Podcast
Questions and Answers
What is the definition of pulmonary hypertension?
What is the definition of pulmonary hypertension?
Which of these is NOT a common clinical course characteristic of community-acquired bacterial pneumonia?
Which of these is NOT a common clinical course characteristic of community-acquired bacterial pneumonia?
What is the primary cause of hemodynamic pulmonary edema?
What is the primary cause of hemodynamic pulmonary edema?
Which of the following can cause pulmonary hypertension?
Which of the following can cause pulmonary hypertension?
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Which of the following is NOT considered a pulmonary vascular disease?
Which of the following is NOT considered a pulmonary vascular disease?
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What is the most common cause of pulmonary arterial obstructions leading to pulmonary hypertension?
What is the most common cause of pulmonary arterial obstructions leading to pulmonary hypertension?
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What is the primary mechanism by which antigenic drift occurs in Influenza virus type A?
What is the primary mechanism by which antigenic drift occurs in Influenza virus type A?
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What is the clinical presentation of pulmonary hypertension?
What is the clinical presentation of pulmonary hypertension?
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Which type of pneumonia is most likely to develop in a patient with a weakened immune system after a long hospital stay?
Which type of pneumonia is most likely to develop in a patient with a weakened immune system after a long hospital stay?
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What is a possible cause of pulmonary hypertension in a patient with systemic sclerosis?
What is a possible cause of pulmonary hypertension in a patient with systemic sclerosis?
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Which of these factors would likely predisposition patients to pulmonary infections?
Which of these factors would likely predisposition patients to pulmonary infections?
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What are the morphological features of pulmonary hypertension?
What are the morphological features of pulmonary hypertension?
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What is the difference between precapillary and postcapillary pulmonary hypertension?
What is the difference between precapillary and postcapillary pulmonary hypertension?
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How does a deficiency of α1-antitrypsin affect lung tissue?
How does a deficiency of α1-antitrypsin affect lung tissue?
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What is the most common origin of pulmonary emboli?
What is the most common origin of pulmonary emboli?
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Which of the following is a possible cause of undifferentiated or multifactorial pulmonary hypertension?
Which of the following is a possible cause of undifferentiated or multifactorial pulmonary hypertension?
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What are the characteristic morphologic changes seen in emphysema?
What are the characteristic morphologic changes seen in emphysema?
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Which of the following is NOT a common risk factor for pulmonary embolism?
Which of the following is NOT a common risk factor for pulmonary embolism?
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What is the clinical significance of a pulmonary embolism dependent upon?
What is the clinical significance of a pulmonary embolism dependent upon?
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What is the typical presentation of a pulmonary infarct?
What is the typical presentation of a pulmonary infarct?
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Which of the following is NOT a symptom of pulmonary embolism?
Which of the following is NOT a symptom of pulmonary embolism?
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What is the primary goal of treatment for pulmonary embolism?
What is the primary goal of treatment for pulmonary embolism?
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What is a saddle embolus?
What is a saddle embolus?
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Which of the following is a non-thrombotic pulmonary embolus?
Which of the following is a non-thrombotic pulmonary embolus?
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What is the term used to describe the structural changes that occur in the airways of individuals with asthma?
What is the term used to describe the structural changes that occur in the airways of individuals with asthma?
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Which of the following is NOT a typical morphological finding in airway remodeling?
Which of the following is NOT a typical morphological finding in airway remodeling?
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Which of the following is a characteristic feature of bronchiectasis?
Which of the following is a characteristic feature of bronchiectasis?
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What is the primary pathological process in idiopathic pulmonary fibrosis?
What is the primary pathological process in idiopathic pulmonary fibrosis?
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Which of the following is a recognized risk factor for the development of lung cancer?
Which of the following is a recognized risk factor for the development of lung cancer?
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What is the most common histological subtype of lung cancer?
What is the most common histological subtype of lung cancer?
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Which of the following is a characteristic feature of a functioning carcinoid tumor of the lung?
Which of the following is a characteristic feature of a functioning carcinoid tumor of the lung?
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What is the most common genetic mutation associated with idiopathic pulmonary hypertension?
What is the most common genetic mutation associated with idiopathic pulmonary hypertension?
