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3. Sys Path 2 > resp notes good 2 > Flashcards

resp notes good 2 Flashcards

1
Q

Bronchopneumonia
- what is it?
- cause
- distribution

A
  • Inflammatory exudates fill alveoli and bronchioles
  • almost always caused by bacteria that have reached the lung by an airborne route, colonize the air spaces of the alveoli and bronchioles, and elicit an inflammatory reaction that fills these air spaces
  • Bronchopneumonia typically has a cranioventral distribution of lesions in the lung.
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2
Q

Airway disease
- what is it? distribution?
- causes

A
  • Inflammation or necrosis specifically affects the bronchi or bronchioles
  • This may be caused by viruses that infect and kill airway epithelium (e.g. influenza virus), or by inflammatory responses that target airways (e.g. asthma/heaves in horses, or chronic bronchitis in dogs and cats)
  • no consistent gross lesions
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3
Q

Interstitial lung disease
- what is it?
- causes?
- distribution?
- lesions? histology?

A
  • Damage to the pulmonary interstitium which we can consider mainly as the alveolar septa.
  • Often, the cause damages the alveolar epithelium or endothelium
  • viral infection, sepsis, or toxic lung injury
  • Lesions of interstitial lung disease typically have a generalized diffuse distribution in the lung
  • Histologic lesions include hyaline membranes, type II pneumocyte proliferation, and interstitial fibrosis
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4
Q

Embolic pneumonia
- what is it?
- cause?
- distribution?

A
  • Inflammation resulting from hematogenous infection, usually caused by bacteria or fungi
  • Embolic pneumonia has a generalized multifocal distribution in the lung
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5
Q

bronchopneumonia
- details of cause
- contributing factors
- pathogenesis
- morphology, histologic appearance
- other lesions that may be present?

A
  • opportunistic bacterial pathogens, that reach the lung via the airways
  • Usually, this requires either exposure to large numbers of bacteria (aspiration pneumonia) or impairment of the normal respiratory defences (by viral infection, stress, etc.)
    <><><><>
  • Bacteria, entering the lungs via the airways, colonize the air spaces of the bronchioles and alveoli. The inflammatory response chases after the bacteria and therefore targets these air spaces, resulting in exudation of fluid (edema), plasma proteins (fibrinogen/fibrin), and infiltration of neutrophils and macrophages
    <><><><>
  • In very early lesions, neutrophils congregate in the lumens of terminal bronchioles and adjacent alveoli.
  • By the time the disease is clinically apparent, alveoli and bronchioles are filled with neutrophils, sometimes fibrin, and edema.
  • But, there is often no damage to the bronchiolar and alveolar epithelium, only filling of the airspaces.
    <><><><>
  • cranioventral distribution of red- purple or tan-white (as acute inflammatory response subsides) discoloration and consolidation
  • Lobular (subacute “smoldering”) vs. lobar (severe acute) distribution
    <><><><>
    Other lesions that may be present include:
  • Fibrin on the pleural surface, as bacteria invade from the alveoli into the pleura. This fibrin will eventually be removed, or organized into fibrous adhesions.
  • Fibrin thickening interlobular septa, giving a marbled appearance to the cut section.
  • Pus that can be squeezed from the airways, but only in subacute or chronic cases. Don’t confuse the normal foamy content of the airways with pus.
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6
Q

major causes of bronchopneumonia in cattle, sheep, and goats:

A
  • Mannheimia haemolytica
  • Histophilus somni
  • Pasteurella multocida
  • Mycoplasma bovis
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7
Q

major causes of bronchopneumonia in swine:

A
  • Actinobacillus pleuropneumoniae
  • Pasteurella multocida
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8
Q

major causes of bronchopneumonia in horses:

A
  • Streptococcus zooepidemicus
  • Rhodococcus equi
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9
Q

major causes of bronchopneumonia in dogs:

A
  • Streptococcus sp.
  • Bordetella bronchiseptica
  • Aspiration pneumonia is particularly important in dogs, and typically results in mixed growth of E. coli and other bacteria within the lung
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10
Q

major causes of bronchopneumonia in cats:

A
  • Bordetella bronchiseptica
  • Pasteurella multocida
  • Streptococcus sp.
  • Mycoplasma felis.
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11
Q

