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1. Cardiorespiratory > Respiratory Pathology > Flashcards

Respiratory Pathology Flashcards

1
Q

What are the defence mechanisms of resp system?

A
  1. Anatomic configuration (coiled nasal conchae, bifurcation at trachea = air turbulence)
  2. Mucosal surface with antimicrobials, neutralizing Ig’s, mucus, ciliated epithelium.
  3. Normal flora
  4. Clearance mechanisms (cough, sneeze, swallow, mucociliary clearance & phagocytosis)
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2
Q

What can cause disruption of resp system defence mechanisms?

A
  1. Viral infection (virus-bacterial synergism)
  2. Immune-compromise/stress
  3. Prolonged antibiotic use
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3
Q

Describe the reactive changes that occur once there is injury to the epithelium of URT.

A

NORMALLY:

  1. Exfoliation of ciliated cells
  2. Ulceration
  3. Rapid dividing cells (basal cells) differentiate into ciliated cells.

WHEN THIS IS OVERWHELMED 2 THINGS CAN HAPPEN:

  1. Goblet cell hyperplasia -> excessive mucus -> reduced mucocilliary clearance
  2. Damage to basal membrane -> scarring (fibrosis) -> squamous metaplasia -> reduced mucocilliary clearance
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4
Q

5 pathological processes: List the circulatory disturbances you can get in your nasal cavity and sinuses.

A
  1. Congestion/hyperaemia: congested blood vessels in lamina propria normal depending on situation
  2. Haemorrhage/epistaxis: hard to tell where the blood is from. Causes: trauma, foreign body, erosion of vessels secondary to inflamm or neoplasia, clotting defects, mycotic infection of guttural pouch, EIPH (horse), ethmoidal haematoma (horse) [protruding mass, confirm by histo, caused by repeated haemmorhage, can press surrounding bone ->necrosis -> facial deformity)
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5
Q

5 pathological processes: List the types of inflammation you can get in your nasal cavity and sinuses.

A
  1. Rhinitis:
    TYPES:
    - serous
    - catarrhal (mucus)
    - purulent/suppurative (neutrophils + mucus = mucopurulent. Usually accompanied by mucosal necrosis & 2 bacterial infection)
    - fibrinous
    *inflamm infiltrates:
    - neutrophils
    - lymphoplasmacytic (chronic, pathogenesis unclear, diffuse/polypoid thickening of nasal passages, hyperplasia of glands, ulcerated epithelium)
    - eosinophilic
    - granulomatous (macrophages; fungi, foreign body, mycobacteria)
  2. Sinusitis
    - Extension of rhinitis.
    - Dental disease -> maxillary sinus (dogs, horse)
    - Dehorning cattle -> frontal sinus
    - Treatment difficult due to poor drainage from sinuses.
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6
Q

List the potential causes of rhinitis.

A
  1. Viral:
    - horse: EHV (equine viral rhinopneumonitis), influenza, adeno
    - ruminants: BVDV (pesti), BHV-1 (infectious bovine rhinotracheitis), gammaherpesvirus (malignant catarrhal fever)
    - dogs: distemper, adeno 1 &2, herpes, para
    - swine: cytomegalovirus (herpes)
    - cats: FHV (feline viral rhinotracheitis), calici
  2. Bacterial
    - ruminants: pasteurella multocida, mannheimia haemolytica, mycoplasma
    - horse: strangles (strep equi ss equi), glanders (burkholderia mallei)
    - pig: atrophic rhinitis (bordetella bronchiseptica, pasteurella multocida)
  3. Fungal
    - Aspergillosis: suppurative/eosinophilic, vascular necrosis, turbinate destruction, mucopurulent, epistaxis, face pain, ulcers, fungal plaques
    - Cryptococcosis: discrete granulomas to mucopurulent exudate
  4. Parasites: larvae in nostrils, mucopurulent, irritation, inflamm, obstruction
  5. Allergic
  6. Foreign body
  7. Irritant inhalation
  8. Idiopathic
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7
Q

5 pathological processes: List the DoG you can get in your nasal cavity and sinuses.

A
  1. SCC (nose, ears, hairless skin)
  2. Papilloma
  3. Adenocarcinoma (glands)
  4. Fibrosarcoma
  5. Osteosarcoma
  6. Chondrosarcoma
  7. Lymphoma (lymphocytes)
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8
Q

5 pathological processes: List the types of circulatory disturbances you can get in your larynx & trachea

A

Laryngeal oedema:

  • can occur 2 to acute inflamm (all species).
  • Can obstruct larynx –> asphyxiation
  • Specific causes: anaphylaxis, irritant gases, trauma, allergic reaction.
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9
Q

5 pathological processes: List the types of inflammation you can get in your larynx & trachea

A
  1. Laryngitis & 2. Tracheitis
    - extensions of inflam of upper/lower RT
    - Viral rhinitis (incl. distemper, BHV (IBR), EHV)
    - Canine infectious tracheobronchitis (kennel cough) (bordetella, CPI, CAV2)
    - nematodes, bacteria
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10
Q

5 pathological processes: List the types of degeneration you can get in your larynx & trachea.

