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Pharmacy 255 > Kidney > Flashcards

Kidney Flashcards

1
Q

What are the 3 functions of the kidney?

A

Excretory
Endocrine - RBC , renin
Metabolic - vitamin D, gluconeogenesis

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2
Q

What is the path of the kidney?

A

Afferent (efferent out) - glomerulus -proximal - descending- ascending (water )- distal - collecting duct

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3
Q

What does renin do?

A

Vasoconstrict and Na and water retention

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4
Q

What gets vasoconstricted from Angio 2?

A

Efferent arteriole

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5
Q

Where is aldosterone secreted from?

A

Adrenal cortex

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6
Q

What is aldosterone’s role?

A

Resort Na for K and retain water

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7
Q

What is ADH job?

A

Retain water

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8
Q

What is ANR’s job?

A

Get rid of water

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9
Q

If GFR is low what is S Cr?

A

Higher

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10
Q

What equation uses GFR and classifies the severity of kidney disease?

A

CKD - EPI

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11
Q

What equation uses s Cr?

A

Cockcroft - gault

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12
Q

What condition must the patient if are using ckd-epi?

A

CKD duh but must be stable

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13
Q

What are the limits of using equations estimate function?

A

Extremes of mass, muscle

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14
Q

What does non-indexed or No normalization mean?

A

Adjusted to patients BSA

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15
Q

How does bun change in kidney disease?

A

Increases

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16
Q

What can also change bun?

A

Eating protein
Gi bleed
Hydration (low h 20 =↑ urea)

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17
Q

What are the ACR ranges of albumin?

A

A 1= <3
A2 = 3-30
A3 = > 30

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18
Q

What range is microalbuminaria?

A

3 - 30

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19
Q

What can cause transient albuminuria?

A

Major exercise , UTI, period,

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20
Q

What does a urinalysis look at?

A

Color, turbidity, casts, glucose, pH,

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21
Q

What are the most common casts, and what causes it?

A

Hyaline - exercise, looks concentrated
Granular - CKD, brown

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22
Q

What is definition of AKI?

A

Sudden decline in renal function

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23
Q

True or false: you can use CKD - EPI if they have AKI?

A

False need stable

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24
Q

What is lab values for AKI?

A

S Cr > 0.3 in 48 hours or > 1.5 times baseline
Urine < 0.5 ml/kg/hr for 6 hrs

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25
Q

What is anuric?

A

< 50ml/day

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26
Q

What is oliguric?

A

< 500mi/day

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27
Q

What is non-oligaric?

A

> 500mi/day

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28
Q

What can change urine output?

A

Dehydration and diuretics

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29
Q

What marker usually shows up first for AKI?

A

↓ urine output ,s Cr takes 4 days

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30
Q

Sx of AKI?

A

Vomit, ab pain, dark urine. Foamy urine, edema, malaise

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31
Q

What can be general causes of AKI?

A

Mostly Anything that changes blood flow to the kidney- sepsis, trauma, burns, drugs(

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32
Q

What can be causes of prerenal azotemia?

A

blood loss, dehydration, HF, hypotension, low glomerular pressure (ACE/ARB, NSAIDS)

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33
Q

WHat are the 4 main types of Intrinsic AKI?

A

Tubular, intersitial, glomerulonephritis and vascular kidney injury

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34
Q

What causes tubular necrosis?

A

toxins mostly aminoglycosides (micins) and myoglobin

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35
Q

WHich type of kidney injury would statins cause?

A

rhabdomyolysis= tubular necrosis= intrinsic AKI

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36
Q

What can cause interstitial nephritis?

A

idiopathic immune response= NSAIDS and penicillin

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37
Q

WHat is a form of vascular kidney injury?

A

renal artery stenosis

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38
Q

WHat are some causes of post renal AKI?

A

obstruction= kidney stones, prostate, cancer, drugs (sulfonamides, MTX, Acyclovir)

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39
Q

What are the general 4 things used to diagnose AKI?

A

history
Lab data- increased S Cr, BUN, acidosis, hyperkalemia
FEna= % of sodium filtered and excreted
Urinalysis- casts

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40
Q

What does a high FEna mean?

A

tubular damage

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41
Q

What does a low FEna mean?

A

pre renal AKI

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42
Q

WHat other things can change FEna value?

A

RAAS and diuretics

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43
Q

If a patient had acute tubular necrosis, what form of cast could they have?

A

cellular

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44
Q

If a patient had increased WBC what can this indicate?

