Respiratory Pathology Quiz
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Questions and Answers

Which of the following disorders is NOT included in the learning objectives outlined for the Respiratory Pathology lectures?

  • Bronchial Asthma
  • Pneumonia (correct)
  • Idiopathic Pulmonary Fibrosis
  • Pulmonary Hypertension

    • What is the main difference between emphysema and bronchiectasis within the context of Chronic Obstructive Pulmonary Disease (COPD)?

  • Emphysema is a reversible condition, while bronchiectasis is irreversible.
  • Emphysema is characterized by airway inflammation, while bronchiectasis involves permanent dilation of the airways.
  • Emphysema is caused by smoking, while bronchiectasis is caused by infections.
  • Emphysema affects the alveoli, while bronchiectasis primarily affects the bronchi. (correct)

    • Which of these conditions would be classified as a restrictive pulmonary disease?

  • Pneumoconiosis (correct)
  • Congenital pulmonary hypoplasia
  • Pulmonary embolism
  • Acute respiratory distress syndrome (ARDS)

    • What is the primary pathophysiologic change that leads to pulmonary hypertension?

    <p>Increased pressure within the pulmonary arteries (A)</p> Signup and view all the answers

    How does atelectasis lead to clinical manifestations?

    <p>It constricts the airways, leading to shortness of breath and difficulty breathing. (B)</p> Signup and view all the answers

    Which of the following is a key distinguishing feature between ARDS and NRDS?

    <p>ARDS can be caused by various factors, while NRDS is primarily seen in newborns. (C)</p> Signup and view all the answers

    Which of the following is NOT a type of restrictive pulmonary disease?

    <p>Bronchiectasis (B)</p> Signup and view all the answers

    What is the most common cause of pulmonary embolism?

    <p>Thrombotic embolism (A)</p> Signup and view all the answers

    What does the term "interstitial edema" refer to in the context of pulmonary edema?

    <p>Fluid accumulation in the interstitial space between the alveoli and capillaries (C)</p> Signup and view all the answers

    Which of the following conditions can contribute to non-cardiogenic pulmonary edema?

    <p>Kidney failure (A)</p> Signup and view all the answers

    Which of the following cellular components are commonly found in alveolar edema due to heart failure?

    <p>Hemosiderin-filled macrophages (B)</p> Signup and view all the answers

    What does "V/Q mismatch" refer to in the context of pulmonary edema?

    <p>A mismatch between the volume of blood flow and the volume of air flow in the lungs (B)</p> Signup and view all the answers

    What is the most common characteristic visualized on a chest X-ray in a patient with pulmonary edema?

    <p>Diffuse pulmonary opacities (D)</p> Signup and view all the answers

    In the context of pulmonary edema, which of the following can contribute to decreased plasma oncotic pressure?

    <p>Liver disease (C)</p> Signup and view all the answers

    Which of the following conditions is NOT associated with increased tendency to clotting and thus can contribute to thrombotic pulmonary embolism?

    <p>Diabetes mellitus (A)</p> Signup and view all the answers

    What is the pathological mechanism underlying the development of pulmonary edema?

    <p>Increased pressure in the pulmonary arteries causes fluid to leak into the interstitial space and then the alveoli (A)</p> Signup and view all the answers

    In the context of extrinsic asthma, what is the primary role of IL-4 during initial immune sensitization?

    <p>IL-4 stimulates B cells to produce IgE antibodies, which bind to mast cells and initiate an allergic response. (C)</p> Signup and view all the answers

    Which of the following is NOT a direct consequence of mast cell degranulation in the immediate phase of allergic asthma?

    <p>Recruitment of additional eosinophils to the site of inflammation. (C)</p> Signup and view all the answers

    What is the primary mechanism by which eosinophils contribute to the persistent inflammation characteristic of the late-phase response in allergic asthma?

