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205 Cards in this Set
- Front
- Back
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You see a patient with the right side of the chest more expanded than the other. Which side has the collapsed lung?
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Right side!
Lung collapses but chest wall expands |
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What is FiO2 at sea level?
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21%
0.21 * 760 mm Hg = 160 mm Hg |
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What is water vapor pressure?
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47 mm Hg
PiO2 = 150 mm Hg at the trachea due to the water vapor |
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What is PAO2?
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Alveolar PO2 = 100 mm Hg
B/c air encounters CO2, further dilutes from 150 at tracheal level |
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What is PvO2? What is venous sat?
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40 mm Hg
75% |
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What is the A-a gradient?
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Alveolar-arterial O2
Tells you the efficiency with with the arteries take oxygen from the alveoli Normal: 8 Older (age 80): 20 **Measure at room air!! (usually) |
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How is shunt defined?
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Blood goes from R heart to L heart without ever having seen ventilation
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What are the 4 ways to negate the alveolus (intrapulmonary shunt)?
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1. Pus
2. Water 3. Blood 4. Atelectasis (collapse) |
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What is the O2Sat for PO2 of:
• 40 • 60 |
• 40 = 75%
• 60 = 90% |
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Can or can't average in shunt:
• Sat • PO2 • O2 content |
• Sat - YES
• PO2 - NO • O2 content - YES |
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What does it mean if you give a patient 100% O2 and the O2sat only goes up a small fraction?
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SHUNT SHUNT SHUNT
(pus, water, blood, atelectasis) |
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What are the 8 causes of hypoxemia?
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1. ↓ P<sub>ATM</sub>
2. ↓ F<sub>I</sub>O2 3. ↑ P<sub>a</sub>CO2 4. ↓ R -------------- 5. Shunt 6. Low V/Q 7. Diffusion -------------- 8. ↓ venous sat (Mixed Venous O2) • Anemia • ↓ CO • Hypoxemia • ↑ O2 consumption (VO2) |
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What do you have to do when you take a room air blood gas?
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A-a gradient!!!
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By how much does an increase/decrease in P<sub>CO2</sub> of 10 decrease/increase pH?
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0.8
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Why is A-a gradient only measured on room air? What is done instead?
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1. Cannula/face mask doesn't give pure O2 = can't calculate accurate F<sub>I</sub>O2
2. ↑ F<sub>I</sub>O2 = ↑↑ A-a gradient!!! Instead, PF ratio: P<sub>a</sub>O2/F<sub>I</sub>O2 Normal: 450 |
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What is the main (mechanistic) cause of pneumonia? What are other causes?
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Aspiration!
• Small amounts at night • ↑ with alcohol Inhalation (TB) Hematogenous (tricuspid valve endocarditis throwing infection) |
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What are the types of pneumonia (CXR)?
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Lobar
Broncho Interstitial Abcess |
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What are the causes of community-acquired pneumonia?
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1. Streptococcus pneumoniae
2. Haemophilus influenzae 3. Mycoplasma pneumoniae 4. Chlamydia pneumoniae 5. Legionella pneumophila 6. Oral anaerobes 7. Influenza, RSV |
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What is the treatment for community-acquired pneumonia?
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Moxifloxacin or levofloxacin
**NOT cipro OR β-lactam + macrolide (ceftriaxone + azithromycin) |
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What is nosocomial pneumonia?
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Hospital-acquired (> 48 hrs after admission - not incubating prior)
Ventilator-associated (>48-72 hrs after intubation) Healthcare-associated |
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What are the causative agents of nosocomial pneumonia?
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Early onset (< 4 days), no risk factors
1. Enteric gram - bacilli 2. MSSA 3. H. influenzae 4. Streptococcus spp. Late onset (> 5 days), risk factors 1. Pseudomonas aeruginosa 2. MRSA 3. Acinetobacter spp. |
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What is the management of nosocomial pneumonia?
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Culture
ABx for most likely cause (local antibiograms, prior exposure, etc.) • Empiric, broad-spectrum • Anti-MDR ABx for late-onset cases (meropenem, linezolid) Focus ABx after micro evaluation Really important to get ABx right ASAP |
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What is the main immune response to TB?
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Cell-mediated: Th1 = resistance to infection
Tissue hypersensitivity - altered cellular reactivity • Caseating granulomas • Reaction to tuberculin (PPD) **Antibodies - little apparent role, maybe in children (BCG vaccine) |
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What part of the lung does primary TB affect? Reactivation TB?
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Lower lobes
Apical posterior lung (upper) |
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What are some other sites of infection by TB?
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Kidney
Vertebral bodies Spleen Meninges |
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What are 3 stains used for acid-fast bacilli?