A

UTI

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45
Q

If crystals were present, what form of AKI would the patient have?

A

post renal

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46
Q

How can we treat pre renal AKI?

A

hydration/ stop diuretics
BP support
perhaps fluid removal
stop/hold nephrotoxic meds

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47
Q

How can we treat intrinsic AKI?

A

stop offender, manage autoimmune

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48
Q

How can we treat post renal failure?

A

catheter, remove obstruction, hydration

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49
Q

What is the range of good potassium?

A

3.5-5.0

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50
Q

What are signs of moderately high potassium?

A

weak, confused, peaked T waves

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51
Q

What are signs of severely high potassium?

A

wide QRS and small p Waves- heart block

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52
Q

If a patient came in with mildly high K, what are we doing?

A

15-60 mg BID-QID of sodium polystyrene or furosemide

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53
Q

WHy might furosemide not work to remove K+?

A

need functional kidneys

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54
Q

Why cant sodium polystyrene be used for severe k+?

A

too slow- one hour

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55
Q

If severely high K+ (>7), what are we doing?

A

calcium gluconate to protect heart
use insulin to drive K into cells
sodium bicarb if metabolic acidosis
then sodium polystyrene

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56
Q

What if all else fails to lower K?

A

dialysis

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57
Q

What are our go to agents if fluid overload?

A

furosemid +/- metalazone

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58
Q

Patient arrives to the ER with metabolic acidosis, what will be done to help?

A

sodium bicarb IV

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59
Q

When should dialysis be used to treat AKi (Hint: AEIOU)

A

A-acidosis
E-electrolytes- high K
I- Toxic ingestions
O- Fluid overload
U- Uremia
TOP 2 for AKI
and BOTTOM for CKD

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60
Q

What is the leading cause of CKD?

A

diabetes and HTN

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61
Q

What are the early stage symptoms of CKD?

A

ASYMPTOMATIC

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62
Q

What population in Canada is at risk for CKD and maybe could benefit from increased screening?

A

First Nations- higher rates of diabetes

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63
Q

What is the clinical definition of CKD?

A

under 60 ml/min GFR WITH or WITHOUT Kidney damage/ACR>3 mg/mmol for at least 3 months

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64
Q

How often should you be screened for CKD if the patient is high risk?

A

annually

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65
Q

When should the patient be refered to a nephrologist?

A

<30 ml/min and > 60 ACR

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66
Q

Why is CKD more prevalent in older people?

A

higher rates of diabetes and HTN

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67
Q

At age 30 what happens to your GFR?

A

lowers by 1 ml/min ish a year

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68
Q

Since we know that with age your kidney function declines, if the patient is >80 and has a GFR under 60 will this always be CKD?

A

No- if no marker of kidney damage

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69
Q

Stages of CKD using GFR

A

G1- >90
G2- 60-90
G3a- 45-60
G3b- 30-45
G4- 15-30
G5- <15/ dialysis

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70
Q

Stages of CKD for albuminuria

A

A1-<3
A2-3-30
A3- >30

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71
Q

If we want to determine GFR which equation will we use?

A

CKD-EPI

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72
Q

What is usually the first sign of CKD if the patient is diabetic and poor sugar control?

A

albuminuria

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73
Q

At what stage of CKD does the patient become symptomatic?

A

> stage 3

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74
Q

What are the symptoms of CKD?

A

fatigue, cloudy urine, edema, SOB, pruritis

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75
Q

What is associated with faster progression of CKD?

A

low GFR and high albuminurea, diabetes, male, african, age

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76
Q

Overview of interventions of delaying progression of CKD?

A

Blood pressure control
RAAs block
SGLT2- diabetic
smoking cessation
avoid nephrotoxins

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77
Q

Explain how HTN can cause and be a complication of CKD.

A

can cause it by damaging the glomerulus
and low GFR can stimulate RAAS to retain more fluids

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78
Q

What is blood pressure target for diabetics?

A

<130/80

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79
Q

What is blood pressure target for high risk?

A

<120/80

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80
Q

What is blood pressure target for most people?

A

<140/80

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81
Q

Who wasn’t included in the sprint trial?

A

diabetics= found that <130 is better in a different study

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82
Q

Who is considered high risk for blood pressure control? Hint AARF

A

A-age >75
A-athersclerosis
R-renal (CKD)
F-framingham risk score>15%

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83
Q

What would a BP target <120 do for diabetics?

