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NAPLEX Prep > Renal Disease > Flashcards

Renal Disease Flashcards

physiology, DIKD, CrCl, CKD, dosing, CKD complications, dialysis

1
Q

proximal tubule function

A

Na Ca and Cl are filtered into the nephron
pH regulated with H and bicarb exchange
SGLT2 transporter is here

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2
Q

where do SGLT2-i work

A

proximal tubule

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3
Q

descending LOH function

A

water reabsorption into the blood

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4
Q

ascending LOH function

A

water reabsorption via ADH (vasopressin)
~25% Na and Cl reabsorption into blood
Ca resorption

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5
Q

where do loops work and on what receptor

A

work on the ascending LOH where they block Na K pump to prevent sodium reabsorption
also block Ca reabsorption and can cause dec MBD with time

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6
Q

distal convoluted tubule function

A

K, Na, Ca, pH regulation
~5% of Na a reabsorbed into the blood here
thiazides work here and increase Ca reabsorption and are therefore bone-protective

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7
Q

collecting duct function

A

connect kidney to ureter
H2O and electrolyte final balancing via ADH and aldosterone
MRAs work here to dec Na and H2O reabsorption without affecting K

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8
Q

aldosterone function

A

increases K excretion in collecting duct

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9
Q

risk factors for DIKD

A

dec renal BF (HF, CKD, HLD, dec BP)
inc age
nephrotoxins

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10
Q

what are the major nephrotoxins

A

AGs
Amph B
loops
vanco
cisplatin
cyclosporine
NSAIDs
polymixins
radiographic contrast dye
tacrolimus

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11
Q

what is the BUN

A

amount of nitrogen in the blood that comes from urea, a waste product of protein metabolism
as renal disease progresses, kidneys are unable to filter urea out of the blood as it should
normal <20

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12
Q

what is Scr

A

waste product of muscle metabolism
norm 0.6-1.3

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13
Q

what GFR is stage 3a

A

45-59

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14
Q

what GFR is stage 3b

A

30-44

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15
Q

what GFR is stage 1

A

> /= 90

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16
Q

what GFR is stage 2

A

60-89

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17
Q

what GFR is stage 5

A

</= 15

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18
Q

what GFR is stage 4

A

15-29

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19
Q

how do we delay CKD progression

A

treat comorbidities DM and HTN
finerenone

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20
Q

first line for CKD + HTN +/- hyperalbuminuria

A

ACE or ARB

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21
Q

what is the BP target for CKD and HTN

A

SBP <120

22
Q

what is an adverse effect of ACEi/ARBs that is expected with initiation? When do we hold ACEi/ARB?

A

inc Scr </=30% from baseline

hold when SCr increases over 30% from baseline

23
Q

first line for patients with CKD + DM

A

SGLT2-i

24
Q

what medication prevents CKD progression? What are the criteria for starting it?

A

finerenone

start when on SGLT2-i and on max tolerated ACEi or ARB + eGFR 25+

25
Q

which drugs require CrCl adjustments

A

ABX (SMX/TMP, B lactams except anti staph and CTX, AGs, fluconazole, FQ, vancomycin)

Cardiac (LMWH, xarelto for afib, xarelto for afib, dabigatran for afib, most statins)

H2RAs

others (bisphosphonates, lithium gabapentin, metformin, morphine, pregabalin, codeine)

26
Q

what drug(s) are CI at CrCl <60

A

nitrofurantoin

27
Q

what drug(s) are CI at CrCl <50

A

TDF
voriconazole IV

28
Q

what drug(s) are CI at CrCl 30

A

TAF
NSAIDs
dabigatran (DVT/PE)
rivaroxaban (DVT/PE)
MRAs
duloxetine
bisphosphonates

29
Q

what drug(s) are CI at eGFR <30

A

metformin
SGLT2i
meperidine

30
Q

what are the complications of CKD

A

MBD
anemia of CKD
hyperkalemia
metabolic acidosis

31
Q

what is considered microalbuminuria

A

UA 30-300

32
Q

what is considered macroalbuminuria

A

UA >300

33
Q

what are treatment options of MBD in CKD

A

restrict dietary phosphate
phosphate binders
calcimimetics
Vit D analogs

34
Q

why do patients with MBD in CKD have inc serum phosphate, low vitamin D levels and variable Ca levels

A

kidney damage prevents phosphate clearance which stimulates PTH and increases bone resorption

dec EPO production decreases active Vit D production and therefore dec Ca absorption from gut –> PTH overcompensates by stimulating bone resorption to inc serum Ca

Ca levels vary due to dec GI absorption and increased Ca resorption from bone

35
Q

sevelamer
brand name
MOA
dosing
ADE

A

Renvela
non Ca-based phosphate binder that binds phos in gut and is eliminated

800-1600mg TID W MEALS
ADE NVD :////

36
Q

sevelamer is CI in

A

bowel obstruction

37
Q

sevelamer effects on lipid panel

A

can decrease TG and LDL by 15-30%

38
Q

what drugs does sevelamer interact with/binds them

A

levothyroxine
FQ
TTC

39
Q

sevelamer can dec absorption of what from the gut

A

phos (obv)
Vitamins D E K
folic acid

40
Q

what are the calcium based phosphate binders
what is the concern

A

ca acetate
ca carbonate

concern for hypercalcemia

41
Q

what are the vitamin D analogs
MOA?
concern?

A

increase Ca absorption in the gut
calcitriol (Rocaltrol)
calcifediol (Rayaldee)
doxercalciferol

hypercalcemia risk?

42
Q

cincalcet
brand
MOA
dosing
ADE

A

Sensipar
calcimimetic
30-180mg PO daily with food
hypocalcemia risk

43
Q

hyperkalemia
K = _____
s/sx

A

K >5
s/sx : muscle weakness, bradycardia, arrhythmias

44
Q

drugs that cause hyperkalemia

A

ACE-i
ARB
aliskerin
SMX/TMP
MRAs (aldosterone antagonists)
TPN
K supplements
NSAIDs
CYA, tacro

45
Q

steps to treat hyperkalmenia

A

d/c sources of hyperkalemia
stabilize cardiac membranes
move it intracellularly
remove it in the gut

46
Q

how do we shift K into the cell in hyperkalemia

A

regular insulin + dextrose to prevent hypoglycemia
sod bicarb if acidotic
albuterol

47
Q

how do we remove potassium in hyperkalemia

A

loops
HD
SPS (Kayexalate)
SZC (Lokelma)
patiromer

48
Q

lokelma
generic
dosing
administration

A

sodium zirconium cyclosilate
10 grams PO TID W MEALS

separate other drugs by 2 hours before and after
in 3tbsp of water each time

49
Q

Kayexalate
generic
dosing
CI
administration

A

sodium polystyrene sulfate
15 grams PO QD-QID
CI GI necrosis

50
Q

Kayexalate can cause GI necrosis especially when combined with ___________

A

sorbitol

51
Q

what characteristics of the drug / HD / PD can increase removal by dialysis

A

dec MW/size
dec Vd
dec ppb
high flux (large pore size)
high efficiency (inc SA)
inc dialysis BF rate

NAPLEX Prep (57 decks)

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