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TXP: Pulm/ Tox. And Rheumatology > Week 4: Drug Induced Cardiac/Kidney/Lung Disease > Flashcards

Week 4: Drug Induced Cardiac/Kidney/Lung Disease Flashcards

1
Q

QTc prolongation and Torsades de points(TdP)

what is it:

A

QTc prolongation: lengthening of the qt interval due to increased positive ions, which increases risk for TdP

TdP: lifethreatening polymorphic ventricular tachycardia triggered by premature ventricular beating during qtc prolongation
*not all QTc leads to TdP

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2
Q

normal QTc (must ocrrect for HR)

A

men: <470 ms
women: <480 ms

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3
Q

drug induced QTc dx

A

QTc >/ 500 ms
OR
QTc of >/ 60 ms from baseline

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4
Q

Common medications that cause QT prolongation

also note**

A

ABCDEF

A:antiarryhtmics (amiodarone,sotalol, dofetilide) (classIII antiaryhtmics)

B: Antibiotics (fluroquinolones[lexoflox,ciproflox,], macrolides[erythromycin,azithromycin])

C: antipsyChotics(Class I worse than Class II)

D: AntiDepressants:( !!Citalopram!!, TCA’s)

E:AntiEmetics (ondansetron)

F: Antifungals (-azole antifungals)

and many many more

notes: DDII or organ function may increase levels of these medications
*additive qt prolongation occurs when one or more than one offending agent

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5
Q

risk factors that lead qt prolongation-> TdP

A

nonmodifiable:
>65 years old
female gender (already have longer qt interval than men)
genetic predisposition
cardiac disease

modifiable:
diuretic treatment( due to electrolyte imbalance during treatment)
electrolyte abnormalities
>1 ST-prolonging agent
organ function

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6
Q

approch to drug induced qt prolongation

A

avoic qtc interval prolongation drugs in pts w. pretreatment intervals >450 msec

reduce dose or d/c prolonging agents if qtc increases >60msec from pretreatment value

d/c prolonging agent if qtc increases >500msec

maintain k>4 and Mg>2

avoid concaminant administratoin of qtc interval prolonging drugs

avoid qtc interval-prolonging drugs in patients with a hx of drug induced tdp

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7
Q

Treatment of Tdp

A

goal: increase HR even faster to avoid introduction of early beat

1.D/C offending agents that can potentially cause prolonged qt (and avoid admin. more qt prolonging agents

  1. *!! IV magnesium!! push or infusion (mg is a safe positive ion to admin in an acute setting)
    *if pt does not have a pulse, admin as push
    *if pt still has a pulse , can give infusion
    *pay attention to other electrolytes such as K+, and Ca may need to be repleted

3.Transcutaneous pacing

  1. isoproterenol infusion: beta agonist to increase chronitropy and inotropy of heart. DRUG OF CHOICE in Tdp, however $$ and not always available, alternatives are epinephrine or atropine

if at any point the pt is hemodynamically unstable, cardioversion or defribillation is required

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8
Q

Drug induced HF causes

A

sodium and volume retention

direct cardiotoxicity-> cardiomyopathy

negative inotropy

*some drugs or drug classes can cause more than one of these mechanisms

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9
Q

drug induced HF

drugs that causeHF due to NA and fluid retention

A

NSAIDS
steroid
thiazolidinediones (TXDs)

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10
Q

drug induced HF

drugs that cause HF due to cardiomyopathy

A

chemo agents

biologic agents

alcohol

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11
Q

drug induced HF

drugs that cause HF due to negative inotropy

A

Non-dihydropyridine calcium channel blockers

beta blockers

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12
Q

considerations for drugs that cause HF due to sodium and fluid retention

A

nsaid(also increase systemic vascular resistance) and steroids:
in pts w. HF,
avoid if possible!!
if necessary: minimize dose and duration

TZDS: BBW: avoid in pts with NYHA III-IV HF

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13
Q

considerations for drugs that cause HF due to cardiomyopathy

A

chemo agents: anthracyclines, alkylating agents

biologic agents: Trastuzumab

alcohol: direct toxic effect on the myocardium

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14
Q

Anthracycline induced cardiomyopathy

most common agents:
moa:
mechanism of damage:
chemoprotective agent to help w. cardiomyopathy