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Which of the following is NOT a characteristic feature of Goodpasture syndrome?
Which of the following is NOT a characteristic feature of Goodpasture syndrome?
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What is the most common pattern of metastasis to the lung?
What is the most common pattern of metastasis to the lung?
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What is the typical age range for individuals diagnosed with idiopathic pulmonary hypertension?
What is the typical age range for individuals diagnosed with idiopathic pulmonary hypertension?
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Which of the following best describes the mechanism of injury in Goodpasture syndrome?
Which of the following best describes the mechanism of injury in Goodpasture syndrome?
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What is the main distinguishing characteristic of Granulomatosis and polyangiitis (GPA)?
What is the main distinguishing characteristic of Granulomatosis and polyangiitis (GPA)?
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What is the significance of hemosiderin-laden macrophages in the lung tissue of individuals with Goodpasture syndrome?
What is the significance of hemosiderin-laden macrophages in the lung tissue of individuals with Goodpasture syndrome?
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Which of the following is a common symptom of both Granulomatosis and polyangiitis and Goodpasture syndrome?
Which of the following is a common symptom of both Granulomatosis and polyangiitis and Goodpasture syndrome?
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Which of the following is a condition that may predispose to pulmonary infection?
Which of the following is a condition that may predispose to pulmonary infection?
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Which of the following bacteria is most likely to cause pneumonia in an immunocompromised patient due to chemotherapy?
Which of the following bacteria is most likely to cause pneumonia in an immunocompromised patient due to chemotherapy?
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What is a predisposing condition for aspiration pneumonia?
What is a predisposing condition for aspiration pneumonia?
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What is a hallmark characteristic of aspiration pneumonia?
What is a hallmark characteristic of aspiration pneumonia?
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What is a possible outcome of aspiration pneumonia?
What is a possible outcome of aspiration pneumonia?
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Which of the following fungal organisms is commonly associated with pneumonia in immunocompromised patients?
Which of the following fungal organisms is commonly associated with pneumonia in immunocompromised patients?
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Flashcards
Airway remodeling
Airway remodeling
Structural changes in the airways due to chronic inflammation, often seen in asthma.
Asthma triggers
Asthma triggers
Environmental and genetic factors that can worsen asthma symptoms and attacks.
Bronchiectasis
Bronchiectasis
Chronic condition involving dilation and damage of the bronchial tubes, often linked with infections.
Fibrosing restrictive lung diseases
Fibrosing restrictive lung diseases
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Granulomatous lung diseases
Granulomatous lung diseases
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Lung carcinoma types
Lung carcinoma types
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Carcinoid tumor
Carcinoid tumor
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Hyperplasia-dysplasia-carcinoma sequence
Hyperplasia-dysplasia-carcinoma sequence
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Congenital lung abnormalities
Congenital lung abnormalities
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Atelectasis
Atelectasis
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Hemodynamic pulmonary edema
Hemodynamic pulmonary edema
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ALI/ARDS
ALI/ARDS
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Antigenic drift
Antigenic drift
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Obstructive lung disease
Obstructive lung disease
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Chronic bronchitis
Chronic bronchitis
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Atopic asthma
Atopic asthma
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Acute Lung Injury
Acute Lung Injury
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Morphology of DAD
Morphology of DAD
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Pulmonary Embolism (PE)
Pulmonary Embolism (PE)
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Risk Factors for PE
Risk Factors for PE
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Saddle Embolus
Saddle Embolus
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Pulmonary Infarcts
Pulmonary Infarcts
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Signs of PE
Signs of PE
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Prevention of PE
Prevention of PE
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Aspiration Pneumonia
Aspiration Pneumonia
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Opportunistic Organisms
Opportunistic Organisms
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Mixed Flora in Aspiration
Mixed Flora in Aspiration
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HIV-Related Lung Disease
HIV-Related Lung Disease
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Necrotizing Pneumonia
Necrotizing Pneumonia
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Idiopathic pulmonary hypertension
Idiopathic pulmonary hypertension
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BMPR2 mutation
BMPR2 mutation
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Goodpasture syndrome
Goodpasture syndrome
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Symptoms of Goodpasture syndrome
Symptoms of Goodpasture syndrome
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Granulomatosis and polyangiitis
Granulomatosis and polyangiitis
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Anti-neutrophil cytoplasmic antibodies (PR3-ANCAs)
Anti-neutrophil cytoplasmic antibodies (PR3-ANCAs)
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Pulmonary infection predispositions
Pulmonary infection predispositions
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Defense mechanisms of lungs
Defense mechanisms of lungs
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Pulmonary Hypertension
Pulmonary Hypertension
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Causes of Pulmonary Hypertension
Causes of Pulmonary Hypertension
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Symptoms of Pulmonary Hypertension
Symptoms of Pulmonary Hypertension
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WHO Classification 1
WHO Classification 1
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WHO Classification 2
WHO Classification 2
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Chronic Lung Diseases
Chronic Lung Diseases
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Pulmonary Vascular Morphology
Pulmonary Vascular Morphology
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Right Ventricular Hypertrophy
Right Ventricular Hypertrophy
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Study Notes
Learning Objectives
- List and briefly describe common congenital lung abnormalities.