A

NOT improve progression/ESRD
may even worsen it

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84
Q

What is salt restriction for people?

A

<2 grams. but as much as you can

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85
Q

Good technique for BP testing?

A

sit upright, feet flat, arm su[ported, dont talk or move

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86
Q

What is limit for alchol for BP?

A

1-2 drinks a day

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87
Q

What is first line for BP control?

A

ACE/ARB, diuretic, long acting CCB

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88
Q

What is first line for HTN if albuminurea too?

A

ACE/ARB- is the absolute best!

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89
Q

MOA of ACE/ARB

A

dilate efferent arteriole

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90
Q

When should ACE/ARB not be used?

A

angioedema, renal artery stenosis= >30% decrease of GFR when starting, pregnant, hypotension and high K+

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91
Q

What monitoring for ACE/ARB?

A

BP, SCr, K, ACR

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92
Q

If patient is at target BP but not yet max dose of ARB what is the next step?

A

keep increasing dose and maybe back off other BP meds

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93
Q

A patient has been on perindopril for 10 years and has just now got a GFR under 30 ml/min. What should be done?

A

DO NOT SWITCH/ STOP- just monitor more

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94
Q

Is it okay to combo ACE/ARB?

A

NO- hurts kidneys (K+),

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95
Q

What is an example of a direct renin inhibitor?

A

aliskiren

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96
Q

Compare with ACE, how does Aliskiren stack up?

A

more s/e such as stroke, renal issues, hyper K, hypotension

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97
Q

What benefits are given when adding a MRA?

A

lower proteinuria, slow progression,

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98
Q

Cons of MRA?

A

MORE hyper K and gynecomastia

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99
Q

What are the steroidal MRAs?

A

spirinolactone, eplerenone (less s/e)

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100
Q

What are the non steroidal (selective) MRAs?

A

finerenone- much less side effects better for diabetics

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101
Q

Since finerenone is so good. Can we use this for HF instead of steroidal ones?

A

NOOO, dont use

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102
Q

When is it an issue for thiazides?

A

<30 ml/min- go to a loop now

103
Q

What are DHP-CCB and what benefit do they have?

A

amlodipine- better BP control and preffered than thiazides in diabetics NOT FOR KIDNEY

104
Q

What is an issue with amlodipine?

A

May cause fluid retention and edema

105
Q

What are Non-DHP CCBs and what benefit do they have?

A

diltiazem, verapamil
decreases proteinuria, no renal adjusting

106
Q

Issues with Non-DHP CCB?

A

lots of DI and CI, constipation

107
Q

Is beta blockers a good addition?

A

it can yes, but may need to renal adjust under 30 ml/min

108
Q

Is alpha 2 agonists good? what is one?

A

clonidine- adjuctive, CNS side effects

109
Q

Is alpha 1 blockers good? what is some?

A

terazosin, adjunctive

110
Q

What is role of direct vasodilators and what is the drug?

A

hydralazine- adjunct- may cause fluid retention

111
Q

What is average protein loss in urine?

A

40-80 mg

112
Q

What is level that is considered proteinuria?

A

> 150

113
Q

What is nephrotic syndorme?

A

hyper lipids, low albumin, edema, embolism risk

114
Q

How can lupus effect your kidneys?

A

increase proteinuria

115
Q

What is role for SGLT2i?

A

lowered mortality and GFR decline, more for HF

116
Q

Issue with SGLT2i?

A

dapagliflozin well tolerated but volume depletion may be an issue

117
Q

If a diabetic person was to keep their sugars in check how does it reduce their risk?

A

40% less albuminuria
37 less complications

118
Q

What is general A1C target?

A

<7 maybe <6.5 if patient is VERY healthy

119
Q

What is an issue with looking at A1C in CKD

A

at stage 4-5 less accurate

120
Q

When do you have to discontinue metformin?

A

<30 ml/min

121
Q

If needing adjuct sugar control and is already on metformin and SGLT2 what is the next agent?

A

GLP-1 agonist

122
Q

Pros of metformin

A

cheap, no hypoglycemic, NO weight gain

123
Q

Why do we have to adjust dose or discontinue metformin if low GFR?

A

risk of lactic acidosis= 50% mortality

124
Q

What is kidney benefit of SGLT2i?

A

protects kidney, narrows afferent

125
Q

Patient is at target A1C but not at optimal SGLT2i dose what is next step?

A

keep increasing but lower other meds

126
Q

How far down can dapa be used for?

