Nephrology Flashcards

1
Q

Labs to assess kidney function

A

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

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2
Q

Problems with MDRD

A

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

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3
Q

Problems with CrCl

A

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

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4
Q

Problems with GFR

A

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

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5
Q

Problems w/ 24 hr urine

A

cumbersome, prone to error

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6
Q

What do you not use to assess AKI

A

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

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7
Q

AKI definition

A

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

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8
Q

AKI risk factors

A

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

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9
Q

Causes of AKI

A

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

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10
Q

When you hear pre-renal what should you think

A

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

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11
Q

Pre-renal AKI can be caused by

A

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

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12
Q

Treatment for Pre-renal

A

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

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13
Q

Postrenal is caused by

A

kidney stone, enlarged prostate, CA

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14
Q

Intrinsic is caused by

A

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

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15
Q

Medications known to cause AKI

A

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

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16
Q

Acute interstitial nephritis

A

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

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17
Q

Acute interstitial nephritis is caused by

A

Medications, infections, lupus, lymphoma, leukemia, sarcoidosis

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18
Q

Acute tubular necrosis

A

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

19
Q

Nephrotoxic ATN caused by

A

aminoglycosides, amphotericin B, Cisplatin, contrast media, vancomycin

20
Q

Treatment AKI

A

volume control with RRT and diuretics

21
Q

start RRT if

A

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

22
Q

Chronic kidney disease definition

A

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
Q

Stage 1 CKD

A

kidney damage with normal or inc GFR

24
Q

Stage 2 CKD

A

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

25
Q

Stage 3 CKD

A

moderate dec GFR, 30-50 ml/min

26
Q

Stage 4 CKD

A

severe dec GFR, 15-29 ml/min

27
Q

Stage 5 CKD

A

kidney failure,

28
Q

CKD risk factors

A

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

29
Q

Why do you not want to use CrCl for CKD

A

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

30
Q

CKD manifestations

A

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

31
Q

Management of CKD

A

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

32
Q

Treating fluid overload

A

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

33
Q

Diuretics for Fluid overload

A

not for stage 5, do not use thiazides if CrCl

34
Q

Treating hyperkalemia

A

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

35
Q

Hyperphosphatemia causes

A

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

36
Q

Treating hyperphosphatemia

A

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

37
Q

MOA of phosphate binders

A

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
Q

Dosage of Phosphate binders

A

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

39
Q

ADRs of phosphate binders

A

constipation, GI upset

40
Q

hyperparathroidism treatment

A

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

41
Q

Calcitriol (rocaltrol)

A

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

42
Q

Paricalcitol (Zemplar)

A

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

43
Q

Docercalciferol (Hectoral)

A

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

44
Q

Dyslipidemia in CKD

A

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