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Ziehl-Neelsen
Kinyoun - don't need to heat Fluorochrome (auramine-rhodamine) - can use 20x or 40x to see |
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What are the 4 main drugs against TB?
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Isoniazid
Rifampin Ethambutol Pyrazinamide |
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What is the current regiment for active TB treatment?
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4 drugs for 2 months (IREZ) + 2 drugs (IR) for 4 months
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What is MDR TB?
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Resistance to AT LEAST rifampin and isoniazid
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What is XDR-TB?
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Resistant to:
• Rifampin • Isoniazid • ≥ 3 second-line drugs |
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What is interstitial lung disease?
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AKA diffuse parenchymal lung disease
Disease of alveolar wall • Includes interstitium (space between alveolar epithelium and capillary endothelium) |
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What are the subcategories of DPLD?
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1. DPLD of known cause (drugs, CVD)
2. Idiopathic interstitial fibrosis • IPF • NON-IPF 3. Granulomatous (sarcoidosis) 4. Other |
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What are some causes of Pneumoconiosis (DPLD)?
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Inorganic dusts:
Silica → Silicosis Asbestos → Asbestosis Hard metal alloys → giant cell pneumonitis Beryllium → Berylliosis |
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What are some causes of hypersensitivity pneumonitis?
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Organic dusts:
• Immune reaction Mold hay → farmer's lung Bird proteins → bird fancier's disease |
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What types of collagen vascular diseases can cause DPLD?
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Rheumatoid arthritis
SLE Scleroderma Sjogren's Polymyositis, dermatomyositis MCTD Ankylosing spondylitis |
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What is the histologic pattern of IPF called?
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Usual interstitial pneumonia
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What is IPF? What organs does it affect?
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Chronic fibrosing interstitial pneumonia
Limited to lungs Restrictive lung disease! |
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What is the pathogenesis of IPF?
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Repeated stimulus
↓ Sequential lung injury ↓ *Inflammation Aberrant wound healing ↓ Fibrosis *Damage most sensitive to type I cells (thin, unlike type II which are cuboidal and make surfactant) |
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What are some signs and symptoms of IPF?
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Symptoms:
• SOB - insidious • Non-productive cough Signs: • Crackles/rales ("velcro") • Clubbing • Cor pulmonale |
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What is seen on CXR in IPF?
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<b>Reticular/nodular infiltrates</b>
Honeycombing (end stage) |
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What is a better test than CXR for imaging of DPLD?
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High-res CT
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What are the characteristics of UIP (histology)?
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1. Heterogeneity - alternating zones of fibrosis, inflammation, honeycombing, and normal
→ Different stuff going on in different places 2. Patchy thickening of alveolar septa 3. Fibroblastic foci 4. Honeycomb lung (end stage) |
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What is non-specific interstitial pneumonia (NSIP)? How is it different from IPF?
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Non-IPF idiopathic interstitial pneumonia
1. Ground glass opacities on CXR 2. Intact alveolar walls on histology (although not completely normal) 3. Much better prognosis (cellular > fibrotic > IPF) |
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What is sarcoidosis?
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• Multi-system disorder (unlike IPF), including lung
• Young/middle-aged • Interstitial lung disease + enlargement of thoracic lymph nodes <b>• Non-caseating granulomas w/o infection/foreign body</b> • TH1 response |
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What are some "other" types of DPLD?
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1. Pulmonary Langerhans cell hystiocytosis (cysts + nodules + young)
2. Lymphangioleiomyomatosis (women) 3. Pulmonary alveolar proteinosis 4. Pulmonary vasculitides (Wegeners', etc.) ... |
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What can be diagnosed by bronchoscopic transbronchial biopsy? What do you need for IPF?
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Granulomatous (sarcoid.)
Neoplasm Infection IPF needs surgical lung biopsy |
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How is ILD treated?
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1. Remove offending agents
2. Corticosteroids • IPF - rare • Sarcoidosis - common 3. Cytotoxic/immunosuppressives 4. Antioxidants (n-acetylcysteine) --- 5. Oxygen 6. Flu vaccines 7. Supervised exercise (pulmonary rehab) 8. Transplant |
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How are non-tuberculous mycobacterium and fungal infections transmitted?
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Environmentally - NOT person-to-person
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How does NTM present?
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Chronic, low-grade pneumonia
Hard to diagnose because they're found everywhere - + acid-fast |
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What is MAC? What diseases does it cause?
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M. avium + M. intracellulare
• Pulmonary disease • Disseminated disease (AIDS) → now, rare • Cervical lymphadenitis in kids |
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What is Lady Windermere syndrome?
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MAC!!
