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Respiratory > Pathology of parenchymal lung disease > Flashcards

Pathology of parenchymal lung disease Flashcards

1
Q

Examples of mechanical defence mechanisms

A

Ciliated epithelium
Mucus
Cough (damaged by neuromuscular problem- strokes)

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2
Q

Examples of immunological defence mechanisms

A

IgA and antimicrobials in mucus
Resident alveolar macrophages and dendritic cells
Innate/ adaptive immune responses

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3
Q

Describe the gas exchange surface

A

Thin
Type 2 pneumocytes/ epithelium differentiate to type 1, produce surfactant
Type 1 pneumocytes- gas exchange
Vessels and cells

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4
Q

What is the parenchyma?

A

The parts of the lungs involved in gas transfer including the alveoli, interstitium, blood vessels, bronchi and bronchioles

  • Respiratory bronchiole
  • Terminal bronchiole
  • Alveolar rings, ducts, septum
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5
Q

How might pneumonia present?

A

-Shortness of breath
-Cough
-Haemoptysis (coughing up blood)
-Pyrexia (temperature)
=Elevated neutrophils
=Right basal crepitations and consolidation

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6
Q

Describe pneumonia

A
  • Greatest cause of deaths due to infection in the developed world
  • 15% of all deaths of children under 5
  • Caused by range of pathogens= bacteria, fungi, virus
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7
Q

What are the categories of pneumonia?

A

-Community acquired
-Hospital acquired
-Health care associated
-Aspiration associated
-Immunocompromised host
-Necrotising/ abscess formation
=Resistance

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8
Q

What pathogens are associated with Community acquired pneumonia?

A
  • Streptococcal pneumoniae
  • Haemophilus influenzae
  • Moraxella catarrhalis
  • Staphylococcus aureus
  • Klebsiella pneumoniae/ Pseudomonas aeruginosa
  • Mycoplasma pneumoniae
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9
Q

What are the pathogens associated with hospital acquired/ health care associated pneumonia?

A

-Gram negative rods= Enterobacteriaceae, Pseudomonas
-Staph aureus (usually methicillin resistant)
=more immunosuppressed, at least 48 hours prior to symptom onset

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10
Q

What pathogens are associated with aspiration pneumonia?

A

Anaerobic oral flora mixed with aerobic bacteria

No control over larynx

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11
Q

What pathogens are associated with Pneumonia in the immunocompromised host?

A
  • Cytomegalovirus (organ transplant-liver)
  • Pneumocytis jiroveci (PCP)
  • Mycobacterium avium-intracellulare
  • Invasive aspergillosis
  • Invasive candidiasis
  • Unusual bacterial, virus and fungal organisms
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12
Q

What pathogens are associated with necrotising/ abscess formation?

A

Anaerobes, S. aureus, Klebsiella, S. pyogenes

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13
Q

Describe the cellular response to infection

A
  • Neutrophils= chemotaxis, degranulation, reactive oxygen species, extracellular traps, phagocytosis
  • Macrophages(alveolar resident recruit)= cytokine and chemokines, phagocytosis (bacteria and dead cells), antimicrobial peptides, resolution (also involves T cells, dendritic cells and epithelial cells)
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14
Q

What is the clinical presentation of pneumonia?

A
  • Cough
  • Sputum= stimulates goblet cells so production of mucus
  • Pyrexia
  • Pleuritic chest pain= irritated pleura (rubbing)
  • Haemoptysis= vasodilation, rupture of small blood vessels
  • Dyspnoea
  • Hypoxia= not effective gas exchange, pus filled alveoli
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15
Q

What are the types of pneumonia?

A
  • Bronchopneumonia

- Lobar pneumonia

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16
Q

Describe the appearance of bronchopneumonia

A
  • Most common pattern
  • Patchy consolidated areas of acute suppurative inflammation
  • Often elderly with risk factors (cancer, heart failure, renal failure, stroke, COPD)
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17
Q

Describe the appearance of lobar pneumonia

A
  • Rust coloured sputum
  • S. pneumoniae
  • Consolidation of a large portion of a lobe or of an entire lobe
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18
Q

What are the general risk factors for pneumonia?