Aspiration pneumonia
- pathogenesis
- distribution
- differentiating factors

A
  • Aspiration introduces massive numbers of low-virulence bacteria directly into the lung, overhelming even the healthiest defences
    <><><><>
  • Focal/unilateral distribution, in contrast to the usually bilateral and more-or-less symmetrical distribution of other bronchopneumonias.
  • Foul smell, abundant necrosis, and green discoloration; because of the large number of bacteria aspirated and the fact that many are anaerobes.
  • Culture reveals a mixed population of environmental bacteria, rather than the 1 or 2 recognized pathogens isolated from other bronchopneumonias.
  • Plant material (herbivores) or meat (carnivores) may be visible histologically.
    <><><><>
    <><><><>
    In carnivores (especially dogs), the lesions are as described above if the aspirated material contains food or numerous bacteria. But alternatively, dogs can aspirate relatively sterile gastric acid that damages bronchiolar and alveolar epithelium, and thus makes an interstitial lung disease. This is uncommon, and most dogs with aspiration pneumonia have cranioventral, focal, lobar, or unilateral pneumonia as described above.
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12
Q

normal ideal resolution to bronchopneumonia vs what unfortunate sequlae are possible

A
  • lesions of bronchopneumonia can resolve if the infection is eliminated
    > Fibrin is removed by plasmin (fibrinolysis), and neutrophils undergo apoptosis
    <><><><>
  • If the infection cannot be eliminated, then the inflammatory response will continue
    > sequelae include:
  • chronic suppurative bronchopneumonia
  • abscess formation
  • bronchiectasis (dilated bronchi that are filled with pus)
  • sequestrum formation
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13
Q

Causes of airway disease?
tissues affected?

A
  • infectious agents, hypersensitivity reactions, and toxins
  • airways = bronchi and bronchioles (+/- trachea, nasal tissues)
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14
Q

how do viruses cause airway disease?

A
  • infect airway epithelial cells and induce acute epithelial injury
  • some also infect and damage alveolar epithelium
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15
Q

important viral causes of airway disease in cattle

A
  • Bovine respiratory syncytial virus
  • bovine herpesvirus-1 (infectious bovine rhinotracheitis)
  • bovine coronavirus,
  • bovine parainfluenza virus
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16
Q

important viral causes of airway disease in sheep and goats

A
  • BRSV
  • (Maedi-visna virus and enzootic nasal tumour virus are important but don’t cause airway disease).
17
Q

important viral causes of airway disease in swine

A
  • Influenza
  • (PRRS virus and Porcine circovirus are important but they cause interstitial lung disease rather than airway disease)
18
Q

important viral causes of airway disease in horses

A
  • Equine herpesviruses-1 & -4
  • equine influenza virus
19
Q

important viral causes of airway disease in dogs

A
  • Canine coronavirus
  • canine distemper virus
  • canine adenovirus-2
  • canine parainfluenza virus
  • canine influenza virus
20
Q

important viral causes of airway disease in cats

A
  • Feline herpesvirus
  • feline calicivirus
21
Q

can bacterial infections cause airway disease?

A

Bacterial infections can cause bronchitis, although severe infections more typically result in bronchopneumonia.

22
Q

Examples of hypersensitivity reactions that result in airway disease

A
  • asthma (heaves) in horses
  • asthma in cats
  • chronic bronchitis in dogs and cats
23
Q

Toxins & chemical irritants as a cause of airway disease - some common causes and how they cause damage

A
  • can cause airway disease, alveolar disease, or both
  • Smoking, dusts, & gases directly irritate or kill the airway epithelium > bronchitis, bronchiolitis
  • some toxins (eg. 3-methylindole) must be metabolized to reactive intermediates
    > Clara cells with cytochrome p450 transform xenobiotics to reactive intermediates in the process of detoxifying them > these reactive intermediates may induce tissue damage before they are conjugated and excreted
24
Q

Morphology of airway disease

A

There are often no gross lesions. Histologic lesions include inflammation centred on airways, and/or necrosis of ciliated epithelium

25
Q

Functional consequences of airway disease

A
  • airway narrowing: inflammatory mediators (leukotrienes, other eicosanoids, or cytokines) > smooth muscle contraction (bronchoconstriction)
  • airway obstruction: inflammation and edema of the airway wall, and exudates and necrotic cells within the lumen
    <><><><>
    The functional effects of airway obstruction are:
  • Increased resistance to airflow through the airways
  • Increased respiratory effort (dyspnea)
  • Failure to ventilate the alveoli, thus leading to hypoxemia and hypercapnia.
    <><><><>
    <><><><>
  • if alveolar hypoxia is widespread (due to widespread airway lesions), then generalized pulmonary vasoconstriction may lead to pulmonary hypertension and cor pulmonale.
  • Cor pulmonale refers to pulmonary hypertension and right heart failure as a consequence of lung disease.
26
Q

