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Pharmacology II > Drug-Induced Pulmonary Disease > Flashcards

Drug-Induced Pulmonary Disease Flashcards

1
Q

How many medications can cause lung injury?

A

350 and they all manifest in a variety of ways

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2
Q

What is the most common drug induced respiratory problem?

A

Drug-induced bronchospams

Usually seen in patients with pre-existing bronchial hyper-reactivity

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3
Q

What are the mechanisms of bronchospams?

A 
Anaphylaxis (IgE-mediated)
Penicillins
Sulfonamides
Serum
Cephalosporins
Can occur with any drug

Cyclooxygenase inhibition
Aspirin/NSAIDs

Pharmacologic effects
β -adrenergic blockers

Direct airway irritation
Smoke
N-acetylcysteine

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4
Q

What is the aspirin triad (Samter’s syndrome)?

A

Asthma
Nasal Polyps
And aspirin intolerance

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5
Q

Aspirin/NSAID bronchospasm- presentation

A

Bronchospasm, rhinorrhea, conjunctivitis, flushing
Urticaria, periorbital edema, abdominal pain
Can present separately or blended

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6
Q

Aspirin/NSAID bronchospasm- sx resolution

A

Diminish within 24-48 hours

urticaria may continue 1-2 wks.

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7
Q

Aspirin/NSAID bronchospasm- diagnosis

A 
No in vitro diagnostic test to confirm or establish aspirin sensitivity
Provocation challenge
Respiratory reactions
30 -150mg (average 60 mg)
Completed in hospital
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8
Q

Aspirin/NSAID bronchospasm- management

A

Avoid aspirin and nonselective NSAIDs
Cross sensitivity
Ibuprofen (98%)
Naproxen (100%)

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9
Q

Aspirin/NSAID bronchospasm- desensitization and leukotriene modifiers

A

Elimination of reactions by slowly increasing doses of oral aspirin

Leukotriene modifiers
Dose response curve shifted

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10
Q

Aspirin/NSAID bronchospasm- therapy options

A 
Therapy options
COX-2 selective NSAIDs (Celecoxib)
Generally can be used safely in patients with ASA induced asthma
Acetaminophen
5% of ASA sensitive patients react
< 1000 mg
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11
Q

Aspirin/NSAID bronchospasm- cross-sensitivity

A

Up to 80% of ASA-sensitive patient had AE to yellow azo dye tartrazine (FD&C Yellow No.5)
Colors food, drinks, drugs, cosmetics
FDA requires labeling

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12
Q

The use of ________ might increase the risk of asthma and allergic disease when used early in life?

A

Acetaminophen

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13
Q

Beta blocker bronchospasm

A

Effects seen with oral, IV or ophthalmic administration
Rarely seen in patients without pulmonary disease
Reaction can be fatal
Primarily with non-selective β-blockers
Patients taking β -blockers without incident for long periods of time may experience fatal asthma attacks

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14
Q

Beta blocker bronchospasm- symptoms

A 
Symptoms
Increased pulmonary symptoms
Decreased pulmonary function tests
Decrease in FEV1 or peak expiratory flow
Death
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15
Q

Beta blocker bronchospasm- Mechanism

A

Direct inhibition of β2-receptors may result in bronchoconstriction

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16
Q

Beta blocker bronchospasm- management

A

Inhaled bronchodilator for bronchospasm
Avoidance
If necessary, use selective β-blockers
Use lowest dose possible

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17
Q

Will treatmeant with beta blockers in patients with COPD reduce the risk of exacerbations and improve survival?`

A

It might

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18
Q

Sulfite induced bronchospasm

A 
Potassium metabisulfite
Preservative in food and wine
Injectable epinephrine, isoproterenol
Rare in general population
1-5% in patients with asthma
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19
Q

Sulfite induced bronchospasm- patient presentation

A

Severe wheezing, chest tightness and dyspnea after ingestion

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20
Q

Sulfite induced bronchospasm- Diagnosis

A

History

Re-challenge- in a controlled setting

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21
Q

Sulfite induced bronchospasm- mechanism

A

Sulfite converted to sulfur dioxide in acidic or warm environment
Sulfur dioxide causes direct stimulation of parasympathetic receptors
IgE-mediated (anaphylactic reactions)
Reduced concentration of sulfite oxidase enzyme reported in sulfite-sensitive asthma patients
Catalyzes oxidation of sulfites to sulfates

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22
Q

Sulfite induced bronchospasm- management

A

Avoidance
Read labels
Pharmacologic agents
» Manufacturers of drugs for the treatment of asthma have discontinued use of sulfites
Food products
» Labeling required on packaged foods that contain sulfites at 10 ppm or more

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23
Q

Sulfite induced bronchospasm- pretreatment

A

Cromolyn, anticholinergics, cyanocobalamin

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24
Q

Inhaled agents bronchospasm

A

Nonspecific bronchial irritant effect
Usually NOT caused by medication
Propellant, delivery, pH, osmolality, temperature, preservative
Albuterol, cromolyn, inhaled corticosteroids, pentamidine, N-acetyl cysteine

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25
Q

Is the bronchospasm from inhaled medications caused by the medication itself?