A

most common agents: doxorubicin, daunorubicin

moa: Topoisomerase 2B (TOP2B) mediator for anthracycline induced cardiopyopathy

mechanism of damage:
*TOP2B: in all cells, including cardiomyoctes
*inhibition of TOP2B (anthracyclines) causes DNA breakdown and cell death
->increase free radicals and cell death
->defective mitochondrial biogenesis

*dexazoxane binds to TOP2B to prevent anthracycline binding(helps prevent cardiotoxicity of anthracyclines

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15
Q

risk factors for anthracycline toxicity

A

treatment related
*cumulative dose of anthracycline (>400mg/m^2)
*dosing schedules
*previous anthracycline therapy
*radiation therapy
*co-administration of potentially cardiotoxic agents

Patient related
*age
preexisting CV disease or risk factors
*obesity
*smoking
*gender

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16
Q

maximum dose of anthracyclines (doxorubicin)

A

Lifetime dose of 550 mg/m^2

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17
Q

is anthracycline cardiotoxicity reversible or irreversible

A

IRREVERSIBLE

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18
Q

Trastuzumab induced cardiomyopathy

moa of drug:
moa of cardiomyopathy
is it reversible or irreversible

A

moa: trastuzumab is a HER2 receptor antagonist that can be used in certain types of breast cancer
moa of cardiomyopathy: inhibition of HER2 receptors->
* increased reactive o2 species (ROS)
*reduced NOS expression
*reduced NO bioavailability
*increased angiotensin
cardiotoxicity is usually REVERSIBLE once drug is d/c

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19
Q

risk factors for development of trastuzumab induced cardiomyopathy

A

1.advanced age

  1. presence of cv comorbidities
  2. previous treatment with anthracyclines
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20
Q

Trastuzumab precautions and BBW

A

nO CI, bu recommended to avoid in pts with a hX of HF. evvaluate LVEF in all patients prior to and during treatment

BBW: associated w. symptomatic and asymptomatic reductions in left ventricular ejection fraction and development of HF

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21
Q

Treatment of Trastuzumab induced cardiomyopathy

A

dose adjustments based on LVEF
consider dose reduction or discontinuation if HF develops

consider using HF meds during treatment if EF declines
*ACE/ARBS
*beta-blockers

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22
Q

HF due to negative inotropy

drug considerations

A

NON-DHP CCB: avoid in pts w. EF<40%
BB: avoid in acute HF exacerbation

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23
Q

General mechanisms of drug induced myocardial ischemia and acute coronary syndrome

A

1.increased myocardial oxygen demand
2. decrease myocardial oxygen supply
3.drug induced ACS

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24
Q

Drug induced myocardial ischemia and acute coronary syndrome

INCREASED MYOCARDIAL DEMAND

Disease and Mechanism
Examples

A

disease and mechanism: incfreased HR and contractility

examples: cocaine, beta agonists, sympathomimetics, withdrawal of b blockers, potent vasodilators

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25
Q

Drug induced myocardial ischemia and acute coronary syndrome

DECREASED MYOCARDIAL SUPPLY

Disease and Mechanism
Examples

A

sidease and mechanism: increased coronary resistance (vasospasm

ex: cocaine, antimigraine agents (triptans)

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26
Q

Drug induced myocardial ischemia and acute coronary syndrome

DRUG INDUCED ACS

Disease and Mechanism
Examples

A

disease and mechanism:
A) coronary arthery thrombosis/vasospasm
ex: cocaine, oral contraceptives, NSAIDS, estrogens, antimigraine agents
B)Increased cardiovascular risk
ex: cocaine, NSAIDS estrogens, HIV agents, oral contraceptives, rosiglitazone

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27
Q

cocaine induced myocardial infarction

moa
prevelance

A

*25% of MI in 18-45 y.o is a ssociated w. frequent cocain euse

moa: sympathomimetic crisis, cocaine inhjibits the reuptake of norepineohrine leadint to increased norepineohrine concentrations and enhanced alpha 1 mediated vasoconstriction

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28
Q

treatment of cocaine induced MI

A

chest pain:
*aspirin
*benzodiazipines(cheat sympathomimetic crisis)

persistent HTN
*benzos
*IV nitroglycerin

other acute ACS trtmt
*possible aboid acute BB
*otherwise proceed as normal

Longterm ACS treatment
*possibly avoid beta speciic blockers
*drug abuse counseling

