Pulmonary Pathology Flashcards

1
Q

Describe basic respiratory system anatomy

A
  • Trachea, right / left principal bronchus, lobar bronchi (secondary), segmental bronchi (tertiary), terminal bronchioles, respiratory bronchioles, alveolar ducts / sacs, alveoli
  • From conducting to respiratory areas we see a loss of cartilage, mucous secreting cells, goblet cells, cilia and cells become progressively flattened
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2
Q

What are characteristics of the trachea

A
  • Pseudo-stratified columnar ciliated epithelium
  • Goblet cells
  • C-shaped cartilage
  • Smooth muscle at opening of C-shaped hyaline cartilage
  • Serous / mucous glands
  • Conducting
  • Connects upper respiratory tract to lungs via bronchial tree, posterior wall is fibrous tissue
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3
Q

What are characteristics of the bronchi

A
  • Pseudo stratified columnar ciliated
  • Goblet cells
  • Pieces of hyaline cartilage
  • Smooth muscle encircles lumen
  • Serous / mucous glands
  • Conducting
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4
Q

What are characteristics of the bronchioles (terminal and respiratory)

A
  • Bronchioles / Terminal: Simple columnar ciliated, exocrine / club cells, supported by smooth muscle and elastic fibres, conducting
  • Respiratory: Simple cuboidal, some ciliated, exocrine cells, smooth muscle, respiratory
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5
Q

What are characteristics of the alveolar ducts / alveoli

A
  • Alveolar Duct: Mostly simple squamous, respiratory
  • Alveoli: Simple squamous, type I (pneumocytes, squamous epithelium 95%) and type II (pneumocytes, cuboidal epithelium, surfactant producing), respiratory
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6
Q

What are obstructive lung diseases

A
  • Increase in resistance to airflow due to partial / complete obstruction of the airways
  • Obstruction is worse with expiration, more force required
  • Decreased expiratory flow rate
  • FEV1 sec to FVC (deepest breath) ratio is decreased
  • FEV1/FVC is ≤ 70% in adults and < 85% in children
  • Types: Chronic bronchitis, emphysema, asthma, ARDS
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7
Q

What is chronic bronchitis (OLD)

A
  • Cough with sputum production ≥ 3 months in 2 consecutive years
  • Aetiology (smoking)
  • Hypertrophy of submucosal mucus glands, hyperplasia of goblet, hyper secretion of mucous
  • Simple: Productive cough (no airflow obstruction)
  • Asthmatic: Cough, intermittent bronchospasm and wheezing
  • Obstructive: Cough and outflow obstruction
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8
Q

What is emphysema (OLD)

A
  • Damaged / enlarged alveoli
  • Aetiology (smoking or a1-antitrypsin deficiency)
  • Dyspnea, lungs enlarged
  • Permanent dilation of air spaces distal to terminal bronchioles
  • Destruction of alveolar walls (loss of elastic recoil)
  • Asymptomatic until 1/3 of parenchyma is destroyed
  • Reactive oxygen species / free radicals attract neutrophils
  • Increased neutrophil elastase, pro-inflammatory cytokines, neutrophils and macrophage elastase
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9
Q

What is asthma (OLD)

A
  • Chronic inflammation of airways (hyper-reactive)
  • Recurrent episodes of wheezing, breathlessness, chest tightness and cough caused by reversible bronchospasm
  • Status Asthmaticus: Severe, prolonged / continuous, rare, can be fatal
  • Extrinsic: Type I HS (IgE)
  • Intrinsic: Non-immunological, aspirin, viral infections, cold, exercise and stress
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10
Q

What are restrictive lung diseases

A
  • Intrinsic lung diseases, limited potential of lung to expand), reduced lung compliance and reduced TLC, FVC and FEV1, progressive breathlessness and cough
  • Diffuse and chronic involvement of pulmonary connective tissue (alveolar interstitium)
  • Types: Acute interstitial disease (ARDS), chronic interstitial diseases (idiopathic pulmonary fibrosis, pneumoconiosis, sarcoidosis, hypersensitivity pneumonitis)
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11
Q

What is ARDS (RLD)

A
  • Acute respiratory distress syndrome
  • Caused by infection, burns, gas inhalation, protein-rich edema (hypoxemia)
  • Can be fatal within a few days (lung damage / fibrosis)
  • Diffuse alveolar capillary and epithelial damage
  • Leakage of proteins and fibrin into alveoli and hyaline membrane, severe fluid buildup
  • Bright eosinophilic hyaline membrane, regenerative hyperplasia of type II cells, collapsed alveoli and proteinaceous debris present
  • Lungs are large and dusky red, firm and airless by palpation
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12
Q

