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Lab Modules > Module 6 - Drug Level Monitoring > Flashcards

Module 6 - Drug Level Monitoring Flashcards

1
Q

List 5 indications for drug monitoring

A
  • Therapeutic confirmation
  • Dose optimization
  • Suspected toxicity
  • Assess for inefficacy
  • Non-adherence vs. treatment failure
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2
Q

What are some ideal drug characteristics?

A
  • Clinically necessary
  • Drug level = clinical outcome
  • Established assays
  • Risk of toxicity high/narrow TI
  • Unpredictable dose-response
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3
Q

What is the therapeutic index?

A

window between therapeutic effects and toxic effects

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4
Q

List advantages of population PK

A
  • Provides a “best guess” based on majority of population

- Standardized dosing nomograms, easily available for clinical use

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5
Q

List disadvantages of population PK

A
  • Genetic variability
  • “Compartmental” PK
  • Not very generalizable (very sick individuals)
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6
Q

List advantages of patient-specific PK

A
  • specific to patient

- individualized therapy

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7
Q

List disadvantages of patient-specific PK

A
  • time-consuming
  • requires special knowledge
  • intensive monitoring
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8
Q

Describe the elderly

A
  • Decreased organ function
  • Decreased Vd (increased adipose tissue, decreased muscle mass)
  • Absorption (decreased GI motility, increased pH, decreased blood flow)
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9
Q

Describe infants

A
  • Underdeveloped liver enzymes (decreased metabolism)
  • Underdeveloped renal clearance
  • Gastric acidity (12 years)
  • Infants increase TBV
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10
Q

Describe males

A
  • Larger body size
  • Increased muscle mass (increased sCr)
  • Lower % body fat
  • Higher CYP 1A2, 2D6, and CYP 2E1 activity, higher p-glycoprotein activity
  • Faster renal and hepatic clearance
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11
Q

Describe females

A
  • Smaller body size
  • Decreased muscle mass (decreased sCr)
  • Higher % body fat
  • Higher CYP 3A activity, lower p-glycoprotein activity
  • Slower renal and hepatic clearance
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12
Q

Describe ethnicity

A

PK characteristics most likely to result in ethnic differences

  • Gut or hepatic first-pass effects
  • High plasma protein binding
  • Hepatic metabolism as major route of elimination
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13
Q

List examples of ethnic differences regarding drugs

A
  • Rosuvastatin: Asians require lower doses
  • Carbamazepine: Han Chinese higher risk of SJS and TENS
  • Warfarin: African Americans require higher doses, Asians require lower doses than caucasians
  • Tacrolimus: Black patients require higher doses than caucasians
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14
Q

How does pregnancy affect absorption?

A
  • Morning sickness (n/v)

- GI motility reduced

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15
Q

How does pregnancy affect distribution?

A
  • Increased Vd (TBW increases by 8L)

- Decreased plasma albumin (dilution)

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16
Q

How does pregnancy affect metabolism?

A

-CYP enzymes induced by hormones

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17
Q

How does pregnancy affect excretion?

A

-Higher cardiac output, higher renal blood flow (GFR increases by 50%), higher clearance

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18
Q

How does obesity affect the body?

A
  • renal clearance increased
  • lipophilic drugs = higher Vd
  • hydrophilic drugs = ? Vd
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19
Q

How does being really skinny affect the body?

A

-muscle wasting, low body weight, low body fat (Vd altered)

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20
Q

How does renal disease affect the body?

A
  • Bioavailability may be increased or decreased
  • Vd increased
  • Protein binding decreased
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21
Q

How does hepatic disease affect the body?

A
  • Decreases metabolism
  • Phase 1 > Phase 2
  • Cirrhosis&raquo_space; chronic hepatitis
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22
Q

What are the clinical uses for ahminoglycosides (gentamicin/tobramycin) ?

A
  • Concentration-dependent, bactericidal antibiotic with gram-negative coverage (including Pseudomonas)
  • Used conservatively due to potential for serious adverse effects (ototoxicity/nephrotoxicity)
  • Usually used in an inpatient setting (IV)
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23
Q

Describe absorption of aminoglycosides

A

Oral: poor absorption
IM: rapid absorption (peak within 30-120 mins)
IV: 30-60 min infusion, slow bolus or continuous infusion (peak 30 mins after infusion)

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24
Q

Describe the distribution of aminoglycosides

A

Vd = 0.2 - 0.3 L/kg (ECF), significantly affected by volume status

Vd = 0.35 - 0.4 L/kg in the critically ill

protein binding = 10%

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25
Q

Describe the metabolism of aminoglycosides

A

unchanged; no major metabolites

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26
Q

Describe the excretion of aminoglycosides

A
  • t1/2 = 2-3 hours
  • kidney, unchanges
  • fe = 85-95%, directly related to renal function
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27
Q

What is the equation we use for half life of aminoglycoside?

