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USMLE Step 2 (Subject) / Respiratory (Lesson)

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• Restrictive lung disease Characterized by loss of lung compliance. Result in ↑ lung stiffness and ↓ lung expansion. Etiology:- Alveolar (edema, hemorrhage, pus)- Interstitial lung disease (idiopathic interstitial pneumonias)- Idiopathic pulmonary fibrosis (IPF)- Inflammatory (sarcoid, cryptogenic organizing pneumonia)- Neuromuscular (myasthenia, phrenic nerve palsy, myopathy)- Thoracic wall (kyphoscoliosis, obesity, ascities, pregnancy, ankylosing spondylitis)
• Interstitial lung disease A heterogenous group of disorders characterized by inflammation and/or fibrosis of the interstitium. - Advanced disease: Cystic spaces devlop in the lung periphery ("honey-combing"). Subgroups:(1) Exposure related: "coal worker's pneumoconiosis", asbestosis, silicosis, berylliosis, hypersensitivity pneumonitis, radiation-induced injury(2) ILD associated with systemic disease or connective tissue diseases: polymyositis/dermatomyositis, sarcoidosis, amyloidosis, vasculitis, CREST syndrome(3) Idiopathic: idiopathic pulmonary fibrosis, cryptogenic organizing pneumonia, acute interstitial pneumonia(4) Medications: Amiodarone, busulfan, nitrofurantoin, bleomycin, radiation Presentation:- Shallow, rapid breathing; dyspnea with exertion; chronic nonproductive cough- Cyanosis, inspiratory squeaks, fine or "Velcro-like" crackles, clubbing, or right heart failure Diagnosis:- CXR/CT (initial test): Reticular, nodular, or ground-glass pattern; "honey-comb" pattern- PFTs: ↓ TLC, ↓ FVC, ↓ DLCO (initial test), normal FEV1/FVC. - Serum markers of connective tissue diseases if clinically indicated.- Surgical biopsy (definitive test): Often to confirm a diagnosis of IPF Treatment:- Supportive: Avoid exposure to causative agents.- Medications: Anti-inflammatory, immunosuppresive agents (eg, corticosteroids), antifibrotic agents (pirfenidone, nintedanib) for IPF.- Surgery: Lung transplantation may be indicated at late stages of IPF.
• Antifibrotic agents - Pirfenidone - Nintedanib
• Hypersensitivity pneumonitis Alveolar thickening and noncaseating granulomas 2° to environmental exposure (eg, mold, hot tubs, cockatiels, down feather antigens). Presentation:- Acute: Dyspnea, fever, malaise, shivering, and cough starting 4-6 hours after exposure. Gather a job/travel history to determine exposure.- Chronic: Progressive dyspnea; examination reveals fine bilateral rales. Diagnosis:- CXR/CT: Variable - Upper lobe fibrosis is common in chronic disease Treatment: Avoid exposure; corticosteroids
• Eosinophilic pulmonary syndromes A diverse group of disorders characterized by eosinophilic pulmonary infiltrates and abnormal peripheral blood eosinophilia.  Includes:- Allergic bronchopulmonary aspergillosis- Löffler syndrome- Acute eosinophilic pneumonia- Drug-induced (eg, NSAIDs, nitrofurantoin, sulfonamides) Presentation:- Dyspnea, cough, potentially blood-tinged sputum, and/or fever Diagnosis:- CBC: Peripheral eosinophilia- CXR: Pulmonary infiltrates Treatment: Removal of extrinsic cause or treatment of underlying infection (eg, helminths) if identified. Corticosteroid treatment may be used.
• Chronic obstructive pulmonary disease (COPD) A chronic pulmonary disease that presents with progressive shortness of breath caused by airway inflammation. It is subdivided into chronic bronchitis and emphysema. - Chronic bronchitis: productive cough for at least 3 months each year for 2 consecutive years- Emphysema: permanent dilatation of pulmonary air spaces distal to the terminal bronchioles. Etiology:- Smoking- Air pollution, exposure to dusts- Recurrent pulmonary infections- α1-antitrypsin deficiency- Primary ciliary dyskinesia Classification:- Airflow limitation in patients with FEV1/FVC < 70%GOLD 1: mild; FEV1% ≥ 80%GOLD 2: moderate; FEV1% 50-79%GOLD 3: severe; FEV1% 30-49%GOLD 4: very severe; FEV1% < 30% GOLD A: ≤ 1 Exacerbation/year + Mild symptomsGOLD B: ≥ 1 Exacerbation/year + Severe symptomsGOLD C: ≥ 2 Exacerbations/year + Mild symptomsGOLD D: ≥ 2 Exacerbations/year + Severe symptoms- Emyphysema: Centrilobular (smokers, upper lobes) / Panlobular (α1-antitrypsin deficiency, lower lobes) Clinical features:- Dyspnea, cough- Cachexia, cyanosis, tachypnea, tachycardia- Advanced disease: Distended neck veins, barrel chest, use of accessory muscles, peripheral edema Diagnostics:- Physical exam: Hyperresonance on percussion, inspiratory coarse crackles and wheezing- Spirometry: FEV1/FVC < 70% (Tiffeneau-Pinelli index), ↓ FVC, ↓ FEV1, ↑ Residual volume, ↑ Intrathoracic gas volume, ↑ Total lung capacity, DLCO ↔ in chronic bronchitis and ↓ in emphysema- Post-bronchodilator test: ΔFEV1 ≤ 12%- ABG: Hypoxic hypercapnic respiratory acidosis Treatment:1. General considerations- Smoking cessation- Vaccinations: pneumococcal (every 5-6 years), influenza (annual)- Pulmonary rehabilitationGOLD A: No long-term treatment, but is treated when symptomaticGOLD B: Monotherapy with long-acting bronchodilatorGOLD C: Combination therapy with inhaled corticosteroids and long-acting bronchodilatorGOLD D: Combination therapy with inhaled corticosteroids, long-acting parasympatholytics and/or long-acting β2-agonists- Short-acting parasympatholytics: ipratropium bromide- Short-acting β2-agonists: salbutamol, fenoterol- Long-acting parasympatholytics: tiotropium bromide- Long-acting β2-agonists: salmeterol, formoterol- Inhaled corticosteroids: budesonide, fluticasone, beclomethasone- PDE type 4 inhibitors (PDE = phosphodiesterase): roflumilast- Continuous oxygen therapy: PaO2 ≤ 55 mm Hg or SaO2 ≤ 88 % at rest 
• Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) Etiology- 80% of cases are caused by infection - Common causative agents: Haemophilus influenzae, Streptococcus pneumoniae, viruses- Other triggers: drugs (e.g., beta blockers), allergens, air pollution, stress Clinical features:- Worsening of respiratory symptoms (cough, expectoration, dyspnea)- Fever accompanied by chills- Normal treatment does not relieve symptoms Treatment:- Oxygen if O2 < 92% (beware of potential risk of hypercapnia)- Beta agonists: inhaled short-acting beta adrenergic agonists (e.g., albuterol, levalbuterol)- Anticholinergics: short-acting anticholinergic agents (e.g., ipratropium bromide)- Glucocorticoids: prednisolone (oral or IV)- Antibiotic treatment if ≥ 2 cardinal symptoms. Empiric therapy includes macrolides (eg, azithromycin), respiratory fluoroquinolones (eg, levofloxacin, moxifloxacin), or penicillin/beta-lactamase inhibitors (eg, amoxicillin-clavulanate)- Mechanical ventilation: indicated for patients with severe AECOPD→ Non-invasive ventilation (NIV): most commonly NIV with bilevel positive airway pressure (BiPAP)→ Invasive ventilation (i.e., intubation): only if NIV is contraindicated or not tolerated- Supportive care: Bedrest in recumbent position, avoid tobacco use, thromboprophylaxis
• Asthma Allergic asthma:- Cardinal risk factor: atopy- Environmental allergens: pollen (seasonal), dust mites, domestic animals, mold spores- Allergic occupational asthma: from exposure to allergens in the workplace (e.g., flour dust) Nonallergic asthma:- Triggers: cold air, viral infections, tobacco smoke, medications (β-blockers, aspirin/NSAIDs), exercise. Clinical features:- Persistent, dry cough- End-expiratory wheezes - Shortness of breath- Chest tightness Diagnosis:1. Pulmonary function tests (spirometry)- Obstructive lung disease with increased airway resistance → ↓ FEV1, ↓ Tiffeneau index (FEV1/FVC ratio)- Obstruction is reversible with bronchodilators → diagnostic confirmation via post-bronchodilator test- Post-bronchodilator test: Obstruction is reversible with bronchodilators (increase in FEV1 by ≥12%)2. Methacholine challenge test (bronchoprovocation test)- Second-line diagnostic test if pulmonary function testing is nondiagnostic.3. Chest x-ray: Usually only indicated in patients with severe asthma to exclude differential diagnoses (e.g., pneumonia, pneumothorax)- ABGs Classification of asthma severity:- Intermittent: Symptoms ≤ 2 days/week, FEV1 > 80%- Mild: Symptoms ∼ 2 days/week, nighttime 3-4 times/month, FEV1 > 80%- Moderate: Symptoms most days, nighttime 1-2 times/week, FEV1 60-80%- Severe: Daily symptoms, most nights, FEV1 < 60% Treatment:Acute management- For mild symptoms: short-acting beta agonist- For exercise-induced asthma: short-acting beta agonist prior to exerciseLong-term management- Intermittent: PRN short-acting β2-agonist- Mild: Daily low-dose inhaled corticosteroid; PRN short-acting β2-agonist- Moderate: Daily low- or medium-dose inhaled corticosteroid + long-acting β2-agonist; PRN short-acting β2-agonist- Severe: Daily high-dose inhaled corticosteroid + long-acting β2-agonist; PRN short-acting β2-agonist; Consider omalizumab or systemic steroids if refractory.- Alternative treatment: Leukotriene pathway modifiers, theophylline, cromolyn sodiumInhaled corticosteroids do not take full effect until they have been used for approx. 1 week!- Preferred treatment in children: inhaled corticosteroids
• Status asthmaticus Extreme asthma exacerbation that does not respond to initial treatment with bronchodilators Clinical features:- Initially: orthopnea, tachypnea, tachycardia, hypoxemia and cyanosis, hypercarbia- Signs of imminent respiratory arrest→ Drowsiness/confusion→ Paradoxical thoracoabdominal movement→ Bradycardia→ Absent wheezing→ Absent pulsus paradoxus (indicative of respiratory muscle fatigue) Treatment:- Short-acting beta agonist- Inhaled anticholinergics (e.g., ipratropium)- Systemic glucocorticoids- Supplemental oxygen and/or helium-oxygen mixture (heliox)- Intravenous magnesium sulfate- Non-invasive ventilation (NIV)- Indications for intubation: use of accessory muscles, decreased oxygen saturation, inability to speak in full sentences, inadequate response to initial therapy, normalizing PCO2 or pH
• Bronchiectasis Etiology:- Airway obstruction (eg, cancer)- Rheumatic disease (eg, RA, Sjögren), toxic inhalation- Chronic or prior infection (eg, aspergillosis, mycobacteria)- Immunodeficiency (eg, hypogammaglobulinemia)- Congenital (eg, cystic fibrosis, alpha-1-antitrypsin deficiency) Clinical features:- Chronic productive cough with copious mucopurulent sputum- Dypnea- Hemoptysis- Digital clubbing Diagnostics:- Chest x-ray (best initial test)→ “Tram track” lines→ Thin-walled cysts (i.e., dilated bronchi forming sacs), possibly with air-fluid levels → Late-stage bronchiectasis: honeycombing- High-resolution computer tomography (HRCT): confirmatory test→ Dilated bronchi with thickened walls; possible signet-ring appearance and tram track lines→ Cysts, especially at bronchial ends in lower lobes, and honeycombing- Sputum culture and smear: to determine infectious etiology (i.e. bacteria, mycobacteria, and fungi)- Pulmonary function tests: Obstructive pattern- Bronchoscopy: to visualize tumors, foreign bodies, or other lesions Treatment:- Bronchopulmonary hygiene and chest physiotherapy: postural drainage, hydration, directed cough- Antibiotic therapy of exacerbations- Smoking cessation- Vaccinations (i.e. seasonal influenza vaccine, pneumococcal vaccine)- Inhaled bronchodilators