A
  • Chronic disease
  • Immunologic deficiency
  • Immunosuppressive agents
  • Leukopenia
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19
Q

What are the local risk factors for pneumonia?

A
  • Loss or suppression of the cough reflex (drugs)
  • Injury to the mucociliary apparatus (viruses, gases)
  • Accumulation of secretions (CF, obstruction- tumour)
  • Impaired alveolar macrophages function (alcohol, tobacco)
  • Pulmonary congestion and oedema
20
Q

What are the complications of pneumonia?

A

Local:
-Abscess formation (poor blood supply)
-Parapneumonic effusion (aseptic oedema, visceral and pleura space)
-Empyema (same plus bacteria)- chronic= chest drain
Systemic:
-Sepsis (hyperdilation)
-ARDS (Acute respiratory distress syndrome)
Multi-organ failure
Not resolving- cancer?- allows stagnation behind tumour (6 week scan after pneumonia to check)

21
Q

Describe Acute Respiratory Distress syndrome

A
  • Incidence 10-14/100,000/yr
  • Mortality rate= 40%
  • Clinical diagnosis= hypoxia (PaO2/FiO2 <300mmHg), Non-cardiogenic pulmonary oedema
  • Causes= direct (pneumonia, aspiration, hyperoxia, ventilation), indirect (sepsis, trauma/DAMPs, pancreatitis, acute hepatic failure)
22
Q

What is Bronchiectasis?

A
  • The permanent dilation of one r more large bronchi (chronic infection, altering bronchial defence= impaired)
  • Typically affects the 2nd to 8th order of segmental bronchi (largest central airways more robust)
23
Q

What are the causes of diffuse or multifocal bronchiectasis?

A
  • Infection (mycobacterial, childhood infection= pertussis bacterial/ Viral RSV/ adenovirus/ measles)
  • Hereditary (Cystic fibrosis, primary ciliary dyskinesia, Alpha-1-antitrypsin deficiency)
  • Congenital
  • Immunodeficiency (hypogammaglobulinemia, HIV, Lung transplantation)
  • Allergic bronchopulmonary aspergillosis
  • Connective tissue disorders (rheumatoid, Sjogren’s Syndrome)
  • Inflammatory bowel disease (ulcerative colitis, Crohn’s disease)
  • Chemical injury/ aspiration (Inhalation of SO2, NO5, H2S, gastric aspiration)
  • Idiopathic
24
Q

Describe Cystic Fibrosis

A
  • Multi-system disorder affecting lungs, GI tract etc
  • F508 (autosomal recessive) most common in CFTR
  • Altered ion transportation
  • Viscous mucoid secretions due to H20 resorption
25
Q

Describe Tuberculosis

A
  • Extremely common worldwide (more common in developing world)
  • Immune response very important (11% of TB cases attributable to HIV 2000)
26
Q

What are the predisposing factors of TB?

A
  • Alcoholism
  • Diabetes mellitus
  • HIV/ AIDS
  • Some ethnic groups
27
Q

What is the treatment for TB?

A
  • Socio-economic conditions
  • Drugs- triple antibiotic therapy
  • Prevention= BCG vaccination
28
Q

What happens at 3-4 weeks in primary TB?

A
  • M. TB multiples within alveolar macrophages (naïve, unable to kill)
  • Bacterium resides in phagosomes and carried to regional lymph nodes, from there to circulation
29
Q

What happens at 3-8 weeks in primary TB?

A
  • Onset of cellular immunity and delayed hypersensitivity
  • Activated lymphocytes further activate macrophages to kill
  • Primary infection arrested in most immunocompetent people
  • Few bacilli may survive dormant
30
Q

What is a Ghon complex?

A

lesions consist of a Ghon focus along with pulmonary lymphadenopathy within a nearby pulmonary lymph node (hilar)
Subpleural lesion + hilar lymph node

31
Q

Describe progressive primary TB

A
  • Infection not arrested (minority: infants, children, immunocompromised)
  • Tuberculosis bronchopneumonia (infection spreads via bronchi, results in diffuse bronchopneumonia, well developed granulomas do not form)
  • Miliary TB (infection spreads via blood-stream, organisms scanty, multiple organs= liver, lungs, spleen, kidneys, meninges, brain)
32
Q

Describe secondary TB

A
  • Also termed post-primary TB
  • Reactivation of old, often subclinical infection
  • Occurs in 5-10% of cases of primary infection
  • More damage due to hypersensitivity (apical region of lung/ tubercles develop locally, enlarge and merge/ erode into bronchus and cavities develop/ may progress to tuberculous bronchopneumonia)
33
Q

What are other causes of granulomatous pulmonary inflammation?

