Pulmonology Flashcards
Opacification, consolidation, air bronchograms
lobar consolidation= PNA
hyperlucent lung fields with flattened diaphragms
COPD
heart > 50% AP diameter, cephalization, Kerly B lines & interstitial edema”
CHF
Cavity containing an airfluid level
abscess (staph or anaerobes)
“Upper lobe cavitation, consolidation +/- hilar adenopathy”
TB
transudative pleural effusion most likely?
CHF, nephrotic, Cirrhotic
if exudative pleural effusion w/ low pleural glucose?
Rheumatoid Arthritis
if exudative pleural effusion w/ high lymphocytes?
TB
if exudative pleural effusion that is bloody?
Malignant or PE
If exudative pleural effusion most likely?
parapneumonic effusion, TB, empyema, cancer, SLE, RA, Pancreatitis
Lights criteria Transduative if?
Pleural fluid protein: Serum Protein ratio = ≤ 0.5
Pleural Fluid LDH: serum LDH ratio = ≤ 0.6
Pleural Fluid LDH = < ⅔ the upper limit of normal serum LDH
Pleural fluid has ph 7.5, glucose 102, cholesterol 25, protein 4, specific gravity 1.003 what type of fluid is it?
Transudative Pleural effusion
Pleural fluid has ph 7.34, glucose 45, cholesterol 72, protein 53, specific gravity 1.020 what type of fluid is it?
Exudative Pleural effusion
Pleural fluid is clear, decreased cell count, low levels of protein, albumin and LDH what type is it?
Transudative pleural effusion
Pleural fluid is cloudy, increased cell count, high level of protein, albumin, and LDH, what type is it?
Exudative Pleural effusion
Pt. has SOB, tachypnea, Pleuritc chest pain with hemoptysis and is tachycardic and decreased PO2 what does this pt. have?
Pulmonary emoblism
tx: with heparin
pest diagnostic test is pulmonary angiography
what is the most common cause of ARDS?
Sepsis
other: gastric aspiration, trauma, low perfusion, pancreatitis
ARDS pathyphysiology?
Tissue damage (pulmonary or extrapulmonary) → release of inflammatory mediators (e.g., interleukin-1) → inflammatory reaction → injury to alveolar capillaries and endothelial cells leading to: Exudation of neutrophils and protein-rich fluid (hyaline membrane) into the alveolar space → diffuse alveolar damage (DAD) to type I and type II pneumocytes → decrease in surfactant → intrapulmonary shunting → late stage: proliferation of type II pneumocytes and infiltration of fibroblasts → progressive interstitial fibrosis
Diagnosis of ARDS
- ) PaO2/FiO2 < 200 (<300 means acute lung injury)
- ) Bilateral alveolar infiltrates on CXR
- ) PCWP is <18 (means pulmonary edema is noncardiogenic)
Tx of ARDS
Mechanical ventilation with PEEP
with high RR and low tidal volume
Obstructive lung disease
COPD (Emphysema, chronic bronchitis) Asthma
Restrictive lung disease
Interstitial lung dz (sarcoid, silicosis, asbestosis. Structural- super obese, MG/ALS, phrenic nerve paralysis, scoliosis
COPD dx?
postbronchodilator FEV1/FVC < 0.70
Productive cough >3mo for >2 consecutive yrs= Chronic bronchitis
Emphysema= permanent dilatation of pulmonary air spaces distal to the terminal bronchioles
COPD treatment?
1st line = ipratropium (SAMA), tiotropium (LAMA), budenside and or fluticasone, PDE4 inhibitor (roflumilast). 2nd line = Beta agonists salmeterol, formoterol (LABA) salbutamol, fenoterol(SABA). 3rd line= Theophylline