A

Laryngeal hemiplegia

  • degeneration of L recurrent laryngeal nerve & atrophy of L & dorsal cricoarytenoid muscles
  • Distorts & partially obstructs larynx
  • Horses have stertorous breathing (roaring)
  • idiopathic or secondary to nerve damage (guttural pouch mycosis, enlarged LN, iatrogenic, neck trauma, neoplasia)
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11
Q

5 pathological processes: List the DoG you can get in your larynx & trachea

A

Larynx: papilloma, SCC, rhabdomyoma
Trachea: carcinoma, chondroma, oestochondroma

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12
Q

5 pathological processes: List the problems you can get in the guttural pouch

A
  • Same pathogens as pharynx
  • Guttural pouch mycosis (Aspergillus)
  • Empyema (sequel to strangles - S. equi ss equi)
  • drainage problems similar to those of sinuses
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13
Q

List the defence mechanisms of the LRT.

A
  1. Mucociliary clearance, sneezing, coughing, swallowing. Entraps molecules >2um
  2. Bronchial-associated lymphoid tissue (BALT)
  3. Alveolar macrophages
  4. Pulmonary intravascular macrophages
  5. Oxygen & free radical scavengers
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14
Q

Describe the reactive changes that occur when there is injury to bronchi.

A
  1. Exfoliation of ciliated cells
  2. Ulceration
  3. Rapid dividing cells regenerate as ciliated cells
    PERSISTENT INJURY:
  4. Goblet cell hyperplasia > excess mucus > reduced mucocilliary clearance
  5. Damage to basal membrane > scarring (fibrosis)> squamous metaplasia (reduced mucociliary clearance)
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15
Q

Describe the reactive changes when there is injury to bronchioles.

A
  1. Acute and mild injury > exfoliation of bronchiolar ciliated cells> ulceration>mitotic divisions of Clara cells> regeneration
  2. Acute and severe injury: exudate is infiltrated by fibroblasts > nodules of fibrovascular tissue> polyp formation> obstruction
  3. Persistent injury> exfoliation of bronchiolar ciliated cels > ulceration > goblet cell metaplasia (usually NO goblet cells in bronchioles) > catarrhal exudate
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16
Q

Describe the reactive changes when there is injury to alveoli.

A
  1. alveolar injury
  2. pneumocytes 1 detach
  3. Increased permeability
  4. Leakage of plasma fluid
  5. Proliferation of pneumocytes 2
  6. Differentiation into pneumocytes 1 (to regenerate surface of alveolar space)

*NOTE: pneumocyte= alveolar cells. Pneumocyte 1 = gas exchange (sqaumous). Pneumocyte 2 = surfactant production (cuboidal)

17
Q

5 pathological processes: List the circulatory disturbances you can get in your lungs

A
  1. Congestion (blood gets stuck in lungs usually related to HF) /hyperemia (inflammation)
  2. Oedema
    - Cardiogenic: increased hydrostatic P
    - Non-cardiogenic: inflammation or direct damage to pneumocytes type 1 (viral and toxic)
    - Concentration of protein
  3. haemorrhage
    - trauma, DIC, coagulopathies, vasculitis, sepsis
  4. Acute respiratory distress syndrome
    - alveolar and/or endothelial damage -> increased permeability and leakage of fluid and protein->forms hyaline membrane -> pneumocyte type 2 proliferation -> exchange of gas is impaired
  5. Embolism and infarct
    - infarct when circulation compromised by emboli (thrombo, spetic, tumour), dirofilaria immitis etc.
    - first microscopic lesions are haemmorhage > necrosis & inflamm cells> haemosiderophages are present a few days later.
    - sterile emboli => fibrotic scars
    - septic emboli => abscess formation
18
Q

Pathological processes: List the INFLATION disturbances you can get in your lungs

A
  1. Atelectasis (alveoli spaces collapse)
    - incomplete distention of alveoli (but normal cellular composition) due to: compression (tumour), contraction (fibrosis in lung/pleura not allowing enough space for alveoli to dilate), congenital
    - grossly: red with firm liver-like consistency and slightly depressed surface. May sink in fixative.
  2. Emphysema
    - enlargement of airspaces distal to terminal bronchiole, with destruction of alveolar septa (large clear areas)
    - secondary to air outflow obstruction) or bronchopneumonia (plug of exufate in bronchi and bronchioles)
    - Alveolar (usually) or interstitial
19
Q

5 pathological processes: List the types of inflammation you can get in lungs.