Right middle lobe OR left lingular bronchiectasis Older (> 60), white, female, tall, thin Associated with CF Tx with macrolides (clarithromycin, azithromycin) plus other drugs for 12-18 mo!! |
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How does M. kansasii present?
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Mimics pulmonary TB
Less difficult than MAC, but still must treat for 18mo. |
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What does thermally dimorphic mean?
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Fungi that are hyphae in environment, yeast in tissue
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How do fungal infections transfer?
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Inhalation of conidia → pulmonary infection → dissemination
Not transferred between animals/humans (except for weird case) |
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Histoplasma capsulatum
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Ohio/Mississippi river valleys
SOIL-based = excavation, construction Mycelial phase - ambient temp Yeast phase - 37<sup>o</sup>C Granulomas - caseating or non-caseating --- Flu-like illness - most self-limiting Ghon complex - scar in parenchyma and calcified lymph node • Mimics TB!! |
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What is the "sweet spot" of infectious size to get into the alveoli?
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2-5μm
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How is histoplasmosis treated?
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Acute - not
Chronic - amphotericin B, itraconazole |
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Blastomyces dermatitidis
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Southeastern, south central states, Great lakes states
Moist SOIL Can spread to bone, skin Non-caseating granulomas, giant cells, but also <b>NEUTROPHILS</b> ---- Mimics bacterial pneumonia, TB, malignancy, other fungal infections |
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How is blastomyces treated?
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Asymptomatic - not
Immunosuppressed, symptoms - itraconazole |
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Coccidioides immits (california)
Coccidioides posadasii |
Mycelia, Spherule (intead of yeast)
Southwest USA SOIL Conidia inhaled, form spheres which subdivide into endospores → rupture and release ---- Most asymptomatic/subclinical • Pulmonary nodule - looks like cancer • Chronic fibrotic pneumonia • Disseminated - skin, bone/joints, <b>meningitis</b> → requires lifelong treatment!! Tx: Severe: amphotericin B, fluconazole, itraconazole |
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What is PE a complication of?
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DVT
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Which 4 groups are at an increased risk of PE mortality?
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1. Age > 60
2. Cancer 3. COPD 4. CHF |
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What is the pathophysiology of PE?
What happens to pulmonary pressures, airway resistance and lung compliance? |
1. V/Q mismatch = hypoxemia, ↑ A-a gradient; ↑ airway resistance
2. ↑ PVR + PHTN 3. Alveolar hyperventilation (reflex + compensation) 4. ↑ airway resistance (bronchiolar constriction) 5. ↓ pulmonary compliance (↓ surfactant, edema, hemorrhage) |
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What is the mechanism of hypotension in PE?
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↑ PVR
= cor pulmonale • ↑ HR • ↓ RV/LV preload • Interventricular septal shift →→ RV ischemia + ventricular interdependence = ↓ CO |
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What are the 3 main syndromes seen in PE?
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1. Pleuritic pain (+/- hemoptysis)
2. SOB 3. Shock, syncope |
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How accurate is clinical diagnosis alone in diagnosing PE?
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Not very.
"Wells clinical prediction score" |
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When is D-Dimer useful?
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Low/intermediate clinical suspicion
Because NPV is very high |
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How is PE managed?
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1. Prevention!!!
2. Fluids for hypotension (rarely pressors) 3. O2, bronchodilators for V/Q mismatch 4. Anticoagulation |
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What is the pathogenesis of COPD?
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Noxious agent (tobacco smoke, pollutants, occupational)
+ Genetic (<b>α1-antitrypsin deficiency</b>) Infection Asthma Other = COPD |
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What are the main inflammatory cells involved in COPD?
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NEUTROPHILS
CD8+ lymphocytes Fibroblasts |
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What are the 3 main problems in COPD?
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1. Emphysema = parenchymal destruction
• ↓ elastic recoil (think plastic bag) • ↓ tethering 2. Small airway problem • Peribronchial fibrosis - constricted like tight rubber band • Loss of alveolar attachments 1 + 2 make it very hard to expire!! 3. Chronic bronchitis = ↑ mucus in lungs from ↑ neutrophils |
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What are 2 characteristics of COPD seen on CXR?
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Hyperinflation!!
1. Flattening of diaphragm 2. Retrosternal clear space |
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What does COPD look like on CT?
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Black cystic sacs with clear alveolar markings
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What does spirometry of COPD show?
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1. Ramp
2. ↓ FEV1 = ↓ FEV1/FVC → concave-like flow-volume loop |
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How is COPD staged? What is the problem with it?
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FEV1 level
Does not correlate well with quality of life/exercise capacity |
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What is the physiologic reason people with COPD have trouble exercising?
