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Pulm Therapeutics > Exam 2: just fing do it man > Flashcards

Exam 2: just fing do it man Flashcards

1
Q

Co-morbidities with CF

A

-depression
-anxiety
-asthma
-acid reflux
-CF related diabetes
-sinus disease

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2
Q

What age range can Ivacaftor be used?

A

age > 4 months

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3
Q

what age range can lumcaftor/ivacanftor be used?

A

age > 2 yrs

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4
Q

what age range can tezacaftor/ivacaftor be used?

A

age > 6 yrs

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5
Q

what age range can elexacaftor/tezacaftor/Ivacaftor be used?

A

age > 6 yrs

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6
Q

Ivacaftor use in CF

A

MOA: facilitates opening of chloride channel (CFTR potentiator), mostly used in class 3 or 4 mutations
-indicated for pts aged > 4 months and >1 of 97 mutations
–> G55ID + R117H mutations

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7
Q

Tezacaftar + Ivacaftor use in CF

A

-Tezacaftor component fixes the defective CFTR protein so it can move to the proper place on the airway cells surface (CFTR corrector)
-indicated in pts age >6 y/o who have HOMO or HETERO genes copies of F508del

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8
Q

Lumacaftor/Ivacaftor use in CF

A

-lumacaftor component fixes the defective CFTR protein so it can move to its proper place (CFTR corrector)
-indicated for pts aged >2 yrs who have HOMO F580del mutations

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9
Q

Elexacaftor/Tezacaftor/Ivacaftor use in CF

A

-E & T component fix the defective CFTR protein so it can move to the proper place (CFTR correctors)
-indicated for pts aged > 6 y/o who have. at least 1 copy of the F508del mutation or 1 of 177 other mutations
**does NOT carry the limitations of T+I so it can be more widely used

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10
Q

Impact on the rate of decline of FEV1 with the use of the CFTR modulators

A

-acute PE rate was decreased with the use of each CFTR modulator
-showed decreased rate in the decline of lung funcction over a longer period of time therefore- these pts improved their health acutely + stayed healthier for longer
*take each modulator with fat containing meal
*dose reduction is required in moderate-severe hepatic function

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11
Q

CYP3A inhabitation (mod) DDI in CF

A

ex: erythromycin, fluconazole
I: once daily dose
T + E: QOD dosing

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12
Q

CYP3A inhibition (strong) DDI in CF

A

ex: clarithromycin, Itarconazole
I/T/E: twice weekly dosing

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13
Q

CYP3A induction DDI in CF

A

ex: rifampin, carbamazepine, phenobarbital, phenytoin, st. John’s wort
AVOID use!

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14
Q

Complimentary therapy to aid in obstruction in CF

A

-can use physiotherapy (vest treatment)
-mucolytics: Dornase alfa
-hydrating agents: hypertonic saline
-bronchodilators: albuterol

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15
Q

Complimentary therapy to aid in infection in CF

A

-inhaled tobramycin
-inhaled aztreconam
-systemic antibiotics
-annual vaccinations (flu)

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16
Q

Complimentary therapy to aid in inflammation in CF

A

1: azithromycin

-high dose ibuprofen

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17
Q

Non-pharm tx for CF lung disease

A

**Physiotherapy: high frequency chest wall oscillation - used by 80% (others: postural drainage, positive expiratory pressure, oscillatory PEP and exercise)
**influenza vaccine is recommended for pts w/ CF, starting at age 6 months

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18
Q

Dornase alfa in CF tx

A

-25 mg inhalation 1-2 x daily (shows improvement in FEV1; decreased rates of APEs)
AEs: voice hoarseness and rash
–> recommended for all ages > 6

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19
Q

Hypertonic saline in CF tx

A

-7%
-pulls water into the airway, helps to decrease the thickness of the secretions, making them easier to expel
–> decreases rates of APEs
AEs: bronchospasm (mitigate w/ albuterol) –> recommend for chronic use in ages > 6

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20
Q

Bronchodilator use in CF TX

A

-used in ~ 90% of pts with CF
-some pts with CF also have an asthmatic component in which cases there may be a benefit observed with using albuterol
-may be utilized to improve deposition of inhaled medications

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21
Q

Azithromycin in CF tx

A

-most commonly used anti-inflammatory in CF
-most clear indication in pts > 6 y/o chronically infected w/ pseudomonas arginosa
-dosing is based on weight:
–> pts < 25 kg: 10mg/kg PO MWF
–> pts < 40 kg: 250mg PO MWF
–> Pts > 40 kg: 500 mg PO MWF
SEs: nausea, diarrhea, wheezing w/ some antibiotic resistance in smaller studies

