USMLE (Fach) / Respiratory (Lektion)

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• Lung cancer Leading cause of cancer death. Risk factors: Smoking, radon, asbestos, family history. Presentation: cough, hemoptysis, bronchial obstruction, wheezing, pneumonic "coin" lesion on CXR or noncalcified nodule on CT.- Squamous and small cell carcinoma are central.- Adenocarcinoma and large cell carcinoma are peripheral. Sites of metastases from lung cancer: adrenals, brain, bone (pathologic fracture), liver (jaundice, hepatomegaly).In the lung, metastases (usually multiple lesions) are more common than 1° neoplasms. Most often come from breast, colon, prostate, and bladder cancer. Complications: Superior vena cava syndrome, Pancoast tumor, Horner syndrome, paraneoplastic syndromes, recurrent laryngeal nerve compression (hoarseness), effusions (pleural or pericardal).
• Bronchial carcinoid tumor Location: Central or peripheralExcellent prognosis, metastasis rare. Symptoms due to mass effect or carcinoid syndrome (flushing, diarrhea, wheezing). - CXR shows hazy infiltrates. Histology: Nests of neuroendocrine cells; chromogranin A ⊕.
• Respiratory tree Conducting zone: - Large airways consist of nose, pharynx, larynx, trachea, and bronchi. Small airways consist of bronchioles that further divide into terminal bronchioles (large number in parallel → least airway resistance).- Warm, humidifies, and filters air but does not participate in gas exchange → "anatomic dead space."- Cartilage and goblet cells extend to the end of bronchi.- Psuedostratified ciliated columnar cells primarily make up epithelium of bronchus and extend to beginning of terminal bronchioles, then transition to cuboidal cells. Clear mucus and debris from lungs (mucociliary escalator).- Airway smooth muscle cells extend to end of terminal bronchioles (sparse beyond this point). Respiratory zone:- Lung parenchyma; consists of respiratory bronchioles, alvoelar ducts, and alveoli. Participates in gas exchange.- Mostly cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli. Cilia terminate in respiratory bronchioles. Alveolar macrophages clear debis and participate in immune response.
• Lung anatomy Right lung has 3 lobes separated by horizontal and oblique fissure.Left lung has 2 lobes and lingula (homolog of middle right lobe) separated by oblique fissure. Instead of a middle lobe, left lung has a space occupied by the heart. Relation of the pulmonary artery to the bronchus at each lung hilum is decribed by RALS – Right Anterior, Left Superior. Carina is posterior to ascending aorta and anteromedial to descending aorta. Right lung is a more common site for inhaled foreign bodies because right main stem bronchus is wider, more vertical, and shorter than the left. If you aspirate a peanut:- While supine – usually enters right lower lobe.- While lying on right side – usually enters right upper lobe.- While upright – usually enters right lower lobe. Needle positioning for tension pneumothorax – ICS2.
• Determination of physiologic dead space VD = VT x (PaCO2 - PECO2)/PaCO2 VD = physiologic dead space = anatomic dead space of conducting airways plus alveolar dead space. Apex of healthy lung is largest contributor of alveolar dead space. Volume of inspired air that does not take part in gas exchange.VT = tidal volumePaCO2 = arterial PCO2PECO2 = expired air PCO2 Physiologic dead space – approximately equivalent to anatomic dead space in normal lungs. May be greater than anatomic dead space in lung diseases with V/Q defects.
• Ventilation Minute ventilation = Total volume of gas entering lungs per minuteVE = VT x RR Alveolar ventilation = Volume of gas that reaches alveoli each minuteVA = (VT - VD) x RR Normal values:- Respiratory rate (RR) = 12-20 breaths/min- VT = 500 mL/breath- VD = 150 mL/breath
• Lung and chest wall Elastic recoil – tendency for lungs to collapse inward and chest wall to spring outward. At FRC, inward pull of lung is balanced by outward pull of chest wall, and system pressure is atmospheric. At FRC, airway and alveolar pressures equal atmospheric pressure (called zero), and intrapleural pressure is negative (prevents atelectasis). The inward pull of the lung is balanced by the outward pull of the chest wall. System pressure is atmospheric. PVR is at a minimum. Compliance – change in lung volume for a change in pressure; expressed as ∆V/∆P and is inversely proportional to wall stiffness. High compliance = lung easier to fill (emphysema, normal aging), lower compliance = lung harder to fill (pulmonary fibrosis, pneumonia, NRDS, pulmonary edema). Surfactant increases compliance. Hysteresis – lung inflation curve follows a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation.
• Respiratory system changes in the elderly ↑ lung compliance (loss of elastic coil)↓ chest wall compliance (↑ chest wall stiffness)↑ RV↓ FVC and FEV1Normal TLC↑ ventilation/perfusion mismatch↑ A-a gradient↓ respiratory muscle strength
• Hemoglobin Hemoglobin (Hb) is composed of 4 polypeptide subunits (2 α and 2 β) and exists in 2 forms:- Deoxygenated form has low affinity for O2, thus promoting release/unloading of O2.- Oxygenated form has high affinity for O2 (300x). Hb exports positive cooperativity and negative allostery. ↑ Cl-, H+, CO2, 2,3-BPG, and temperature favor deoxygenated form of oxygenated form (shifts dissociation curve right → O2 unloading). Fetal Hb (2α and 2γ subunits) has a higher affinity for O2 than adult Hb, driving diffusion of oxygenation across the placenta from mother to fetus. ↑ O2 affinity results from ↓ affinity of HbF for 2,3-BPG. Hemoglobin acts as buffer for H+ ions. Myoglobin is composed of a single polypeptide chain associated with one heme moiety. Higher affinity for oxygen than Hb.