A
  • Other infection= fungi
  • Sarcoidosis
  • Rheumatoid arthritis
  • Berrylosis
  • Hypersensitivity pneumonitis
  • Aspiration pneumonia
  • Langerhans Cell Histiocytosis
34
Q

Describe fibrosing diseases of the lung

A
  • Restrictive chronic lung disease
  • Dyspnoea, (cough), tachypnoea, crepitation, cyanosis (late stage)
  • Pulmonary function tests= reduced transfer factor and total lung capacity
  • Ground glass changes in lower zones on x-ray
35
Q

Describe the pathogenesis of idiopathic pulmonary fibrosis

A

Unclear

  • Cause unknown
  • Persistent epithelial injury/ activation
  • Innate and adaptive immune response
  • Pro-fibro genic factors
  • Abnormal intracellular signalling
  • Proliferation and collagen production
  • Fibrosis
36
Q

Describe what IPF looks like under the microscope/ morphology

A

Usually interstitial pneumonia

  • Subpleural accentuation
  • Spatial and temporal heterogeneity
  • Fibroblastic foci
  • Mixed inflammatory infiltrate
  • Excess alveolar macrophages
37
Q

Describe asbestos

A
  • Occupational lung disease= exposure in shipyards, building trade
  • Several diseases= pleural plaques (benign), asbestosis (progressive fibrosis), mesothelioma, adenocarcinoma
  • Issues surrounding compensation for patient and families
  • Other occupational factors= silica, coal dust, berrylium
38
Q

Describe hypersensitivity pneumonitis

A
  • Type 3 hypersensitivity (Ab/Ag complex within the lung)
  • Various causative agents= Farmer’s, Pigeon fancier’s, mushroom picker’s lung (and hot tub)
  • Most resolve when agent of exposure removed but can be chronic
39
Q

What are the local complications of Bronchiectasis?

A
  • Distal airway damage/ loss and lung fibrosis
  • Pneumonia
  • Pulmonary abscess formation
  • Haemoptysis
  • Airway colonisation by aspergillus
  • Aspergilloma
  • Tumourlet formation
40
Q

What are the physiological and systemic complications of bronchiectasis?

A 
Physio= respiratory failure, cor pulmonale
Systemic= metastatic abscess, amyloid deposition
41
Q

Describe infection in bronchiectasis

A 
Impaired bacterial clearance
-Altered anatomy
-Thickened mucus
-Impaired immune cell function
Colonisation
-Pseudomonas Aeruginosa
-Klebsiella, Moraxella
-S. pneumoniae, H. influenzae
42
Q

Describe the pathogenesis of bronchiectasis

A
  • Airway injury
  • Inflammation +/- infection
  • Cough increases airway pressure/ destruction of airway wall, loss of elastic tissue and fibrosis
  • Airway dilation
  • Distal lung changes with fibrosis/ retained secretion and infection
43
Q

What is traction bronchiectasis?

A

Dilation of airways due to parenchymal fibrosis

  • Parenchymal inflammation
  • New collagen formation
  • Collagen contracts
  • Loss of lung volume
  • Pulling open of airways
  • Airway dilation
44
Q

What is the pattern of bronchiectasis?

A

Based on imaging appearances

  • Cylindrical
  • Sacular
  • Varicose
  • Cystic
45
Q

What are the classifications of bronchiectasis

A

-More useful to think in terms of anatomical distribution of disease
-Closer linkage with aetiologies
=Localised bronchiectasis
=Diffuse/ multifocal bronchiectasis

46
Q

Describe localised bronchiectasis

A
  • Bronchial obstruction= neoplasm, foreign body, external compression (middle lobe syndrome), allergic bronchopulmonary aspergillosis
  • Infection= TB, Necrotising bacterial/ viral infection
  • Gastric acid aspiration
  • Traction bronchiectasis
  • Idiopathic

Respiratory (41 decks)

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