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COPD = ↓ elasticity
→ lung more expanded than normal = ↑ FRC But, normal TLC. TLC - FRC = inspiratory capacity (IC) → IC is ↓ As breathing rate increases, normally can inspire more air up to a maximum of IC. If IC is low (like in COPD) + increased breathing rate makes it lower = SOB "IC/TLC = lung ejection fraction" |
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What is the usefulness of IC/TLC?
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"Lung ejection fraction"
Predicts mortality! Much higher rate if < 25% |
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What is the management of COPD?
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Additive with stages
1. Bronchodilators (short-acting) 2. Bronchodilators (long-acting) + rehab 3. Glucocorticoids 4. O2, surgical treatments *Anticholinergics (ipratropium) |
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What are some big differences between asthma and COPD?
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Asthma:
• Eosinophiles • CD4+ • Fully reversible COPD: • Neutrophils • CD8+ • NOT fully reversible |
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What is the Starling equation?
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![Q = K[(P<sub>MV</sub> - P<sub>IS</sub>)-σ(π<sub>MV</sub> - π<sub>IS</sub>)]
Changes in K or σ = exudative
Changes in P, π = transudative](https://ctools.umich.edu/access/content/user/aturin/Images/starling.png)
Q = K[(P<sub>MV</sub> - P<sub>IS</sub>)-σ(π<sub>MV</sub> - π<sub>IS</sub>)]
Changes in K or σ = exudative Changes in P, π = transudative |
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What is the main purpose of the pleura?
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To prevent pulmonary edema
e.g. CHF Fluid accumulates first in pleural space = ↑ P<sub>PL</sub> = ↑ P<sub>IS</sub> = ↓ hydrostatic flow into interstitial space |
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How does hanging or thoracentesis lead to pulmonary edema?
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Hanging: constricted trachea = lots of effort to inhale = ↓↓P<sub>PL</sub> = ↓↓P<sub>IS</sub>
Thoracentesis - pulling out too much fluid can cause P<sub>PL</sub> to ↓ |
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What drives fluid clearance from the alveoli?
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Na/K-ATPase (and Na, Cl channels on apical side)
= movement of H2O transcellularly Also paracellularly |
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What is the difference in the fluid in cardiogenic and non-cardiogenic pulmonary edema?
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Cardiogenic = water, ↓ protein
Non-cardiogenic = ↑ protein, cellular content |
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What defines ARDS?
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1. Diffuse alveolar damage
2. ↑ microvascular permeability 3. Non-cardiogenic pulmonary edema 4. SHUNT (V/Q = 0) 5. NO LA hypertension PF ratio < 300 = acute lung injury PF ratio < 200 = ARDS |
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What is the pathophysiology of ARDS?
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Inflammation
Increased permeability (alveolar-capillary membrane) = σ → 0 |
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What drives pulmonary edema formation in ARDS?
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Microvascular hydrostic pressure
σ → 0, so there is essentially no oncotic term in the Starling equation anymore |
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What are the 3 stages of ARDS?
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Edematous (1-2d)
Exudative (2-7d) Proliferative (weeks) - fibrosis as an attempt to heal |
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How long does it take for PPD to become positive after TB infection?
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3-8 weeks
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What things can cause granuloma formation in the lung?
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1. TB: caseating (sometimes non)
2. Churg-Strauss: caseating 3. Wegener's: caseating 4. Histoplasmosis: caseating or non 5. Blastomycosis: non-caseating 6. Sarcoidosis: non-caseating (rarely caseating) 7. Berylliosis - non-caseating granulomas |
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What are epithelioid cells?
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Stimulated macrophages found in TB granulomas
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How can TB be cultured?
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Lowenstein-Jensen (solid egg)
Solid agar - 3-8wk Liquid broth - 1-3wk |
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What is the mediastinum?
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Extrapleural space bounded by anatomic landmarks (diaphragm, sternum, vertebrae, first rib)
Anterior Posterior Superior Middle |
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What % of asymptomatic mediastinal tumors are benign?
What % of symptomatic mediastinal tumors are malignant? Which compartment are most of them found? |
90%
25-40% Anterior, superior |
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What is the difference between true thymic hyperplasia and follicular thymic hyperplasia?
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True: epithelial + lymphocytic ↑
Follicular: lymphocytic ↑ only • 75% of pts with myasthenia gravis |
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What is the most common tumor of the superior/anterior mediastinum?
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Thymoma
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What age do patients present with thymoma? What disease is it associated with?
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50-60
Myasthenia gravis |
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How are thymomas classified?