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• Lung cancer Pathologic types are divided into two subgroups:- Small cell lung cancer (SCLC) – 25% of lung cancers- Nonsmall cell lung cancer (NSCLC) – 75% of lung cancers; includes squamous cell carcinoma, adenocarcinoma, large cell carcinoma, and bronchoalveolar cell carcinoma Risk factors:- Cigarette smoking – accounts for > 85% of cases (lowest association for adenocarcinomas)- Exposure to carcinogens: passive smoking, asbestos, arsenic, radon, uranium- Family history (genetic predisposition) Staging: - NSCLC is staged via the primary TNM system.- SCLC is staged differently:→ Limited – confined to chest plus supraclavicular nodes, but not cervical or axillary nodes→ Extensive – outside of chest and supraclavicular nodes Clinical features: - Pulmonary symptoms: Cough, hemoptysis, progressive dyspnea, chest pain- Constitutional symptoms: Anorexia, weight loss, weakness, fever- Superior vena cava (SVC) syndrome – occurs in 5% of patients→ Most commonly occurs with SCLC→ Findings: facial fullness; facial and arm edema; dilated veins over anterior chest, arms, and face; jugular venous distention (JVD)- Phrenic nerve palsy – occurs in 1% of patients- Recurrent laryngeal nerve palsy (3% of patients) – causes hoarseness- Horner syndrome: unilateral facial anhidrosis, ptosis, and miosis- Paraneoplastic syndromes: SIADH, ectopic ACTH secretion, PTH-like hormone secretion, hypertrophic pulmonary osteoarthropathy, Eaton–Lambert syndrome Diagnostics:1. Chest x-ray and comparison to previous images if available2. CT imaging for further evaluation indicated if→ New lesion detected on chest x-ray→ Changes (e.g., enlargement) compared to previous chest x-ray→ No previous CXR is available3. Assessment of lesion size and probability of malignancy (based on CT findings and patient characteristics)- Increased probability of malignancy: History of smoking, age > 40 years, other (e.g., positive family history, asbestos exposure)4. PET if CT inconclusive or high probability of malignancy (> 8 mm)5. Bronchoscopy and biopsy6. Staging: CT scan (chest, liver, adrenal glands) and blood tests Treatment:- NSCLC: Surgical resection ± adjuvant chemotherapy (radiation therapy is only required if the resection margins are not tumor free)- SCLC: → Limited: Polychemotherapy + radiation therapy→ Extensive: Polychemotherapy
• Pleural effusion Transudative effusion: ↑ Capillary hydrostatic pressure and/or ↓ Capillary oncotic pressure- Congestive heart failure- Hepatic cirrhosis- Nephrotic syndrome Exudative effusion: ↑ Capillary permeability- Pneumonia- Malignancies (e.g., lung cancer, metastatic breast cancer, lymphoma, mesothelioma) - Tuberculosis- Pleural empyema- Collagen vascular diseases (e.g., SLE, rheumatoid arthritis)- Pancreatitis- Hemothorax- ChylothoraxPEs can cause transudative and exsudative effusion. Clinical features:- > 300 mL required for effusion to become evident- Pleuritic chest pain- Dry, nonproductive cough, and dyspnea Diagnostics:1. Chest x-ray: Blunting of costophrenic angle2. Ultrasound, recumbent x-ray CT scan to assess if fluid is free moving or loculated- Loculated → Thoracocentesis- < 1 cc → Observe- CHF → Diuresis and observe- Tappable → Thoracocentesis Light’s criteria:- Protein (pleural)/protein (serum) > 0.5- LDH (pleural)/LDH (serum) > 0.6- LDH > two-thirds the upper limit of normal serum LDH Treatment:- Treat underlying condition (e.g., loop diuretics for acute congestive heart failure, antibiotics for pneumonia).- Therapeutic thoracentesis (chest tube) to remove fluid- Tube thoracostomy: in recurrent pleural effusion or for urgent drainage of infected and/or loculated effusions± Systemic antibiotics such as clindamycin, meropenem, and piperacillin-clavulanate for 4-6 weeks  - Video-assisted thoracoscopic surgery (VATS)- Pleurodesis: chemical or surgical obliteration of the pleural space
• Acute respiratory distress syndrome (ARDS) Definition:- Acute onset (<1 week)- Bilateral infiltrates on chest imaging- Pulmonary edema not explained by fluid overload or CHF- Abnormal PaO2/FiO2 ratio→ 200-300: Mild→ 100-200: Moderate→ < 100: Severe Etiology:- Sepsis, eg, secondary to trauma, infection- Aspiration of gastric contents- Shock- Massive transfusions- Pancreatitis- Drug overdose, toxic inhalations Clinical features:- Tachypnea and tachycardia- Cyanosis, dyspnea, and diffuse crackles- Fever, cough, and chest pain may also be present Diagnostics:- ABGs: Initially, hypoxemic respiratory failure with ↓ PaO2 and respiratory alkalosis → PaO2/FiO2 ≤ 300 mm Hg; hypercapnic respiratory failure develops with disease progression.- Chest x-ray→ Diffuse bilateral infiltrates (perihilar bat wing or butterfly distribution of infiltrates)→ Air bronchogram→ Atelectasis→ Pleural effusions- Pulmonary artery catheter – enables a determination of PCWP→ If PCWP is low (<18 mm Hg), ARDS is more likely→ If PCWP is high (>18 mm Hg), cardiogenic pulmonary edema is more likely Treatment:- Oxygenation – try to keep O2 saturation >90%- Mechanical ventilation using high PEEP and low-tidal volumes- FiO2 < 0.5 to avoid oxygen toxicity- Standard tidal volume: ~ 6 mL/kg body weight
• Pulmonary hypertension Mean pulmonary arterial pressure ≥ 25 mm Hg at rest Classification of pulmonary hypertension (WHO) by cause:Group 1: Pulmonary arterial hypertension (PAH)→ Idiopathic→ Hereditary (e.g., BMPR2 mutation)→ Drug-induced: sympathomimetic appetite suppressants (e.g., diethylpropion), amphetamines, cocaineGroup 2: Left heart disease (e.g. valvular heart diseases, left-to-right shunt)Group 3: Chronic lung diseases and/or hypoxemia→ COPD, emphysema→ Obstructive sleep apnea→ Interstitial lung diseaseGroup 4: Chronic thromboembolic occlusion of the pulmonary vesselsGroup 5: Unclear multifactorial mechanisms Clinical features:- Dyspnea and/or syncope on exertion- Fatigue- Chest pain – exertional- Physical examination: → Loud P2, right-sided S3→ Left parasternal heave, right ventricular heave→ Pansystolic murmur of tricuspid regurgitation→ Nail clubbing, jugular vein distention, ascites, peripheral edema, hepatomegaly Diagnostics:- Doppler echocardiography (best initial test)→ Hypertrophy and/or dilation of the right heart ventricle→ Dilation of the coronary sinus→ Estimation of pulmonary arterial pressure- Right heart catheterization (confirmatory test)→ mPAP ≥ 25 mmHg at rest→ Pulmonary capillary wedge pressure: ≥ 15 mmHg in PH due to left heart disease- ECG: right axis deviation due to right ventricular hypertrophy- Chest x-ray→ Pronounced central pulmonary arteries→ Right heart hypertrophy (prominent right heart border)→ Signs of underlying cause (e.g., nodular opacities in interstitial lung disease, barrel chest in COPD) Treatment:- Diuretics- Physical exercise- Oxygen therapy- Vasoactive agents: Calcium channel blockers, prostacyclin analogs (e.g., iloprost), endothelin receptor antagonists (e.g., bosentan), PDE 5 inhibitors (e.g., sildenafil)