A

Dettli equation

*if CrCl is known

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28
Q

Who is allowed high dose ahminoglycosides?

A

only for patients with good renal function (>60 mL/min)

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29
Q

Can high dose ahminoglycosides be used as mono therapy?

A

no

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30
Q

Describe the monitoring for aminoglycosides

A
  • Obtain levels pre-3rd dose (traditional), pre 2nd dose (high dose)
  • Peak: 30 mins post infusion
  • Trough: 30 mins prior to next dose
  • Watch sCr, urea and urine output at least 2-3x/week
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31
Q

2 toxicities associated with aminoglycosides

A
  • ototoxicity

- nephrotoxicity

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32
Q

Describe ototoxicity caused by aminoglycosides

A
  • Overt, 2-10% of patients, 43% subclinical; onset > 5 days

- Audiometry (hearing test) if treatment is > 72 hours

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33
Q

Describe nephrotoxicity caused by aminoglycosides

A
  • Onset 6-10 days
  • Proximal tubule reabsorption, can bind to renal membranes and cause acute tubular necrosis
  • Labs will show: increased sCr, decreased eGFR, increased urea and impaired urinary concentrating ability
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34
Q

What are the goals of aminoglycoside therapy?

A
  • keep levels within range
  • shortest possible treatment duration
  • once daily dosing (if good renal function)
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35
Q

What are some clinical uses of vancomycin?

A
  • Antibiotic with slow bactericidal activity against GP, including MRSA, alternative to pens/cephs in severe allergy
  • Used in inpatient or outpatient IV therapy
  • Used orally against C. dif infection
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36
Q

What is the best predictor of clinical efficacy for vancomycin?

A

AUC/MIC = 400 (up to 600 for MRSA)

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37
Q

Describe absorption of vanco

A
  • Oral < 10%
  • Intraperitoneal 54-65% (peak approx 6 hours)
  • IM erratic absorption
  • IV (peak after completion of infusion)
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38
Q

Describe distribution of vanco

A 
Vd = 0.4-1.0 L/kg
fu = 50%
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39
Q

Metabolism of vanco

A

very small amount of liver metabolism

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40
Q

Excretion of vanco

A

t1/2 = 6-8 hours with normal renal function

IV = 80-90% urine (as unchanged drug)

Oral: primarily feces

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41
Q

What equation can be used for finding half life of vancomycin if CrCl is known?

A

Matzke

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42
Q

Describe the monitoring of vancomycin

A
  • Obtain levels pre-3rd dose (assess Css)
  • Peak: 1-2 hours post infusion (distribution)
  • Trough: 15-30 mins prior to next dose
  • Repeat weekly (stable patients) or as needed for unstable patients
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43
Q

Describe the consequences of toxic levels of vanco

A

Nephrotoxicity (controversial)

  • “mississippi mud” - problems with fermentation methods
  • now 95% pure, drastically reduced nephrotoxicity
  • Not nephro or ototoxic unless combined with aminoglycosides
  • Suggested risk factors: trough > 20 mg/L, concomitant treatment with nephrotoxic agents, prolonged therapy (>7 days) and ICU stay
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44
Q

Goals of vancomycin?

A

hit hard and fast (optimize therapy)

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45
Q

Clinical uses of phenobarb

A
  • Management of seizures

- Sedative/hypnotic (withdrawal management-unlabeled use)

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46
Q

metabolism of phenobarb

A

hepatic; inactive metabolites

phenobarbital is an INDUCER

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47
Q

excretion of phenobarb

A

long half life (5 days in adults, 2.5 days in children)

35-50% fu in urine

remainder eliminated in feces

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48
Q

What equation do we use for phenobarb?

A

WAGNER !!!

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49
Q

Css target for phenobarb?

A

15-30 mg/L

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50
Q

Describe drug level monitoring for phenobarb

A
  • Bc of the very long half life, it will take 3 weeks to reach Css
  • Can measure 1 hour after IV load or in 5-7 days if PO
  • If sub-therapeutic, can consider a loading dose to get patient to Css
  • Monitor levels at same time of day (consistency)
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51
Q

What are some other lab monitoring parameters for phenobarb?