A
  1. Bronchitis/Bronchiolitis
    - extension of pneumonia or primary
    - acute or chronic (mucus)
    - feline asthma:
    • Early stage: mucosal edema, eosinophils
    • Advanced: bronchoconstriction, excess mucus, smooth muscle & submucosal glands hyperplasia, obstruction of bronchi & bronchioles, eosinophils.
  2. Pneumonia:
    TYPES
    (a) Bronchopneumonia: cranioventral distribution Most common type.
    Usually aerogenous pathogens (pasteurella multocida, bordetella bronchiseptica, strep spp, mannheimia haemolytica, actinobacillus pleuropneumoniae, mycoplasma) . Defence overwhelmed. Bronchoaspiration (force-feeding, passing nasogastric tube, vomit, anesthesia, cleft palate).
    Cranioventral consolidation (bronchiole mucosa injury -> hyperaemia -> permeability oedema -> recruitment of leukocytes -> increased vascular changes: fibrinous exudate and haemorrhage -> lung consolidation [alveolar spaces filled with stuff]). Suppurative and/or fibrinous (more severe- pleural involvement common): resolution or progression to chronic stage (BALT hyperplasia, goblet cell hyperplasia, bronchiectasis [wider thicker tubes], fibrosis; unresolved fibrinous pneumonia = bronchiolitis obliterans.

(b) Interstitial pneumonia (pneumonitis): diffuse
Injury on alveolar wall (endothelium, BM & alveolar epithelium) bronchiolar interstitium.
Grossly: failure of lungs to collapse, rib impressions, no exudates in airways
pathogenesis: injury to pneumocytes via aerogenous (virus, toxic gas)/injury to alveolar capillary & BM via haematogenous (septicemia, DIC, toxins/endotoxin, free radicals)
- Acute: diffuse alveolar damage, hyaline membranes, thickened alveolar wall (neutrophils, oedema), type 2 pneumocyte hyperplasia, mild.
- Chronic: persistent injury, fibrosis, lymphocytes, macrophages, fibroblasts, myofibroblasts. Type 2
pneumocyte hyperplasia & persistence, sqaumous metaplasia, smooth muscle hyperplasia in bronchioles & pulmonary arterioles.

(c) Embolic pneumonia: multifocal. Injury haematogenous: bacteria disrupt endothelium and BM -> spread from vessel to interstitium -> inflamm reaction assoc with blood vessels -> unresolved acute lesions may progess to pulmonary abscesses.
SOURCES: hepatic abscesses rupture into caudal VC (cattle), bacterial skin or hoof infections, contaminated catheter, endocarditis R heart.

(d) Granulomatous pneumonia: multifocal/nodular
- Nodular & random distribution
- Grossly, can be mistaken with neoplasia
- Pathogen enters aerogenous or haematogenous
- Fungi (crypto, asperigullus), mycobacteria (tuberculosis), rhodococcus equi, foreign bodies, FIP (cats)

20
Q

5 pathological processes: List the pigments and tissue deposits you can get in your lungs

A

Anthracosis

  • heavy black carbon deposits
  • Common incidental PM finding in city animals
21
Q

5 pathological processes: List the DoG you can get in your lungs

A
  1. Primary neoplasias: uncommon, adenocarcinomas most common
  2. Metastatic neoplasia: common.
    - Can be epithelial, mesenchymal (spindle) or round (free) cells.
    - metastases from mammary, uterine or thyroid carcinomas, hemangiosarcoma, osteosarcoma, malignant melanoma or lymphoma
22
Q

5 pathological processes: List the circulatory disturbances you can get in your pleura.

A
  1. Pleural effusion
    - accum of fluid in thoracic cavity
    - thoracocentesis: cytology, protein content & cell counts
    (a) Hydrothorax: oedematous fluid (pure transudate), clear, colourless, no coagulation, can occur in generalised oedema (CHF or hypoproteinemia/nephrotic syndrome), mesothelial hyperplasia and fibrosis may occur.
    (b) Haemothorax: blood in thoracity cavity, atelectasis of lungs. Secondary to trauma, or erosion of vessel wall by neoplasia or inflammation, coagulopathies.
    (c) Chylothorax: accumulation of chyle, rupture of major lymph vessel (thoracic duct). Trauma, neoplasia, lymphangitis, iatrogenic.
    2
23
Q

5 pathological processes: List the types of inflammation you can get in your pleura.

A
  1. Pleuritis/pleurisy
    - direct implantation through penetrating wound, rupture of pulmonary abscess. haematogenous, secondary to adjacent pneumonia (pleuropneumonia), usually bacterial cause. TYPES:
    - fibrinous: chronic may –> fibrosis & adhesions between visceral and parietal pleurae (commonly arises from fibrinous bronchopneumonia)
    - granulomatous: mycobacterial, FIP, nocardial, actinomyces
    - purulent: may lead to accum of purulent material in cavity (pyothorax or thoracic empyema), can result in severe toxaemia
    - haemorrhagic
  2. Pyothorax
24
Q

5 pathological processes: List the DoG you can get in your pleura.

A

Mesothelioma

  • rare except for koalas
  • thoracic, pericardial or peritoneal mesothelium
  • can be congenital in calves
  • multiple discrete nodules on pleural surface
  • malignant but rarely metastasise
25
Q

5 pathological processes: List OTHER disorders you can get in your pleura.

A

Pneumothorax

  • air in pleural cavity from ruptured airways (spontaneous) or damaged thoracic wall (penetrating wound)
  • Must be expelled to maintain (-) pressure so lungs expand properly
  • can lead to collapsed lung (atelectasis)

1. Cardiorespiratory (4 decks)

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