A

can start at >25, if already started= until dialysis

127
Q

Can SGLT2i cause AKI?

A

prob not but theoretical

128
Q

Pros of GLP-1?

A

weight LOSS, low hypoglycemic

129
Q

What are GLP-1 agonists?

A

semaglutide

130
Q

What does smoking do to your kidneys?

A

increases BP and HR, and lower renal flow

131
Q

What are some nephrotoxic drugs?

A

NSAIDS, lithium, aminoglycosides, calcineurin

132
Q

What is sad mans

A

S-SU
A-ACE
D-diuretics
M-metformin
A-ARB
N-NSAIDs
S-SGLT2i

133
Q

What is the leading cause of death of people with CKD?

A

CVD

134
Q

When should statins be given for CKD?

A

> 50 and GFR<60 regardless of LDL

135
Q

Can you be on a statin if also doing dialysis?

A

yes if initiated before

136
Q

What is recommended dose for statins of dialysis?

A

atorvastatin=20
Rosuvastatin=10

137
Q

What is recommended dose for statins of general people?

A

ator 80 and rosuvastatin 40

138
Q

Which statin is renally eliminated?

A

rosuvastatin

139
Q

Is ASA useful?

A

not for 1* prevention

140
Q

Which has lower mortality, dialysis or transplant?

A

trasnplant

141
Q

When do we need RRT?

A

serositis (electrolyte issues), cant control BP, malnutrition even with supplements, cog impairment
GFR=10

142
Q

What is most common dialysis?

A

hemodialysis

143
Q

Explain hemodialysis.

A

blood taken out, filtered and returned
3 x a week for 3-5 hours each time

144
Q

What vascular access is given for HD?

A

AV fistula
graft
catheter in neck

145
Q

What is always given to patients on HD?

A

anticoag during procedure
and renal vitamin

146
Q

What is benefit of home HD?

A

better tolerated but more frequent

147
Q

Complications of HD?

A

fatigue, hypotension, N/V, loss of water sol vitamins (B+C)

148
Q

Explain peritoneal dialysis

A

use own peritoneal membrane to act as a filter

149
Q

What is difference between continuous ambulatory PD and automated PD?

A

CAPD- manual exchange 4-5 x a day
APD- at night and may also need CAPD

150
Q

Pros of PD?

A

more freedom and less visits and preserves kidneys

151
Q

Complication of PD?

A

inflammation and infection of peritoneal

152
Q

When is CRRT done?

A

for hemodynamically unstable patients

153
Q

At what stage does sodium and water imbalance begin to take shape?

A

stage 4

154
Q

What corrections can be done for water and Na imbalance?

A

salt and water restriction
diuretics

155
Q

When can we not use thiazides?

A

GFR<30

156
Q

How much Na loss occurs with loops vs thiazides?

A

25% and 4%

157
Q

What monitoring should be done for diuretics?

A

electrolytes=K+ every 3-6 months once stable

158
Q

How does metabolic acidosis occur from CKD?

A

no ammonia to buffer the H+

159
Q

How can we treat metabolic acidosis?

A

325-500 mg BID-TID of sodium bicarbonate

160
Q

What are we concerned about with treatment for metabolic acidosis?

A

if kidneys are not functioning well the drug will cause sodium loading

161
Q

What is normal range of K+?

A

3.5-5

162
Q

WHich drugs are we concerned about hyperkalemia?

A

potassium sparing diuretics, ACE, NSAIDS

163
Q

What drugs can we give to lower K+

A

sodium polystyrene sulfonate (kayexalate), patiromer, soidum zirconium cyclosilicate

164
Q

Which K binder is the fastest? What about slowest?

A

SZC
Patiromer

165
Q

Which K binder uses Ca?

A

patiromer

166
Q

Which K binder is selective for K+

A

SZC

167
Q

Which K binder is the least tolerable?

A

Gi really bad with SPS

168
Q

What is the mechanism for CKD-MBD?

A

more serum phosphate due to less excretion and it binds to Calcium
low absorption due to less vitamin D as it binds to phosphate and less activated
No calcium= PTH to resorb bone and try to get kidney to resorb calcium and get rid of phosphate
Calcium can also calcify in the blood

169
Q

When should we monitor bone in CKD?

A

stage 4-5

170
Q

What will labs show for CKD-MBD?

A

high phosphate
Low calcium
High PTH

171
Q

If low calcium is present is it okay to just load up on calcium?

A

No hypercalcemia is really bad=CV

172
Q

What is symptoms of low calcium?

