resp 1 lectures Flashcards

1
Q

club cells
- location and function

A
  • in smaller airways
  • progenitor cells to replace damaged ciliated epithelium
    > metabolize and detoxify chemicals and drugs in some species
    > secrete proteins that help to regulate the inflammatory response
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2
Q
  • Nasal cavity and nasopharynx functions
A

– Air conduction
– Removal of large particulates
– Warming and humidification of air
– Olfaction

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3
Q

Trachea, bronchi, bronchioles functions

A

– Air conduction
– Defence

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4
Q

Alveoli function

A

gas exchange

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5
Q

Cells in the Respiratory Tract: Trachea & bronchi

A
  • Ciliated epithelial cells
  • Goblet cells & mucosal glands
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6
Q

Cells in the Respiratory Tract: Bronchioles

A
  • Few ciliated epithelial cells or goblet cells,
    no mucosal glands
  • Club cells: non-ciliated cells
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7
Q

Cells in the Respiratory Tract: Alveoli

A

*Type I pneumocytes (membranous)
*Type II pneumocytes (cuboidal) > progenitors, surfactant
*Alveolar macrophages

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8
Q

Pulmonary Intravascular Macrophages
- in vessels of what animals? not normally in?
- functions?

A

*Macrophages in blood vessels of:
cat, horse, ruminants, pig
*But not normally in:
dog, rodents, humans
*Removal of particulates from blood (bacteria, opsonized RBCs, …)

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9
Q

Anatomic Patterns of Pneumonia

A
  1. Bronchopneumonia
  2. Airway disease
  3. Interstitial lung disease (aka interstitial pneumonia)
  4. Embolic pneumonia
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10
Q

Bronchopneumonia
- cause
- gross lesions
- hitso lesions

A
  • Cause: airborne bacterial infection, with infection of airspaces
  • Gross lesions: usually cranioventral consolidation
  • Histologic lesions:
    > Neutrophils & edema fill alveoli and bronchioles
    > Often no damage to airway or alveolar epithelium
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11
Q

Airway disease
- what is it?
- cause
- common examples

A
  • Inflammation and/or necrosis of bronchi and/or bronchioles
  • Cause: viruses, bacteria, hypersensitivity
  • Examples
    > Influenza virus: bronchial and bronchiolar necrosis
    > Chronic bacterial bronchitis
    > Chronic bronchitis in dogs
    > Equine, feline, human asthma
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12
Q

Interstitial lung disease “Interstitial pneumonia”
- what is the interstitium?
- what is it?
- cause
- gross lesions
- histo lesions
- repair?

A
  • Interstitium = alveolar septa and other connective tissue
    <><><><>
  • Injury to alveolar epithelium or endothelium
  • Cause: viruses, sepsis, toxins, hypersensitivity, idiopathic
  • Gross lesions: diffusely rubbery
  • Histologic lesions:
    > Hyaline membranes
    > Repair: proliferation of type II pneumocytes, interstitial fibrosis
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13
Q

Embolic Pneumonia
- what is this?
- lesions?

A
  • Blood-borne showering of the lungs by bacterial or fungal pathogens, (ddx= metastatic neoplasia)
  • Lesions: generalized, randomly distributed foci of suppuration ± necrosis, centred on blood vessels
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14
Q

Horse, embolic pneumonia with aspergillus, pethogenesis?

A

Colitis > loss of mucosal barrier > hematogenous spread of Aspergillus

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15
Q

Anatomic Patterns of Pneumonia, summary with brief cause

A
  1. Bronchopneumonia: Inflammatory exudates fill the air spaces
  2. Airway disease: Inflammation or injury to bronchi / bronchioles
  3. Interstitial lung disease (interstitial pneumonia): Injury to alveolar epithelium (or endothelium)
  4. Embolic pneumonia: Blood-borne insult
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16
Q

The Need for Lung Defences

A
  • Most bacterial respiratory pathogens are carried by apparently healthy animals
  • The lungs are constantly challenged with pathogens from the nasopharynx and in inhaled particles
  • The lung must remain sterile for optimal function
17
Q

how fast do lungs cleat pathogens, eg. M. haemolytica?

A

only ~25% of pathogen after 2 hours, ~10% at 4…

18
Q

Multi-layered System of Lung Defence

A
  1. Mucociliary clearance
  2. Proteins in lung lining fluid
  3. Resident Alveolar Macrophages
  4. Recruited cells…
19
Q

what is mucociliary clearance?
- purpose, mechanism

A

Mucociliary clearance & cough rapidly eliminates inhaled particles
* Periciliary layer (hypophase) and mucous layer
* Trapping of particles by mucus
* Clearance of mucus to the nasopharynx

20
Q

Proteins in lung lining fluid
- what do they do?
- which ones?

A

Proteins in lung lining fluid block colonization, kill or opsonize bacteria that reach the lung
* Antibody
* Surfactant proteins A & D
* Defensins
* Lactoferrin
* Lactoperoxidase

21
Q

Resident Alveolar Macrophages - functions

A
  • Phagocytosis of particles & bacteria
  • Killing pathogens
  • Recruitment of inflammatory cells
  • “Housekeeping” in the alveoli
22
Q

Recruited cells for lung defence
- which ones, and what do they do?

A

…enhance lung defences
* Neutrophils, monocyte- derived macrophages: phagocytose & kill bacteria
* B lymphocytes: antibody blocks colonization, kills bacteria, opsonization
* T lymphocytes: activate macrophages-> increased microbicidal functions

23
Q

Summary of Lung Defences

A
  • Particle entrapment
  • Mucociliary clearance & cough
  • Proteins in lung lining fluid
  • Alveolar macrophages
  • Recruitment of neutrophils & monocyte-derived macrophages
  • Immune responses: neutralize pathogens, block colonization, enhance cell function
24
Q

shipping fever - usually presents as what type of pneumonia

A

Fibrinopurulent bronchopneumonia

25
Q

Pneumonia and pleuritis =
- how does it develop?

A

Pleuropneumonia
- Most cases have an underlying bronchopneumonia, with pleuritis developing as bacteria migrate into the pleural space

26
Q

Earliest lesions of bronchopneumonia: 3 hours post-infection.

A

neutrophils in distal bronchioles, no clinical signs yet

27
Q

Sequelae of Bovine Bacterial Pneumonia

A
  • Acute: death due to sepsis
    <><>
  • Chronic bronchopneumonia
  • Pleural adhesions, lung fibrosis
    <><>
  • Abscessation
  • Sequestrum formation
  • Bronchiectasis
28
Q

Bronchiectasis - what is this?

A

Pooling of exudates > Neutrophil-mediated degradation of bronchial wall

29
Q

Sequestrum formation… what is a sequestrum?

A

mass of necrotic tissue surrounded by fluid exudate… cannot be removed & persists

30
Q

Abscess, Bronchiectasis, Sequestrum: Clinical Importance?? Clinical Outcome??

A
  • Permanent
  • Inaccessible to many antibiotics
  • Refuge for pathogens > relapse
31
Q

Summary: Bronchopneumonia progression

A
  • Multilayered system of lung defences
  • Compromised lung defence > air-borne infection by opportunistic pathogens
  • Cranioventral consolidation;
    Histologic lesions: bronchioles and alveoli filled with neutrophils ± fibrin
  • Resolution;
    Chronic bronchopneumonia,
    abscessation, bronchiectasis, sequestration
32
Q

Feedlot calf, liver abscess erodes into hepatic vein and caudal vena cava
> Acute showering of lung with myriad bacteria
- what is the pattern of lung disease?

A

c) Interstitial lung disease