A

No its caused by the other chemicals that are in the drug

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26
Q

Inhaled agents- bronchospasm- Ethylenediamine tetraacetic acid (EDTA)

A 
Stabilizing agent
Mechanism
Calcium chelation property
Benzalkonium chloride
Bacteriostatic agent
Found in some albuterol nebulization multi-dose vials

Mechanism
Mast cell degranulation

Management
Change therapy

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27
Q

Ace Inhibitors-cough- risk factors

A

Female
Asian descent
Elderly
Heart failure

28
Q

Do patients with asthma or COPD appear to be at an increased risk for development of a cough with ace inhibitor use?

A

No

29
Q

Ace Inhibitors-cough- symptoms

A

Cough
Tickle to debilitating cough with insomnia and vomiting
Dry, nonproductive, hacking cough
Patients have normal spirometry and chest xray

30
Q

Ace Inhibitors-cough- mechanism

A 
Not fully known
Usually attributed to accumulation of bradykinin and substance P
Bradykinin
Stimulate cough reflex
Substance P
Cause bronchoconstriction
31
Q

Ace Inhibitors-cough- management

A

Cough may resolve within a few weeks
Usually stop medication
Cough resolves within a few days to a month after discontinuation
Usually unresponsive to cough suppressants or bronchodilators

32
Q

Fentanyl cough

A

IV formulation
Unclear mechanism
Associated with young age and absence of smoking
History of asthma/COPD not predictive

33
Q

What is narcotic induced non-cardiogenic pulmonary edema most commonly assoiciated with?

A

IV heroin use

Also can be seen with morphine, methadone, meperidine, and propoxyphene

34
Q

Narcotic induced non-cardiogenic pulmonary edema- mechanism

A

Idiosyncratic reaction
Often seen when Moderate and high doses are used
Mechanism is unknown

35
Q

Narcotic induced non-cardiogenic pulmonary edema- sx

A

May be comatose with depressed respirations, dyspnea and tachypnea
Varies from cough to severe cyanosis and hypoxia
Decreased pulmonary function tests
Appear within minutes of IV administration up to 2 hours

36
Q

Narcotic induced non-cardiogenic pulmonary edema- treatment

A 
Clinical improvement within 24-48 hours
Pulmonary function abnormality may last up to 12 weeks
Treatment
Naloxone, oxygen, ventilatory support
Mortality less than 1%
37
Q

What is the presentation of pulmonary edema?

A 
Persistent cough
Tachypnea
Dyspnea
Tachycardia
Rales on auscultation
Hypoxemia
Decreased lung compliance
38
Q

What is pulmonary edema reported with?

A 
Hydrochlorothiazide
Contrast media
IV bleomycin, cyclophosphamide and vinblastine (oncology agents)
Terbutaline (used as tocolytic)
Salicylate overdose
39
Q

What is the management for pulmonary edema?

A

DC medication, supportive care

40
Q

What is pulmonary infiltrates with eosinophilia most frequently associated with?

A

Nitrofurantoin

Para-aminosalicylic acid (not a drug that you will rx to pts, anti-infective topical)

41
Q

Pulmonary esoinophilia- presentation

A

Fever, nonproductive cough, dyspnea, cyanosis, bilateral pulmonary infiltrates and eosinophilia in blood

42
Q

Pulmonary eosinophilia- nitrofurantoin

A

Occurs within 1 month of therapy

Complete recovery within 15 days of DC of medication

43
Q

What is excessive amount of connect tissue in the the intersitial spaces of the lung?
Hint- normal airspaces and blood vessels are replaced by fibrotic tissue; lungs become small and stiff and is secondary to chronic inflammatory dz?

A

Chronic pulmonary fibrosis

44
Q

What can chronic pulmonary fibrosis lead to?