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22
Q

inhaled antibiotics in CF tx

A

**systemic antibiotics should NOT be used for suppression therapy!
-provide high concentration directly to the site of infection, targets bacterial colonization to decrease the number of exacerbations & systemic absorption is generally minimal ( = good safety profile)

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23
Q

Inhaled tobramycin in CF tx

A

-TOBI: nebulizer, 300 mg inhaled BID: 28 days ON, 28 days OFF
-TOBI Podhaler, 112 mg: dry powder device, inhaled BID: 28 days ON and 28 days OFF (more preferred product, easier to use and faster)
SEs: voice alterations & tinnitis

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24
Q

Inhaled Aztreonam in CF tx

A

-Aztronam 75 mg: inhaled TID- 28 days ON, 28 days OFF
-nebulize solution: administered over ~2-3 mins using altera nebulizer
SEs: bronchospasm (pre-treat with SABA)

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25
Q

Pancreatic enzyme replacement therapy (PERT)

A

-brand names: creaon, pancraeze, pertzye, ultresa, viokace, zenpep
-dosing is based on lipase component
-enternal feeding is useful for: children falling off the growth curve & adults not gaining/maintaining weight

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26
Q

Dosing for PERT *

A

Infants: 2000-5000 units per 120 ml of formula
Children < 4 y/o: 1000 units/kg with meals and 1/2 dose with snacks
Children > 4 y/o & adults: 400-500 units/kg with meals & 1/2 dose with snacks
-mean dose = 1800-1950 units/kg/meal

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27
Q

Decrease dose of PERT when:

A

-pt on high doses with good effects
-pt having side effects

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28
Q

Increase dose of PERT when:

A

-poor weight gain
-pt experiencing bloating, inc # of fatty stools

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29
Q

Empiric dosing for Vits in CF *

A

ADEK
-age < 12 months: 1 ml po qd
-age 1-3yrs: 2 ml PO ad
-age 4-10 yrs: 1 tab PO qd
-age > 10: 2 tab PO QD

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30
Q

Vitamin D dosing in CF

A

-age 1-11: D3 1000 IU QD
-age > 11 y/o: D3 2000 IU QD
if after 3 months level < 30 ng/L:
-age < 5: D3 50,000 IU MFW x 1 month
-age > 5 y/o: D3 50,000 QD x 1 monht

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31
Q

other vitamins to consider in CF

A

-vit K (supp during IV antibiotic tx): phytonadione 5 mg PO twice weekly
-ferrous sulfate
-poor weight gain? zinc sulfate: 1 mg/kg/day divided BID

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32
Q

Symptoms of acute worsening of CF

A

-cough
-increased sputum production
-SOB
-chest pain
-loss of appetite
-weight loss
-lung function decline

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33
Q

Treatment of acute CF

A

-INCREASE vest tx, dornsae alfa, hypertonic saline and bronchodilator

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34
Q

CF exacerbation w/ hx of MSSA (NO PA)

A

anti-staphyloccal penicillin/cephalosporin

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35
Q

CF exacerbation w/ hx of MSSA AND PA

A

double PA coverage: aminoglycosides + cefepime

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36
Q

CF exacerbation w/ hx of MRSA (no PA)

A

vancomycin or Linezolid

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37
Q

CF exacerbation w/ hx of MRSA AND PA

A

double PA coverage: aminoglycoside + B-lactam (ceftazidine)

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38
Q

Aminoglycosides goal peak and trough

A

peak: 10-12
trough: < 15
-draw serum initially and then every 3-7 days after dosing regimen

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39
Q

Vancomycin trough

A

10-20

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40
Q

drug related risk factors for developing drug-induced pulmonary disease

A

-dose or administration rate
-treatment duration
-oxygen therapy
-radiation therapy
-cumulative dose

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41
Q

patient related factors for developing drug-induced pulmonary disease

A

-age (extremes)
-RA or pre-exsiting lung disease
-impaired renal/hepatic function
-genetics

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42
Q

drug-induced interstitial pneumonitis/fibrosis

A

*most common one
-onset: can be acute or chronic
-symptoms: nonproductive cough, sudden onset of dyspnea, fever, rash, eosinophilia (chronic: slowly progressing breathlessness, decreased physical activity)
-PE: crackles on expiration + clubbing
-chest CT will show fibrosis

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43
Q

antimicrobials that can cause DIP/F

A

-nitrofurantoin: occurs due to an imbalance of oxidant/anti-oxidant
-presents as acute eosinophilic pneumonia or chronically as pulmonary fibrosis
-can show up 8 months to 16 years after use