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29
Q

Mechanism of NSAID induced Toxicity

A

NSAID moa: blocks cox enzyme

Cardiovascular effects
COX enxymes> vascular vasodilation and decrease platelet aggregation
cox inhibition: MI, stroke

GI mucosa
cox enzymes: increase gastric acid, increase bicarbonate, increase mucosal blood flow
cox inhibition: peptic ulcers, bleeding

Kidneys
cox enzymes: afferent arteriolar vasodilation-> increase GFR
increase sodium and water retention
cox inhibition: Na/H1O retention, HTN, AKI

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30
Q

NSAID BBW

A

may increase risk of serious CV thrombotic events,MI, STROKE, which can be fatal. may increase w. duration of use. pts w. cv disease or rosk factors for cv disease may be at greater risk

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31
Q

risk factors for acute MI with NSAIDS

A

when: risk of MI early in theraypu
rapid onset (w.in 7 days)

how much: NSAID use increases risk by about 20-50%

which NSAIDs: no diff btw. selectgive and non selective NSAIDs

which doses: higher doses, higher risk
1200mg/day ibuprofen
750 mg/day naproxen

duration: doesnt appear to increase risk
not been well studied

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32
Q

Drug Induced Kidney Disease

Category: hemodynamic mediated renal injury
basic patho:
exs:
notes:

A

Category:
basic patho: reeuction in glomerular pressure due to alterations in arteriole tone

exs:* ACE/ARBS: efferent arteriole dilation via decreased angiotensin II
*NSAIDS: afferent arteriole constriction via decreased PGE2 production
*SGLT2 inhibitors: deliver Na to macula densa cellsafferent arteriole constriction via tubuloglomerular feedback
*calcineurin inhibitors: afferent arteriole constriciton

notes:
*net effects is a loss of autoregulation-> increase risk of decreased intraglomerular hydrostatic pressure-> decreases GFR
*combos of these drug s w. low volume state (dehydration) is highest risk for AKI

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33
Q

hemodynamic mediated renal injury

Prerenal injury

A

Prerenal:
basic patho: reduced blood flow to kidney
ex: diuretics
note: decrease effective circulatory volume if over diuresis occurs

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34
Q

Drug Induced Kidney Disease

Category: intrinsic renalinjury
basic patho:
exs:

A

Drug Induced Kidney Disease

Category: hemodynamic mediated renal injury
basic patho:
1. Glomerular nephritis
exs: Gold, Allopurinol

  1. Acute tubular necrosis
    ex: Aminoglycosides, amphotericin B, IV contrast media
  2. acute interstitial nephritis
    ex: PCNs, NSAIDs, PPIs, sulfa drugs
  3. vasculitis: PTU, Levamisole ,Allopurinol, Phenytoin
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35
Q

Drug Induced Kidney Disease

Category: post renalinjury
basic patho:
exs:

A

Drug Induced Kidney Disease

Category: post renalinjury
basic patho: nephrolithiaisis
exs: topiramate, furosemide, acyclovir, sulfonamides, allopurinol

36
Q

risk factors for drug induced renal disease

A

elderly (age>65 y.o)

CKD

concaminant nephrotoxins

renin dependent state (low effective circulating volume; ex HF, cirrhosis)

known allergy to drug

duration of therapy

DM/HTN

37
Q

keys to prveent drug induced kidney disease (DIKD)

A

direct prevention to underlying mechanism of injusry

!!!avoid nephrotoxic meds (and combos of ) in high risk pts!!

maintain adequate perfusion (i.e hydration)
a. IV isotonic crystaloids in pts at risk of AKI

TDM (if possible

38
Q

Prevention of drug induced kidney disease: proactive monitoring

A

kidney function monitorinf w. an intensity that matches the risk of kidney injury
markers: SCr, BUN, eGFR, urinary output
frequency: yearly to hourly based on clnical context

novel urinary biomarkers
‘*kidney injury molecule 1 (KIM1-ATN
*neutrophil gelatinase associated lipocalin (NGAL)(ischemic injury)
*insulin like growth factor binding protein 7(IGFBP7 and tissue inhibitor of metalloproteinase2 (TIMP-2)-markers of cell cycle arrest