A

numb, tingly, myalgia

173
Q

What are the three Lab calciums?

A

ionized= Active
Total= all, misleading
corrected- estimated active

174
Q

What is target PTH in dialysis and what is too high PTH?

A

2-9 x upper limit
50 x

175
Q

What does adynamic bone disease mean?

A

low bone turnover= low pth

176
Q

What all stims more PTH?

A

too much phosphate
low vitamin D
low Calcium

177
Q

What does FGF-23 do?

A

Maintain Ca and PO4
suppress formation of vitamin D to lower phosphate in Gi
causes Po4 excretion and increases PTH

178
Q

What is calciphylaxis?

A

calcification of small bnlood vessels= sepsis, ulcers, gangrene

179
Q

What foods are high in phosphates?

A

packaged meat, peanut butter, nuts, cola

180
Q

Is it okay to add K binder to orange juice to drink it?

A

NOOOOO it has K+ in it

181
Q

When do you take phosphate binders?

A

beginning of a meal so nothing gets absorbed

182
Q

Is phosphate binders enough?

A

No must restrict diet too

183
Q

What are the general phosphate binders and what info about each?

A

Calcium(carbonate) based-tums, 500 with meals, be careful of too high Ca and constipation
Sevelamer HCl- bad GI effects, $$
Lanthanum- same as above but chewable
Sucroferric oxyhydroxide- iron base= black stool

184
Q

For a K+ binder is it okay to use calcium citrate?

A

No- increases aluminum and toxicity

185
Q

How can Vitmain D therapy help MBD?

A

stims absorption of calcium from Gi and suppress PTH

186
Q

WHat is the evidence for vitamin D therapy?

A

VERYYYYYY uncertain, dont use unless severe

187
Q

What are our vitamin D analogues?

A

calcitriol and alfacalcidol
Dose= 0.25-1 mcg daily

188
Q

Is nutritional Vitamin D good?

A

can suppress but less so AND less hyper Ca and PTH

189
Q

How does calcimimetics work and what is an example?

A

increase sensitivity of Parathyroid
Cinacalcet- for dialysis

190
Q

Do calcimimetics raise Ca and PO4?

A

no

191
Q

What are s/e of calcimimetics?

A

N/D/V, HYPOCALCEMIA

192
Q

What are the antiresorptive treatment?

A

Prolia
Alendronate- caution under 35ml/min

193
Q

How often should labs be monitored if MBD-CKD?

A

MONTHLY

194
Q

If no drugs are working what can we do for people with bone issues?

A

partial removal of parathyroid

195
Q

What issue can arise after operation for parathyroid?

A

hungry bone syndrome, will build a bunch of bone

196
Q

How can adynamic bone disease occur?

A

too much treatment for PTH
= no remodeling

197
Q

How can osteomalacia occur with CKD?

A

softens due to no calcitriol or aluminum deposition

198
Q

How can vascular calcification occur?

A

smooth muscle change into osteoblast like cell

199
Q

WHen is ferritin not accurate?

A

raised in inflammation

200
Q

What is level of anemia in males and females?

A

<130 for men and < 120 for females

201
Q

What do RBC’s look like in CKD anemia?

A

normal. just not enough

202
Q

How does anemia happen in CKD? and at what GFR levle?

A

<10 ml/min
loss of EPO
OR
iron low due to low Gi absorb

203
Q

What tests show Iron is low?

A

low TSAT and low ferritin

204
Q

If ferritin is increased what can this mean?

A

anemia of chronic and iron supp not helpful

205
Q

WHat is hemoglobin, TSAT, ferritin goal if anemic

A

100-110
>20%
>100 if no dialysis
>200 if HD

206
Q

Why isnt hemoglobin goal higher?

A

CVD risk

207
Q

If on ESA what else is needed?

A

Iron supplementation

208
Q

How long must you be on oral iron therapy before IV

A

1-3 months

209
Q

What is dose of iron a day?

A

100-200 daily in 2-3 doses

210
Q

What are the iron formulations?

A

Oral: Gluconate, sulfate, fumerate
IV: Sucrose, sodium ferris, isomaltoside

211
Q

What are the side effects of IV iron?

A

WELL tolerated
maybe some hypotension- lower infusion rate

212
Q

What stims EPO production?

A

low O2 in blood

213
Q

WHat is difference between Epoetin and Darbepoetin?