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44
Q

Antineoplastic agents that can cause DIP/F

A

**bleomycin
-busulfan
-carmustine
-cyclophosphamide
-gemcitabine

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45
Q

Bleomycin in DIP/F

A

-cytokine
-inflammatory cells & free O2 radical induction
-presents weeks to months, can progress to fibrosis

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46
Q

Aminodarone as agent that can cause DIP/F**

A

-via direct toxic effect –> SUPER common
-can happen 4 weeks - 6 yrs
-dose dependent: yes, smaller doses over year (> 2 yrs) or larger doses over shorter time frames (~ 400 mg/day for > 2 months)
-age > 60: 3x increase in risk of toxicity for each subsequent decade

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47
Q

Treatment of DIILD: immunotherapy check point inhibitors: grade 1

A

-consider holding med + reassessing medication in 1-2 weeks

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48
Q

Treatment of DIILD: immunotherapy check point inhibitors: grade 2

A

hold meds
-give prednisone/methylpred 1-2 mg/kg/day –> treat until grade 1 & taper over 4-6 weeks
No improvement? treat as grade 3

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49
Q

Treatment of DIILD: immunotherapy check point inhibitors: grade 3,4

A

-PERMANANT D/C
-methylpred 1-2 mg/kg/day - taper over 4-6 weeks
No improvement? Infiximab, IVIG, or MMF

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50
Q

Treatment of DIILD: MTORI’s: grade 2

A

-dose reduce or hold meds
-prednisone 0.75-1 mg/kg/day

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51
Q

Treatment of DIILD: MTORI’s: grade 3

A

-hold medication
-prednisone 0.75 - 1 mg/kg/day

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52
Q

Treatment of DIILD: MTORI’s: grade 4

A

-PERMANENTLY D/C med
-prednisone 0.75-1 mg/kg/day

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53
Q

Treatment of DIILD: Bleomycin

A

Prednisone 0.75 mg/kg/day for 4-6 weeks, then taper
Prevention: do chest xray q 1-2 weeks, and DLCO monthly

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54
Q

Treatment of DIILD: Carmustine

A

Prednisone 60 mg PO BID then 30 mg PO daily then taper by 10 mg po weekly then 5 mg PO weekly

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55
Q

Treatment of DIILD: Aminodarone

A

Prednisone 0.5mg-1 mg/kg/day - continue for several months to up to a year
Prevention: baseline spirometry, DLCO, chest xray then q 3-6 months if clinically indicated

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56
Q

BOOP

A

-acute inflammatory response in lung
-nonproductive cough, dyspnea, bilateral crackles, occasionally a fever & rash

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57
Q

BOOP: medications that can cause & tx

A

Meds: minocycloine, nitrofurantoin, bleomycin, aminodarone, sulfazalaine, carbamazepine, cocaine
tx: D/C agent, possible to add steroids

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58
Q

Eosinophilic Pneumonias

A

-infiltration of pulmonary intersistium w/ eosinophilia, drug or toxin mediated
-dry cough, dyspnea, chest pain, fever, BL ground glass opacities

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59
Q

Eosinophilic Pneumonias: medications that can cause & TX

A

Meds: daptomycin, nitrofurantoin, minocycline, mesalamine, sulfasalazine
tx: acute- treat with steriods, chronic is not as common

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60
Q

Hypersensitivity Pneumonitis

A

-immediate is more common –> can lead to asthma exacerbations
-symptoms: urticaria, angioedema, rhinitis, dyspnea,
-chest xray: localized or bilateral alveolar infiltrates
meds involved: NSAIDs, methotrexate
-tx: d/c agent, ANTIHISTAMINES + possibly steroids

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61
Q

Drug induced pulmonary edema

A

-caused by: narcotics, heroin (IV), morphine, methadone, propoxyphene, naloxone, nalmefene, hydrochlorothiazide
Symptoms: cough, crepitation, cyanosis/hypoxemia
-chest xray: will show acinar infiltrate + normal heart size
-dose dependent: moderate to high doses narcotics
-onset: mins to 2 hrs
-remits: 24-48 hours (symptoms)
treatment: naloxone, oxygen, ventilator support

62
Q

Drug induced lupus

A

-involves the lungs in 50-70% of all cases, mechanism = hypersensitivity –> can exacerbate underlying lupus or cause disease
-common meds: PROCAINAMIDE, hydralazine, isoniazid or anti- TNF alpha
symptoms: fever, myalgia, rash, arthralgia, arthritis, serosites, pruritic pain
-onset: up to 3 yrs after initiation
tx: withdraw agent, will return to normal after 6 weeks