- Define atelectasis and describe the principal types.
- Distinguish hemodynamic pulmonary edema from pulmonary edema arising from microvascular injury. Understand and recognize morphologic changes seen with hemodynamic pulmonary edema.
- Describe acute lung injury/acute respiratory distress syndrome (ALI/ARDS), and understand the associated pathogenesis, morphologic changes, and clinical course.
- Describe pulmonary vascular diseases, their pathogenesis and courses, including pulmonary embolism, pulmonary hypertension, and pulmonary hemorrhage syndromes.
- Relate factors predisposing patients to pulmonary infections.
- List and briefly describe common causative organisms in community-associated bacterial pneumonia.
- Describe the morphologic changes and clinical course of community-acquired bacterial pneumonia.
- List common viruses implicated in community-acquired viral pneumonia.
- Explain the concept of antigenic drift and antigenic shift as observed in influenza virus, type A.
- Relate the pathogenesis of influenza virus pneumonia, and the morphologic features of viral pneumonia generally.
- Describe health care-associated pneumonia, hospital-associated pneumonia, aspiration pneumonia, the type of patients typically affected, and the organisms commonly implicated.
- Describe lung abscess, its pathogenesis, morphologic features, and clinical course.
- Discuss fungal causes of chronic pneumonia, epidemiologic features, and clinical and pathologic findings.
- Describe pneumonia in an immunocompromised patient, and list common causative organisms.
- Briefly discuss pulmonary disease in HIV-infected patients.
- Define obstructive lung disease and explain common pulmonary function test findings.
- Describe clinically important subtypes of emphysema, anatomic patterns of involvement, clinical associations, pathogenesis, and morphologic changes seen in emphysema. Explain why emphysema is an obstructive lung disease and relate its clinical course.
- Describe the effect of a₁-antitrypsin deficiency on lung tissue.
- Define chronic bronchitis and relate its pathogenesis, morphologic features, and clinical features.
- Describe asthma and relate the pathogenesis of atopic asthma. Give examples of stimuli known to precipitate asthma.
- Describe the changes seen in "airway remodeling."
- Relate genetic and environmental factors known to predispose and precipitate asthma.
- Describe the morphologic changes and clinical course of asthma.
- Describe bronchiectasis, and list examples of precipitating causes. Relate the pathogenesis, morphologic features, and clinical course.
- Describe the general features of chronic diffuse (restrictive) lung diseases.
- Describe the clinical features, pathogenesis, and morphologic findings of fibrosing restrictive lung diseases, including idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, cryptogenic organizing pneumonia, autoimmune disease-associated lung disease, pneumoconiosis, and therapy-related lung diseases.
- Describe the morphologic features of usual interstitial pneumonia.
- Describe the pathogenesis, morphologic findings, and clinical features of granulomatous lung diseases, including sarcoidosis and hypersensitivity pneumonitis.
- Relate the clinical and morphologic findings in smoking-related interstitial lung diseases, including desquamative interstitial pneumonia and respiratory bronchiolitis-associated interstitial lung disease.
- Describe the clinical and morphologic features of pulmonary Langerhans cell histiocytosis.
