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Pharm II > Drug-induced Pulmonary disease > Flashcards

Drug-induced Pulmonary disease Flashcards

1
Q

what is the most common drug-induced respiratory problem?

A

Drug-Induced Bronchospasm

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2
Q

Drug-induced bronchospasm is seen in pts with

A

pre-existing bronchial hyper-reactivity

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3
Q

what drugs may cause anaphylaxis?

A

Any; Penicillins
Sulfonamides
Serum
Cephalosporins

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4
Q

what directly irritates the airway?

A

Smoke

N-acetylcysteine

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5
Q

what is the Aspirin triad / Samter’s Syndrome

A

Asthma, nasal polyps and aspirin intolerance

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6
Q

how does aspirin/NSAID bronchospasm present?

A

Can present separately or blended

Bronchospasm, rhinorrhea, conjunctivitis, flushing
Urticaria, periorbital edema, abdominal pain

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7
Q 
Based off the proposed mechanism of aspirin intolerance in patients with asthma, which of the following agents could potentially be used for treatment?
Albuterol
Theophylline
Salmeterol
Zileuton
Omalizumab
A

Zileuton

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8
Q

How do you dx aspirin/NSAID Bronchospasm

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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9
Q

how can you manage aspirin/NSAID Bronchospasm? 3

A 
-Avoid aspirin and nonselective NSAIDs
Cross sensitivity
Ibuprofen (98%)
Naproxen (100%)
-Desensitization
Elimination of reactions by slowly increasing doses of oral aspirin
-Leukotriene modifiers
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10
Q

what are treatment options for aspirin/NSAID Bronchospasm

A

-COX-2 selective NSAIDs (Celecoxib)
Generally can be used safely in patients with ASA induced asthma
-Acetaminophen
5% of ASA sensitive patients react

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11
Q

Up to 80% of ASA-sensitive patient had AE to

A

yellow azo dye tartrazine (FD&C Yellow No.5)

Colors food, drinks, drugs, cosmetics

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12
Q

Use of what early in life might increase risk of asthma and allergic disease

A

acetaminophen

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13
Q

Beta Blockers Bronchospasm effects are seen with what ROA

A

oral, IV or ophthalmic

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14
Q

Beta Blockers Bronchospasm effects are rarely seen in pts w/o?

A

pulmonary disease

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15
Q

Beta Blockers Bronchospasm in what type of b blockers

A

non-specific

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16
Q

Patients taking β -blockers without incident for long periods of time may experience

A

fatal asthma attacks

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17
Q

what are symptoms of Beta Blockers Bronchospasm

A

Increased pulmonary symptoms
Decreased pulmonary function tests

Decrease in FEV1 or peak expiratory flow
Death

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18
Q

what is the mechanism of Decrease in FEV1 or peak expiratory flow
Death

A

Direct inhibition of β2-receptors may result in bronchoconstriction

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19
Q 
Based on the proposed mechanism of beta blocker induced bronchospasm, which of the following agents could potentially be used for treatment of bronchospasm?
Albuterol
Salmeterol
Ipratropium
Pirbuterol
Metaproterenol
A

Ipratropium - need an anticholinergic because you dont want to have a battle at the receptor (never give ag and antag of the same receptor

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20
Q

how do you manage Beta Blockers Bronchospasm

A

Inhaled bronchodilator for bronchospasm

Avoidance
If necessary, use selective β-blockers
Use lowest dose possible

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21
Q

Treatment with beta blockers in patients with ___ may reduce the risk of exacerbations and improve survival

A

COPD

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22
Q

how does Sulfite Induced Bronchospasm present?

A

Severe wheezing, chest tightness and dyspnea after ingestion of potassium metabisulfite

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23
Q

what is the mechanism of Sulfite Induced Bronchospasm

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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24
Q

how do you manage sulfite induced bronchospasm?

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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25
Q

how do you pretreat for sulfite induced bronchospasm?

A

Cromolyn, anticholinergics, cyanocobalamin

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26
Q

what happens when edta (stabilizing agent) is inhaled? and where is it found?

A 
Calcium chelation property-->
Benzalkonium chloride
Bacteriostatic agent
Found in some albuterol nebulization multi-dose vials
Mast cell degranulation
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27
Q

how do you manage edta induced bronchospasm

A

change therapy

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28
Q

ACE inhibitors cause

A

cough

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29
Q

ACE inhibitor cough May begin within____ after initiating therapy

A

days to 12 months

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30
Q

Patients with asthma or COPD ____to be at increased risk for ACE inhibitor cough

A

do not appear

31
Q

what are symptoms of ACE inhibitor cough

A

Tickle to debilitating cough with insomnia and vomiting
Dry, nonproductive, hacking cough –>Usually unresponsive to cough suppressants or bronchodilators
Patients have normal spirometry and chest xray

32
Q

what is the mechanism of ACE inhibitor cough

A

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

33
Q

how do you manage ACE inhibitor cough

A

Cough may resolve within a few weeks
Usually stop medication

Cough resolves within a few days to a month after discontinuation

34
Q

Fentanyl- Cough is related to what ROA?

A

IV

35
Q

what is Fentanyl- Cough associated with? what is not predictive of it?

A

Associated with young age and absence of smoking

COPD/asthma

36
Q

Narcotic Induced Non-Cardiogenic Pulmonary Edema is most commonly associated with?

A

heroin IV

37
Q

what other drugs might Narcotic Induced Non-Cardiogenic Pulmonary Edema be assoc with?