63
Q

Normal QtC values

A

men: < 470 ms
women: < 480 ms

64
Q

Drug induced QT prolongation values/parameters

A

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

65
Q

Common meds that can cause QTc prolongation (ABCDEF)

A

A: antiArrhythmics (aminodarone, sotalol, dofetilide)
B: antiBiotics (flouroquinolones, macrolide) –> levo, cipro, erythromycin (DDi or organ function may increase levels of these medications
C: antipsyChotics (class 1)
D: antiDepressants (citalopram, TCAs)
E: antiEmetics: (ondasteron)
F: antiFungals (-azole antifungals)
**additive QT: prolongation occurs with one or more than one offending agent

66
Q

Risk factors for Torsades De Pointes: non-modifiable

A

-> 65 y/o
-female gender
-genetic disposition
-cardiac disease

67
Q

Risk factors for Torsades De Pointes: modifiable

A

-diutetic tx
-electrolyte abnormalities
- > 1 QT prolonging agent
-organ function

68
Q

approach to drug induced QT prolongation

A

-avoid QTc interval prolonging drugs in patients w/ pretreatment intervals > 450 ms
-reduce dose of d/c prolonging agents if QTc increases > 60 ms
-d/c prolonging agent if QTc increases to > 500 ms
-MAINTAIN K > 4 AND MG > 2 (anything below these values has shown to inc risk of TdP
-avoid concomitant administration of QTc interval prolonging drugs
-avoid use of QTc interval-prolonging drugs in pts with a hx of drug induced TdP

69
Q

Treatment of drug induced Torsade de pointes

A

1- d/c the offending agent that can potentially cause prolonged QT
2- magnesium IV push or infusion (based on pulse)
3- transcutaneous pacing (pads that send electric stim to speed up the heart)
4-Isoproterenol infusion ($$, alts are: epinephrine or atropine)
if at any point the pt is hemodynamically unstable, cardioversion or defibrillation is required

70
Q

3 main causes of drug induced HF

A

1- sodium and volume retention
2- direct cardiotoxicity –> cardiomyopathy
3- negative ionotropy

71
Q

HF due to sodium and fluid retention

A
  • NSAIDs, steroids & TZDs
    NSAIDs & steroids: in pts with HF: AVOID is possible
    -TZDs: BBW- avoid in pts with NYHA III-IV
72
Q

HF due to cardiomyopathy

A

-chemotherapeutic agents, biological agents, & alcohol
-chemo: anthracyclines, alkylating agents
-bio: Trastuzumab
-alcohol: direct toxic effects on the myocardium

73
Q

HF due to negative ionotropy

A

-non-dihydropyridine calcium channel blockers (diltiazem or verapamil)
-beta blockers

74
Q

Anthracycline induced cardiomyopathy

A

classic hallmark drug that causes cardiotoxicity + cardiomyopathy from chemo
–> most common: doxorubicin, daunorubicin
-TOP2B is the mediator for anthracycline induced cardiomyopathy

75
Q

Anthracycline induced cardiomyopathy: mechanism of damage

A

–> TOP2B: causes cell death in all cells, including cardiac myocytes
-inhibition of TOP2B causes DNA breakdown + cell death via increased free radicals of oxygen and defective mitochondrial biogenesis

76
Q

Anthracycline induced cardiomyopathy: treatment

A

Dexrazoxane: binds to TOP2B to prevent anthracycline binding + helps prevent the cardiotoxicity portion of the drug
limit anthracycline dose to 550 mg/m2

77
Q

Risk factors for drug induced HF (treatment related)

A

-cumulative dose of anthracycline ( > 400 mg/m2)
-dosing schedule
-previous anthracycline therapy
-radiation therapy
-co administration of potentially cardiotoxic agents

78
Q

Risk factors for drug induced HF (patient related)

A

-age
-preexisting cardiovascular disease or risk factors
-obesity
-smoking
-gender (maybe?)

79
Q

Trastuzumab induced cardiomyopathy

A

-Trastuzumab is a HER2 receptor antagonist that can be used in certain types of breast cancer –> the cardiomyopathy is usually reversible (slowly) once drug is discontinued!
-risk factors for development of cardiomyopathy: advanced age, presence of CV comorbidities, previous tx with anthracyclines

80
Q

what are 4 things that are occur due to inhibition of HER2 receptors that lead to HF?