- Discuss clinicopathologic features of pulmonary alveolar proteinosis and surfactant function disorders.
- Discuss the epidemiology, etiology, and pathogenesis of lung carcinoma.
- Describe the clinical and pathological characteristics of major histologic subtypes of lung carcinoma. Identify common mutational abnormalities associated with these subtypes.
- Understand precursor lesions to lung carcinoma.
- Describe typical and atypical carcinoid tumor of the lung, and the clinical features of a functioning carcinoid tumor.
- Describe common patterns of metastases to the lung.
- Describe malignant mesothelioma, its epidemiologic, clinical, and pathologic features.
- Describe the morphologic and clinical characteristics of sinonasal and nasopharyngeal tumors, including nasopharyngeal angiofibroma, sinonasal papilloma, olfactory neuroblastoma, and nasopharyngeal carcinoma.
- Describe benign mass-forming lesions of the larynx, including reactive nodules and squamous papillomas.
- Describe the clinical characteristics and morphologic features of squamous cell carcinoma of the larynx. Understand the hyperplasia-dysplasia-carcinoma sequence.
Congenital Anomalies
- Pulmonary hypoplasia: Decreased weight, volume, and acini for age/body weight; compression of lung(s) in utero (e.g., diaphragmatic hernia); severe cases are fatal shortly after birth.
- Foregut cyst: Bronchogenic, esophageal, or enteric.
- Pulmonary sequestration: A segment of lung tissue without airway connection and with systemic circulatory supply (not pulmonary).
Atelectasis
- Resorption atelectasis: Complete airway obstruction, air in dependent lung is resorbed, mediastinum shifts toward affected lung.
- Compression atelectasis: Fluid, tumor, or air accumulate in pleural space, preventing normal expansion—mediastinum shifts away from affected lung.
- Contraction atelectasis: Pulmonary or pleural fibrosis prevents normal expansion, irreversible.
Pulmonary Edema
- Hemodynamic pulmonary edema: Intra-alveolar fluid accumulation due to increased hydrostatic pressure in pulmonary circulation. Fluid accumulation is basally at first, alveolar capillaries are congested, and an intra-alveolar transudate is observed, pink and granular appearance. Hemosiderin-laden macrophages (heart failure cells) may be present with chronic pulmonary edema; the lungs may become edematous, brown, and indurated. Decreased oxygenation and increased infection risk.
- Microvascular injury pulmonary edema: Injury to or inflammation of alveolar vascular endothelium and/or respiratory epithelium; infectious or toxic insults; can be localized or diffuse.
Acute Lung Injury/Acute Respiratory Distress Syndrome (ALI/ARDS)
- Inflammation-induced vascular permeability, leading to diffuse pulmonary edema and rapid onset of hypoxemia.
- Several predisposing factors, including infectious agents, physical injury, toxic substances, and hemodynamic disturbances.
- Sepsis, diffuse pulmonary infection, gastric aspiration, and trauma contribute to >50% of cases.
- Pathogenesis: Endothelial activation, neutrophil accumulation and activation, accumulation of intra-alveolar fluid and hyaline membranes, resolution of injury.
- Morphology: Grossly heavy, firm, and wet lungs; microvascular changes observed include congested interstitial and intra-alveolar edema, necrosis of type I and type II pneumocytes, presence of hyaline membranes, and collapse of some alveoli—interstitial scarring can also occur.
- Clinical course depends on cause and severity. Mortality is approximately 40%.
Pulmonary Embolism
- Important cause of morbidity and mortality in hospitalized adults.
- 95% originate in deep veins of the legs.
- Risk factors: post-surgical (hip/knee), severe trauma/burns, disseminated cancer, congestive heart failure, OCPs/pregnancy, primary hypercoagulable state, immobility.
- Clinical significance depends on extent of pulmonary artery blood flow obstruction, size of occluded vessel, patient's cardiovascular health, and number of emboli.
- Consequences: Increase in pulmonary artery pressure from blockage of flow and vasospasm, ischemia of downstream pulmonary parenchyma, sudden death (often due to blockage of blood flow through lungs or acute right-sided heart failure).
- Usually >60% of pulmonary vasculature obstructed.