39
Q

What is the fluid of choice fo rprevention of AKI

A

ballance crystalloids (lactated ringers, plasma liteA)

isotonic iV crystalloids as fluid of choice for prevention of acute kidney injury

foudnd to have improved renal in jury outcomes

40
Q

prevention of drug induced AKI

A

maintain adequate fluid intake

avoic concaminant nephrotoxins

in high risk pts, start w. lowest dose of drugs that affect renal hemodynamics
*monitor Scr, BUN, K+, weights closely )q2weeks as outpt until stable
*titrate slowly
*hold diuretics while initiating/titrating these agents
*avois NSAID+ACE/ARB combo in CKD, heart disease, or liver disease

41
Q

treatment of prerenal/hemodynamic kindey in jury

A

D/C offending agent

provide sufifcient fluids to maintain effective circulating volume

monitor kidney function and electrolyes

42
Q

Intrinsic renal in jury

Acute Tubular Necrosis (ATN)

causative agents and presentation

A

1 cause of in hopsital acute kidney injury

causative agents: aminoglycosides, amphotericin B*(conventional»liposomal),
IV contrast media

presentation: acutely progressive increase in SCr and BUN with decrease in GFR and urine outpit (oligouria and nonoligouria are both common

urinalysis: proteinuria. cellular debirs, mussy brown color, and granular casts

metabolic acidosis

hyperkalemia

FeNa>1%

Mg waisting (cisplastin)

43
Q

aminoglycosides and ATN

A

nephrotoxicity is related to torugh concentrations, importance of TDM and PK individualization

goal troughs:
gentamicin and tobramycin: </2mg/L
Amikacin </8mg/L

Extended interval dosing (e.g q24 hrs may reduce risk of nephrotoxicity
goal trough. undetectable
*no difference in risk of nephrotoxicity, maybe some reduce risk
*optimizes pk/pd relationship in comparison to traditional dosing

44
Q

mgt of ATN

A

supportive care
d/c drug and other nephrotoxic drugs

non-nephrotoxic alternatives

mainteain hydration

kidney replacement therapy

renal dose dopamine (2-5mg/kg/min)?
pharmacologic diuresis

45
Q

contrast induced nephropathy risk factors

A

CKD GFR<60

DM, age, LVEF<40%

Low effective circulating volume

concaminant nephrotoxic agents

large dose volume iodinated contrast

high osmolal contrast

ionic contrast

short time interval btw 2 ocntrast administrations

46
Q

prevention of CIN

A
  1. sodium based hydration- gold standard
    Saline hydration(normal saloine)
    maintain output >/150 ml/hr post contrast (need to flush the contrast out of the kidneys)
  2. sodium bicarb (not graded): recommended if pt has another indication for bicarb

3.N-acetylcysteine (NAC)-conflicting evidence, possible benefit, contreversial
1200 mg PO BIDx4 doses (if high risk factors, can add

47
Q

examples of contrast media available agents

A

3 classes (high, low, and iso)
examples of high: Diatrazoate (1550)
metrizoate (2100)

Low: Iohexol (884)
*note: low osmolal agents are still higher than plasma osmolality

iso: iodixanol:290

48
Q

monitoring parameters for CIN

A

SCr and BUN q12hrs for 2 days then q24hrs for 5-7 days (as inpt)

urine output with strict ins and outs x 4 days

medication regimen review (avoid nephrotoxic meds)

49
Q

Acute interstitial nephritis (AIN)

A

Type 4 cell mediated immune reaction

immune activation/hypersensitivity->leukocyte infiltration->inflammation-> AIN

50
Q

drug induced AIN causative agents

A

BETA LACTAMS
NSAIDS
SULFA CONTAINING DRUGS
PPIs

others include
vanco
diuretics
allopurinol
anti epileptics

51
Q

treatment of drug AIN

A

stop offending drug

avoid cross reacting drugs

supportive care

steroids (EARLY INTERVENTION)

52
Q

AIN steroid protocol example

A

corticosteroid dosing protocols are not standardized

early, aggressive steroid therapy may improve long term renal outcomes

53
Q

Vancomycin associated AKI mechanism

A

mechanism: unclear: AIN plays a role but reports of ATN, oxidative stress, complement fixation, etc.