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Whether chief neoplastic cell is spindled or epithelioid:
(decreasing prognosis) A = spindled B = epithelioid AB = both B1: lymphocytes > epithelial cells B2: lymphocytes = epithelial B3: lymphocytes < epithelial C: thymic carcinoma |
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What is the Masaoka staging system for thymomas?
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Based on status of capsule
1 - no invasion into capsule 2 - some capsule invasion 3 - invasion of neighboring tissues 4 - metastasis |
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Where are lymphomas found in the mediastinum?
What is the most common type of NHL in children? Adults? |
Anterior, superior
Hodgkin disease = most common Acute lymphoblastic leukemia/lymphoma (T-cell) = most common in children Large B-cell lymphoma - adults |
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What is pathognomonic of Hodgkin disease on histology?
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Reed-Sternberg cells
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Where in the mediastinum are germ cell tumors found?
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Anterior
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What are the types of germ cell tumors?
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Teratoma (most common)
Seminoma (most common malignant) Other ("mixed", embryonal, yolk sac, choriocarcinoma) |
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What are the germ cell tumor markers?
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Choriocarcinoma - β-hCG
Yolk Sac - AFP Dysgerminoma - LDH Embryonal - LDH, β-hCG |
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What are type I and type II GCTs?
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Type I: YOUNG
• Teratomas • Yolk sac tumors No gains in 12p Good prognosis Type II: Post-pubertal • Seminomas • Teratomas • Mixed GCT Gains in 12p Worse prognosis |
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Where are neuroendocrine tumors of the mediastinum found?
What tumors do they resemble? What is the most common hormone secreted? |
Anterior, superior
Carcinoid tumors *Associated with MEN-I 5% of the time ACTH |
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What is distinguishing of neuroendocrine tumors on histology?
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Salt and pepper chromatin pattern
+ chromogranin stain |
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Where are neurogenic tumors found in the mediastinum?
What are the two most common? |
Posterior
1. Schwannoma = neurilemmoma 2. Neurofibroma (associated with neurofibromatosis-1) |
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What is a ganglioneuroma and where is it found in the mediastinum?
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Posterior
Tumor from sympathetic ganglia or adrenal gland = Schwann cells + ganglion cells |
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Why do ganglioneuromas present with diarrhea?
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Secretion of VIP!
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What do nodules of neuroblast do to a ganglioneuroma?
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↑ malignant potential
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What are some cysts of the mediastinum?
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1. Thymic
• Anterior, superior • Congenital = unilocular • Acquired = multilocular, secondary to inflammation 2. Bronchogenic • Middle 3. Gastroenteric • Posterior • Vertebral abnormalities |
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Where does chronic fibrosing medastinitis present?
What are the types? |
Middle, anterior
1. Infection - e.g. histoplasmosis, TB 2. IgG type 4 plasma-cell mediated sclerosing disease |
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What is the biggest cause of lung cancer in non-smokers?
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Radon
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What are the general types of lung cancer?
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Non-small cell (85%)
• SCC • Adenocarcinoma • Large cell CA Small cell CA (15%) → most associated with smoking behaviors |
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What are some strategies for prevention of lung cancer?
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1. Smoking cessation
2. ↓ exposure to smoke, radon 3. Diet 4. Chemoprevention (e.g. ↓ β-carotene) |
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How many cancers are detected at early stage? What is the mortality?
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15-20% stage I
5-10% stage II 40-80% mortality ANYWAY! |
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What is the most useful method of screening that improved mortality?
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CT screening
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What is Pancoast's tumor?
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Superior sulcus tumor
Hard to detect as it's under the first rib Often invades brachial plexus (40%) |
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What are some paraneoplastic syndromes?
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1. SIADH - small cell
2. Cushings - small cell 3. ↓Ca (calcitonin) 4. ↑ Ca (PTH-rP) - squamous 5. ↑ Gonadotropin - small cell, squamous cell 6. Lambert-Eaton - anti-Ca antibodies • strength improves with exercise/repeated motion • Small cell 7. Hypertrophic osteoarthropathy • Pain • Clubbing • NOT small cell |
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What is ERCC1?
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Limiting factor in nucleotide excision repair
ERCC1- patients respond better to chemo |
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What is erlotinib?
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Small molecule inhibitor of EGFR-kinase
20% increase in 1-year survival |
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What is crizotinib?
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EML4-ALK inhibitor
Also massively good results like erlotinib |
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What determines a good gefitinib response?
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EGFR mutation +!!
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What are the two most common types of lung tumors?
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Malignant epithelial
Metastatic |
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What are some genetic mutations seen in lung cancer?
|
p53
K-ras EGFR myc Rb |
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What are the precursor lesions in SCC, adenoCA, and carcinoids?
|
SCC:
• Hyperplasia • Metaplasia • Dysplasia • CIS Adenocarcinoma • Atypical adenomatous hyperplasia (AAH) Carcinoids • Bronchial neuroendocrine cell proliferation |
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What are some characteristics of SCC of the lung?