- Saddle embolus: Large embolus lodging in the main pulmonary artery or at the bifurcation.
- Small emboli travel peripherally, causing infarction and ischemic hemorrhage.
- Infarcts typically involve lower lobes, and most cases are multiple. Infarcts are initially hemorrhagic (red-blue) and turn to scar tissue.
- Signs and symptoms: Severe chest pain, dyspnea, and shock; Smaller emboli may be silent and cause transient chest pain and cough. Risk of recurrent PE in patients is approximately 30%.
- Prevention includes early mobilization, elastic stockings, graduated compression stockings, and anticoagulants; treatment involves anticoagulation and supportive measures.
- Non-thrombotic emboli: Rare but potentially lethal—air, fat, amniotic fluid and talc common types.
Pulmonary Hypertension
- Defined as mean pulmonary arterial pressure >20 mmHg.
- May be caused by: Decrease of cross-sectional area of pulmonary vascular bed, or increased pulmonary vascular blood flow.
- Clinically: dyspnea, fatigue, syncope, chest pain, right ventricular hypertrophy, death due to cor pulmonale.
- WHO Classification:
- Pulmonary arterial hypertension (PAH): Fibromuscular remodeling of distal pulmonary arterioles - genetic or molecular events, certain toxic drugs (e.g. methamphetamines), liver disease, HIV, or other conditions.
- Pulmonary hypertension associated with left heart disease
- Chronic obstructive or interstitial lung diseases and/or hypoxia: Severity is variable.
- Pulmonary arterial obstructions: Thrombotic mechanical obstruction is common.
- Undifferentiated or multifactorial causes (e.g., schistosomiasis).
- Frequently associated with a medial hypertrophy of pulmonary muscular and elastic arteries, pulmonary arterial sclerosis, and plexiform lesions (tufts of capillaries spanning lumens of dilated small arteries).
Pulmonary Hemorrhage Syndromes
- Goodpasture syndrome: Kidney and lung injury due to presence of anti-basement membrane antibodies. Usually presents as progressive glomerulonephritis (kidney disease) and necrotizing hemorrhagic interstitial pneumonitis. Common symptoms: hemoptysis, dyspnea. Treatment: plasmapheresis and immunosuppressants.
- Granulomatosis and polyangiitis (formerly Wegener's granulomatosis): Necrotizing vasculitis; presents with upper respiratory tract (URT) signs and symptoms (e.g. cough, hemoptysis, chest pain, chronic sinusitis, epistaxis, nasal septal perforation), can also involve kidneys, lungs, etc. High correlation (90% of cases) with anti-neutrophil cytoplasmic antibodies (PR3-ANCAs).
Pulmonary Infections
- General Considerations: Very common; 8th leading cause of mortality in the US. Underlying systemic conditions (immunodeficiency, chronic diseases, etc.) can predispose to pulmonary infections. Defense mechanisms to pulmonary infections can be compromised (e.g. cough reflex, impaired ciliary function, mucus stasis, decreased pulmonary macrophage activity, pulmonary edema).
- Community-Acquired Bacterial Pneumonia: Predisposing conditions include: age (young or old), chronic disease (COPD, diabetes, CHF), and absent splenic function (encapsulated bacterial infections). Common causative organisms include Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Legionella pneumophila.
- Morphology: Consolidation (solidification) of lung tissue results from bacterial invasion, leading to alveolar filling with inflammatory cells & exudate. Patterns: bronchopneumonia (patchy involvement) and lobar pneumonia (entire lobe consolidation). Stages of consolidation include congestion, red hepatization, grey hepatization, and resolution.
- Clinical course: abrupt fever, shaking chills, productive cough (rust colored sputum), opaque/focal opacities on x-ray. Complications including abscess, empyema (pleural involvement), and bacteremia.
- Community-Acquired Viral Pneumonia: Common organisms include influenza viruses (A, B, and C), RSV, human metapneumovirus, adenovirus, and rhinoviruses, coronaviruses. Predisposing factors include young age, elderly, malnutrition/alcoholism, and chronic illness. Inflammation & damage to defense systems (ciliary mechanism) lead to bacterial superinfection.