A

-increased reactive oxygen species (ROS)
-reduced NOS expression
-reduced nitric oxide bioavailability
-increased angiotensin II
*all 4 lead to an increased vascular resistance

81
Q

Warnings & BBW of Trastuzumab

A

-no contriindications based on manufacturer but it is recommended to avoid in pts with a hx of HF –> evaluate LVEF in all pts to and during tx.
BBW: associated with symptomatic + asymptomatic reduction in LVEF + development of HF

82
Q

treatment of Trastuzumab induced cardiomyopathy

A

-dose adjustments based on LVEF
-consider dose reduction or discontinuation if HF develops
-consider using HF medications drug tx if EF declines ( ACE/ARB or beta-blockers)

83
Q

HF due to negative inotropy

A

-non-dihydropyridine calcium channel blockers: avoid in pts with EF < 40%
-beta-blockers: avoid in acute HF exacerbations

84
Q

mechanisms of drug induced myocardial ischemia + acute coronary syndrome: increased myocardial oxygen demand

A

-increased HR & contractility –> cocaine, B-agonists, sympathomimetics, withdrawal of B-blockers, potent vasodilators

85
Q

mechanisms of drug induced myocardial ischemia + acute coronary syndrome: decreased myocardial oxygen supply

A

-increased coronary resistance (vasospasm) –> cocaine, anti-migraine agents (triptans)

86
Q

mechanisms of drug induced myocardial ischemia + acute coronary syndrome: drug induced ACS

A

-coronary artery thrombosis/vasospasm –> cocaine, oral contraceptives, NSAIDs, estrogens, anti-migraine agents
-increased cardiovascular risk: cocaine, estrogens, NSAIDs, HIV agents, oral cantroceptives, rosiglitazone

87
Q

cocaine induced myocardial infarction

A

-MI caused by vasospasm + vasoconstriction of coronary arteries
sympathomimetic crisis: cocaine inhibits the reuptake of norepinephrine leading to increased NE concentration + enhanced alpha 1 mediated vasoconstriction

88
Q

Treatment of cocaine induced myocardial infarction: chest pain

A

-aspirin
-benzodiazepines

89
Q

Treatment of cocaine induced myocardial infarction: persistent hypertension

A

-benzodiazepines
-IV nitroglycerin

90
Q

Treatment of cocaine induced myocardial infarction: others + long term

A

-possibly avoid beta blockers (eh choice)
-drug abuse counseling

91
Q

Mechanism of NSAID induced cardiotoxicity

A

-PG12 & TXA2: vascular vasodilation + decreased platelet aggregation
–> affects the vasculature of out coronary arteries, which are what brings that oxygenated blood to our heart muscles—BLOCKING this causes vasoconstriction in these arteries = decrease the amount of oxygen that can be delivered to the heart muscles
-physiologic effect of COX inhibition = MI, stroke

92
Q

NSAID BBW

A

may cause an increased risk of serious cardiovascular thrombotic events, MI, and stroke which can be fatal. this risk may increase with duration of use. Pts with cardiovascular disease or risk factors for cardiovascular disease may be at greater risk

93
Q

Risk factors for acute MI with NSAIDs

A

-risk of MI is highest early in therapy = rapid onset ( 7 days)
-NSAID use increases risk by about 20-50%
-higher doses = higher risk!

94
Q

Risk factors for acute MI with NSAIDs: Ibuprofen & Naproxen doses

A

> 1200 mg/day Ibuprofen
750 mg/day Naproxen

95
Q

risk factors for drug induced renal disease* (ON EXAM)

A

-elderly (age > 64 yrs)
-CKD (existing)
-concomitant nephrotoxins
-renin-dependent state (low effective circulating volume: HF, cirrhosis)
-known drug allergy
-duration of therapy
-DM/HTN

96
Q

keys to prevent drug induced renal disease (ON EXAM)

A

-direct prevention strategy to underlying mechanism of kidney injury
*avoid nephrotoxic medications (and combinations there of) in high risk pts
-maintain adequate kidney perfusion –> intravenous isotonic crystalloids in pts at risk of AKI
-therapeutic drug monitoring
-balanced crystalloids (mimic plasma electrolyte concentrations

97
Q

*causative agents of pre-renal hemodynamic-mediated injury (ON EXAM)

A

-ACEi
-ARBS
-NSAIDS
-diutretics (loop)
-calcineurin inhibitors (cyclosporine + tacrolimus)

98
Q

Tx of pre-renal + hemodynamic- mediated injury

A

-d/c offending agent (NSAIDS)
-provide sufficient fluids to maintain effective circulating volume (.9% sodium cl)
-monitor kidney function and electrolytes

99
Q

what does ACE + loop diuretic + HF = ? (ON EXAM)

A

NO NSAID USE!
-combo is very common to manage disease state
-patient is “on-the -edge” of kidney injury, addition of NSAIDs puts them over the edge due to hemodynamic effects
*NSAIDs are the #1 cause of community based drug-induced AKI!