airway disease
- optimal resolution
- possible sequelae

A

The airway epithelium heals quickly following an acute one-time insult, as follows:
Viral infection → Necrosis → Sloughing of necrotic epithelial cells with exposure of basement membrane → Flattening and stretching of surviving epithelial cells to cover the basement membrane → Clearing of exudates by mucociliary clearance, macrophages and proteolytic enzymes → Proliferation of surviving epithelial cells → Differentiation into normal epithelium
<><><><>
Healing is usually perfect following viral infections, but may not occur if there is repetitive injury or with overwhelming damage
<><><><>
Sequelae:
2. Increased susceptibility to bacterial pneumonia > loss of ciliated epithelium
3. Atelectasis and/or emphysema may occur as a result of airway obstruction.
4. Bronchiectasis
5. Bronchiolitis obliterans fibrosa > fibrous tissue in airway lumen
6. Mucous and squamous metaplasia, neoplastic transformation

27
Q

interstitial pneumonia (aka interstitial lung disease)
- causes

A
  • Infectious agents: many viruses, migrating larva (e.g. Dictyocaulus, Ascaris suum), protozoa (e.g. Toxoplasma)
  • Sepsis
  • Toxins that are activated by biotransformation: 3-methylindole (fog fever), paraquat, mouldy sweet potatoes, Perilla mint, … These are rarely recognized in Ontario.
  • Toxins that cause direct injury without biotransformation: chlorine gas, 100% oxygen, acid aspirated from vomitus, silo gas, noxious gases
  • Chemical injury from aspiration of gastric acid, or smoke inhalation from fires, or inhalation of toxic gases like ammonia, chlorine, nitrogen oxides (silo gas)
  • Hypersensitivity: allergic alveolitis in housed adult dairy cattle. This is uncommon.
  • Pneumoconiosis: inhalation of inorganic dusts can cause chronic interstitial lung disease. Asbestosis, silicosis, and many other occupational exposures are well-recognized in humans, but are rare in domestic animals.
28
Q

interstitial lung disease pathogenesis

A
  • damage to alveolar epithelium or endothelium (various mechanisms, depend on insult)
  • The endothelium and the epithelium are both important barriers to water movement across the air- blood barrier. Damage to either of these cell types causes alveolar edema.
    <><>
  • acutely: formation of hyaline membranes
  • 3 days after injury to type I pneumocytes: type II cells proliferate > necessary for repair, but poor oxygen exchange > eventually differentiate in acute cases
  • In less favorable circumstances, type II pneumocytes persist and interstitial fibrosis develops > permanently impairs gas exchange, reduces the compliance
  • with severe damage, fibrosis may develop before the tissue has time to heal
    <><><><>
  • hypoxemia, reduced lung compliance, increased work of breathing, and reduced functional lung volume
29
Q

what are hyaline membranes?

A
  • a mixture of plasma proteins, surfactant proteins, and dead type I pneumocytes
  • When the alveolar epithelium is damaged, these substances form a membrane that lines the inner surface of the alveolus
  • Think of hyaline membranes as a scab covering the alveolar surface
  • Hyaline membranes are a diagnostic indicator that there has been damage to the alveolar epithelium
30
Q

functional effects of interstitial lung disease

A
  • alveolar edema, hyaline membranes, type II pneumocytes, and interstitial fibrosis > obstruction to gas exchange in the alveolus
  • reduction in compliance of the lung
  • functional lung volume is reduced
    <><><><>
    hypoxemia, reduced lung compliance, increased work of breathing, and reduced functional lung volume
31
Q

interstitial lung disease morphology

A
  • usually diffuse, occasionally checkerboard
  • rib impressions, failure of lungs to collapse
  • firm, heavy and wet (edema), reddened
  • +/- interlobular edema/emphysema (cattle, pigs, horses)
    <><><><>
    Histology:
  • edema and hyaline membranes in acute stages
  • proliferation of type II pneumocytes and interstitial fibrosis if chronic
32
Q

embolic pneumonia
- general causes?
- vs interstitial lung disease?
- distribution?
- more specific causes?

A
  • blood-borne bacteria or fungi
    <><><><>
  • If an abscess ruptured into a large vein, then massive numbers of bacteria would suddenly attack the lung, and this would cause a diffuse interstitial lung disease
  • But here we are discussing a less fulminant disease, where low numbers of bacteria might seed a tiny area of the lung today, and another cluster colonizes a different area of lung tomorrow, and another the next day
  • Each of these tiny colonies grows to form an abscess, and those abscesses together have the generalized multifocal distribution that indicates embolic pneumonia
    <><><><><><><><>
  • right-sided valvular endocarditis
  • omphalitis
  • jugular venipuncture
  • traumatized and infected ears in pigs
  • liver abscesses in feedlot cattle
  • udder cleft dermatitis in dairy cows

3. Sys Path 2 (47 decks)

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