-
vitamin E's chemical name. is it antioxidant or oxidant?
-
oxidants are ___ _____, partially reduced oxygen metabolites.
highly reactive
-
mechanism of drug induced pulmonary disorder?
- increased production of oxidant
- inhibition of antioxidant system
- so oxidant/antioxidant system is not balanced
-
histology: is drug induced damage similar or different from idiopathic damage?
similar
-
what is the tissue separating respiratory blood flow from alveolar space?
interstitium
-
via what mechanism do O2 and CO2 pass btwn capillary?
diffusion
-
acute pulmonary edema symptoms. two categories? (II)
- dyspnea, chest discomfort, tachypnea, hypoxemia, alveolar flooding
- lead to acute respiratory distress syndrome (ARDS)
- cardiogenic vs. non-cardiogenic
-
cardiogenic acute pulmonary edema (II) symptoms. causal agents?
- increased pressure, vague fatigue, mild pedal edema, exertional dyspnea
- (left heart cannot pump well so fluid backed up in lungs)
- caused by fluid overload and contrast media
-
non-cardiogenic acute pulmonary edema (II). describe onset and pathophys. what agents cause?
- immediate to days onset --> rapid alveolar flooding
- caused by chemotherapy agents, naloxone, opiates
- (alveolar damage, not heart)
-
pulmonary hypertension (III).
symptoms. pathophys. causal agents.
- asymptomatic early then dyspnea, fatigue, chest pain. could be life threatening and chronic
- burden on right ventricle . remodel and large size to compensate the pressure from lungs
- stimulant appetite suppressant, maternal SSRI during pregnancy (high chance of pHTN with newborn)
-
what is the most common drug induced lung disease?
D) intersitital lung disease
-
symptoms of interstitial lung disease (IV).
- progressive dyspnea or non-productive cough
- hemoptysis, wheeze, chest pain
- interstitial opacities on CXR.
-
progressive dyspnea or non-productive cough
hemoptysis, wheeze, chest pain
interstitial opacities on CXR.
A) interstitial lung disease
-
dyspnea, chest discomfort, tachypnea, hypoxemia, alveolar flooding.
D) acute pulmonary edema
-
asymptomatic, dyspnea, chest pain, fatigue.
D) pulmonary htn
-
three types of interstitial lung disease. (IV)
- interstitial infiltrate/pneumonia
- pulmonary fibrosis
- bronchiolitis oliterans organzing pneumonia
-
pulmonary fibrosis.
C) intersitital lung disease
-
bronchiolitis oliterans organizing pneumonia.
A) interstitial lung disease
-
what changes on CXR does interstitial infiltrate/pna (interstitial lung disease IV) have?
fluid or cells btwn alveolus and capillary
-
interstitial infiltrate/pna (interstitial lung disease IV) causal agents.
- most common pulmonary tox of methotrexate
- nitrofurantoin, epidermal growth factor receptor antagonist
-
pathophys of pulmonary fibrosis (IV).
- scarring of lung parenchyma and accumulation of excessive connective tissue
- often secondary to a chronic inflamm process.
-
causal agent of pulmonary fibrosis (IV).
chemotherapy agent, amiodarone, ergot derivative, nitrofurantoin, illicit IV drug ("talc lung")
-
pathophys of bronchiolitis obliterans organizing pnemonia (IV) (BOOP)
inflamm of lung characterized by alveolar fibrosis
-
causal agents of BOOP (IV).
- antimicrobials
- cyrotoxic drugs
- "statins"
- amiodraone
- etc.
-
pathophys of pulmonary eosinophilia (V). how is this confirmed?
- eosinophils in alveolar space, interstitium or both.
- confirmed by excessive eosinophils in biopsy or bronchoalveolar lavage
-
how does pulmonary eosinophilia present in CXR? (V)
typically ground glass opacities in peripheral and upper lobe distribution
-
causal agents of pulmonary eosinophilia (V)
- antimicrobial, NSAID, amiodarone, nitrofurantoin
- (these were all part of hypersensitivity chart)
-
pathophys of pleural inflamm and symptoms? (VI)
- asymptomatic --> acute pleuritis --> pleural thickening
- pleural effusion - chest pain, dyspnea, cough
-
pleural effusion.
D) pleural inflammation
-
causal agents of pleural inflammation (VI).
- nitrofurantoin
- ergot alkaloids
- amiodarone
-
pathophys of diffuse alveolar hemorrhage (VII).
bleed from pulmonary capillaries --> RBC accumulate in alveolar space.
-
symptoms of diffuse alveolar hemorrhage (VII)?
hemoptysis, cough, progressive dyspnea --> intraalveolar clotting
-
intra-alveolar clotting
B) diffuse alveolar hemorrhage
-
causal agents of diffuse alveolar hemorrhage (VII)?