100
Q

acute tubular necrosis causative agents

A

#1 cause of in hospital acute kidney injury
-aminoglycosides *
-amphoterian B (conventional&raquo_space; liposomal) *
-IV contrast media *
-anti-neoplastic agents (platins, alkylating agents)
-direct cellular toxicity
-prolonged ischemia

101
Q

ATN clinical Presentation

A

-acutely progressive, inc Scr and inc BUN, w/ dec GFR and dec urine output
-muddy brown color + granular casts
-metabolic acidosis
-hyperkalemia
-FeNa > 1%
-magnesium wasting

102
Q

Aminoglycosides and ATN

A

-10-25% nephrotoxicity rates (up to 58%)
-highest when used with: vancomycin, amphotericin, contrast media, NSAIDs
*nephrotoxicity is related to trough concentrations, importance of therapeutic drug monitoring + PK individualization

103
Q

Goal trough concentrations of aminoglycosides in ATN

A

-gentamicin + tobramycin: < 2 mg/L
-amikacin: < 8 mg/L
-extended interval dosing may reduce the risk of nephrotoxicity –> goal trough concentrations = UNDETECTABLE

104
Q

management of ATN

A

supportive mainly
-d/c offending agent
-maintain hydration + euvolemia
-electrolyte management
-kidney replacement therapy if severe ATN

105
Q

Contrast media & ATN, risk factors (ON EXAM)

A

-CKD, GFR < 60 ml/min
-DM, age, LVEF < 40%
-low effective circulatory agents
-large dose (volume) iodinated contrast *
-high osmolal contrast
-ionic contrast *
-short time interval between 2 contrast administrations*

106
Q

Prevention of Contrast (CIN)

A

*saline hydrations: .9% sodium chloride: 1.5 ml/kg/hr 12 hours prior and 12 hours after –> maintain urine output of > 150ml/hr post contrast
*N-acetylcystine (NAC): given to pts who are at HIGH risk of contrast induced neuropathy –> 1200 mg PO BID x 4 doses ( 2 before and 2 after contrast)

107
Q

What monitoring parameters should be used prior to and following coronary catheterization? (in regards to CIN)

A

-serum creatinine and BUN q 12 hrs for 2 days then Q 24 hrs for 5-7 days
-urine output with strict ins/outs for 4 days
-medication regimen (avoid nephrotoxic medications)

108
Q

what treatments should a pt receive to prevent contrast induced nephropathy?

A

*0.9% sodium chloride IV at 100mL/hr 12 hours before and for 12 hours
(NAC 1200 mg PO BID x 4 doses ALWAYS an add on and only in HIGH risk pts)

109
Q

Acute Interstitial nephritis (AIN) (ON EXAM)

A

-immune activation/hypersensitivity –> leukocyte infiltration –> AIN
clinical triad: eosinophils, fever, rash

110
Q

Drugs that induce AIN (ON EXAM)

A

*beta-lactams
*NSAIDs
*Sulfa-containing drugs
* PPIS
*vancomycin
-diuretics
-allopurinol
-anti-epileptics

111
Q

Treatment of Drug-induced AIN

A

-stop the attending agent (duh)
-avoid cross-reacting drugs
-supportive care
- steroids?
–> SURE! early, aggressive steroid therapy MAY improve long term renal outcomes
ex) methylprednisolone 250-500mg IV daily x 3 days then prednisone 1 mg/kg/day to taper over 8-12 weeks

112
Q

Vancomycin associated AKI (ON EXAM)

A

mechanism: unclear, prevalence: 0-42%
Risks:
-elevated trough concentrations
***24 hr AUC > 600 mcgh/mL
*daily dose > 4 g
-duration of therapy > 7 days
-severity of illness
-weight > 101.4 kg
*concomitant nephrotoxic agents (piperacillin/tazobactam)!

113
Q

Prevention of vancomycin associated AKI

A

-stewardship
-concomitant drug use: avoid with aminoglycosides, use caution with pip/tazo (use cefepime if needed)
-monitoring:
–> frequent monitoring in high risk pts
–> avoid trough > 15-20 mg/L; avoid AUC > 600

114
Q

Nephorolithiasis (said wont be on exam but..)

A

common causative agents: topiramate, sulfonamide, furosemide
-goal urine output = > 2.5 L/day
-treatment: hydration to induce diuresis

115
Q

drug induced chronic kidney disease: lithium: pathogenesis

A

-chronic interstitial nephritis, minimal change disorder, focal segmental glomerulosclerosis (GSGS) –> IRREVERSIBLE damage = STOP the lithium
-nephrogenic diabetes insipidus –> prevents the kidney from responding to ADH = pee our a lot of water, can be managed with amiloride
-distal tubular acidosis

116
Q

Drug induced chronic kidney disease: lithium - risk factors

A

-duration of therapy
-episodes of acute lithium toxicity
-CUMULATIVE lithium exposure!