54
Q

risk factors for vancomycin AKI

A

elevated trough concentrations

24-hr AUC>600 mcg*h/mL

daily dose>4g

duration of therapy>7 days

severity of illness

weight>101.4 kg

concaminant nephrotoxic agents (pip/tazo)

55
Q

prevention of vanco associated AKI

A

stweardship

avoid nephrotoxic concaminnat drugs
avoid aminoglycosides if possible
caution with pip/tazo (cefepime)

monitoring: frequent monitoring in high risk patients
avoid trough 15-20 mg/L; avoid AUC 400-600

56
Q

refresher: definition of AKI

A

increase of 0..3 mg/dl in a 48hr period
ORRR
50% from baseline in a 7 day period

57
Q

Nephrolithiasis common causative agents

A

topiramate

sulfonamides

furosemides

58
Q

nephrolithiasis preventin and treatment

A

maintain adequate hydration

goal output >/2.5L/ day

treatment: hydration to induce diuresis
*pain management
*lithostipsy-shockwave disintegation of ston epassage

59
Q

rhabdomylysis

mechanism
causative agents
prevention
management

A

mechanism:intra tbuular precipitation of myoglobin from muscle breakdown

drugs: statins and stain fibrate combos

prevention: avoid statin interactions, counsel pts on muscular symptoms

management: d/c offenidng agent, aggresive IV fluid admin, +/- urinary alkalization
targe t UOP~3ml/kg/hr
if urine pH<6.5, alternate sodium chloride and sodium bicarb iv fluids

60
Q

Lithium induced CKD

patho:
lithium target range(general)
risk factors:
prevention:
treatment:

A

patho: chornic interstitial nephritis, minimal change disease, focal segmental glomerulanecrosis, NEPHROGENIC DIABETES INSIPIDUS(can be managed by ameloride), distal tubular acidosis
,

incidence: 1.2%

lithium target range: 0.5-1

risk factors: duration of therapy, episodes of acute lithium toxicity.!! CUMULATIVE LITHIUM EXPOSURE. (CHORNIC EXPOSURE)

prevention: routine TDM of lithium, avoiding dehydration, monitoring renal function over time, avoid drug interactions (HCTZ)

treatment: D/C lithium, hydration, amiloride 5-20 mg daily (treats polyuria and polydipsia), avoid orher nephrotoxic drugs, monitor renal function

*amiloride doesnt trat the ckd, just the symptomsof drug induced diabetes insipidus

61
Q

Role of Liver

A

metabolism
*aminoacids, carbs,lipids (bile)

synthesis
*proteins (albumin, clotting factors, etc.)
*cholesterol and tgl
*thrombopoeitin

Detoxification
*food
drugs
herbals

Detoxification

62
Q

problems w. a diseased liver

A

decreased amino acid metabolism

decreaed protein synthesis

incrfeased bilirubin

altered carb metabolism

reduced cholesterol production

reduced detoxification

63
Q

Hepatic Labs

A

Liver function Tests

aminotransferases (AST,ALTCGT,ALP)
*best markers of acute injury
*in cirrohissis(chronic), these normalize, so not a good marker of liver function in chronic disaease

synthetic function
*albumin (normal albumin levels: 3.4-5.4 g/L
*PT/INR
*good markers in choronic liver funciton evaluation

jaundice

64
Q

aminotransferases

lrvrld:
maerkers for what kind of injury

A

AST
ALT
*both levels 5-40
*found in hepatocytes
*hepatocellular injury markers

ALK PHOS()ALP)
*found in cells of bile ducts (bile canniculi) normal levels (30-140)
*cholestatic injury markers

65
Q

bilirubin

A

derived from degredation of hemoglobin from rbc’s

normal values: ~1

66
Q

jaundice

A

physical manifestation of hyperbilirubinemia

*accumulation of hyperbilirubinemia

67
Q

causes of liver disease

A

alcohol
hepatitis ABCDE
biliary tract disease
nonalcoholic fatty liver disease
drug induced
genetic/metabolic

68
Q

Drug Induced Liver Injury (DILI)

etiology

A

range from asymptomatic elevations in lab liver tests to overt liver failure

etiology not completely known

most common road block in drug development

APAP most common cause

69
Q

adili DEFINITION

A

newer definition

*total bili>2.5 mg/dL and any elevation in ALT, AST, or ALP

ALT>5x ULN
AST>5X ULN
ALP>2x ULN
INR>1.5 w. elevated AST, ALT, ALP

70
Q

types of DILI

A

Hepatocellular
*AST AND ALT elevation
*R=[ALT/ULN]/[ALP/ULN]>/5

CHOLESTATIC (something preventing bile moving to duodenum)
*alp elevation
R=[ALT/ALP/ULN]</2