    <p>Eosinophils release ECF, MBP, and eosinophil peroxidase, which damage airway epithelial cells and contribute to sustained inflammation. (D)</p> Signup and view all the answers

    Which of the following best describes the role of eosinophil IL-5 receptor antagonists in the treatment of allergic asthma?

    <p>These antagonists inhibit the binding of IL-5 to its receptor on eosinophils, thereby reducing eosinophil activation and inflammation. (D)</p> Signup and view all the answers

    Which of the following is a key distinguishing feature of the immediate phase response compared to the late-phase response in allergic asthma?

    <p>The immediate phase is mediated by mast cell degranulation, while the late phase involves the accumulation of eosinophils and the release of their cytotoxic mediators. (D)</p> Signup and view all the answers

    Which of the following is a characteristic feature of chronic bronchitis that contributes to the clinical presentation of a "blue bloater"?

    <p>Increased goblet cell hyperplasia leading to excessive mucus production (A), Alveolar destruction resulting in reduced gas exchange and hypoxemia (B), Pulmonary hypertension due to increased resistance in the pulmonary vasculature (D)</p> Signup and view all the answers

    Which of the following is a characteristic of the acute exudative phase of Diffuse Alveolar Damage (DAD)?

    <p>Increased alveolar capillary permeability (B)</p> Signup and view all the answers

    The release of which type of cell plays a crucial role in the progression of DAD?

    <p>Neutrophils (C)</p> Signup and view all the answers

    Which of the following correctly describes the role of surfactant in the lungs?

    <p>Surfactant reduces surface tension, preventing alveolar collapse (A)</p> Signup and view all the answers

    What is the primary cause of the 'white out' seen in X-rays during the acute exudative phase of DAD?

    <p>Accumulation of fluid in the alveoli (C)</p> Signup and view all the answers

    How does the organizing phase of DAD differ from the acute exudative phase?

    <p>The organizing phase is characterized by fibroblast proliferation and collagen deposition (A)</p> Signup and view all the answers

    Which of the following is a potential outcome leading to honeycomb lung formation?

    <p>Fibrosis and remodeling of lung tissue (A)</p> Signup and view all the answers

    Which cell type is primarily responsible for the repair of the respiratory epithelium after DAD?

    <p>Type II pneumocytes (B)</p> Signup and view all the answers

    Which of the following is NOT a potential cause of Diffuse Alveolar Damage?

    <p>Bacterial pneumonia (B)</p> Signup and view all the answers

    What is the primary characteristic that differentiates Neonatal Respiratory Distress Syndrome (NRDS) from Adult Respiratory Distress Syndrome (ARDS)?

    <p>Immature surfactant production (A)</p> Signup and view all the answers

    Which of the following correctly represents the relationship between Diffuse Alveolar Damage (DAD) and Acute Respiratory Distress Syndrome (ARDS)?

    <p>DAD is a specific type of lung injury that can lead to ARDS. (C)</p> Signup and view all the answers

    Flashcards

    Respiratory Disorders

    Conditions affecting the airways and lungs leading to breathing difficulties.

    Pulmonary Hypertension

    Increased blood pressure in the pulmonary arteries, leading to heart strain and shortness of breath.

    Atelectasis

    Collapse of lung tissue that prevents gas exchange, caused by blockage or pressure.

    Acute Respiratory Distress Syndrome (ARDS)

    Severe lung condition characterized by rapid onset of widespread inflammation and fluid buildup in the lungs.

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    Chronic Obstructive Pulmonary Disease (COPD)

    Progressive disease that makes it hard to breathe, including emphysema and chronic bronchitis.

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    Restrictive Pulmonary Disease

    Disorders that limit lung expansion, reducing lung volume and causing difficulty in breathing.

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    Congenital Pulmonary Hypoplasia

    Underdevelopment of the lungs present at birth, often leading to respiratory failure.

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    Pulmonary Edema

    Accumulation of fluid in the lungs causing respiratory distress.

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    Cardiogenic Pulmonary Edema

    Pulmonary edema caused by heart failure or mitral stenosis leading to increased pressure.

