Lecture 25 Flashcards

1
Q

What does injury to the ciliated bronchial epithelium result in

A

Degeneration, detachment and exfoliation

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2
Q

What does injury to the ciliated bronchial epithelium follows with

A
  • Inflammation, cell proliferation, cell differentiation and repair
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3
Q

What is the exudate like with injury to the bronchi

A
  • Fibrinous, catarrhal, purulent, fibronecrotci
    • Chronic inflammation - also goblet cell hyperplasia and excess mucus production
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4
Q

Explain the chronic injury to the bronchi

A

Can lead to squamous metaplasia of bronchial epithelium -> breakdown of mucociliary clearance

Goblet cell hyperplasia -> chronic catarhal inflammation

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5
Q

What can chronic bronchitis lead to

A
  • Bronchiectasis
    • Pathological and permanent dilation of the bronchus from accumulation of exudates
    • Partial destruction of the bronchial wall
      • Due to proteolytic enzymes and free radicles from neutrophils and macrophages
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6
Q
A

Severe Bronchiectasis

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7
Q

Why is the epithelium susceptible to injuty

A
  • High vulnerability to oxidants and free radicles
  • Presence of club cells righin antioxidants which generate toxic metabolites
  • Alevolar macropages and leukocytes accumulate
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8
Q

What is bronchiolitis

A
  • Classified as necrotizing, suppurative, catarrhal of granulomatous
  • In severe injury, the exudate becomes infiltrated with fibroblast and forms microscopic polyps inside the bronchiolar lumen
    • May block air flow
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9
Q

What are the chronic injury to bronchioles

A
  • Peribronchiolar lymphoid hyperplasia
  • Mild persistent injury
    • Goblet cells proliferate and change the properties f bronchiolar secretions
      • Goblet cell metaplasia
    • Mucous needs to be cleared by coughing
      • As there is partial or coplete blockage of the lumen of bronchioles by mucus hypersecretion
  • Pulmonary emphysema and atelectasis occur
    • CHaracteristically seen in chronic obstructive pulmoary disease
    • Recurrent airway obstruction = heaves in horses
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10
Q

What is reccurent airway obstruction in horses

A
  • Haves
  • Signs
    • Recurrent respiratory distress
    • Chronic cough
    • Poor atletic performance
    • Airway neutrophilia and mucous hypersecretion
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11
Q

What is hypothesis of RAO

A

Dust paticles upregulate production of cytokines by alveolar macrophages which attracts neutrophils

  • Neutrophils induce bronchiolar damage
  • Goblet metaplasia
  • Preibronchial accumulation of lymphocytes and esinophils and interstitial fibrosis
  • Peribronchial fibrosis and epithelial cell hyperplasia are inconsistent findings
  • Alveolar emphysema may be present
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12
Q
A

Goblet cell metaplasia

Alcian blue stain to show mucus

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13
Q
A

ROA - emphysema

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14
Q
A

ROA - mucous and exudate in airway

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15
Q
A

RAO - mucous and exudate in airways

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16
Q

What is feline asthma

A
  • Feline allergic bronchitis/bronchiolitis
    • Reccurent bronchoconstriction, coughing or dyspnoea
    • Poorly understood
17
Q

Describe Type I pneumocytes

A
  • Very susceptibleto aerogenousand haematogenous injury -> swelling and vacuolation
  • Repair is possible as long as the basement membrane is intact
  • Cuboidal pneumocytesproliferate
18
Q

Describe type Ipneumocytes

A
  • Line the denuded alveolar basement membrane and differentiate into Type I pneumocytes
    • In diffuse injury, the proliferating Type II pneumonocytes give the appearance of glandualar structure called - epithelialisation
19
Q
A

Pulonary epithelialialisation: proliferating Type II pneumonocytes

20
Q

What injury to the alveoli

A
  • Loss of type I pneumocytes
    • Means damage to blood-air barrier and alveolar capillaries leak plasma
    • Alveolar macrophages remove fluid and cellular debris
  • If injury is persistent, fibroblasts proliferate leading to intra-alveolar fibrosos
    • Extensive alveolar fibrosis seen in toxic and allergic pulmonary disease
  • Fibrosis has a major effect on lung function
21
Q

What is the most important leukocyte in lung inflammation

A

Alveolar macrophages

  • Rapid recruitment and migration of leukocytes into alveoli
    • Alveolar fulid contains large amounts of inflammatory mediators
    • Large capillary network
    • Neutrophils recruited into alveolar spaces within minutes of local and systemic inflammatory response
22
Q

What is pulmonary oedema

A
  • Protein leakage from flasma into alveoli and formation of fibrin can be rapid
    *
23
Q

What is the formation of ‘hyaline membranes’

A
  • Plasma proteins mixed with necrotic Type I pneumonocytes and pulmonary surfactant can form eosinophilic membranes along alveolar septa
24
Q
A

Hyaline membranes - cows lung

25
Q

What is chronic inflammation pneumonia

A
  • Shift from neutrophils to mononuclear cells
    • Increased in IL-4, interferon-gamma and interferon-inducible protein to attract lymphocytes and mactophages
  • Macrophages and lymphocytes release growth factor
    • Recruitment and proliferation of fibroblast
  • Fibroblasts and fibrocytes
    • Synthesise and secrete large amounts of extracellulat matrix
  • Causes fibrosis and obliteration of alveolar spaces
26
Q

What are the systemic effects of pneumonia

A

Inflammatory mediators from inflammation of the lungs have effects on other tissues and body systems

27
Q

What is pulomnary hypertension and right sided heart failure due to

A
  • The effects of increased pulmonary blood pressure in chronic alveolar inflammation and
  • The effects of inflammatory mediators on the contracibility of smooth muscle of the pulmonary and system vasculature
28
Q

What is persistent alveolar injury

A
  • Restoration of alveolar structure does not occur
  • Lesions can progress to an irreversible stage
  • Tissue can be replaced by fibrous tissue