A

sCr: Reduce dose in renal impairment

LFT’s: caution in hepatic impairment

CBC: can cause agranulocytosis, thrombocytopenia, megaloblastic anemia

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52
Q

What are some consequences of toxic levels of phenobarb?

A

CNS side effects

35-80mg/L = sedation and ataxia

> 65 mg/L = stupor and coma

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53
Q

Clinical uses of phenytoin?

A
  • Management of seizures
  • Trigeminal neuralgia
  • Seizure prophylaxis after neurosurgery
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54
Q

What kinetics does phenytoin follow?

A

Michaelis-Menten dose-dependent kinetics

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55
Q

Phenytoin acts as an _____

A

inducer (important for drug interactions

56
Q

Can you do ratio dose adjustments for phenytoin?

A

NO WAY

use orbit plot!!

57
Q

Phenytoin may need corrections for what two things?

A
  • uremia

- hypoalbuminemia

58
Q

How will phenytoin be adjusted for hypoalbuminemia?

A
  • Less albumin = less protein binding = more free drug

- Adjusted will be higher than measured

59
Q

How will phenytoin be adjusted for uremia +/- hypoalbuminemia ?

A
  • Urea binds to albumin and displaces phenytoin (more free drug)
  • Adjusted will be higher than measured
60
Q

What are some drug level monitoring timelines for phenytoin?

A
  • Very long half life (may take 3 weeks to reach Css)
  • Draw first level: 1hr after IV load or 24h after PO load
  • Second level: 2-3 days after starting
61
Q

What are some other lab monitoring parameters for phenytoin?

A

CBC: leukopenia, agranulocytosis, thrombocytopenia, granulocytopenia

LFTs: hepatitis, acute hepatic failure

Albumin: critical illness, renal/hepatic disease (decrease albumin = increased free drug)

62
Q

What are some consequences of toxic levels of phenytoin?

A

nystagmus, taxis, nystagmus, diminished mental capacity, involuntary muscle movements, seizures, death

63
Q

What is valproic acid used for?

A
  • Management of seizures
  • Mood stabilizer
  • Migraine prophylaxis
64
Q

metabolism of VPA

A

primarily hepatic

65
Q

VPA acts as an ______

A

inhibitor

66
Q

____ VPA concentration and dose relationship is linear

A

free

67
Q

Describe drug level monitoring timeline of VPA

A
  • draw first level within 5 days of starting therapy

- if t1/2 = 10 hour then Css at 50 hours (approx 2-3 days)

68
Q

What are other lab monitoring parameters for VPA

A

LFTs: baseline and frequently during first 6 months (small risk of hepatic failure with genetic disease)

CBC: platelets at baseline and then periodically due to thrombocytopenia

69
Q

Consequences of toxic levels of VPA

A

sedation, lethargy, ataxia

cerebral edema, coma, bone marrow, depression

70
Q

What is carbamazepine used for?

A
  • management of seizures
  • trigeminal neuralgia
  • mood stabilizer
  • neuropathic pain
71
Q

Describe the metabolism of carbamazepine

A

hepatic with active metabolite

72
Q

Carbamazepine can have ___________ (induces it’s own metabolism) which is complete 3-5 weeks after initiation

A

autoinduction

73
Q

Describe the drug level monitoring timeline of carbamazepine

A
  • Autoinduction: complete by 6-7 weeks (including 2-3 weeks for initial dose titration)
  • Takes 2-3 weeks for new Css to occur if dose adjustments are made or interacting drugs are added or adjusted
74
Q

Describe some other lab monitoring parameters for carbamazepine

A
  • electrolytes (hyponatremia)
  • sCr and urea: renal failure
  • CBC and differential: DRESS syndrome, bone marrow depression
  • TSH
  • LFTs
  • pregnancy test (teratogenic)
75
Q

What are some consequences of carbamazepine?

A

ataxia, sedation, n/v, decreased consciousness, hallucinations, belligerence, abnormal movements, seizures and coma

76
Q

What are some clinical uses of lithium?

A
  • Mood stabilizer

- Unlabeled: augmentation of antidepressants, PTSD, conduct disorder in children, cluster headaches

77
Q

Describe the metabolism of lithium

A

not metabolized

78
Q

The formula:

Cl(Li) = 0.288 (CrCl)

is for _______ patients

A

non-manic

79
Q

The formula:

Cl(Li) = 0.432 (CrCl)

is for _______ patients

A

manic

80
Q

What is the conversion between mmol and mg of lithium?