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    Non-cardiogenic Pulmonary Edema

    Pulmonary edema not caused by heart issues, often due to low plasma oncotic pressure or injury.

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    Oncotic Pressure

    The pressure exerted by proteins in plasma that pulls fluid into the blood vessels.

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    Alveolar Edema

    Fluid in the alveoli leading to impaired gas exchange and respiratory distress.

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    Chest X-ray Findings in Edema

    Diffuse pulmonary opacities indicating fluid in the lungs, presenting a 'white out' appearance.

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    Pulmonary Embolism

    Sudden obstruction of a lung artery by a blood clot or other material.

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    Thrombotic Embolus

    Blood clot causing obstruction in the pulmonary artery, often due to increased clotting tendency.

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    Heart Failure Cells

    Hemosiderin-laden macrophages in the lungs from chronic heart failure related edema.

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    Gastric Content Injury

    Chemical injury to alveolar epithelium caused by gastric contents.

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    Drugs and Toxins

    Substances causing chemical injury to the respiratory membrane via systemic or inhalation routes.

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    DAD Effects

    Diverse Acute Damage (DAD) increases alveolar capillary permeability, leading to fluid leakage.

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    Acute Exudative Phase

    Initial stage of lung injury with cell injury and fluid leakage into alveoli.

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    Bilateral Patchy Infiltrates

    Fluid leak in acute phase presents as 'white out' on X-ray due to edema.

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    Macrophage Activation

    First immune response in lung injury leading to recruitment of neutrophils.

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    Neutrophil Role

    Recruited neutrophils release enzymes causing further damage to alveolar walls.

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    Hyaline Membrane Formation

    Fluid organizes into a layer in the alveoli, affecting gas exchange ability.

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    Surfactant

    A mixture of phospholipoproteins secreted by type II pneumocytes, reducing surface tension.

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    NRDS

    Neonatal Respiratory Distress Syndrome caused by insufficient surfactant in infants.

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    Pathogenesis of Chronic Bronchitis

    Inhaled irritants lead to chronic inflammation and mucus production in bronchi.

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    Goblet Cell Hyperplasia

    Increase in goblet cells in the airways, leading to excess mucus production.

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    Mucus Hypersecretion

    Excessive mucus accumulation in the airways, leading to blockage.

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    Bronchial Wall Destruction

    Damage to the bronchial walls leading to conditions like emphysema.

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    Blue Bloater

    Nickname for chronic bronchitis patients due to cyanosis from hypoxia.

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    Bronchial Asthma

    Airway obstruction due to hypersensitivity and inflammation.

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    Intrinsic Asthma

    Non-allergic asthma triggered by irritants or infections.

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    Extrinsic Asthma

    Allergic asthma triggered by environmental allergens.

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    Mucus Plugging

    Formation of mucus plugs in airways, obstructing airflow.

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    Cor Pulmonale

    Right heart failure due to pulmonary hypertension from chronic lung disease.

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    TH2 Cells

    T helper cells that produce interleukins promoting allergic responses.

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    IgE Production

    Immunoglobulin E generated by B cells, important in allergic reactions.

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    Immediate Phase Response

    Rapid allergic reaction where mast cells release mediators causing bronchoconstriction.

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    Late Phase Response

    Sustained allergic response involving eosinophils and inflammation.

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    Study Notes

    Respiratory Pathology Lectures

    • Course name: IBSSD 1534/1515
    • Instructor: Luigi Strizzi, MD, PhD
    • Department: Pathology
    • University: Midwestern University

    Learning Objectives

    • Students will become familiar with respiratory nomenclature and terminology.
    • Students will understand the pathophysiology of various respiratory disorders and how these affect clinical manifestations.
    • Students will learn the key macroscopic and microscopic features of different respiratory disorders.