117
Q

Drug induced chronic kidney disease: lithium - prevention

A

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

118
Q

Drug induced chronic kidney disease: lithium - treatment

A

-D/C lithium
-hydration
*amiloride 5- 20 mg qd (treats polyuria and polydipsia)
-avoid other nephrotoxic drugs
-monitor renal function

119
Q

Drug induced liver injury (DILI): role of the liver

A

-metabolism: amino acids, carbs, lipids
-synthesis: proteins, cholesterol + triglycerides, thrombopoietin
-detoxification: foods, drugs

120
Q

Problems with a diseased liver

A

-decreased amino acid metabolism
-decreased protein synthesis
-increased bilirubin
-altered carbohydrate metabolism
-reduced cholesterol production
-reduced detoxification
(If any of these are happening acutely = bad new bears!)

121
Q

AST in DILI*

A

-mainly found in hepatocytes, also found in cardiac muscle, skeletal muscles, kidneys, brain
Normal lab values: 5-40
(used for acute situations)

122
Q

ALT in DILI*

A

-found in hepatocytes (felt to be more specific for liver injury than AST)
-normal values: 5-40
(used for acute situtations)

123
Q

Cholestatic in DILI*

A

-something preventing bile from moving from the liver to the duodenum –> immunoaltergenic problem with the metabolic packaging of the bile

124
Q

Bilirubin in DILI

A

-derived from degeneration of hemoglobin from RBCs
-total bilirubin = conjugated + unconjugated (< 1.2)
–> unconjugated: in serum and lipophilic ( < 1.0)
–> conjugated: glucoconidated in hepatocytes + transported into biliary canalicui ( < 0.2)

125
Q

Jaundice

A

physical manifestation of hyperbilirubinema (yellow)
-accumulation of unconjugated or conjugated bili, bili deposits in skin and sclera, filtered by kidney

126
Q

Causes of liver disease

A

-alcohol
-hepatitis A, B, C, D, E
-biliary tract disease
-non-alcoholic fatty liver disease
**drug induced
-genetic/metabolic: hemochromatosis, alpha 1 antitrypsin deficiency, Wilson’s disease

127
Q

Drug induced liver injury (some facts)

A

-can range from asymptomatic elevations in a lab liver test to overt liver failure
-most common road block in drug development
-responsible for 13% of acute liver failure events –> most common cause of death in acute liver failure
** APAP is the most common cause! (antibiotics next in line)

128
Q

Drug induced liver injury definition/test parameters

A

-total bili > 2.5 mg/dL & ant elevation in:
–> ALT (> 5x ULN)
–> AST ( > 5x ULN)
–> ALP ( > 2x ULN)
–> INR > 1.5 with elevated AST, ALT, or ALP

129
Q

Types of DILI : Hepatocellular *

A

-direct toxicity from the drug killing hepatocytes
-AST and ALT elevation
–> R = (ALT/ULN) / (ALP/ULN) >/= 5

130
Q

Types of DILI: Cholestatic*

A

-something is preventing the bile from moving from the liver to the duodenum
-ALP elevation
–> R = (ALT/ULN) / (ALP/ULN) </= 2

131
Q

Types of DILI: Mixed*

A

–> R = (ALT/ULN) / (ALP/ULN) = 2-5

132
Q

Amox-Clav & DILI things

A

1 on the DILIN list

-known to cause cholestatic jaundice, can also cause hepatocellular injury
-associated with the HLA-DRBI*15 allele
Symptom onset: 2-45 days after ingestion
Management: supportive care, will self resolve after removing the offending agent

133
Q

DILIN and herbal & dietary supplements:

A

STAY AWAY from:
-hydroxycut & NO-XPLODE (body building things)

134
Q

Can you give a pt amox-clav after a DILIN?

A

-only 40-60% of pts show a recurrence of DILI after a rechallenge test dose
-many ots may not encounter problems unless given long term therapy ( up to 12 weeks) with the offending agent
*re challenge may only be considered if the pt had only cholestatic injury!!!
(DO NOT rechallenge if pt had hepatocellular injury!!)