A

8.12 mmol = 300 mg

81
Q

Can you do linear dose adjustments for lithium?

A

Yes

82
Q

How do ACEi interact with Li ?

A

ACEi decrease renal blood flow, reduces aldosterone, both causing increased Na+ and Li+ reabsorption

83
Q

How do NSAIDs interact with Li ?

A

NSAIDs decrease renal blood flow (PG inhibition), increase Na+ and Li reabsorption

84
Q

How does dehydration interact with Li ?

A

increase Li reabsorption

85
Q

How does HYPOnatremia interact with Li ?

A

increase Li reabsorption

86
Q

How does HYPERnatremia interact with Li ?

A

decrease Li reabsorption

87
Q

How do thiazides affect Li ?

A

Promote Na and H20 loss in distal tubule causing increased Na and Li reabsorption in proximal tubule

88
Q

How does caffeine/theophylline osmotic diuretics affect Li ?

A

increase Li excretion

89
Q

What is the acute mania target for lithium?

A

0.8-1.2 mmol/L

90
Q

What is the maintenance target for lithium?

A

0.6-0.8 mmol/L

91
Q

Describe the drug level monitoring timeline for lithium

A
  • Initiation of therapy: draw level in 2-3 days (for safety reasons) - Css at 5 days
  • Once Css achieved, every 1-2 weeks until stable, then every 6-12 months if disease is well-controlled
  • Draw level ideally 12 hours after the last dose
92
Q

What are some consequences of toxic levels of lithium?

A

fine tremors, GI upset, muscle weakness, fatigue, polyuria, polydipsia, coarse tremors, slurred speech, confusion, delirium and vomiting, seizures, coma, death

93
Q

What are some other lab monitoring parameters for lithium?

A
  • electrolytes
  • renal function
  • thyroid function
  • pregnancy test
  • fasting glucose
  • fasting lipid panel
  • prolactin
  • CBC
94
Q

What is the bottom line for immunosuppressant drug monitoring?

A

Don’t meddle with these drugs unless you have a very good reason to or have a specialized practise

95
Q

What are some clinical uses for cyclosporine?

A
  • Transplant rejection prophylaxis

- Immunomodulatory therapy (levels not monitored)

96
Q

Describe the metabolism of cyclosporine

A

Hepatic via CYP 3A4 (drug interactions). Forms at least 25 metabolites, the most active ones having only 10-20% immunosuppressive activity. Extensive first pass effect with oral administration

97
Q

Does cyclosporine follow proportional kinetics?

A

yes

98
Q

concentration of cyclosporine at ___h post dose is ideal

A

2

99
Q

What does C2h correlate with?

A

AUC which clinically correlates with organ rejection rates

100
Q

Describe the drug level monitoring timeline of cyclosporine

A

Initially: every 1-2 days (even if Css is not reached), Css is at 2-5 days depending on half life, then q3-5 days

Maintenance: monthly

Ideally 2h post dose (C2 level) or prior to next dose (trough)

Target levels based on type of transplant and transplant protocol

101
Q

What are some consequences of cyclosporine toxic levels?

A

nephrotoxicity, neurotoxicity, hypertension, hyperlipidemia, hirsutism, gingival hyperplasia

102
Q

What are some other lab monitoring parameters of cyclosporine?

A
  • Electrolytes and uric acid: hyperkalemia, hyperuricemia, hypomagnesemia
  • CBC: infections (immunosuppressive), leukopenia, thrombocytopenia, anemia
  • Renal (sCr, urea): structural kidney damage
  • LFTs: hepatotoxicity, hepatitis
  • Lipid panel: low cholesterol can increase cyclosporine levels, hyperlipidemia (TGs)
103
Q

What are some clinical uses for tacrolimus?

A
  • Transplant rejection prophylaxis (kidney, liver, heart)

- Rheumatoid arthritis that is not responsive to DMARD therapy

104
Q

Prograf = _____ release

A

immediate

105
Q

Advagraf = ______ release

A

extended

106
Q

Metabolism of tacrolimus

A
  • extensive CYP 3A4 metabolism (drug interactions)
  • 8 metabolites
  • equipotent to parent drug
107
Q

What are some factors affecting tacrolimus blood concentrations?

A
  • genetics
  • age, disease, race, diet
  • pre-existing factors
  • blood concentration
  • clinical status
  • transplanted organ and time after transplant
  • concomitant therapy (drug interactions)
108
Q

What do targets of tacrolimus levels depend on?