• Pulmonary embolism Etiology:- Deep vein thrombosis: Typically popliteal or femoral veins→ Risk factors: obesity, immobility, malignancy, pregnancy, dehydration, hypercoagulability, use of contraceptives, previous DVT - Fat embolism during major surgical interventions (e.g., endoprosthesis replacement, osteosynthesis)- Other: air embolism, amniotic fluid embolism, cement embolism Clinical features:- Acute onset of symptoms, often triggered by a specific event (e.g., on rising in the morning, sudden physical strain/exercise)- Dyspnea and tachypnea (> 50% of cases)- Sudden chest pain (∼ 50% of cases), worse with inspiration- Cough and hemoptysis- Possibly decreased breath sounds, dullness on percussion, split-second heart sound audible in some cases- Tachycardia (∼ 25% of cases), hypotension- Jugular venous distension- Low-grade fever Diagnostics:- Hemodynamically stable patients (systolic BP > 90 mmHg) with high probability of PE (Wells score > 4) → CTA → Unless strongly contraindicated (e.g., high risk of bleeding, recent surgery), administer immediate anticoagulation with unfractionated heparin before conducting a CTA→ If too unstable for CTA →  echocardiography - In patients with a low or medium probability of PE (Wells score ≤ 4) → measure D-dimer levels (+ ABG evaluation + CXR)→ If positive (D-dimers ≥ 500 ng/mL) → CTA → If negative → PE unlikely → consider other causes of symptoms- Arterial blood gas (ABG) test:→ Respiratory alkalosis: ↓ paO2 < 80 mmHg, ↓ paCO2, ↑ pH→ ↑ Alveolar-arterial (A-a) gradient: compares the oxygenation status of alveoli to arterial blood→ ↓ O2 saturation- Chest x-ray→ Atelectasis→ Pleural effusions→ Hampton's hump = wedge-shaped opacity in the peripheral lung with its base at the thoracic wall; caused by pulmonary infarction → Westermark sign = embolus leads to diminished perfusion of downstream lung tissue, which appears hyperlucent on radiograph- Ventilation/perfusion scintigraphy: in patients with severe renal insufficiency or contrast allergy- Pulmonary angiography: Gold standard but only conducted if CT angiography unavailable Treatment:- Initial anticoagulation (0-10 days): Low molecular weight heparin (LMWH) or fondaparinux- Long-term anticoagulation and prophylaxis (3-6 months): Anticoagulation treatment is indicated for a minimum of three months. Agents: Warfarin (target INR 2–3), LMWH, direct oral anticoagulants- Life-threatening embolism: Recanlization (e.g., thrombolytics, embolectomy)
• Interstitial lung disease Etiology:- Idiopathic pulmonary fibrosis (most common)- Cryptogenic organizing pneumonia (COP)- Environmental lung disease: Coal worker's pneumoconiosis, silicosis, asbestosis, beryllosis- Drug-induced: Amiodarone, nitrofurantoin, bleomycin, phenytoin, methotrexate- ILD associated with granulomas: Sarcoidosis, histiocytosis X, Wegener granulomatosis, Churg-Strauss syndrome- Hypersensitivity reactions- Connective tissue disorders: rheumatoid arthritis, scleroderma, SLE, mixed connective tissue disease- Radiation pneumonitis Clinical features:- Exertional dyspnea- Nonproductive cough- Fatigue Diagnostics:- Signs: Rales at the bases, digital clubbing, signs of pulmonary hypertension and cyanosis- PFT: Restrictive lung disease (e.g., low lung volumes, high/normal FEV1/FVC ratio), decreased DLCO- Chest x-ray→ Normal in approximately 10% of patients.→ Increase in reticular opacities (sign of fibrosis)→ Ground-glass opacities and honeycombing- CT or HR-CT: Irregular thickening of the interlobular septa, honeycombing, and bronchiectasis- Biopsy Treatment:- Corticosteroids and immune modulators- Lung transplantation in end-stage ILD
• Sarcoidosis Bimodal distribution: 25-35 years old with a second peak for females 45-65 years oldSex: F > M (2:1)Prevalence: higher among African-Americans in the US Clinical features: - Constitutional symptoms: Fever, malaise, weight loss, anorexia- Lungs: dry cough, dyspnea (especially with exercise)- Skin (25% of cases): Erythema nodosum, lupus pernio- Eyes (25% of cases): Anterior uveitis, posterior uveitis, conjunctivitis- Heart (5% of cases): Arrhythmias, heart block - Musculoskeletal system (25%-50%): Arthralgias and arthritis- Nervous system (5%): Bell palsy, optic nerve dysfunction, papilledema, peripheral neuropathy Lofgren's syndrome:1. Migratory polyarthritis2. Erythema nodosum3. Bilateral hilar lymphadenopathy Heerdfolt syndrome:1. Parotitis2. Bell's palsy3. Uveitis Diagnostics:- Chest x-ray (best initial test)Staging:Type 0: Normal findingsType I: Bilateral hilar lymphadenopathy (reversible)*Type II: Bilateral reticular or ground glass opacities with hilar lymphadenopathy → disseminated, reticulonodular infiltratesType III: Bilateral reticular or ground glass opacities without hilar lymphadenopathyType IV: Lung fibrosis- Lab tests: ↑ inflammatory markers, ↑ calcium, ↓ CD4+ T cells, ↑ angiotensin-converting enzyme (ACE)- Biopsy (Gold standard): non-caseating granulomas with giant cells- PFTs Treatment:- Isolated pulmonary sarcoidosis: usually no treatment required, as the disease is often asymptomatic and non‑progressive with a high rate of spontaneous remissions- Symptomatic or extrapulmonary sarcoidosis:→ First line: glucocorticoids→ Second line: alternative immunosuppressive therapy (e.g., methotrexate or azathioprine), possibly in combination with glucocorticoids→ Antimalarial drugs (e.g., chloroquine, hydroxychloroquine)
• Histiocytosis X Chronic interstitial pneumonia caused by abnormal proliferation of histiocytes (related to Langerhans cells of the skin). - Most patients (90%) are cigarette smokers. - Variants of disease include eosinophilic granuloma (localized to bone or lung), and two systemic forms –Letterer-Siwe disease and Hand-Schüller-Christian syndrome. Clinical features:- Dyspnea and nonproductive cough.- Spontaneous pneumothorax, lytic bone lesions, diabetes insipidus Diagnostics:- CXR has a honeycomb appearance- CT scan shows cystic lesions Treatment: - Corticosteroids are sometimes effective.- Lung transplantation may be necessary.