A

Restrictive airway disease

Can be fatal if process is not stopped

45
Q

Pulmonary fibrosis- causes

A

Idiopathic pulmonary fibrosis is rare

Drug induced pulmonary fibrosis
~ 50 causative agents

Prevalence increases with increasing cumulative dose

46
Q

What are the chemotherapeutic agents that cause pulmonary fibrosis?

A 
Bleomycin
Busulfan
Carmustine
Methotrexate
Amiodarone- not chemo but causes pulmonary fibrosis
47
Q

Pulmonary fibrosis-acute phase

A 
Non-productive cough
Acute dyspnea
Tachypnea
Lung crackles
PFTs- Initially normally, reduced carbon dioxide diffusing capacity
Arterial blood gases- Hypoxemia
48
Q

Pulmonary fibrosis- chronic phase

A 
Slow progression
Dyspnea on exertion
Fatigue
Non-productive cough
Lung crackles
Clubbing

PFTs
Restrictive disease, decreased vital capacity
Reduced carbon monoxide diffusing capacity

49
Q

Pulmonary fibrosis- time of onset

A

Acute sx have been seen after 1st dose of bleomycin

Patients have died up to 15 years after receiving therapy.

50
Q

Pulmonary fibrosis- diagnosis

A

Known exposure to causative drug

No known symptoms, physical findings, laboratory tests or histopathologic findings specific to pulmonary fibrosis

51
Q

Pulmonary fibrosis- management

A

Discontinuation of medication

+/- prednisone

52
Q

Amiodarone pulmonary toxicity- risk factors

A

Men
Increases with age
Pre-existing lung disease
Dose/duration- Usually >400 mg/day; seen with 200 mg/day for 6-12 months
Occurs 4 weeks to 6 years after initiating therapy

53
Q

Amiodarone pulmonary toxicity- clinical course

A

Variable- some patients don’t do that bad and some do really bad
Progressive dyspnea, malaise, nonproductive cough
Rapidly progressive acute respiratory distress syndrome

54
Q

Amiodarone pulmonary toxicity- proposed mechanism

A

Accumulation of amiodarone and metabolite in lung tissue
Interfere with normal processing of phospholipids
Breakdown of phospholipid-laden macrophages results in pulmonary inflammation and fibrosis

55
Q

Amiodarone pulmonary toxicity- monitoring

A

Monitor PFTs and CXR at baseline
CXR every year
PFTs if symptomatic

56
Q

Amiodarone pulmonary toxicity- management

A

Majority of patients improve with DC of medication
Clinical improvement 1-2 months
PFTs and CXR may take up to 18 months
+/- corticosteroids

57
Q

What are the medications that cause pulmonary HTN?

A 
Anorexic agents- used for weightloss
Fenfluramine and dexfenfluarmine (not on the market)
Part of “fen-phen”
Phentermine
20% of diagnosed cases
Onset between 23 days and 27 years
58
Q

Pulmonary HTN- symptoms

A

Generally non-specific
Exertional dyspnea: most common
Chest pain
Syncope

59
Q

Pulmonary HTN- mechanism

A

unknown

60
Q

Pulmonary HTN- Management

A

DC medication
Improvement within 1-3 months

1997: FDA requested withdrawal of fenfluramine and dexfenfluamine (valvular damage)

Phentermine
Case reports of pulmonary hypertension
Association not supported

61
Q

Oxygen toxicity- presentation

A

Cough, chest pain, dyspnea
Masked in ventilator dependent patients
Lungs become progressively stiffer
Ability to oxygenate is compromised

62
Q

Oxygen toxicity- normal cellular respiration

A

Oxidants are counterbalanced by antioxidant defense system (prevents tissue destruction)

63
Q

Oxygen toxicity- excess oxygen (hyperoxia)

A

Produces highly reactive, partially reduced oxygen metabolites
Superoxide anion, hydrogen peroxide, hydroxyl radical, singlet oxygen, hypochlorous acid
Overwhelm antioxidant system

64
Q

Oxygen toxicity- lung damage determinants

A

Fraction of inspired oxygen–50-100%

Duration of exposure- Inversely proportional to fraction of inspired oxygen

65
Q

Oxygen toxicity- lung damage

A

Acute phase: edema with alveolar hemorrhage

Subacute or chronic phase: collagen and elastin deposition in alveolar walls

66
Q

What does the lung damage in oxygen toxicity lead to?

A

Thickening of gas exchange area and fibrosis

67
Q

Oxygen toxicity-course

A

+/- improvement in lung function

May see improvement months to years following exposure

Pharmacology II (23 decks)

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