- antiplatelet/anticoagulant
- chemotherapeutic agents
-
pathophys of diffuse alveolar damage (VIII).
alveolar epithelial cells sloughed --> edematous interstitium with chronic inflamm of alveolar walls
-
s&s of diffuse alveolar damage (viii)
dyspnea, pulm infiltrate, ARDS
-
causal agents in diffuse alveolar damage (viii)
- chemotherapy
- nitrofurantoin
- narcotics
- carbamazepine
-
when does drug hypersensitivity syndrome (ix) occur?
within 8 wks of treatment
-
s&s of drug hypersensitivity syndrome (ix)
fever, rash, organ involvement (derm, hematol, lymph, pulm)
-
how does drug hypersensitivity syndrome (ix) present pulmonary disorder?
- lymphoid interstitial pneumo
- interstitial lung dz
- eosinophil pneumo
- pleural effusion
-
causal agents of drug hypersensitivity syndrome (ix)
- aromatic anticonvulsant (esp carbamazepine, phenytoin, phenobarb)
- allopurinol
- sulfonamides
-
differential dx of drug induced pulm disorder?
- idiopathic pulm fibrosis
- viral infxn
- military TB
- pneumocystis jirovecci
- SLE
- wegener's granulomatosis
- radiation pneumonitis
- viral bronchiolitis obliterans
-
risk factors:
____ of cytotoxic meds
combination
-
risk factors: multiple exposures (increase risk of hypersensitivity rxn).
which meds?
- nitrofurantoin
- sulfasalazine
-
risk factors: higher dose.
which meds
- bleomycin, busulfan, carmustine
- amiodarone
- methotrexate
-
risk factors: increased age.
which meds?
-
risk factor: young age.
which med
carmustine
-
risk factors: radiation therapy and oxygen therapy.
which meds?
- bleomycin
- cyclophosphamide
- mitomycin
- carmustine
-
risk factors of drug-induced pulm disease for bleomycin
- higher dose
- increased age
- radiation/oxygen therapy
-
risk factors of drug-induced pulm disease for carmustine
- higher dose
- young age
- radiation/oxygen therapy
-
risk factors of drug-induced pulm disease fornitrofurantoin
- multiple exposure
- increased age
-
morbidity/mortality prognosis of pulm fibrosis
5 month
-
morbidity/mortality prognosis of pulm htn
2-3 yrs from symptom presentation
-
morbidity/mortality prognosis of carmustine
15 years
-
morbidity/mortality prognosis of amiodarone
- ZERO if early recognition
- but 64% if untreated!!!
-
survival may improve with _______.
early recognition and cessation of therapy
-
important prevention: do NOT exceed ____.
toxic dose
-
what to monitor for amiodarone?
- CXR and PFT q4-6 mo
- b/c usually presents with diffuse reticular infiltrates
-
manage acute pneumonitis/hypersensitive pneumonitis?
- d/c med
- prednisone 40-80 mg daily
-
manage chronic fibrosis
- d/c med
- consider prednisone if not improving
-
manage bleomycin /carmustine-induced pulm tox.
- avoid high concentration inspired Oxygen (b/c rapid deterioration)
- corticosteroids (variable response. carmustine generally less inflamm component)
-
manage methotrexate /amiodarone induced tox.
- AVOID corticosteroids
- (may respond but fulminant resp failure has occurred)
-
manage nitrofurantoin, sulfasalazine tox.
respond WELL to corticosteroids (b/c hypersensitivity related)
-
manage alkylating agent, busulfan, mephalan, chlorambucil-induced tox.
- permanent d/c
- no corticosteroids
-
when do you NOT use corticosteroids?
A) chlorambucil
-
when do you use corticosteroids?
D) sulfasalazine
-
when do you use corticosteroids?
A) carmustine
-
what does "corticosteroid response" mean?
improve of sympt of lung fxn within 10 days of therapy
-
oxygen: what concentration should you use?
use lowest possible oxygen concentration.
-
if receiving drug with high incidence of toxicity, early report of S&S is important. what are those?
- dyspnea on exertion
- dry non-productive cough
- acute dyspnea
- chest pain
-
drugs commonly cause pulm disorder. list 7
- amiodraone
- bleomycin
- busulfan
- carmustine
- methotrexate
- mitomycin
- nitrofurantoin
-
define bronchospasm.
constriction of the air passages of the lung by spasmodic contraction of the bronchial muscles
-
define aspirin induced asthma.
inflamm disease of the airways with exacerbation of pre-existing asthma and rhinitis after ingestion of aspirin and many other NSAIDs
-
what's samter's triad ("aspirin triad")
characterized by aspirin sensitivity + asthma + nasal polyposis
-
what is the highest incidence in aspirin induced asthma. two things that lead a higher risk?
- bronchospasm
- asthama and nasal polyps (samter's triad)
-
beta blocker induced bronchospasm has been fatal with what med?
opthalm timolol
-
bronchospasm can also be part of any ___ reaqction. (food, drug, latex, bee sting)
anaphylaxis
-
mechanism of aspiring induced asthma.
- COX enzyme inhibited thus arachidonic acid shifts towards lipoxygenase path. thus more leukotriene and then bronchospasm
- genetic likely - increased LT synthase (pro-inflam) and dec PG-E2 (anti-inflam)
-
mechanism of beta-blocker induced bronchoconstriction.