MIXED:
R=[ALT/ULN/ALP/ULN=2-5

71
Q

Causes of DILI

what is #1 cause of DILI in DILIN

A

1 on the Drug induced liver disease network (DILIN)

amox-clav
known to cause cholestatic jaundice
can cause hepatocellular injury

associated w. HLA-DRB1*15 allelle

symptom onset 2-45 days

Treatment: supportive care, will self resolve

72
Q

DILI network

A

prospective ongoing observational study assessing causation, w. intent to create a national data base of DILI reports, excluding APAP

criteria of inclusion:
*total bili>2.5 mg/dL and any elevation in ALT, AST, or ALP

ALT>5x ULN
AST>5X ULN
ALP>2x ULN
INR>1.5 w. elevated AST, ALT, ALP

ABX should be on our radar for causing DILI, esp. augmentin, after APAP

73
Q

DILIN: HErbal and Dietary supplements

A

16% of DILI cases were du eto herbals and dietary supplements

bodybuilding had more cholestatic, nonbuilding had more hepatocellular injury

74
Q

DILN: mortality/transplant and patterns of injury

A

cholestatic injury less associated w. mortality and transplant

75
Q

rechallenging i nDILI

A

rechannelenge may only be considered if pt had only cholestatic injury

do not rechallenge if pt had hepatocellular injury
if mized: used shortest duration of therapy possible

in general, avoid rechallengin unless no alternative exists

76
Q

APAP overdose PK

A

rapid PO absorption wihtin 2 hours

APAP crosses BB and placenta

meTABOLISM: 25% extracted through pass metabolism

77
Q

APAP toxicity mechanism and toxic acute dose

A

elimantion processes(glutathione) become saturated

toxic acute dose considered >/7.5 g in adults or >/150 mg/kg in children

78
Q

predisposing factors for APAP toxicity

A

cyp2e1 induction (anticonvulsants, isoniazid, chornic etoh users), recued glutathione stores(malnurished) decreased sulfation and glucuroniation

79
Q

manisfestation of APAP toxicity

A

N&V, malaise, pallor, diaphoresis

doesnt occur until 24-36 hrs post ingestion w. increase in AST

max hepatotoxicity occurs btw 72-96 hrs

not uncomon to se AST,ALT >10000

can see changes in INR, bilirubin, glucose, lactate, phosphate and pH +/- renal failure

those thaqt survive make a ocmplete recovery

80
Q

APAP toxiicty management

A

activated charcoal in pts who present within 1-2 hours of ingestion

N-Acetylcysteine therapy (NAC) is crucial

supportive care
*IV fluids
*management of N/V
corrwction of hypoglycemia
*vit. K /FFP

81
Q

NAC mOA

A

serves as glutathione substitute detoxifying NAPQI

precursor to glutathione resulting in increased glutathione production

follows more nontoxic metabolism thorugh increased sulfation, resulting in less NAPQI production

appears to preserve multiorgan function in severe toxiicty thorugh unknown mechanisms

82
Q

NAC efficacy

A

efficacy nearly complete in trial data when adminstered within 8hrs of APAP overdose

decision to treat based on APAP serum levels plotted on the rumack-mathew nomogram

available in PO and IV formulations

83
Q

what if the APAP level is outside 4-24 hr window

A

prior to hour 4:
*consider activated charcoal
wait and recheck at hour 4 to asess whether or not nac is indicated

after hour 24: if AST is elevated regardless of APAP level,begin NAC

after 24 hours or unknown late ingestion w. detectable APAP level, beginNAC

84
Q

IV vs PO NAC

A

equallt efficacious

chois eshould be based on side effect profile, whether or not failure is present, and extrahepatic involvement

dosings:
Po: 72 hr protocol
IV: 20 hour protocol

AE:
Po:bad taste, N/v in50% of pts (pretreat w. antiemetics)
IV:anaphylactoid (rash, flushing,nromchospasm) in 17% of pts

notes:
Po: NAC delivery may be delayed up to an hour
po therpay should be changed to IV if liver failure develops
*solution shoul dbe diluted to 5% w. a soft drink and covered to cover smell
IV: preffered in pts w. liver failure, pregnancy and in ability to tolerate PO
*give over 60 min to avoid

85
Q

treatment duration of NAC

A

anywhere from 20-72 hrs

continue if on going liver failure present, elevated pt/inr encephalopathy

detecatable apap or ongoing hepatocyte damage

TXP: Pulm/ Tox. And Rheumatology (7 decks)

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