agonists (stimulate Na/K/ATP pump)
27
bind K+ and allow it to excrete through GI tract to lower hyperkalemia
cation exchangers
28
separate --- --- by 3 hours from all other medications precautions of constipation, GI obstruction, hypomagnesemia
cation exchangers
29
ion-exchange resin that binds potassium in gut for excretion with risk of bowel necrosis (choose other cation exchangers), exchange calcium for potassium
kayexalate (sodium polystyrene sulfonate)
30
cation exchange drug that may worsen edema, exchanges sodium for potassium
sodium zirconium cyclosilicate (lokelma)
31
this cation exchanger can cause hypomagnesimia
patiromer (veltassa)
32
hyperphosphatemia can be chronic due to
secondary hyperparathyroidism presenting as joint pain, soft tissue and joint calcifications
33
how do you prevent hyperphosphatemia
restrict diet to 800-1000mg/day of phosphorous - dairy, meat, fish, grains "instant" products, spreadable cheeses, soft drinks typically not until stage 5 CKD
34
mineral bone disorder begins as GFR falls
<60
35
mineral bone disorder contributing factors
-decreased phosphorous excretion -decreased production of D3 - reduced absorption of calcium in GI tract -decreased free calcium concentrations -direct stimulation of PTH
36
consider -- --- --- with fatigue, M/S and GI pain, bone pain, fractures
mineral bone disorder
37
consequences of mineral bone disorder
renal osteodystrophy and vascular calcification
38
bind dietary phosphage in gut to prevent absorption, excreted in feces, MUST be taken with food, treating for mineral bone disorder
phosphate binders - calcium carbonate (Tums) - calcium acetate
39
DO NOT USE CALCIUM BASED IN DIALYSIS PATIENTS WHO ARE
HYPERCALCEMIC >10.2 OR PTH <150
40
use ---- if hypercalcemia or when calcium intake exceeds recommended amount
sevelamer phosphate binder (first line in stage 5 CKD) Gi sx common
41
dissociates in upper GI so lanthanum ions can bind to phosphorous in GI tract, must be chewed and completely taken with food, contraindicated if GI obstruction, fecal impaction, or ileus
lanthanum carbonate (phosphate binder)
42
bind iron in GI tract and only for dialysis patients
oral iron - sucroferric oxyhydroxide with insignificant increase in serum iron (dark stool) - ferric citrate with iron absorption (must check iron before studying, GI ADRs)
43
all phosphate binders need monitoring
serum phosphate and calcium levels
44
stimulate calcium absorption and suppress PTH syntehsis
vitamin D analogues (calcitriol, paricalcitol)
45
vitamin D analogues are for
stage 3-5 CKD and vitamin D level <30, can treat/prevent secondary hyperparathyroidism recommended: 600-1000 units/day
46
with vitamin D analogues, monitor --
serum calcium and phosphorous levels, PTH must correct high calcium and/or phosphorous before starting vitamin D
47
discontinue vitamin D analogues if calcium is
>10.2 9.5-10.2 = decrease dose by 50%
48
vitamin D inactive forms
ergocalciferol (D2) -- weekly/monthly cholecalciferol (D3) -- daily
49
active vitamin D 3
calcitrol paricalcitrol doxercalciferol
50
adrs of vitamin d analogues
may increase phosphorous, must maintain balance of Ca, phosphates, PTH levels
51
increase sensitivity of calcium-sensing receptor on parathyroid glands to reduce PTH secretion, calcium, phosphorous levels for dialysis patients with PTH >300 and Ca >8.4
calcimimetics (cinacalcet)
52
Hyperphosphatemia is/isn't a CI for calcimimetics
Is NOT -- vitamin D cannot be used with hyperphosphatemia though
53
What are ADRs of calcimimetics
**hypocalcemia**, N/V, HOTN caution with seizure disorders extensive metabolism by 3A4 and 2D6 monitor serum calcium and PTH
54
Overview of MBD treatment ADRs
phosphate binders = constipation, hypercalcemia vitamin d analogues = hypercalcemia, hyperphosphatemia, vitamin D toxicity calcimimetics = hypocalcemia, nausea, vomiting
55
administer phosphate binders with
meals
56
monitor regularly
serum calcium, phosphate, PTH
57
If CKD and mild metabolic acidosis, treat if
serum bicarb <22 with sodium bicarbonate 650-1300 PO/TID or sodium citrate/citric acid
58
If CKD and sever uncompensated acidosis, <7.2, treat with
IV sodium bicarb
59
sodium bicarb ADRs
hypernatremia, hypocalcemia, hypokalemia, metabolic alkalosis, edema
60
CKD anemia in CKD 3-5 --
decreased erythropoietin production, shorter life span of RBCs, blood loss during dialysis, iron deficiency
61
CKD + anemia evaluation
CrCl <60ml/min OR Hgb <13 (M), <12 (W) reticulocyte count iron studies serum B12 and folate
62
stimulate RBC production in bone marrow, counteracting anemia used in patients with anemia (Hgb <10) due to ESRD
erythropoiesis-stimulating agents
63
treat iron deficiency
first and maintain iron supplementation
64
epoetin alfa (epogen)
recombinant human EPO
65
darbopoetin alfa
long acting ESA
66
ESA black box warning
increase risk of death, MI, stroke, thromboembolis, thrombosis, tumor progression
67
ESA ADRs
HTN, HA, arthralgia, N/V, pruritus, rash use lowest effective dose to reach lowest Hgb sufficient to reduce need (increased risk of death with Hgb >11)
68
monitoring parameters of ESAs in CKD
hemoglobin target 10-11 iron status blood pressure
69
with diabetes in CKD
tight gluocse control with HgA1C <7% utilize SGLT2 inhibitors: empagliflozin, dapagliflozin, canagliflozin (decrease albuminuria, decrease GFR loss)
70
CKD + HTN
non-dialysis patient goal <120 renal transplant goal 130/80 ACEI/ARB (reduces progression, protects kidney)
71
monitoring with ACEI/ARB
monitor Cr, potassium, titrate every 1-3 months to achieve maximal reduction, dose adjustments may be needed to prevent hyperkalemia
72
dose adjustments with lowered renal function
antibiotics anticoagulants cardiac meds lipid-lowering therapy narcotics antipsychotic/epileptic hypoglycemic antiretrovirals miscellaneous

Clinical Pharmacology 2 (12 decks)

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