• Berylliosis Workers at risk:- Workers in high-tech fields, where alloys are often utilized (e.g., aerospace, nuclear, and electronics plants, ceramics industries, dental material production, and dye manufacturing) Characteristic featuers:- Noncaseating granulomatous disease affecting the lungs and skin- Chronic beryllium disease: Progressive dyspnea may occur within a few days of high-grade exposure. Diagnostics:- Chest x-ray:→ Reticular interstitial pattern (similar to sarcoidosis), affecting the upper lobes→ In some cases, hilar lymphadenopathy- Beryllium lymphocyte proliferation test Treatment: Glucocorticoids
• Silicosis Workers at risk:- Sandblasting, mining (e.g., coal mining), construction (e.g., tunnel construction), ceramics production, glass manufacturing, and working in foundries. Acute: short-term exposure to a large amount of crystalline silica dustChronic: long-term exposure to crystalline silica dust (>15 years) Clinical features:- Dyspnea, cough- Pleuritic pain- Fever, weight loss, fatigue- Cyanosis- Respiratory failure- Special form: Caplan syndrome (pneumoconiosis in combination with rheumatoid arthritis) → rapid development of basilar nodules and mild obstruction of ventilation Diagnostics:- Chest x-ray→ Eggshell calcification = well-defined, sickle-shaped calcification of the rims of hilar lymph nodes→ Bilateral diffuse ground glass opacities in the upper lobe- PFTs: mix of restrictive and obstructive lung disease- Biopsy Complications:- Tuberculosis: advanced silicosis increases the risk of tuberculosis. - Lung cancer: silicosis doubles the risk for developing lung cancer.
• Asbestosis Risk factors:- Occupations involving the manufacture or demolition of ships, plumbing, roofing, insulators, heat-resistant clothing, and brake-lining- Smoking Clinical features:- Long latent period- Exertional dyspnea- Dry cough → productive cough- Digital clubbing - Bilateral fine, basal end-inspiratory rales Diagnostics:- Chest x-ray:→ Diffuse bilateral infiltrates predominantly in the lower lobes→ Interstitial fibrosis→ In some cases, pleural effusion- HR-CT- PFTs: Restrictive ventilatory defects- Biopsy: microscopic asbestos (ferruginous) bodies and evidence of fibrosis Complications: Increased risk of bronchogenic carcinoma (smoking is synergistic) and malignant mesothelioma.
• Pneumococcal vaccination - Indication For all adults age ≥ 65, PCV13 vaccine is recommended followed by the PPSV23 vaccine 12 months later. For people age < 65 with certain high-risk conditions, sequential PCV13 and PPSV23 are also recommended.High-risk conditions:- Chronic heart disease- Lung disease- Sickle cell disease- Diabetes- Alcoholism- Cirrhosis- Leaks of cerebrospinal fluid or cochlear implant- Hodgkin disease, lymphoma or leukemia- Kidney failure- Multiple myeloma- Nephrotic syndrome- HIV infection or AIDS- Organ transplant- Long-term steroids, certain cancer drugs, radiation therapy- Smoker - Asthma
• Pleural empyema Accumulation of pus in the pleural cavity Etiology: - Infected parapneumonic pleural effusion- Untreated hemothorax that becomes infected- Ruptured lung abscess- Thoracic trauma Clinical features:- Pleuritic chest pain- Shortness of breath- Low-grade fever- Cough Diagnosis:- Chest x-ray:→ May resemble pleural effusion with blunting of the costophrenic angle; often loculated→ Large empyema: diffuse consolidation of the lung- Chest CT: very good at differentiating empyema from pleural effusion→ Split pleura sign: thickening of visceral and parietal pleura caused by fibrin that adheres to the surfaces, which results in vascular proliferation→ Septations- Thoracocentesis: pleural fluid analysis: Low glucose (< 60 mg/dL) and pH < 7.2 Treatment:- Chest tube (thoracostomy) to remove empyema fluid→ Intrapleural administration of fibrinolytic agents (to improve chest tube drainage of empyema fluid) may be considered.
• Allergic rhinitis Etiology:- Type I hypersensitivity reaction- Genetic predisposition to atopy Clinical features:- Recurrent episodes of sneezing, nasal congestion, rhinorrhea, and post-nasal drip- Itchy nose and throat- Pale, boggy nasal mucosa with hypertrophic turbinates- Nasal polyps may be seen in long-standing cases of allergic rhinitis. - Cobblestone appearance of the posterior pharyngeal wall- "Allergic shiners": Infraorbital edema & darkening- "Allergic salute": Transverse nasal crease- "Allergic facies": High-arched palate, open-mouth breathing Diagnostics:- RAST (radioallergosorbent test): measures serum concentrations of IgE antibodies against a specific allergen- Prick and intradermal tests to identify the allergen Treatment- Avoid exposure to the putative allergen (e.g., allergen, dust).- Intranasal sprays: → Antihistamines (e.g., azelastine) → Decongestants (α1-sympathicomimetics such as phenylephrine, oxymetazoline, xylometazoline) → Corticosteroids (e.g., budesonide, fluticasone) → Sodium cromoglycate→ Ipratropium bromide
• Aspirin exacerbated respiratory disease (AERD) A chronic condition characterized by Samter's triad; exacerbated by a pseudoallergic sensitivity reaction to aspirin and other NSAIDs (NSAID intolerance). Clinical features: Samter's triad 1. Asthma2. Chronic/recurrent rhinosinusitis3. Nasal polyps Diagnosis: NSAID/aspirin challenge test Treatment: avoid NSAIDs; aspirin desensitization
• Post-nasal drip syndrome (= Upper airway cough syndrome) Abnormally increased nasal mucus secretion that drips down the back of the throat and can lead to coughing, a feeling of obstruction in the throat, and throat clearing. Etiology:- Allergies- Cold temperatures- Viral or bacterial infections- Dry air Treatment:- First line: First-generation antihistamines (eg, diphenhydramine, chlorpheniramine)
• Ludwig's angina Etiology:- Mixed infection (Viridans streptococci and anaerobes)- Usually arising from an infected mandibular molar, an infection of the upper airways, or acute lingual tonsillitis- Predisposing factors: diabetes mellitus, alcoholism, immunocompromise Clinical features:- Submandibular space infection- Fever, mouth pain, stiff neck, difficulty swallowing, trismus- Anaerobic, gas-producing bacteria may cause crepitus- Airway obstruction may occur! Diagnostics:- CT scan of the neck: Rules out abscess Treatment:- IV antibiotics (eg, ampicillin-sulbactam, clindamycin) - Removal of the inciting tooth
• Retropharyngeal abscess Epidemiology:- Generally the most dangerous deep neck infection- Most common in children < 5 years of age  Etiology:- Pathogen: Streptococci (viridans Streptococci, S. pneumoniae), Staphylococci (including MRSA), Haemophilus influenzae, oral anaerobes (Peptostreptococci, Bacteroides species), often in a polymicrobial environment - Direct or indirect causes: Contiguous or lymphatic spread from oral (most common) or upper respiratory tract infections- Local penetrating pharyngeal trauma (e.g., from small bones such as of fish or chicken, or medical instruments) Clinical features:- Features of tonsillitis and trismus (minimal)- Neck asymmetry with unilateral swelling of the posterior pharyngeal wall (possible fluctuance) → inability to extend neck- Torticollis- Anterior cervical lymphadenopathy- Respiratory distress  Diagnosis:- Contrast-enhanced CT: shows hypodense lesion in retropharyngeal space, soft-tissue swelling, peripheral ring enhancement, mass effect - Gram stain and culture of aspirated abscess fluid and blood to identify causative pathogen- Lateral neck x-ray: shows a widened prevertebral (soft tissue) space (gas in the retropharyngeal space and lordosis) Treatment:- Airway management is always the first step if the patient has signs of respiratory distress- Hospitalization for all children and any patient with respiratory compromise- IV broad-spectrum antibiotics: empiric options include ampicillin-sulbactam or clindamycin. - Needle aspiration or incision and drainage of abscess immediately in patients with a compromised airway or other life-threatening complications Complications:- Airway obstruction- Spread of infection to carotid sheath (internal carotid artery erosion, jugular vein thrombophlebitis) and then mediastinum (acute necrotizing mediastinitis with widened mediastinum on chest x-ray) - Infection can spread and enter the skull base (epidural abscess) or the posterior mediastinum (pericarditis).