• Cyanide poisoning Inhibits aerobic metabolism via complex IV (cytochrome C oxidase) inhibition → hypoxia unresponsive to supplemental O2 and ↑ anaerobic metabolism.  Etiology:- Inhalation injury (eg, fires)- Nitroprusside Findings:- Almond breath odor- Pink skin- Cyanosis- Rapidly fatal if untreated- Lactic acidosis (high anion gap) Treatment:- Induced methemoglobinemia: First give nitrites (oxidize hemoglobin to methemoglobin, which can trap cyanide as cyanmethemoglobin), then sodium thiosulfates (convert cyanide to thiocyante, which is renally excreted).- Hydroxycobalamine
• Oxygen content of blood O2 content = (1.34 x Hb x SaO2) + (0.003 x PaO2)Hb = hemoglobin levelSaO2 = arterial O2 saturationPaO2 = partial pressure of O2 in arterial blood Normally 1g Hb can bind 1.34 mL O2; normal Hb amount in blood is 15 g/dL.O2 binding capacity ≈20.1 mL/O2/dL of blood.With ↓ Hb there is ↓ O2 content of arterial blood, but no change in O2 saturation and PaO2. O2 delivery to tissues = cardiac output x O2 content of blood. CO poisoning: Normal Hb concentration, ↓ O2 saturation of Hb, normal PaO2, ↓ total O2 contentAnemia: ↓ Hb concentration, normal saturation of Hb, normal PaO2, ↓ total O2 contentPolycythemia: ↑ Hb concentration, normal saturation of Hb, normal PaO2, ↑ total O2 content
• Pulmonary circulation Normally a low-resistance, high-compliance system. PO2 and PCO2 exert opposite effects on pulmonary and systemic circulation. A ↓ in PAO2 causes a hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung. Perfusion limited – O2 (normal health), CO2, N2O. Gas equilibrates early along the length of the capillary. Diffusion can be ↑ only if blood flow ↑.Diffusion limited – O2 (emphysema, fibrosis, exercise), CO. Gas does not equilibrate by the time blood reaches the end of the capillary. Diffusion: Vgas = A (area) x Dk (diffusion coefficient of gas) x (P1-P2)/T (alveolar wall thickness)- A ↓ in emphysema- T ↑ in pulmonary fibrosis DLCO is the extent to which CO, a surrogate for O2 passes from air sacs of lung into blood.
• Pulmonary vascular resistance PVR = (Ppulm artery - PL atrium)/cardiac output ∆P = Q x R, so R = ∆P/QQ = cardiac output (flow) R = 8ηl/πr4
• Response to exercise ↑ CO2 production↑ O2 consumption↑ ventilation rate to meet O2 demand.V/Q ratio from apex to base becomes more uniform.↑ pulmonary blood flow due to ↑ cardiac output.↓ pH during strenuous exercise (2° to lactic acidosis). No change in PaO2 and PaCO2, but ↑ in venous CO2 content and ↓ in venous O2 content.
• Flow-volume loops Obstructive lung disease- RV: ↑- FRC: ↑- TLC: ↑- FEV1: ↓↓- FVC: ↓- FEV1/FVC: ↓- Loop shifts to the left Restrictive lung disease- RV: ↓- FRC: ↓- TLC: ↓- FEV1: ↓- FVC: ↓- FEV1/FVC: – or ↑- Loops shifts to the right
• Sarcoidosis Characterized by immune-mediated, widespread noncaseating granulomas, elevated serum ACE levels, and elevated CD4+/CD8+ ratio in bronchoalveolar lavage fluid.- More common in African-American females. Often asymptomatic except for enlarged lymph nodes. CXR: Bilateral adenopathy and coarse reticular opacities.CT: Extensive hilar and mediastinal adenopathy. Associated with Bell palsy, uveitis, granulomas (epithelioid, containing microscopic Schaumann and asteroid bodies), lupus pernio (skin lesions on face resembling lupus), interstitial fibrosis (restrictive lung disease), erythema nodosum, rheumatoid arthritis-like arthropathy, hypercalcemia (due to ↑ 1α-hydroxylase-mediated vitamin D activation in macrophages). Treatment: steroids (if symptomatic)
• Berylliosis Pneumoconiosis Associated with exposure to beryllium in aerospace and manufacturing industires. - Granulomatous (noncaseating) on histology and therefore occasionally responsive to steroids.- Affects upper lobes- Reticular, interstitial pattern (similar to sarcoidosis) ↑ risk of cancer and cor pulmonale.
• COPD exacerbation Triggers:- Viral infection: Rhinovirus, influenza, parainfluenza- Bacterial infection: Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae- Air pollution, pulmonary embolism Clinical presentation- Increased dyspnea and/or cough- Change in sputum color or quality- Increased respiratory rate, wheezing- Pursed lip breathing with prolonged expiration - Arterial blood gas: Hypoxemia, CO2 retention- CXR: Hyperinflation & flattened diaphragm
• Methemoglobulinemia Etiology:- Exposure to substances that increase methemoglobin levels (most common cause)- Nitrate or nitrite (eg, from dietary intake or polluted/high altitude water levels)- Drugs: benzocaine 0–3% of total hemoglobin: physiological>3%: visible cyanosis (a brownish-blue or greyish coloration of the skin and membranes)>20%: clinical symptoms of oxygen deprivation, brown blood ("chocolate-colored blood") Treatment:- Methylene blue: Reduces methemoglobin to hemoglobin.- Vitamin C
• Foreign body aspiration Most frequently occurs in the right mainstem bronchus. Triad:- Dyspnea- Cough- Focal wheezing

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