Naplex Chapter 12 Renal Disease And Dosing

Front 1

what are the 2 primary types of dialysis

Back 1

HD-hemodialysis
and
PD-peritoneal dialysis

Front 2

whats the diff between HD and PD

Back 2

HD= done 3 x a week, blood is filtered through a machine via diffusion and convection

PD= glucose soln (dialysate) is pumped into perioteneal cavity and peritoneal membrance acts as the dialyzer, done by the patient daily

Front 3

factors that effecr drug removal in dialysis

Back 3

1) molecular size- high flux dialyzers have larger pore size-improved vanco clearance

2) Protein binding- dialysis only removes the unbound portion of drug

3) VD, if drug has a large VD, dialysis is not really effective-digoxin + amiodarone

4)plasma clearance-hepatic drugs won't really be cleared via dialysis

5) dialysis membrane- low-flux, med, high flux-pore size

Front 4

what is an indicator of kidney damage

Back 4

protein or albumin (micro or macroalbunuria) in the urine- the filter or glomerulous isn't working to keep it out of urine

Front 5

what is used as a marker of renal function

Back 5

serum creatinine, but not precise cause it's due to degree of muscle

Front 6

what is BUN

Back 6

blood urea nitrogen measures amount of nitrogen that comes from waste product urea.

increases with renal impairment, but not an independent marker

Front 7

what occurs in the proximal tubule

Back 7

water, Na, and Cl are mainly reabsorbed here

Front 8

where do loop diuretics work?

Back 8

they inhibit Na K, pump in the ascending limb of the loop of henle- 25% of Na is reabsorbed here, making it a potent drug

Front 9

what meds work on the distal convoluted tubule

Back 9

thiazides, only 5% of Na is reabsorbed here, thus thiazides are weaker diuretics than loops

Front 10

thiazides also effect what other cation

Back 10

Calcium, it increases it, so it has a positive effect on bone

Front 11

some common drugs that should not be used in severe renal impairment

Back 11

bisphosphonates, dabigatrin, duloxetine, Li, glyburide, metformin, NSAIDs

Front 12

Stages of CKD
Stage 1 GFR

Back 12

>90 mL/min

Front 13

Stages of CKD
Stage 2 GFR

Back 13

60-89 ml/min

Front 14

Stages of CKD
Stage 2 GFR

Back 14

30-59 ml/min

Front 15

Stages of CKD
Stage 3 GFR

Back 15

15-29

Front 16

Stages of CKD
Stage 4 GFR

Back 16

<15 or dialysis, yeah you are screwed

Front 17

gabapentin should have a dose reduction when the CrCl is what?

Back 17

when CrCl <60 to minimize sedation and accumulation of the drug

Front 18

reglan or metoclopramide should also be dose adjusted in renal dysfunction, why?

Back 18

drug conc increases, causing dopamine blockade....EPS and drowsiness

Front 19

what drugs have been shown to prevent the progression of nephropathy in diabetes and non-diabetic patients with proteinuria

Back 19

ACEI + ARB

note they help in non-diabetics with proteinuria

Front 20

what is the goal BP for a kidney disease patient

Back 20

<130/80

Front 21

what happens initially with the start of an ACEI and ARB

Back 21

a 30% increase in serum creatinine

Front 22

Is a 30% increase in serum creatinIne due to ACEI initiation a reason to stop therapy?

Back 22

NO!

if >30% then need to stop

Front 23

when starting an ACEI or ARB in CKD pt how long should you monitor labs and what labs should be monitored

Back 23

monitor 1-2 weeks

K and SCr

Front 24

patients with CKD should have what else monitored

Back 24

Ca, PTH, PO4 and watch for signs of anemia

Front 25

what happens to Phosphorous and PTH levels in CKD

how to help alleviate

Back 25

phosphorous is not eliminated, so builds up- dumb body cranks up PTH to help, causing hyperparathyroidism

tx of hyperparathyroidism is control dietary phosphorous and maybe use phosphate binders

Front 26

3 examples of phosphate binders

Back 26

1) aluminum based agent- alternagel, Al is dangerous in CKD-only use short term, but MOST effective

2) Ca based- 1st line, but most CKD ppl are taking vit D-which raises Ca

3) Al and Ca free agents- effective, but most expensive

Front 27

when to use phosphate binders

Back 27

use as meal time- bind dietary phosphorous

if miss dose, taking it later or doubling is no good

Front 28

name 2 Al-Ca free phosphorous medication

Back 28

lanthanum carbonate (Fosrenol)
must chew thoroughly

Sevelamer carbonate-also has benefit of decreasing cholesterol and LDL by 15-30%

Front 29

once the hyperphosphatemia is controlled, how do you control excess PTH

Back 29

By increasing Ca, by using Vitamin D

calcitriol is active form of Vitamin D3 and is used to increase Ca gut absorption, decreasing PTH secretion

Front 30

how does a calcimimetic work

Back 30

Cinacalcet or sensipar- increases sensitivity of ca-sensing receptor on parathyroid gland= less, PTH, less Ca, less Phos

Front 31

treatment of vitamin D deficency

Back 31

<5 give 50,000 IU weekly x 12 weeks, then monthly

5-15 give 50,000 IU weekly x 4 weeks, then monthly

16-30 50,000 IU monthly

ALL FOR 6 MONTHS

Front 32

whats the K level for hyperkalemia

Back 32

>5 mEq/L

Front 33

K excretion is increased by

Back 33

aldosterone, diuretics, and loops

Front 34

what is most common cause of hyperkalemia

Back 34

decreased renal fxn, can be due to combo of renal dysfxn and excess K levels from other drugs

but hyperkalemia generally NOT from a excessive intake of K

Front 35

common drugs that raise K

Back 35

ACEI, ARB, NSAIDs, Bactrim, heparin, OC with drospiernone (YAZ)

Front 36

what may need to be done to monitor for cardio toxicity with hyperkalemia

Back 36

ECG, may need to give IV Ca to stabilize cardiac tissue

Front 37

methods to lower K in hyperkalemia

Back 37

insulin drives K into cells, so give insulin

glucose, which increases insulin

Na Bicarb if metabolic acidosis

possibly albuterol

consider cation exchange resin, sodium polystyrene sulfonate (Kayexelate)-can be give PO or PR

Front 38

when to initiate Na bicarb drugs and what are the drugs

Back 38

when Na Bicarb <22 mEq/L

Na Bicarb
Na citrate/citric acid
Oracrit