    Respiratory Pathology Lectures - IBSSD 1535/1516

    • Major signs and symptoms of respiratory disorders
    • Congenital pulmonary hypoplasia
    • Atelectasis
    • Pulmonary vascular disorders (pulmonary hypertension, pulmonary edema, pulmonary embolism)
    • Acute respiratory distress syndrome (ARDS) & Neonatal respiratory distress syndrome (NRDS)
    • Chronic obstructive pulmonary disease (COPD): emphysema, bronchiectasis, chronic bronchitis, bronchial asthma
    • Restrictive pulmonary disease: idiopathic pulmonary fibrosis, pneumoconiosis, sarcoidosis
    • Neoplasms of the lung

    Major Respiratory Signs/Symptoms

    • Cough (dry or productive)
    • Hemoptysis (coughing up blood)
    • Dyspnea (labored breathing)
    • Tachypnea (increased breathing rate)
    • Cyanosis (desaturated hemoglobin)
    • Acid-base disturbances
    • Pain (pleuritic)
    • Fever
    • Excessive weight loss
    • Wheezing
    • Stridor
    • Changes in key spirometry values (e.g., FEV1/FVC)
    • Hypoexmia (reduced tissue oxygen when Hb O2 saturation is less than 90%)

    Congenital Anomalies

    • Congenital pulmonary hypoplasia: incomplete or defective lung development, often associated with other congenital anomalies.
    • Intrathoracic space-occupying lesions (e.g., diaphragmatic hernia)
    • Renal defects can cause fluid retention and oligohydramnios
    • Urinary obstruction can also cause oligohydramnios
    • Clinical presentation includes incomplete lung development, poor ventilation, defective gas exchange, tachypnea, dyspnea, cyanosis that puts the patient at risk of respiratory infections.

    Atelectasis

    • Atelectasis (collapsed lung) results from inadequate expansion of lung tissue/air spaces.
    • Types:
      • Compression atelectasis: caused by direct physical compression (e.g., air or fluid in the thorax)
      • Contraction atelectasis: caused by fibrosis retraction of the affected lung
      • Obstructive/absorptive atelectasis; caused by airway blockage.

    Pulmonary Vascular Disorders

    • Pulmonary hypertension: increased pulmonary arterial pressure (PAP) greater than 25 mmHg.
    • Chronic pulmonary hypertension can lead to right ventricular (RV) failure ("cor pulmonale").
    • Precapillary or postcapillary, i.e upstream or downstream to pulmonary capillaries

    'Precapillary' Causes of Pulmonary Hypertension (PH)

    • Left-to-right cardiac shunt (ventricular septal defect)
    • Over time, increased pulmonary blood volume and pressure stress on vessel walls leads to thickening of pulmonary arteries, narrowing of vessel lumens, and increased pulmonary vascular resistance (PVR).

    'Postcapillary' Causes of Pulmonary Hypertension (PH)

    • Left-sided cardiac disorders (stenosis of mitral or aortic valves, or LV heart failure).
    • Obstruction of increased resistance to postcapillary blood flow from lungs.

    Pulmonary Edema

    • Accumulation of fluid in the lungs due to imbalance between hydrostatic pressure, oncotic pressure, and lymphatic drainage.
    • Cardiogenic causes: the same factors leading to post-capillary pulmonary hypertension, e.g., mitral stenosis.
    • Non-cardiogenic causes: decreased plasma oncotic pressure (malnutrition), lymphatic blockage, volume overload (kidney failure), damage to respiratory membrane (DAD).

    Pulmonary Embolism

    • Sudden blockage of a major pulmonary artery by a blood clot or other obstruction.
    • Major pathophysiologic consequences: hemodynamic compromise (obstruction → increased resistance to pulmonary blood flow → acute pulmonary hypertension and potentially sudden death) and respiratory compromise (ventilation-perfusion mismatch).
    • Morphology can vary, often involves a "saddle" embolus at the bifurcation of the pulmonary artery resulting in an infracted wedge.