What are the types of ARDS

A
  • Acute (1-6 d): Sloughing of bronchial and alveolar epithelium, neutrophils present, air space filled with protein rich edema fluid, lung injury (neutrophil / platelet dependent), delayed resolution
  • Sub-Acute (7-14 d): Some edema reabsorbed, attempted repair, proliferation of alveolar epithelial type II cells, fibroblast infiltration and collagen deposition
  • Chronic (14 d): Resolution of acute neutrophilic infiltrate, increased mononuclear cells and alveolar macrophages, increased fibrosis and repair of alveoli epithelium
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13
Q

What is interstitial lung disease (RLD)

A
  • Many different lung conditions
  • Forms of interstitial lung disease cause thickening of the interstitium due to inflammation (alveolitis)
  • Scarring (fibrosis, honeycomb lung), edema
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14
Q

What is pulmonary fibrosis (RLD)

A
  • Lung tissue is damaged and undergoes fibrosis
  • Difficulty expanding and increased restriction / air volume in the lungs
  • Idiopathic PF (unknown causes)
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15
Q

What is atelectasis (RLD)

A
  • Incomplete expansion / collapse of lung
  • Caused by obstruction, restriction or preterm
  • Results in reduced gas exchange, rapid shallow breathing, coughing, hypotension, tachycardia, fever, cough, pain
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16
Q

What is pneumoconiosis (RLD)

A
  • Inhalation of dusts / fumes
  • Range from asymptomatic anthracosis to fibrotic lungs with compromised function / hypertension
  • Accumulation of macrophages in lung parenchyma
17
Q

Summarise the different between restrictive vs obstructive lung diseases

A
  • Restrictive: FVC is reduced, airways not obstructed, able to expel air reasonably fast
  • Obstructive: Airway obstruction, slow exhalation, reduced FVC
  • FEV1/FVC ratio is lower in persons with obstructive (> 69%) than with restrictive (88-90%)
18
Q

What is pneumonia

A
  • Caused by bacteria, virus, mycoplasma and fungus
  • Presents as acute or chronic
  • Fibrin-purulent alveolar exudate in (acute bacterial)
  • Mononuclear interstitial infiltrates (viral)
  • Granulomas and cavitation (chronic)
19
Q

What is acute pneumonia

A
  • Community acquired
  • Streptococcus pneumoniae
  • Follows upper respiratory tract viral infection
  • Lung parenchyma filled with inflammatory exudate leading to fibrin-supportive consolidation
  • Onset abrupt, high fever, shaking chills, chest pain, productive mucopurulent cough
20
Q

What is lobar pneumonia

A
  • Acute exudative inflammation of an entire pulmonary lobe
  • Lobe enlargement, loss of spongy appearance
  • Red / grey hepatisation
    Stages:
    1. Alveolar lumen contains serous exudate of rare leucocytes / bacteria
    2. Exudate rich fibrin with bacteria, leucocytes, erythrocytes
    3. Alveolar lumens filled with leukocytic exudate, neutrophils / macrophages
    4. Resolution, exudate within alveolar spaces drained
21
Q

What is broncho pneumonia

A
  • Affects one or more lobes
  • Suppurative peri-bronchiolar inflammation
  • Small yellow-tan patches
  • Multiple small foci of inflammation / condensation
  • Extensive congestion and dilation of BV and areas of poorly circumscribed consolidation
22
Q

What is tuberculosis

A
  • Chronic pneumonia caused by mycobacterium tuberculosis
  • Granulomatous inflammation
  • Tubercular granulomas undergo caseous necrosis
  • Primary (previously unexposed, asymptomatic )
  • Secondary (reactivation of primary lesions, fever / night sweats, malaise, anorexia)
  • Ghon complex (lesion after primary, ghon focus, lymphadenopathy, nearby lymph node)
23
Q

What is miliary tuberculosis

A
  • 5% of progressive primary TB
  • Mycobacterium tuberculosis enter blood stream and infect other organs
  • Cell-mediated immune response activated
  • Macrophages infiltrate and form granuloma
24
Q

List vascular lung diseases

A
  • Pulmonary Embolism

- Pulmonary Hypertension

25
Q

What are neoplastic lung diseases

A
  • Risk Factors: Smoking, radiation exposure, asbestos exposure, air pollution, genetic predisposition
  • Lung Carcinoma: Large (10-15%), small (20-25%), squamous (25-40%) or adenocarcinoma (25-40%)
26
Q

What is red vs grey hepatisation in lobar pneumonia

A
  • Red Hepatisation: Early exudate is full of bacteria, RBC, neutrophils, fibrin, day 3-4, firm, red appearance, liver-like consistency, cut surface is dry and rough
  • Grey Hepatisation: Later exudate contains macrophages, broken down RBC, debris, day 5-7, cut surface wet, greyish purulent liquid drains