- may directly inhibit B2-receptor (2 for lungs, 1 for heart)
- bronchodilator effect of B2 adrenergic compromised
-
mechanism of ACEi induced cough
- accum of substance P and bradykinin --> initiate PG and thromboxane A2 pathways
- substance P: bronchoconstrict
- bradykinin: stimulate cough reflex
-
3 mechanism of sulfite-induced bronchoconstriction
- 1) direct stimulation of parasympathetic receptors
- 2) IgE mediated rxn
- 3) reduced sulfite oxidase (enz to metab sulfur cmpd for excretion)
-
mechanism of EDTA bronchoconstriction
- stabilizing agent that chelates calcium
- can potentiate responsiveness to histamine
-
mechanism of benzalkonium chloride (BAC) bronchoconstriction
- found in some nebulizer solutions
- mast cell degranulation
-
anaphylaxsis is Ig___ mediated.
E
-
which is allergy? (the rest are pseudo and this answer can be pseudo too)
D) sulfite
-
EDTA and BAC induced bronchoconstrictions are... pseudo or real allergy
pseudo allergy
-
aspirin induced asthma is... pseudo or real allergy?
pseudo
-
S&S of bronchospasm
cough, SOB, wheeze, chest tight
-
aspirin induced asthma:
when is onset? what is S&S?
- onset in third decade
- persistent rhinitis and nasal congestion.
-
aspirin induced asthma: when does sensitivity develop?
within 5 yrs
-
aspirin induced asthma:
after exposure, what happens and how soon it happens?
- acute asthma exacerbation with rhinorrhea, conjunctivitis, flushing within 3 hrsoccasional urticaria, periorbital edema, abd pain
-
aspirin induced asthma: how to make diagnosis
by oral challenge and monitoring FEV1 and/or sympts
-
ACEi-induced cough:
symptoms?
dry and persistent tickling sensation in the throat
-
ACEi-induced cough:
when is the onset?
- one day to 12 months after initiation.
- also with increased dose
-
sulfite induced bronchoconstriction: what are symptoms?
wheeze, chest tight, dyspnea
-
latex's clinical presentation.
- contact dermatitis to anaphylaxis.
- perform provocation test to confirm dx.
-
differential dx of asthma and bronchospasm?
- asthma, COPD,
- URT, UR obstruction by tumor
- gastroesophageal reflux
- laryngeal edema
- acute left ventricular failure
- pulmonary emboli
- chronic bronchitis, eosinophilic pnuemonia
- systemic vasculitis
-
risk factors for asthma and bronchospasm?
- pre-existing hyper-reactive lung disease (i.e. asthma, COPD, cystic fibrosis)
- (more severe asthma --> more risk drug-induced asthma)
- this is really important
-
risk factors of asthma and bronchospasm for NSAID-induced?
-
risk factors of ACEi induced cough.
- African and Asian Am
- 2 x more in female
-
is pre-existing hyper-reactive lung disease a risk factor in ACE-i cough?
NOPE!
-
manage aspirin induced asthma
- avoid aspirin and NSAID (b/c this is pseudo allergy thus class effect!) and record
- if high CV risk, may use desensitization to use asa/nsaid (inc dose over 2-3 day, must use daily). then could take other NSAID
- may use APAP or corticosteroid instead
- LT modifier (singulair, accolate) or LT production inhibitor (zileuton) are not conclusively beneficial --> AVOID
-
when would you use desensitization for aspirin induced asthma?
when high CV risk because you need to use ASA
-
can you use LT modifier or production inhibitor if ASA-induced asthma?
-
manage b-blocker induced bronchoconstriction
- use selective b1 adrenergic blocker (atenolol, metoprolol, esmolol, nebivolol)
- selectivity is dose dependent. do not inc dose w/o consulting doctor
-
manage ACEi induced cough.
- d/c med if debilitating - resolves within 1day to 2 wk
- try to dec dose
- switch to ARB
- little evidence to treat cough
-
after d/c med, when does ACEi induced cough resolve?
1 day to 2wk
-
presence of sulfite is required on drug manufacturer product label and foods. t or f
true!
-
important risk factor for drug induced bronchospasm (case study)
prior exposure!
-
if ASA or NSAID cannot be given for cardioprotection, what can you consider? (case study)
clopidogrel (Plavix)
-
random ques: what should formoterol be used with??
- this is long acting bb.
- with corticosteroid!
-
beta 2 and alpha 1 receptor blocker?
-
albuterol MDI vs. nebulizer.
what is in nebulizer that may cause bronchospasm?
benzalkonium chloride
-
non-selective beta blocker?
- sotalol
- propranolol
- timolol
-
beta 1 selective blocker
- metoprolol
- esmolol
- atenolol
- nevibolol
-
SE of corticosteroid
- myalgia, myopathy
- if used >6 mo-1yr, inc glucose, osteoporosis, BP, cataract (inc IOP)
-
when you have ACE i induced cough, why is it okay to use ARB?
- b/c ARB do not affect bradykinin
- ACEi induces bradykinin and substance P
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