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Keratin pearls, INTERcellular bridges
Central in location Smoking 2nd most common subtype |
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What are some characteristics of Adenocarcinoma of the lung?
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Most common
Peripheral (and therefore asymptomatic...can also have pleuritic CP) |
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Which lung cancer may have signet ring cells?
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Adenocarcinoma
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Which lung cancer is treated with tyrosine kinase inhibitors?
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Adenocarcinoma
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What are some characteristics of bronchioloalveolar carcinoma of the lung?
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Subtype of adenocarcinoma
Terminal bronchioles Better prognosis than conventional adenocarcinomas |
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What are some characteristics of small cell carcinoma of the lung?
|
Central
Strong smoking association Paraneoplastic syndrome SMALL CELLS (2-3x lymphocyte) |
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What are some characteristics of large cell carcinoma of the lung?
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Large cells with large nuclei
Central or peripheral |
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What are some characteristics of typical carcinoids of the lung?
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Younger
NOT smoking Central *Hemoptysis |
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How is a typical carcinoid distinguished from an atypical one?
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Cytologic atypia!
= ↑ mitosis, necrosis in atypical case |
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What are some characteristics of solitary fibrous tumors of the lung?
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Benign
Pedunculated, well-circumscribed |
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What is seen on histology of solitary fibrous tumors?
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Spindle cells in dense collagen stroma
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What is malignant mesothelioma associated with?
|
ASBESTOS!!!
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What is the histology of malignant mesothelioma?
|
2 types
1. Sarcomatoid - spindle cells 2. Epithelial - resembles adenocarcinoma |
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How do you differentiate between malignant mesothelioma and adenocarcinoma?
|
Malignant mesothelioma:
• Negative staining for CEA and other epithelial glycoprotein markers |
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ΔP<sub>CO2</sub> = 10 → ΔpH =?
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0.08
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How long does it take the kidney to compensate for a respiratory acidosis/alkalosis?
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~3d
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What are the steps to determining acidosis/alkalosis?
|
1. ID state based on pH/P<sub>CO2</sub>/HCO3
2. Calculate anion gap 3. Compare actual HCO3 to expected compensation • Predicted compensated HCO3 = AG - 12 + actual HCO3 = 24 if compensated/normal |
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What are the causes of metabolic acidosis with ↑ AG?
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↑AG = ↑ acid from somewhere
MUDPILES Methanol Uremia DKA Paraldehyde Iron, INH Lactic acid Ethanol, ethylene glycol Salicylate |
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What are the causes of metabolic acidosis with normal AG?
|
USED CAR
Ureteral diversions Saline Endocrine (↓ adrenal) Diarrhea CA inhibitor Ammonium Cl Renal Tubular Acidosis |
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What are the causes of a ↓ AG?
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↓ unmeasured anions → hypoalbuminemia
↑ unmeasured cations → multiple myeloma (+-charged paraproteins) |
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What are the causes of metabolic alkalosis?
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Vomiting (Cl-responsive) - hypovolemia, so NaHCO3 absorbed instead of NaCl = give NaCl
Cl non-responsive: ↑ adrenal ↓ K+ (H/K opposite) |
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What can cause a respiratory alkalosis with a metabolic acidosis?
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ASA toxicity
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What are the key cells in asthma?
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Eosinophils
TH2 cells Mast cells |
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Asthma prevalence:
• children ? adults • boys ? girls • men ? women |
• children > adults
• boys > girls • men < women |
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What is atopy?
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Body's predisposition to make IgE in response to environmental allergens
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What are the important cytokines in asthma?
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IL-4, IL-13 = stimulate IgE production
Leukotrienes - recruit eosinophils |
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What is the early response/late response in asthma?
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Early:
1. Bronchospasm 2. Edema = 3. Airflow obstruction Late: 1. Inflammation + remodeling 2. Airway obstruction 3. Airway hyperresponsiveness |
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What are the remodeling changes in the airway in asthma?
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1. Subepithelial basement membrane thickening
2. Goblet cell hyperplasia 3. Smooth muscle cell hypertrophy |
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What are some symptoms that are highly suggestive of persistent asthma?
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Any ONE:
1. > 2d/wk of symptoms 2. > 2 nights/mo. awakening 3. > 2d/wk rescue inhaler 4. ≥ 2 exacerbations per year (requiring corticosteroids) |
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How is asthma a clinical diagnosis?
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Requires periods of intermittent, episodic changes in symptoms, lung function
NOT based on physical exam, scans, etc. |
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How does ventilation change with sleep stages?