A

E= shorter, 50-100 2-3 x weekly
D= longer, 0.45 weekly

214
Q

Why do we wait 1-2 months before adjusting EPO dose?

A

because delay of 2-6 weeks with Hemoglobin

215
Q

If HGB rise is too low (<10) after 4 weeks what do we do?

A

increase dose by 25%

216
Q

If HGB rise is too high (>10) after 2 weeks what do we do?

A

lower dose by 25%

217
Q

What are side effects of EPO?

A

hypertension, flu like, CVD

218
Q

What is pure red cell aplasia?

A

s/e of EPO
antibodies against EPO

219
Q

When is it considered EPO resistance?

A

eprex doses>300 U/kg/Week
Aranesp > 1.5 mcg/kg/week

220
Q

What camn cause EPO resistance?

A

iron deficiency, inflammation, bleeding

221
Q

How do HIF-PHIs work and whats an example and what is a S/E?

A

inhibit hypoxia factor= more iron mobilized= more EPO
Daprodustat
malignancy

222
Q

What is the most common heart abdnormality with CKD?

A

LVH

223
Q

How do we treat neuropathy/ neurological complications of CKD?

A

dialysis

224
Q

What is the main concern with pruritis in CKD?

A

effect sleep

225
Q

How can we treat pruritis?

A

gabapentinoids, capsaicin, antihistamines, DIfelikfalin

226
Q

How does Difelikefalin work?

A

It is a kappa opiod agonist for severe pruritis

227
Q

S/e of kappa opiod agonists?

A

dizzy, somnolence, mental changes

228
Q

True or false. Drug induced kidney disease is reversible?

A

True

229
Q

What is the state of the kidney in drug induced kidney disease when the drug is not present?

A

HEALTHY

230
Q

What are the signs and sx of DIKD?

A

metabolic acidosis, proteinuria, changes to electrolytes, low urine, more SCr, malaise, nausea, SOB

231
Q

What is indirect nephrotox?

A

Pre renal

232
Q

What is obstructive nephrotoxicity?

A

Post renal

233
Q

What drugs cause indirect nephrotoxicity?

A

ACE
SGLT
NSAIDs
Calcineurin inhibitors

234
Q

What are some calcineurin inhibitors?

A

cyclosporin and tacrolimus

235
Q

What are the three mechanisms of direct nephrotoxicity?

A

Acute tubular necrosis, interstitial nephritis, glomerulonephritis

236
Q

What drugs can cause acute tubular necrosis?

A

Aminoglycosides, calcineurin, cisplatin

237
Q

How can we lower the chance of tubular necrosis?

A

hydration and go slow

238
Q

What drugs can cause interstitial nephritis?

A

Penicillin, Ciprofloxacin, NSAIDs, PPi, loop diuretics, phytoin

239
Q

What is the MOA of interstitial nephritis?

A

immune mediated injury

240
Q

WHen does interstitial nephritis present? what about for NSAIDs?

A

7-14 days
6 months

241
Q

What will be present in the urine if interstitial nephritis?

A

eosinophils, pyuria

242
Q

What can happen with continuous interstitial nephritis? What drugs can cause chronic?

A

can become progressive and irreversible
lithium and calcineurin

243
Q

What drugs cause obstructive nephropathy?

A

Sulfonamides, acyclovir, MXT, ciprofloxacin

244
Q

How can we lower obstructive nephropathy?

A

water because it super saturates and makes urine more acidic if no water

245
Q

What formula do we use to alter drug dosing in renal failure?

A

cockroft and gault

246
Q

When do we generally start to adjust dosing in renal failure?

A

<60 ml/min GFR
fe >0.5

247
Q

Is it always necessary to adjust dose renally? When do we not have to?

A

NO
if liver is primary
if drug is fairly safe
if immediate need for it
tirtation?

248
Q

What are the steps for drug dosing?

A

Get med history
find out degree of impairment
asses drug
choose less nephrotoxic
appropriate dose
monitor

249
Q

Are Scr levels always accurate?

A

not in extremes of weight
can lag, both for disease and treatment
not in dialysis

250
Q

Which types of AKI resolve the quickest?

A

Pre renal and post renal

251
Q

Which type of molecules does HD remove?

A

unbound, small molecules

252
Q

Do we have to worry about drug removal in PD?

A

NO

253
Q

Which drug do we not necessarily follow the drug monograph for? why?

A

ACE and ARBs because they are so good. may use them below 30 ml/min but must monitor

Pharmacy 255 (16 decks)

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