    Acute Respiratory Distress Syndrome (ARDS)

    • Medical emergency; arises from diffuse alveolar damage (DAD).
    • Results in rapid onset of life-threatening respiratory distress/insufficiency, and severe arterial hypoxemia and cyanosis.
    • High rate of mortality (60%).
    • DAD occurs most often when damage occurs to alveolar epithelial and endothelial pulmonary cells.
    • Important causes of respiratory membrane damage include infections, reduced tissue perfusion (causing ischemic tissue damage), aspiration/gastric content, drugs/toxins.

    Neonatal Respiratory Distress Syndrome (NRDS)

    • Common cause of death in premature infants.
    • Results when surfactant production in type II alveoli cells of premature infants is insufficient.
    • Impaired surfactant production results in reduced surface tension and alveoli collapse, especially during expiration, which impairs oxygen delivery to the blood stream.

    Chronic Obstructive Pulmonary Disease (COPD)

    • Fourth leading cause of death in the US.
    • Includes emphysema, bronchiectasis, chronic bronchitis, and bronchospastic asthma.
    • Emphysema results from destruction of alveolar walls.
    • Cigarette smoke is the major cause, causing direct toxic and free radical damage, inflammation, and release of proteases from neutrophils macrophages resulting in enzymatic destruction of alveolar walls.

    Bronchiectasis

    • Damage to the walls of bronchi and bronchioles resulting in permanent dilation of these structures.
    • Pathogenesis includes obstruction (mucous secretions), microbial proliferation (e.g., S. aureus, K. pneumoniae), inflammation (leukocyte infiltration), damage to the epithelium, and stagnation of cellular debris.

    Chronic Bronchitis

    • Persistent, productive cough for at least three months per year for at least two years.
    • Pathogenesis involves exposure to inhaled irritants like smoking and air pollutants that lead to goblet cell hyperplasia, mucus hypersecretion, and submucosal glandular hyperplasia.

    Bronchial Asthma

    • Bronchial obstruction caused by hypersensitivity and airway inflammation and mucous production.
    • Two types: intrinsic (non-atopic) and extrinsic (atopic).
    • Intrinsic asthma is usually triggered by agents that cause airway irritation (e.g., chemicals, viral respiratory infections).
    • Extrinsic: triggered by immune sensitization to allergens (e.g., pollen, animals).

    Restrictive Pulmonary Disease

    • Reduced expansion/elastic recoil of lung parenchyma.
    • Causes: chest wall disorders, acute/chronic interstitial lung diseases (ARDS, idiopathic pulmonary fibrosis, sarcoidosis, etc).

    Pneumoconiosis

    • Lung disease caused by chronic inhalation of mineral dust particles (coal, silica, asbestos).
    • Large particles are usually trapped in the mucous membrane, whereas small particles can enter alveoli, stimulating the release of fibrogenic factors.
    • Can lead to fibrosis, and pleural space involvement.

    Sarcoidosis

    • Multisystem, chronic granulomatous disease of unknown etiology.
    • Can occur in lungs, skin, eyes, salivary glands, etc.
    • Macrophages activate from T-helper responses to unknown antigens and cause noncaseating granuloma formation.

    Neoplasms of the Lung

    • Benign lesions: adenomas, papillomas, and hamartomas.
    • Malignant lesions:
      • Primary lung cancer: most common cause is cigarette smoking, associated with squamous cell carcinoma, adenocarcinoma, and small-cell lung cancer (SCLC).
      • Secondary lung cancer: arises from tumors of other organs that metastasize to the lung.

    Other topics (depending on the page count):

    • Sleep apnea
    • Ocular manifestations of pulmonary embolism
    • Specific details about certain types of lung cancer (e.g. Pancoast tumor), including associated clinical symptoms.
    • Staging systems for lung cancer.

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    Respiratory Pathology IBSSD 1534/1515 PDF

    Description

    Test your knowledge on various disorders related to respiratory pathology through this quiz. Covering topics such as Chronic Obstructive Pulmonary Disease (COPD), pulmonary diseases, and specific clinical conditions, this quiz will enhance your understanding of the respiratory system and its pathologies.

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