• Aspergillosis Invasive aspergillosis:- Risk factors: Immunocompromise (neutropenia, glucocorticoids, HIV)- Triad of fever, chest pain, hemoptysis- Pulmonary nodules with halo sign (nodules with surrounding grown glass opacities)- Positive cultures- Positive cell wall biomarkers (galactomannan, beta-D-glucan)- Management: Voriconazole +/- caspofungin Chronic pulmonary aspergillosis :- Risk factors: Lung disease/damage (cavitary tuberculosis)- >3 months: Weight loss (90%), cough, hemoptysis, fatigue- Cavitary lesion +/- fungus ball (mobile)- Positive Aspergillus IgG serology- Management: Resect aspergilloma (if possible), azole medication (voriconazole), embolization (if severe hemoptysis) Allergic bronchopulmonary aspergillosis (ABPA):- Chronic exposure to Aspergillus - Asthmatic symptoms (e.g., shortness of breath, wheezing)- Productive cough with brown bronchial mucous casts- Fungus ball in the paranasal sinuses with symptoms of chronic rhinosinusitis- Nonspecific symptoms: weight loss, chronic fatigue; irritation of the skin, mucus membranes, and eyes- History of asthma or cystic fibrosis- Positive Aspergillus antigen skin test OR ↑ IgE levels- Laboratory tests: ↑ ESR and eosinophilia- X-ray and CT: parenchymal opacities; features of bronchiectasis
• Predisposing conditions for aspiration pneumonia - Altered consciousness impairing cough reflex/glottic closure (eg, dementia, drug intoxication) - Dysphagia due to neurologic deficits (eg, stroke, neurodegenerative disease) - Upper gastrointestinal tract disorders (eg, GERD) - Mechanical compromise of aspiration defenses (eg, nasogastric & endotracheal tubes) - Protracted vomiting - Large-volume tube feedings in recumbent position
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• Solitary pulmonary nodules Factors increasing malignant probability:- Large size*- Advanced patient age- Female sex- Active or previous smoking- Family or personal history of lung cancer- Upper lobe location- Spiculated radiographic appearance *Size > 2 cm independently correlates with > 50% malignant probability
• Empiric treatment of community-acquired pneumonia Outpatient:- Macrolide or doxycycline (healthy)- Fluoroquinolone* or beta-lactam + macrolide (comorbidities) Inpatient (non-ICU):- Fluoroquinolone* (IV)- Beta-lactam + macrolide (IV) Inpatient (ICU):- Beta-lactam + macrolide (IV)- Beta-lactam + fluoroquinolone* (IV) *Respiratory fluoroquinolones (eg, levofloxacin, moxifloxacin) are required.
• Long-term home oxygen therapy COPD patients with: 1. Resting PaO2 ≤ 55 mmHg or SaO2 ≤ 88% on room air 2. PaO2 ≤ 59 mmHg or SaO2 ≤ 89% in patients with cor pulmonale, evidence of right heart failure, or hematocrit > 55% The dose of supplemental oxygen should be titrated so that SaO2 is maintained at > 90% during sleep, normal walking, and at rest. Survival benefits of home oxygen therapy are significant when it is used for ≥ 15 hours a day.
• Atelectasis Etiology: - Obstructive atelectasis (most common): e.g., foreign body, mucous plug, malignancy- Compressive atelectasis: e.g., pleural effusion- Adhesive atelectasis: surfactant deficiency or dysfunction, e.g., ARDS, respiratory distress syndrome in premature infants- Cicatrization atelectasis: parenchymal scaring, e.g., tuberculosis and fibrosis- Postoperative atelectasis: often occurs within 72 hours of surgery Clinical features:- Dyspnea, chest pain, tachypnea, tachycardia, cyanosis- Dull percussion note, diminished breath sounds, decreased fremitus over affected lung Diagnostics:- aBGA: hypoxemia, potentially low PaCO2, and respiratory alkalosis- Chest x-ray and CT: evidence of lobar collapse- Bronchoscopy (diagnostic and therapeutic): if etiology is unclear Treatment:- Analgesia- Early mobilization- Deep breathing exercises, directed coughing, and incentive spirometry
• Noninvasive positive-pressure ventilation Indications:- COPD- Cardiogenic pulmonary edema- Acute respiratory failure- Facilitate early extubation Contraindications:- Cardiac or respiratory arrest- Severe acidosis (pH < 7.10)- ARDS- Unstable cardiac arrhythmia/hemodynamic instability- Encephalopathy (GCS < 10)- Gastrointestinal bleed- Inability to protect airway (uncooperative, agitated, high aspiration risk)- Facial or neurological surgery, deformity, or trauma- Recent esophageal anastomosis
• Paraneoplastic syndromes All lung cancers:- General paraneoplastic manifestations: cachexia, increased risk of thrombosis (and lung embolism!)- Dermatomyositis- Acanthosis nigricans NSCLC:- Hypercalcemia of malignancy (squamous cell carcinoma)- Gynecomastia (large cell carcinoma)- Hypertrophic osteoarthropathy → Clubbing of the fingers and toes (Hippocratic fingers)→ Swelling and pain in joints and long bones- Hypercoagulability and thrombophlebitis migrans (adenocarcinoma)- Nonbacterial verrucous endocarditis (adenocarcinoma) SCLC:- Cushing syndrome- Syndrome of inappropriate antidiuretic hormone secretion (SIADH)- Lambert-Eaton syndrome (similar clinical features as myasthenia gravis)- Paraneoplastic cerebellar degeneration- Peripheral neuropathy
