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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
how do you pretreat for sulfite induced bronchospasm?
Cromolyn, anticholinergics, cyanocobalamin
26
what happens when edta (stabilizing agent) is inhaled? and where is it found?
``` Calcium chelation property--> Benzalkonium chloride Bacteriostatic agent Found in some albuterol nebulization multi-dose vials Mast cell degranulation ```
27
how do you manage edta induced bronchospasm
change therapy
28
ACE inhibitors cause
cough
29
ACE inhibitor cough May begin within____ after initiating therapy
days to 12 months
30
Patients with asthma or COPD ____to be at increased risk for ACE inhibitor cough
do not appear
31
what are symptoms of ACE inhibitor cough
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
what is the mechanism of ACE inhibitor cough
-Not fully known -Usually attributed to accumulation of bradykinin and substance P -Bradykinin Stimulate cough reflex -Substance P Cause bronchoconstriction
33
how do you manage ACE inhibitor cough
Cough may resolve within a few weeks Usually stop medication Cough resolves within a few days to a month after discontinuation
34
Fentanyl- Cough is related to what ROA?
IV
35
what is Fentanyl- Cough associated with? what is not predictive of it?
Associated with young age and absence of smoking COPD/asthma
36
Narcotic Induced Non-Cardiogenic Pulmonary Edema is most commonly associated with?
heroin IV
37
what other drugs might Narcotic Induced Non-Cardiogenic Pulmonary Edema be assoc with?
Can also be seen with morphine, methadone, meperidine and propoxyphene
38
what type of rxn is Narcotic Induced Non-Cardiogenic Pulmonary Edema
idiosyncratic
39
symptoms of Narcotic Induced Non-Cardiogenic Pulmonary Edema? how long does it take to appear?
- 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
what is the mechanism for Narcotic Induced Non-Cardiogenic Pulmonary Edema
Unknown
41
when does Narcotic Induced Non-Cardiogenic Pulmonary Edema clinically improve?
24-48 hrs but Pulmonary function abnormality may last up to 12 weeks
42
how do you treat Narcotic Induced Non-Cardiogenic Pulmonary Edema
Naloxone, oxygen, ventilatory support
43
how does pulmonary edema present?7
``` Persistent cough Tachypnea Dyspnea Tachycardia Rales on auscultation Hypoxemia Decreased lung compliance ```
44
what meds have been reported to cause pulmonary edema and how do you manage?
``` Reported with: Hydrochlorothiazide Contrast media IV bleomycin, cyclophosphamide and vinblastine Terbutaline (used as tocolytic) Salicylate overdose ``` DC and support
45
what is Pulmonary Eosinophilia
Pulmonary infiltrates with eosinophilia
46
what is Pulmonary Eosinophilia associated with?
Associated with (most frequently): Nitrofurantoin Para-aminosalicylic acid
47
how does Pulmonary Eosinophilia present?
Fever, nonproductive cough, dyspnea, cyanosis, bilateral pulmonary infiltrates and eosinophilia in blood
48
when does Pulmonary Eosinophilia present with nitrofuran? and when do you recover?
Occurs within 1 month of therapy | Complete recovery within 15 days of DC of medication
49
what is Chronic Pulmonary Fibrosis
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
what does Chronic Pulmonary Fibrosis lead to
Leads to restrictive airway disease
51
what drugs cause Chronic Pulmonary Fibrosis? 5
``` -Chemotherapeutic agents Bleomycin Busulfan Carmustine Methotrexate ``` Amiodarone
52
PE of acute phase of Pulmonary Fibrosis? 6
``` within hrs - days -productive cough Acute dyspnea Tachypnea Lung crackles PFTs Initially normally, reduced carbon dioxide diffusing capacity Arterial blood gases Hypoxemia ```
53
PE of chronic phase of Pulmonary Fibrosis? 6
``` -Slow progression Dyspnea on exertion Fatigue Non-productive cough Lung crackles Clubbing -PFTs Restrictive disease, decreased vital capacity Reduced carbon monoxide diffusing capacity ```
54
Acute symptoms of pulmonary fibrosis have been seen after 1st dose of ______ Patients have died up to 15 years after receiving therapy
bleomycin
55
how do you manage pulmonary fibrosis
d/c med and prednisone
56
what are the risk factors associated with Amiodarone Pulmonary Toxicity
Men Increases with age Pre-existing lung disease
57
how much of a dose causes Amiodarone Pulmonary Toxicity and how long after tx initiation does it start?
Usually >400 mg/day; seen with 200 mg/day for 6-12 months | Occurs 4 weeks to 6 years after initiating therapy
58
what is the clinical presentation of Amiodarone Pulmonary Toxicity
- Progressive dyspnea, malaise, nonproductive cough | - Rapidly progressive acute respiratory distress syndrome
59
what is the mechanism of Amiodarone Pulmonary Toxicity
- 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
what labs must be run if you are on amiodarone?
- Monitor PFTs and CXR at baseline - CXR every year - PFTs if symptomatic
61
how do you manage amiodarone pulmonary tox? when do you improve?
- 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
what drugs may cause pulmonary htn? which 2 were pulled from the market?
pulled:(for valvular damage) Fenfluramine and dexfenfluarmine-Part of “fen-phen” Phentermine
63
what is the onset of pulm htn with phentermine?
23days-27 yrs
64
what are symptoms of drug induced pulm htn
Generally non-specific Exertional dyspnea: most common Chest pain Syncope
65
how do you manage pulm htn
DC medication | Improvement within 1-3 months
66
how will O2 toxicity present?
Cough, chest pain, dyspnea
67
who's O2 toxicity gets masked?
Masked in ventilator dependent patients | Lungs become progressively stiffer
68
what happens in O2 tox? | what happens normally in cell resp?
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
what determines lung damage in O2 tox?
-Fraction of inspired oxygen 50-100% -Duration of exposure Inversely proportional to fraction of inspired oxygen
70
how does acute lung damage occur in O2 tox?
edema with alveolar hemorrhage
71
how does subacute or chronic damage occur in O2 tox
collagen and elastin deposition in alveolar walls
72
what does O2 tox do physically to the lungs?
Leads to thickening of gas exchange area and fibrosis
73
in O2 tox when will you see improvement
May see improvement months to years following exposure

Pharm II (8 decks)

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