DIPD-final Flashcards
what are the 2 most common DIPD
interstitial pneumonitis
pulmonary fibrosis
symptoms
acute: dyspnea and non productive cough (rash uncommon)
chronic: fatigue and extertional dyspnea
clinical findings
increased eosinophils
crackles
finger clubbing
Xray- decreased lung volume and opacities
CT- honeycombing and opacities
PFT- restrictive lung disease
mechanism
risk factors present –> direct toxin exposure –> vascular permeability increased (pneumonitis) –> cell death and impaired repair (pneumonitis) –> accumulation of extracellular matrix (fibrosis)
causative agents for fibrosis
antibiotics
antineoplastics
antiarrhythmics
antibiotics
macroBID with long term use
onset: 8 months
oxidative stress
antineoplastics
busulfan
delayed- 4 years
alveolar damage after months of treatment
carmustine
delayed- years
oxidative stress
EGFRIs (-nib and -mab)
onset 1-9 months
impairs alveolar wall repair
gemcitabine
onset 2 months
endothelial dysfunction due to cytokine release
methotrexate
onset days-years
endothel hyperplasia
antiarrhythmic
amiodarone
onset months-years
cell toxicity
causative agents for pneumonitis
antineoplastics
antineoplatsics
bleomycin (BIP)
onset months
inflammation and oxidative stress due to cytokines
cyclophosphamide
onset months-years
direct alveolar cell damage
ICPs (-lumab)
onset 3 months
autoimmune response
taxanes (-taxel)
onset 2-4 weeks
hypersensitivity and/or direct toxic
treatment
remove offending med
corticosteroid (preziose 0.75-2mg/kg/day) till relief then taper off 4-6 weeks
if corticosteroids fail give
infliximab or IVIG or mycophenolate
organizing pneumonia (BOOP)
inflammatory response in lung parenchyma
presents with
non productive cough
dyspnea
crackles
possible rash and fever
infiltrates seen on scans
causative agents
minocycline
macroBID
bleomycin
IF-A
amiodarone
carbamazepine
treatment
stop offending med
corticosteroids
eosinophilic pneumonia
eosinophil accumulation due to eotaxin, t-cell chemokine, or IL-5)
potentially receptor SHT2A involved
oxidative stress
presents with
dry cough
chest pain
fever
dyspnea
>25% eosinophils in WBC
opacities
causative agents
daptomycin
macroBID
minocycline
mesalamine
sulfasalazine
treatment
stop offending med
vent for hypoxia
corticosteroid
assess treatment response
cancer agent- CTCAE (decrease means its working)
non cancer agent- IFP criteria
increase vital capacity >10% or 200mL
increase diffuse lung capacity >15% or 3mL
increase O2 saturation by 4%
pulmonary reactions without toxicity
drug induced bronchospasm
drug induced cough
drug induced bronchospasm
increase leukotriene concentration in bronchi due to cyclooxyrgenase inhibitor
increased risk in asthma patients
presents with
asthma symptoms:
chest tightness
wheezing
dyspnea
causative agents
nonselective BB (propranolol, nadolol, timolol, labetalol, penbutolol, carvedilol)
aspirin
NSAIDS
treatment
acute- inhaled bronchodilators (albuterol with or without iprattopium)
corticosteroids
chronic- leukotriene modifying agents (montelukast)
if no response then try zileuton
drug induced cough presents with
throat tickle
dry cough
causative agents
ACE (occurs days-months with initation and resolves 4 weeks after discontinuation)
CCB (relaxes sphincter with cause gastric reflux)
opioids ( increase vagal tone by decreasing CNS outflow and induces pulmonary chemo reflexes)