• Lung cancer screening Annual low-dose CT scan  Indications:- 55-80 years old- ≥ 30 pack years or quit < 15 years ago
• Extubation readiness criteria - pH > 7.25 - Fraction of inspired oxygen [FiO2] ≤ 40% - Positive end-expiratory pressure (PEEP) < 5 mmHg - Intact inspiratory effort and sufficient mental alertness to protect airway
• Tracheomalacia Collapsible intrathoracic airway Clinical features:- Respiratory distress- Expiratory stridor
• Pneumocystis pneumonia Interstitial pneumonia caused by the yeast-like fungal organism Pneumocystis jirovecii Risk factors:- HIV Infection: CD4 count: usually < 200/μL- History of PCP infection- Primary immunodeficiency disorders (e.g., severe combined immunodeficiency disorder) - Malignancy (e.g., leukemia, non-Hodgkin lymphoma)- Immunosuppressive treatment (e.g., chronic glucocorticoid therapy) indicated in: Stem cell or organ transplantation- Connective tissue disorders (e.g., systemic lupus erythematosus)- Vasculitides (e.g., polyarteritis nodosa)- Malnutrition Clinical features:- Symptoms typically have a gradual onset (days to weeks) - Low-grade fever and malaise- Dyspnea and non-productive cough- Fatigue, weight loss, chills Diagnostics:If PCP is suspected based on the history and clinical examination, oxygen saturation, the CD4+ count, the beta-D-glucan level should be measured and a CXR conducted. If the CXR is inconclusive, a high-resolution CT scan can be obtained. The diagnosis should generally be confirmed via microscopic identification of P. jirovecii from respiratory secretions. - Bilateral crackles and rhonchi- Pulse oximetry: oxygen saturation < 90 % at rest (worsens with exertion)- CD4 count: typically < 200/μL- ↑ Beta‑D‑glucan- Confirmatory test: microscopic identification of P. jirovecii in specimenobtained via bronchoalveolar lavage or induced sputum, with methenamine silver staining and immunofluorescence- Chest X‑ray: Typically symmetrical, diffuse interstitial infiltrates extending from the perihilar region Acute treatment:- High‑dose TMP/SMX for up to 3 weeks- Glucocorticoids: add in the case of severe respiratory insufficiency (either PaO2 < 70 mm or arterial‑alveolar oxygen gradient ≥ 35 Hg). - Alternatives if allergic to TMP/SMX or treatment of choice is ineffective→ Oral trimethoprim + dapsone→ Oral atovaquone→ Oral primaquine + clindamycin→ Moderate/severe disease: Oral primaquine + IV clindamycin
• Peritonsillar abscess Epidemiology:- Most common deep neck infection- Most common in adolescents and young adults Etiology:- Pathogens: Streptococcus pyogenes (most common), Streptococcus anginosus, viridans streptococci, Staphylococcus aureus, and Haemophilus species, often in a polymicrobial environment - Acute bacterial tonsillitis Clinical features:- Features of tonsillitis: fever, malaise, severe sore throat, dysphagia, and odynophagia- “Hot potato” voice (muffled speech), drooling, or halitosis- Trismus- Uvula shifted to the contralateral side, with inferior and medial displacement of tonsil- Unilateral fluctuant, swollen, erythematous tonsil with exudates (ipsilateral bulging of the palatine arch)- Ipsilateral cervical lymphadenopathy (and neck swelling) Diagnosis:- Usually a clinical diagnosis- Gram stain and culture of aspirated abscess fluid, and throat culture to identify causative pathogen- Contrast-enhanced CT if there is a clinical suspicion of other diagnoses or complications Treatment:- Airway management is always the first step!- IV antibiotics with good gram-positive and anaerobic coverage: empiric clindamycin or ampicillin-sulbactam - Incision and drainage or needle aspiration (surgical drainage): risk of airway obstruction, complications, or immunodeficiency. - Tonsillectomy indicated if: Unresponsive to drainage and antibiotics, recurrent tonsillitis or peritonsillar abscess, or other complications occur Complications:- Can become life-threatening due to airway compromise- Further spread of infection into the parapharyngeal space, retropharyngeal space, mediastinum (mediastinitis), or fascia (necrotizing fasciitis)- Aspiration pneumonia- Internal jugular vein thrombosis or thrombophlebitis- Bacteremia and sepsis
• Acute bronchitis Etiology: Viruses (> 90% of cases): Influenza A and B, Parainfluenza, Adenovirus, RSV, Rhinovirus, Coronavirus Clinical features:- Cough > 5 days- Resolves in 2-3 weeks- Sputum (∼ 50% of cases), especially as infection progresses - Runny nose and sore throat (likely symptoms of the preceding or simultaneous URI) - Chest pain and dyspnea- Headache- Malaise- Myalgias- No fever Diagnostics: Acute bronchitis is a clinical diagnosis- Auscultatory findings: Wheezing, rhonchi, coarse crackles Treatment:- Rest and adequate hydration- NSAIDs - Antibiotics: generally not recommended!