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1. Stage 1 = periodic
2. Slow wave sleep = regular 3. Tonic REM (eyes not moving) = mostly regular 4. Phasic REM = irregular |
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What are the types of apnea?
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Obstructive
• Abnormalities in the airway • Apnea - cessation of respiration for at least 10 sec • Hypopnea - airflow in/out of airways is less than 50% normal = oxygen desaturation • Enough to arouse and "wake someone up" Central • Failure to initiate breath - airways are fine |
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What do the Venturi effect and Bernoulli principle say about flow in a tube?
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Higher flow = more negative pressure on outside of tube = more likely to collapse
e.g. sucking a milkshake through a straw |
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What is Loop Gain?
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The loop cycle from a monitor → processor → effector (e.g. the themostat and heater in a room)
In apnea: • Give a disturbance and see how someone response (top is normal) (apnea = vigorous response, narrow tolerance) |
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What is the role of hormones in apnea?
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1. Estrogen protective, Testosterone contributes to central problems
2. Insulin resistance/diabetes/metabolic syndrome contributes to OSA • includes IGF in acromegaly 3. Hypothyroidisim affects OSA |
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What are some genetic factors in apnea?
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Japanese - HLA*A2, HLA*B39
AA - chromosome 8q, obesity ACE deletion polymorphism - ↓ HTN risk APOE-epsilon4 mutation - neurocognitive issue |
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How is OSA diagnosed?
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Polysomnogram (8hr sleep study)
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What is the Mallampati classification?
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Made by anesthesiologists as scale to visualize uvula, soft palate, tonsils, airway, etc.
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What is the relation between OSA and cardiovascular disease?
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↑ HTN in dose-dependent fashion (sleep heart health study)
↑ sympathetic tone, ↑ SVR, ↑ HR (via α-adrenergic) = more risk for HTN due to receptor changes ↑ negative intrathoracic pressure = ↑ afterload ---- Also ↑ risk of: CAD Stroke MI |
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What is the relation between OSA and cognitive impairment?
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OSA exists for ~10 years before it's diagnosed
= lots of cognitive dysfunction, may or may not be reversible Kids: hyperactive behaviors |
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What is the relationship between OSA and asthma?
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OSA worsens asthma hyperresponsiveness and goes away with Tx
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What are some Tx of OSA?
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1. Lifestyle changes
• Positional therapy 2. Surgical opening 3. Dental devices 4. PAP! |
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What are the criteria for exudative fluid in an effusion? "Light's criteria"
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Pleural protein/serum protein > 0.5
• Leaky membrane leaking protein OR Pleural LDH/serum LDH > 0.6 • Cell damage, cells leaking OR Pleural LDH > 2/3 normal |
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What causes transudative effusions?
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1. CHF (↑ Pmv)
2. Cirrhosis (↓ πmv) 3. Nephrotic syndrome (↓ πmv) 4. Hypoalbuminemia (↓ πmv) 5. Atelectasis (↓ Pis) 6. PE (↓ Pis) → atelectasis 7. Myxedema (hypothyroidism) 8. Urinothorax 9. Fontan procedure 10. Peritoneal dialysis |
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Does a pleural effusion result in hypoxemia?
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NO! - little or no change in oxygenation
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What are the types of parapneumonic effusions (with pneumonia)? And what are the criteria for identifying them?
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1. Uncomplicated - probably Tx with Abx
• pH > 7.30 • or serial pH increasing, not decreasing if pH 7.10-7.30 2. Complicated - bugs in the pleural space • pH < 7.10 • LDH > 1000 IU/L • Glucose < 40 mg/dL • Loculations on imaging studies 3. Empyema - pus in the pleural space 2 and 3 require drainage! |
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What causes high amylase effusions?
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1. Pancreatitis
2. Esophageal rupture 3. Malignancy 4. Other intraabdominal processes |
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What test is highly specific for tuberculous effusion?
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Adenosine deaminase - > 47 IU/L
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What does tension pneumothorax mean?
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Pressure in pleural space is high enough to impede central venous return
• Usually in mechanically ventilated patient |
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What are the classifications of pulmonary HTN?
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1. Idiopathic (primary), PAH
• Fen Phen • Pre-capillary 2. Left heart disease, PVH • Post-capillary 3. Lung disease/hypoxia • PH-lung disease 4. Chronic thromboembolic • Pre-capillary 5. Unclear/multifactorial |
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Which class of PHTN is curable?
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Chronic thromboembolic
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How does PVR compare in the different PHTN classifications?