- Influenza virus: Causes epidemics and pandemics. The viral proteins hemagglutinin and neuraminidase facilitate infection and viral release, respectively. Frequent antigenic drift and shift (genome rearrangement) lead to new viral strains and pandemics. Infection generally involves the upper respiratory tract, and then the infection spreads to the lungs via respiratory epithelium leading to intraalveolar fluid accumulation, cell death, and inflammation. Prominent lung findings: patchy or extensive vascular congestion, inflammation in the interstitial tissue, and edema
- Clinical course depends on host immune status, virulence, and co-occurring conditions.
- COVID-19: Transmission by respiratory droplets. Potential for abnormally increased cytokine response, development of arterial and venous thrombosis. A wide range of clinical presentations, from asymptomatic to severe pulmonary disease and multiorgan failure, depending on host factors.
- Chronic Pneumonia: Infectious agents include endemic fungi in the US (histoplasmosis and blastomycosis) and inhaled soil particles contaminated by bird/bat droppings. Histoplasmosis: Typically a self-limiting infection; possible progression to extensive pulmonary infection (extra pulmonary involvement). Blastomycosis: Typically presents with productive cough, chest pain, headache, anorexia, and fever. Coccidiomycosis: Involves inhalation of airborne arthroscones leading to lung granulomas—involves cell-mediated immunity.
- Hospital-acquired pneumonia: This occurs typically following a hospital stay. Predisposing conditions include mechanical ventilation, severe underlying disease, immunosuppression, and invasive access devices. Common causative organisms are gram-positive cocci (e.g., S. aureus) and gram-negative rods (e.g., Enterobacteriaceae, Pseudomonas spp.).
- Aspiration pneumonia: Occurs when gastric contents are aspirated into lungs. Predisposing factors include debilitation, unconsciousness, or conditions affecting swallowing (stroke). Usually mixed flora is involved, with a high likelihood of chemical irritation causing a potential for necrotizing pneumonia and lung abscess development.
- Pneumonia in an immunocompromised host: May result from any cause of immunosuppression. Organisms are highly opportunistic, including bacteria (Pseudomonas aeruginosa, Mycobacterium spp.), viruses (cytomegalovirus [CMV], herpesviruses), and fungi (Pneumocystis jirovecii, Candida spp., Aspergillus spp., Cryptococcus neoformans, Mucormycoses), and can cause pulmonary infiltrates that may need differentiation from other causes.
- HIV-related lung disease: Contributes to 30-40% of hospitalizations of HIV+ patients. Opportunistic infections often depend on CD4+ T-cell count; a count of >200 cells/mL favors bacterial/tubercular infections vs <200/mL favors Pneumocystis pneumonia. Common accompanying infections include Kaposi sarcoma, non-Hodgkin lymphoma, and lung cancer.
- Lung abscess: Defined as local suppurative process producing lung tissue necrosis. Arises from material aspiration. Antecedent primary lung infections are common causes. Complications include septic embolism caused by infective endocarditis, and the possibility of neoplastic obstruction leading to infection.
Tuberculosis (TB)
- Causative organism: Mycobacterium tuberculosis. Infection via airborne droplets—entry into macrophages, replication within macrophages, seeding of multiple sites, bacteremia. Immune response: Cell-mediated (immune cells attempt to contain infection, three weeks post exposure). Granulomatous inflammation/tissue damage.
- Primary TB: Infection in a previously unexposed patient; development of a "Ghon complex" (focal lung parenchyma consolidation/necrosis, hilar lymph node(s) with caseating necrosis); a focus of pulmonary scarring results. Approximately 5% develop significant disease at this point, often in immunocompromised patients.
- Secondary TB: Arises from dormant primary lesions in a previously sensitized host, often occurring in apices of one or both lungs; widespread systemic dissemination possible. Often involves multiple lesions. Common sites of disseminated involvement include liver, bone marrow, spleen, adrenal glands - disseminated TB may present in single organ (vertebrae: Pott's disease).
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Test your knowledge on pulmonary hypertension and pneumonia with this comprehensive quiz. Explore definitions, causes, clinical presentations, and related diseases. Ideal for students and healthcare professionals alike who are looking to deepen their understanding of respiratory conditions.