A
  • type of solid-organ transplant (heart, kidney, liver)
  • with or without induction therapy
  • concomitant immunosuppressive therapies
  • time post-transplant
109
Q

What are some other lab monitoring parameters for tacrolimus?

A
  • electrolytes and glucose
  • CBC: anemia, leukopenia, thrombocytopenia
  • renal: nephrotoxicity
  • hepatic (LFTs): abnormal liver enzymes
110
Q

Clinical uses of sirolimus

A
  • Labelled: Transplant rejection prophylaxis (kidney)

- Unlabeled: heart transplant, HSCT, other cancers

111
Q

metabolism of sirolimus?

A

hepatic; extensive CYP 3A4 metabolism (drug interactions)

112
Q

What do the target sirolimus levels depend on?

A
  • Type of solid-organ transplant (heart, kidney)
  • Concomitant immunosuppressive therapies (CsA, MMF +/- steroids)
  • Time post-transplant
113
Q

Sirolimus:

Css may take >___ days to occur

A

10

114
Q

What are some other lab monitoring parameters?

A
  • electrolytes
  • CBCs: anemia, leukopenia, thrombocytopenia
  • renal, urine: proteinuria, nephrotoxicity
  • lipid profile: increase TG 50%, increase cholesterol 45%
  • hepatic (LFTs)
115
Q

What are some clinical uses of mycophenolate?

A

-Transplant rejection prophylaxis (kidney, liver, heart)

116
Q

Reliable AUC can be determined with as little as 3 blood samples for mycophenolate; when are these samples taken?

A
  • Trough level before next dose (C1)
  • 30 minutes after dose (C2)
  • 120 minutes after dose (C3)
117
Q

When does mycophenolate reach steady state?

A

3 days

118
Q

What is the most important lab monitoring parameter?

A

CBC: weekly for 1st month, twice monthly for month 2-3 then monthly thereafter

119
Q

What are clinical uses of methotrexate?

A

Low doses: rheumatoid arthritis, psoriasis (usually not monitored)

High doses: cancer (leukaemia’s, breast, head and neck, lung, osteosarcoma)

Others: ectopic pregnancy, Crohn’s disease, bladder cancer

120
Q

Describe the metabolism of methotrexate

A

Partially metabolized by intestinal flora, polyglutamtes formed inside cells are equipotent to methotrexate and elicit effects

121
Q

Methotrexate monitoring levels is important for ___ _____ _____ protocols for monitoring risk of toxicity

A

high dose chemo

122
Q

______ rescue dosing is based on methotrexate levels

A

Leucovorin

123
Q

What are some consequences of methotrexate toxicity?

A
  • hematological
  • GI
  • hepatic
  • renal
  • respiratory
124
Q

What do we need to monitor for methotrexate?

A

Baseline, then Q2-4 weeks x 3 months, then Q3 months:
CBC
sCR, urea
LFTs

Baseline, then annually:
chest radiograph

125
Q

What is digoxin used for?

A
  • Heart failure (inotropy)

- Arrhythmias; supra ventricular tachycardia (chronotropy)

126
Q

metabolism of digoxin?

A

majority: stomach or by intestinal bacteria

127
Q

Digoxin presents as a ___ compartment model

A

2

*takes time to distribute to target tissues

128
Q

When should we take digoxin levels?

A
  • at least 6 hours after dose

- ideally 12 hours after last dose

129
Q

Digoxin equations:

Cl = 1.303 (Crcl) + 20

Who is it for?

A

moderate to severe heart failure (Class 3 or 4)

130
Q

Digoxin equations:

Cl = 1.303 (Crcl) + 40

Who is it for?

A

without heart failure

131
Q

List some factors that affect digoxin volume of distribution and clearance

A
  • CHF
  • eGFR
  • Obese
  • Thyroid
  • Physical activity
  • Age
132
Q

What are the clinical uses?

A

Airway diseases (add-on therapy for severe, chronic asthma, last-line for COPD, neonatal apnea but caffeine is preferred)

133
Q

Metabolism of theophylline

A
  • 85-90% hepatic

- metabolized to active metabolites

134
Q

Describe drug level monitoring timeline for theophylline

A
  • Initial: 30 minutes after IV loading dose, one half-life after starting continuous infusion
  • Oral: 2 days to Css
135
Q

Consequences of toxic levels theophylline

A

vomiting, diarrhea, irritability, insomnia, tachycardia, hypotension, arrthymias, seizures, brain damage, death

Lab Modules (7 decks)

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