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1. Idiopathic - ↑ PVR
2. Left heart disease - ↓ PVR 3. Lung disease/hypoxia - ↑ PVR 4. CTEPH - in between |
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What factors lead to ↑ PVR? (4)
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1. Vasoconstriction (↑ endothelin, ↓ NO, ↓ PGI2)
2. Remodeling of vessel wall • SMC hypertrophy 3. Thrombosis in situ 4. Inflammation |
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What is pathognomonic for ↑ PVR?
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Plexiform lesion from intimal proliferation
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What is the pathology of PAH (class 1)? (4)
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1. SMC hypertrophy and extension distally to nonmuscular PAs
2. Endothelial cell proliferation 3. Inflammatory cell infiltration 4. In situ thrombosis |
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What is the pathology of PH (class 2, 3)?
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1. PA medial thickening
• NO endothelial cell proliferation • YES SMC hypertrophy 2. Occlusive venopathy - intimal thickening (class 2) |
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Who does PAH primarily affect?
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Middle-aged women
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What classes of PHTN are the most common?
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2 (PVH) > 3 (↓O2) > 4 (CTEPH) > 1 (PAH)
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Why don't you see pulmonary edema or pleural effusions with PAH?
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B/c it's a R-sided problem.
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What is the most important screening test for PHTN?
What is the gold standard for diagnosing PHTN? |
Echocardiography!
PA-line (Swan-Ganz) |
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What are treatments for PAH?
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1. Endothelin antagonists (-sentan)
2. PDE5 inhibitors (sildenafil, tadalafil) 3. PGI2 analogues (epoprostenol, treprostinil, iloprost) |
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Are vasodilators used to treat PVH?
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No...
Dilating the PAs with high LA pressure = pulmonary edema PDE5 inhibitors maybe... |
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Are vasodilators used to treat class 3 PHTN (↓ O2)?
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No
Increase V/Q mismatch = worse hypoxemia |
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What is the treatment for CTEPH?
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Vasodilators
Thromboendarterectomy = curative |
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What are the 4 stages of lobar pneumonia?
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What is the defect in CF?
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CFTR gene, found in epithelial cells
• Makes channel that allows Cl to move back and forth Autosomal recessive |
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What organs are affected by CF?
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1. Lungs
• Bronchiectasis • Nasal polyps • Sinusitis 2. GI • Pancreatic insufficiency (can get DM) • Liver - cirrhosis • Bowel - obstruction, meconium ileus 3. Male infertility - absence of vas deferens |
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How is CF diagnosed?
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1. Pilocarpine iontophoresis
• Look at sweat chloride [ ] • CFTR normally makes sweat hypotonic, so CF patients have elevated sweat chloride • > 60 = CF • < 40 = NOT • 40-60 = further testing 2. CF Nasal potential differences • Measure potential differences in response to different infusions 3. Genotyping |
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What are the CF mutation types?
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Class 1 - premature stop codon
Class 2 - ΔF508 - defects in post-translational modification = stuck in ER • Most common Class 3 - Defective activation Class 4 - Decreased conductance Class 5 - Decreased transcript expression Class 6 - Defective regulation of other proteins (turnover disregulated) |
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Which organ is it hardest to predict the function of in CF?
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Lung
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How does CFTR relate to ENaC?
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CFTR DOWNREGULATES ENaC activity
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What is the mechanism for mucus secretion in CF?
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No CFTR = ↑ Na reabsorption = ↑ H2O reabsorption
= less water in periciliary space = thicker mucus = infection |
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How is CF managed?
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1. Multidisciplinary care
2. Mucolytics • Pulmozyme DNAse • Hypertonic saline, mannitol (osmotic = water secretion into airway) 3. Chest PT, exercise, etc. 4. Bronchodilators • β2-agonists • Anti-cholinergics 5. Anti-inflammatory • Corticosteroids • NSAIDs 6. Antibiotics 7. Nutrition (pancreatic insufficiency) + pancreatic enzyme replacement |
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What are chemical chaperones for CF?
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VX-809, VX-770
Get CFTR to cell membrane instead of getting stuck in ER (due to ΔF508) |
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Why is the pneumovax vaccine not useful for young children?
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It's a polysaccharide vaccine and the immune system doesn't respond great in young kids because it's not fully developed.
Prevnar-7, Prevnar-13 fix this by conjugating polysaccharides to proteins |
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Why can't you use penicillin against M. pneumoniae?
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No cell wall!
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Which hospital acquired pneumonia grows with fluorescence and is oxidase +?
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P. Aeruginosa
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What conditions must be met for virus to initiate respiratory disease?
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1. Sufficient "dose" of infectious agent inhaled
2. Must be airborne 3. Must remain alive and viable in the air 4. Must be deposited on susceptible tissue |
