Nephrology Flashcards Preview

Pharmacology > Nephrology > Flashcards

Flashcards in Nephrology Deck (44):
1

Labs to assess kidney function

SCr, BUN, CrCl, GFR, MDRD, Urinalysis, salt/H2O balance, acid/base balance

2

Problems with MDRD

although it is very accurate, very little research, all dosing is based on CrCl

3

Problems with CrCl

serum creatinine is just a "snapshot", weight discrepancies , diet can effect, athletically fit

4

Problems with GFR

less reliable, varies w/ age, ethnicity, and body comp

5

Problems w/ 24 hr urine

cumbersome, prone to error

6

What do you not use to assess AKI

CrCl, too rapid of a change to be accurate, instead use I&Os

7

AKI definition

acute decrease in kidney function over hrs, days or weeks, associated w/ accumulation of waste products and volumes, increase of SCr of .5mg/dL in 24 hrs

8

AKI risk factors

pre-existing CKD, volume depletion/ decrease perfusion, using nephrotoxic agents, obstruction of urinary tract

9

Causes of AKI

Pre-renal (affecting blood flow before kidneys), Postrenal (problem with moving urine out of kidneys), Intrinsic (problem w/ kidney, preventing filtration or urine production)

10

When you hear pre-renal what should you think

Hypoperfusion, it's the most common type of AKI, too

11

Pre-renal AKI can be caused by

dehydration, disruption of bllod flow, dec in BP, emboli, MI, CHF, liver failure

12

Treatment for Pre-renal

usually reversible (hydration, fixing other disease), but can cause CKD,

13

Postrenal is caused by

kidney stone, enlarged prostate, CA

14

Intrinsic is caused by

blood vessel disease, injury to tissue or cells, glomerulonephritis, acute interstitial nephritis, acute tubular necrosis, medications

15

Medications known to cause AKI

Aminoglycosides, NSAIDs, ACE-Is (usually only makes preexisting worse), contrast dye, amphotericin-B

16

Acute interstitial nephritis

sudden decline in kidney function from inflammation of interstitial kidney tissue, usually reversible if treated early (steroids)

17

Acute interstitial nephritis is caused by

Medications, infections, lupus, lymphoma, leukemia, sarcoidosis

18

Acute tubular necrosis

kidney tubule damaged and do not function normally, usually end result of acute renal failure

19

Nephrotoxic ATN caused by

aminoglycosides, amphotericin B, Cisplatin, contrast media, vancomycin

20

Treatment AKI

volume control with RRT and diuretics

21

start RRT if

Renal replacement therapy, Acid/base problem, electrolyte abnormality (usually K), Intoxication, fluid overload, uremia

22

Chronic kidney disease definition

kidney damage lasting more than 3 months, including structural or functional abnormality of the kidney w/ or w/out decreased GFR, with pathologic abnormalities or markers of damage; also GFR

23

Stage 1 CKD

kidney damage with normal or inc GFR

24

Stage 2 CKD

kidney damage w/ mild decrease GFR, 60-80 ml/min

25

Stage 3 CKD

moderate dec GFR, 30-50 ml/min

26

Stage 4 CKD

severe dec GFR, 15-29 ml/min

27

Stage 5 CKD

kidney failure,

28

CKD risk factors

diabetes, HTN, CVD, obesity, age, race, acute kidney injury, malignancy, family hx, hep C, HIV, Lupus, NSAIDS, polycystic kidney disease

29

Why do you not want to use CrCl for CKD

will overestimate renal function if it is moderate to severe, so use MDRD instead

30

CKD manifestations

abnormal sodium-water handling (edema, HTN, CVD), metabolic acidosis, anemia, uremia, abnormal Ca-P metabolism due to lack of Vit D

31

Management of CKD

treat fluid retention/overload, hyperphophatemia/hyperkalemia, hyperparathyroidism, dyslipidemia, anemia, proper drug dosing, prep for RRT

32

Treating fluid overload

restrict Na, avoid excessive amts of H2O at one time, keep all fluids in mind (diet, drugs etc)

33

Diuretics for Fluid overload

not for stage 5, do not use thiazides if CrCl

34

Treating hyperkalemia

restrict intake of Potassium to 3 gm/day, dialysis, calcium gluconate, albuterol, insulin+glucose, sodium polystyrene, sodium bicarbonate

35

Hyperphosphatemia causes

inhibition of Vit D activation, dec in ionized Ca conc, direct stimulation of parathyroid hormone secretion

36

Treating hyperphosphatemia

Diet of 800-1200 mg/day phos, phosphate binders- Calcium carbonate, calcium acetate (phoslo), aluminum hydroxide (amphogel), sevelamer (Renagel), lanthanum (Fosrenol)

37

MOA of phosphate binders

binds to phosphate found in diet and thus it is not absorbed and eliminated in feces, must take with a meal, be wary of hypercalcemia with calcium containing pho binders

38

Dosage of Phosphate binders

calcium acetate (phosplo)- 667 mg PO TID, sevelamer (renagel)- 800 PO TID

39

ADRs of phosphate binders

constipation, GI upset

40

hyperparathroidism treatment

Clacitriol (Rocaltrol), Paricalcitol (Zemplar), Doxercalciferol (Hectoral), Cinacalcet (Sensipar)

41

Calcitriol (rocaltrol)

active vit D, IV or PO, decreased PTH secretion by increasing [Ca] via increased gut absorption, monitor for hypercalcemia

42

Paricalcitol (Zemplar)

IV/PO, IV for ESRD pts, favorable due to decrease risk of hypercalcemia, dose based on PTH levels

43

Docercalciferol (Hectoral)

similar to paricalcitol, must avoid in pt w/ liver failure

44

Dyslipidemia in CKD

elevated LDL, be aggressive w/ treatment to decrease morbidity, frequently in glomerular disease w/ proteinuria