135
Q

Acetaminophen in DILI

A

-rapid PO absorption
-even in overdose the majority of APAP absorption occurs within 2 hrs with complete absorption by hour 4
-APAP crosses BBB and placenta

136
Q

APAP metabolism in DILI

A

-25% extracted through 1st pass metabolism (75% remaining)
-90% hepatic conjugation to inactive metabolites eliminated in urine
- <5% eliminated unchanged in urine
- 5-15% oxidated by CYP2E1 to NAPQ1
**toxic acute dose = > 7.5 grams in adults or > 150 mg/kg in children

137
Q

Manifestations of APAP toxicity in DILI

A

-nausea, vomiting, malaise, apllor, diaphoresis
-liver injury is trypically not seen until 24-36 hours post ingestion w/ increases in AST
-maximal hepatotoxicity generally occurs between 72-96 hrs post ingestion

138
Q

Management of APAP toxicity

A

-can consider activated charcoal in pts who present within 1-2 hrs post ingestion
**NAC is CRUTIAL!
-supportive care: IV fluids, management of N/V, correction of hypoglycemia + vitamin K/FFP

139
Q

NAC mechanism of action (In DILI)

A

-serves as a glutathione substitute detoxifying NAPQ1
-serves as a precursor to glutathione resulting in increased glutathione production
-may also allow for more nontoxic metabolism thought increased sulfating

140
Q

What if the APAP level is outside the 4-24 hr window? prior to 4 hrs

A

-consider activated charcoal
-wait and recheck at hour 4 to assess whether ot not NAC is needed

141
Q

What if the APAP level is outside the 4-24 hr window? after 24 hrs: if AST is elevated regardless of APAP level

A

begin NAC

142
Q

What if the APAP level is outside the 4-24 hr window? after 24 hrs or unknown late ingestion with detectable APAP levels

A

begin NAC

143
Q

PO NAC

A

-dosing: 72 hr protocol
Side effects: bad taste, N/V in 50% of pts
-need pretreatment with anti-emetics, may be difficult to administer to pts with AMS
-NAC delivery may be delayed up to an hour until it can be absorbed in duodenum
-PO therapy should be changed to IV if liver failure develops

144
Q

IV NAC

A

dosing: 20 hr protocol (potentially shorter hospital stay)
Side effects: anaphylactoid reactions (rash, flushing, bronchospasm)
-usually minor but can be severe
-pts can almost always restart without recurrence even if severe rxn occurs
**preferred in pts with liver failure, pregnancy + inability to tolerate PO

145
Q

NAC treatment duration in DILI

A

continue if:
-ongoing liver failure present
-detectable APAP or ongoing hepatic damage

146
Q

~some DILI conclusions~

A

-aside from APAP, antimicrobials = CNS agents are most commonly associated with DILI
-DILI pts can present with hepatocellular damage, cholestatic injury or a mixed hepatocellular/cholestatic etiology
-increases in ALT and AST are associated with hepatocellular damage + increases in ALP are associated with cholestatic injury
-APAP intoxicated pts need to be evaluated with the Rumack-Matthew nomogram + started on NAC therapy if they fall above the treatment line, ideally within 8 hrs of ingestion

147
Q

CJ is a 38-year-old male who presents to the ER with crushing chest pain. He has ST elevations on ECG and his troponin is elevated to 12, and he is diagnosed with a STEMI. His blood pressure is elevated at 210/120. A urine tox screen is run and is positive for THC, cocaine, and opioids. Appropriate acute management of CJ’s STEMI includes which of the following? (Select all that apply)
A: Aspirin 81 mg by mouth
B: Ticagrelor 180 mg by mouth
C: Prasugrel 10 mg by mouth
D: Lorazepam 2 mg IV
E: IV Heparin bolus and infusion

A

B: Ticagrelor 180 mg by mouth
D: Lorazepam 2 mg IV
E: IV Heparin bolus and infusion

148
Q

CJ is a 38-year-old male who presents to the ER with crushing chest pain. He has ST elevations on ECG and his troponin is elevated to 12, and he is diagnosed with a STEMI. His blood pressure is elevated at 210/120. A urine tox screen is run and is positive for THC, cocaine, and opioids. 30 mins later, CJ has received a total of 3 doses of lorazepam 4 mg IV and is still complaining of significant chest pain, and his blood pressure is 190/104. What is the most appropriate medication to treat his chest pain and blood pressure?

A: IV nitroglycerin infusion
B: IV metoprolol 5 mg
C: Aspirin 325 mg by mouth D: Prasugrel 60 mg by mouth E: IV hydralazine 10 mg

A

A: IV nitroglycerin infusion

149
Q

the main mechanism of bleomycin induced pulmonary toxicity is:

A

-enzyme deficiency which in activates the medication

150
Q

what strategy is most effective to prevent aminoglycosides nephrotoxicity?

A

therapeutic drug monitoring and pharmacokinetic dose individualization

Pulm Therapeutics (4 decks)

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