A

Can also be seen with morphine, methadone, meperidine and propoxyphene

38
Q

what type of rxn is Narcotic Induced Non-Cardiogenic Pulmonary Edema

A

idiosyncratic

39
Q

symptoms of Narcotic Induced Non-Cardiogenic Pulmonary Edema? how long does it take to appear?

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
40
Q

what is the mechanism for Narcotic Induced Non-Cardiogenic Pulmonary Edema

A

Unknown

41
Q

when does Narcotic Induced Non-Cardiogenic Pulmonary Edema clinically improve?

A

24-48 hrs but Pulmonary function abnormality may last up to 12 weeks

42
Q

how do you treat Narcotic Induced Non-Cardiogenic Pulmonary Edema

A

Naloxone, oxygen, ventilatory support

43
Q

how does pulmonary edema present?7

A 
Persistent cough
Tachypnea
Dyspnea
Tachycardia
Rales on auscultation
Hypoxemia
Decreased lung compliance
44
Q

what meds have been reported to cause pulmonary edema and how do you manage?

A 
Reported with:
Hydrochlorothiazide
Contrast media
IV bleomycin, cyclophosphamide and vinblastine
Terbutaline (used as tocolytic)
Salicylate overdose

DC and support

45
Q

what is Pulmonary Eosinophilia

A

Pulmonary infiltrates with eosinophilia

46
Q

what is Pulmonary Eosinophilia associated with?

A

Associated with (most frequently):
Nitrofurantoin
Para-aminosalicylic acid

47
Q

how does Pulmonary Eosinophilia present?

A

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

48
Q

when does Pulmonary Eosinophilia present with nitrofuran? and when do you recover?

A

Occurs within 1 month of therapy

Complete recovery within 15 days of DC of medication

49
Q

what is Chronic Pulmonary Fibrosis

A

Excessive amount of connective tissue in the interstitial spaces of the lung
Normal airspaces and blood vessels replaced by fibrotic tissue; lungs become small and stiff
Secondary to chronic inflammatory process

50
Q

what does Chronic Pulmonary Fibrosis lead to

A

Leads to restrictive airway disease

51
Q

what drugs cause Chronic Pulmonary Fibrosis? 5

A 
-Chemotherapeutic agents
Bleomycin
Busulfan
Carmustine
Methotrexate

Amiodarone

52
Q

PE of acute phase of Pulmonary Fibrosis? 6

A 
within hrs - days
-productive cough
Acute dyspnea
Tachypnea
Lung crackles
PFTs
Initially normally, reduced carbon dioxide diffusing capacity
Arterial blood gases
Hypoxemia
53
Q

PE of chronic phase of Pulmonary Fibrosis? 6

A 
-Slow progression
Dyspnea on exertion
Fatigue
Non-productive cough
Lung crackles
Clubbing
-PFTs
Restrictive disease, decreased vital capacity
Reduced carbon monoxide diffusing capacity
54
Q

Acute symptoms of pulmonary fibrosis have been seen after 1st dose of ______
Patients have died up to 15 years after receiving therapy

A

bleomycin

55
Q

how do you manage pulmonary fibrosis

A

d/c med and prednisone

56
Q

what are the risk factors associated with Amiodarone Pulmonary Toxicity

A

Men
Increases with age
Pre-existing lung disease

57
Q

how much of a dose causes Amiodarone Pulmonary Toxicity and how long after tx initiation does it start?

A

Usually >400 mg/day; seen with 200 mg/day for 6-12 months

Occurs 4 weeks to 6 years after initiating therapy

58
Q

what is the clinical presentation of Amiodarone Pulmonary Toxicity

A
  • Progressive dyspnea, malaise, nonproductive cough

- Rapidly progressive acute respiratory distress syndrome

59
Q

what is the mechanism of Amiodarone Pulmonary Toxicity

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
60
Q

what labs must be run if you are on amiodarone?

A
  • Monitor PFTs and CXR at baseline
  • CXR every year
  • PFTs if symptomatic
61
Q

how do you manage amiodarone pulmonary tox? when do you improve?

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

+/- corticosteroids
39 cases
9 patients died
30 got better with DC of medication

62
Q

what drugs may cause pulmonary htn? which 2 were pulled from the market?

A

pulled:(for valvular damage)
Fenfluramine and dexfenfluarmine-Part of “fen-phen”

Phentermine

63
Q

what is the onset of pulm htn with phentermine?

A

23days-27 yrs

64
Q

what are symptoms of drug induced pulm htn

A

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

65
Q

how do you manage pulm htn

A

DC medication

Improvement within 1-3 months

66
Q

how will O2 toxicity present?

A

Cough, chest pain, dyspnea

67
Q

who’s O2 toxicity gets masked?

A

Masked in ventilator dependent patients

Lungs become progressively stiffer

68
Q

what happens in O2 tox?

what happens normally in cell resp?

A

Ability to oxygenate is compromised

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

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

69
Q

what determines lung damage in O2 tox?

A

-Fraction of inspired oxygen
50-100%
-Duration of exposure
Inversely proportional to fraction of inspired oxygen

70
Q

how does acute lung damage occur in O2 tox?

A

edema with alveolar hemorrhage

71
Q

how does subacute or chronic damage occur in O2 tox

A

collagen and elastin deposition in alveolar walls

72
Q

what does O2 tox do physically to the lungs?

A

Leads to thickening of gas exchange area and fibrosis

73
Q

in O2 tox when will you see improvement

A

May see improvement months to years following exposure

Pharm II (8 decks)

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