Mechanism, presentation, workup, treatment

Breakdown by system
PULMONARY
Obesity hypoventilation syndrome
 Presentation: fatigue, dyspnea, difficulty concentrating, hypoventilation (PaCO2>45)
 Mechanism: increased CO2 due to increased mass and SA, sleep disordered breathing,
normal Aa gradient
COPD
 Mechanism: air trapping, hyperinflation
 Presentation: breathe at higher FRC
Asthma
 Presentation: cough, SOB, wheeze, inhale dust mites, mold, pollen
 Mechanism: airway inflamm, bronchial hyperreactivity
 Workup: methacholine challenge
 Treatment: bronchodilator (ICS, albuterol)
Pulmonary arterial hypertension
 Mechanism: BMPR2 mutation have predisposition for dysfunctional endothelial and
smooth muscle cell proliferation, endothelin (vasoconstrictor) production increases,
induces smooth muscle cell prolif, intimal thickening and fibrosis (injury to pulm
arterioles)increased pressure in pulm circulationRV hypertrophy
 Presentation: dyspnea, fatigue, cyanosis, Raynaud/CREST
 Workup: S2 heart sound, RAD on EKG
 Treatment: Bosentan- endothelin antagonist
Emphysema
 Presentation: alpha-1 antitrypsin deficiency (has emphysema but never smoked), at risk
for liver cirrhosis
 Mechanism: centriacinar (neutrophils and macrophages release elastase), panacinar
(alpha-1 antitrypsin deficiency)
Pulmonary embolism
 Presentation: travel! sudden onset SOB/dyspnea and chest pain, immobilization and
recent surgery, calf swelling, hypoxemia and respiratory alkalosis (hypocapnia) due to
hyperventilation
 Mechanism: caused by DVT in lower extrem that embolizes to pulm vasculature,
blockage of pulm circulation results in V/Q mismatch, alveoli can’t oxygenate blood bc
 Mechanism: neutrophils form abscess, release lysosomes containing digestive enzymes,
causing liquefying necrosis
 Workup: CXR shows cavitation with air fluid level
Cystic fibrosis
 Presentation: lethargy, vomiting
 Mechanism: CFTR mutation, can’t reabsorb NaCl, so secrete sweat with high NaCl
(hyponatremia/chloremia),
 Treatment: salt supplementation
Collapsed lung due to bronchial obstruction
  Presentation: decreased breath sounds
 Mechanism: obstruction of mainstem bronchus, trachea deviates because loss of lung
volume
 Workup: CXR hemithorax opacification, tracheal deviation toward opacified side
Pleural effusion/Tension pneumothorax
 Tracheal deviation away from affected lung because excess air or fluid pushes against
mediastinal structures
Lobar pneumonia
 Presentation: cough, SOB, fever, lobe infiltrate on CXR
 Mechanism: community acquired pathogen (Strep pneumo)
Silicosis
 Presentation: history, hilar adenopathy, nodular densities, birefringent particles
 Mechanism: impairs macrophages
 Workup: calcifications, in the peripheral lymph nodes of the upper lobes
Sarcoidosis
 Presentation: malaise, night sweats, cough, WL, skin rash, eye prob
 Mechanism: CD4+ T cell mediated disease, noncaseating granulomas consisting of
epithelioid macrophages and multinucleated giant cells, activated macrophages express
1 alpha hydroxylase, forming 1,25 dihydroxycit D w/o PTH hormone (hypercalcemia)
 Workup: hilar adenopathy
ARDS
 Presentation: pneumonia, sepsis (low bp, high RR)
 Mechanism: injury of pulmonary epithelium, neutrophils recruited causing capillary
damage and leakage of fluid into alveoli
Granulomatosis with polyangiitis
 Presentation: cough, hemoptysis, nephritic syndrome
 Mechanism: necrotizing inflammation and pulm hemorrhage, and kidneys
Small cell lung cancer
 Presentation: weakness, cough, decreased appetite
 Mechanism: SIADH (hyponatremia), Cushing, Lambert Eaton, cerebellar ataxia, stain for
neuroendocrine markers like neural cell adhesion molecule (NCAM), enolase,
chromogranin
Squamous cell lung cancer:
 Presentation: weakness, cough, decreased appetite