• Influenza Seasonal pattern: Most infections occur during the fall and winter.Virus: Influenza virus A and B (and rarely influenza C) Clinical features:- Sudden onset of high fever, chills, headache, muscle/joint aches, fatigue, and malaise- Patients often develop acute bronchitis with a cough that is usually dry but may produce small amounts of clear or blood-tinged sputum.- Hypotension and bradycardia are common (especially among women and older patients) Diagnostics:- Normal or slightly elevated inflammatory markers, relative lymphocytosis- Rapid antigen test: Detection of various influenza A/B antigens via nasal or pharyngealswabs- Serological testing (e.g., via complement fixation): Used to diagnose an infection after it has resolved (not relevant in acute illness) Complications:Primary influenza pneumonia- Hemorrhagic pneumonia with poor prognosis (less common than secondary bacterial bronchitis/pneumonia)- May progress to acute respiratory distress syndrome (ARDS) with respiratory/multiorgan failureSecondary bacterial bronchitis/pneumonia- After flu symptoms have improved, patients suddenly become febrile again and develop a productive cough with large amounts of purulent (sometimes bloody) sputum.- Bacteria: most frequently Streptococcus pneumoniae, but also S. aureus and Haemophilus influenzae- Signs suggestive of secondary infection with S. aureus→ Hyperacute onset of symptoms→ Hypoxemia→ Hemoptysis→ Multiple cavitary lesions on chest x-ray: pneumatoceles- Antibiotics: Penicillinase-resistant agents should be used
• CMV pneumonia Interstitial pneumonitis Etiology: immunocompromised patients (e.g., following bone marrow transplant or in HIV/AIDS patients with CD4 ≤ 50 cells/mm3) Clinical findings: fever, nonproductive cough, dyspnea Diagnostics:- Chest x-ray: diffuse bilateral interstitial infiltrates- Detection of CMV in bronchoalveolar lavage fluid or lung tissue samples following biopsy Treatment: IV ganciclovir (or IV foscarnet) and IV immunoglobulin (IVIG) therapy
• Epistaxis Etiology :- Nose picking (common cause)- Fractures to the middle third of the face, base of the skull, or the nasal septum- Foreign body in the nose- Dry nose (rhinitis sicca)- Nasal septal defects (e.g., deviated nasal septum , septal perforation)- Infections (e.g., granulomatous diseases such as rhinosporidiosis)- Tumors of the nasopharynx and/or paranasal sinuses (e.g., juvenile angiofibroma)- Vascular malformations (e.g., nasal hemangioma, hereditary hemorrhagic telangiectasia)- Medications, drugs (e.g., topical corticosteroids, cocaine)- Bleeding disorders- Hypertension Anterior epistaxis: Bleeding through the anterior nasal aperture∼ 90% of cases- More common among children and young adults- Kiesselbach's plexus (Little's region): Anteroinferior region of the nasal septum in which four arteriesanastamose (the anterior ethmoidal artery, sphenopalatine artery, greater palatine artery, and superior labial artery) Posterior epistaxis: Bleeding through the posterior nasal aperture- Bleeding is therefore not obvious but can be identified by examining the posterior pharyngeal wall, which appears blood-stained- The patient may swallow large amounts of blood and present with hematemesis.- Failure of anterior packing to control bleeding is highly suggestive of posterior epistaxis∼ 10% of cases- More common among elderly individuals Treatment 1. Immediate measures- Fluid resuscitation if the patient is hemodynamically unstable- Elevate the upper body and bend the patient's head forward. - Apply cold packs and sustained, direct pressure by pinching the nose at the nostrils for 5-10 minutes in order to occlude the bleeding vessel.- Apply topical vasoconstrictors (e.g., oxymetazoline, phenylephrine)2. If epistaxis continues after 10-15 minutes- First-line: cauterization of the bleeding vessel using silver nitrate or electrocautery. - Second-line: nasal packing using gauze impregnated with paraffinand antibiotics (covering for Staphylococcus aureus). 3. If epistaxis persists: arterial embolization or endoscopic ligation of the bleeding vessel- Anterior ethmoidal artery for anterior epistaxis- Sphenopalatine artery for posterior epistaxis
• Pharyngeal cancer Pharyngeal cancers include all malignant tumors arising in the nasopharynx, oropharynx, or hypopharynx. Epidemiology:- Age: 50-60 years in nasopharyngeal cancer; approx. 55-70 years in oro- and hypopharyngeal cancer- Sex: ♂ > ♀ - Nasopharyngeal cancer is rare in the United States; most common in patients of Mediterranean and southern Chinese (including Hong Kong) descent Risk factors:- Tobacco consumption- Alcohol use - Further risk factors: nitrosamine consumption from salted/preserved foods, chronic iron deficiency, long-term consumption of carcinogenic food (e.g., aflatoxin), exposure to radiation Associations:- Nasopharyngeal carcinoma: EBV infection- Oropharyngeal carcinoma: human papillomavirus infection- Diseases causing atrophy of the mucosa (e.g., Plummer-Vinson syndrome) Clinical features:- Usually asymptomatic for a long time; first manifestation often swollen cervical lymph node(s)Nasopharyngeal cancer:- Painless lymphadenopathy- Obstruction of the Eustachian tube: recurrent otitis media; conductive hearing loss- Discharge, nosebleeds, impaired nasal breathing- Infiltration of caudal cranial nerves → Garcin syndromeOropharyngeal cancer and hypopharyngeal cancer:- Common early symptom: local lymph node metastases causing enlarged cervical lymph nodes- Severe ear pain- Foreign body sensation, dysphagia, sore throat- Muffled voice Diagnostics:- Panendoscopy with biopsy- Histopathological examination (confirmatory test)- CT or MRI imaging: assesses tumor infiltration depth and invasion of surrounding structures Treatment:- Early or localized pharyngeal cancers→ Complete surgical resection of the tumor (preferred) or→ Radiation therapy- Locally advanced pharyngeal cancers:→ Induction chemotherapy, concurrent chemoradiation or radiation therapy→ Surgical resection only carried out if there is response to induction therapies, or if tumor has well-defined margins→ Additionally, excision of the cervical lymph nodes (neck dissection) may be indicated.- If inoperable, or if the patient rejects surgery: primary radiotherapy or radio- and chemotherapy
• Wells criteria Clinical symptoms of DVT – 3 PE more likely than other diagnoses – 3 Previous PE/DVT – 1.5 Tachycardia (heart rate > 100/min) – 1.5 Surgery or immobilization in the past four weeks – 1.5 Hemoptysis – 1 Malignancy (being treated, in palliative care or diagnosis less than 6 months ago) – 1 - Total score of > 4: PE likely- Total score of ≤ 4: PE unlikely
• Management of parapneumonic effusions Small effusion AND no respiratory distress or hypoxia → Oral antibiotics Moderate/large effusion OR Respiratory distress OR hypoxia → Ultrasound, IV antibiotics, drainage
• Air embolism Etiology:- Surgery: neurosurgical procedures (highest risk); laparoscopic surgery- Trauma- Barotrauma: mechanical ventilation ; decompression sickness- Accidental injection of air (infusion-related errors); intentional injection of air (suicidal/homicidal intent) Venous air embolism:- Sudden hypotension, tachycardia, hypoxia- Distended jugular veins- Mill wheel murmur- Cardiac arrhythmia/arrest- Chest x-ray: air shadows (hyperlucency) in the pulmonary arteries and cardiac chambers- Echocardiography: evidence of air in the (right) cardiac chambers Arterial air embolism:- Focal neurological deficits, impaired consciousness, coma- Acute heart failure, myocardial infarction, cardiac arrhythmias- Acute kidney failure- Ophthalmoscopy: air bubbles within the retinal vessels- CT scan of the brain, abdomen, or pelvis may show ischemic changes in the affected organs. Treatment:- Compression of the suspected site of entry (airtight sealing)- Correction of hypoxia and hypotension- Initiate CPR, if necessary- Position change (venous air embolism): Trendelenburg (head down position) and left lateral decubitus (Durant's maneuver)- Central venous line insertion and direct aspiration of air bubbles from the cardiac chambers

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