Respiratory Pathology Flashcards
What are the defence mechanisms of resp system?
- Anatomic configuration (coiled nasal conchae, bifurcation at trachea = air turbulence)
- Mucosal surface with antimicrobials, neutralizing Ig’s, mucus, ciliated epithelium.
- Normal flora
- Clearance mechanisms (cough, sneeze, swallow, mucociliary clearance & phagocytosis)
What can cause disruption of resp system defence mechanisms?
- Viral infection (virus-bacterial synergism)
- Immune-compromise/stress
- Prolonged antibiotic use
Describe the reactive changes that occur once there is injury to the epithelium of URT.
NORMALLY:
- Exfoliation of ciliated cells
- Ulceration
- Rapid dividing cells (basal cells) differentiate into ciliated cells.
WHEN THIS IS OVERWHELMED 2 THINGS CAN HAPPEN:
- Goblet cell hyperplasia -> excessive mucus -> reduced mucocilliary clearance
- Damage to basal membrane -> scarring (fibrosis) -> squamous metaplasia -> reduced mucocilliary clearance
5 pathological processes: List the circulatory disturbances you can get in your nasal cavity and sinuses.
- Congestion/hyperaemia: congested blood vessels in lamina propria normal depending on situation
- 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)
5 pathological processes: List the types of inflammation you can get in your nasal cavity and sinuses.
- 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) - Sinusitis
- Extension of rhinitis.
- Dental disease -> maxillary sinus (dogs, horse)
- Dehorning cattle -> frontal sinus
- Treatment difficult due to poor drainage from sinuses.
List the potential causes of rhinitis.
- 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 - Bacterial
- ruminants: pasteurella multocida, mannheimia haemolytica, mycoplasma
- horse: strangles (strep equi ss equi), glanders (burkholderia mallei)
- pig: atrophic rhinitis (bordetella bronchiseptica, pasteurella multocida) - Fungal
- Aspergillosis: suppurative/eosinophilic, vascular necrosis, turbinate destruction, mucopurulent, epistaxis, face pain, ulcers, fungal plaques
- Cryptococcosis: discrete granulomas to mucopurulent exudate - Parasites: larvae in nostrils, mucopurulent, irritation, inflamm, obstruction
- Allergic
- Foreign body
- Irritant inhalation
- Idiopathic
5 pathological processes: List the DoG you can get in your nasal cavity and sinuses.
- SCC (nose, ears, hairless skin)
- Papilloma
- Adenocarcinoma (glands)
- Fibrosarcoma
- Osteosarcoma
- Chondrosarcoma
- Lymphoma (lymphocytes)
5 pathological processes: List the types of circulatory disturbances you can get in your larynx & trachea
Laryngeal oedema:
- can occur 2 to acute inflamm (all species).
- Can obstruct larynx –> asphyxiation
- Specific causes: anaphylaxis, irritant gases, trauma, allergic reaction.
5 pathological processes: List the types of inflammation you can get in your larynx & trachea
- 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
5 pathological processes: List the types of degeneration you can get in your larynx & trachea.
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)
5 pathological processes: List the DoG you can get in your larynx & trachea
Larynx: papilloma, SCC, rhabdomyoma
Trachea: carcinoma, chondroma, oestochondroma
5 pathological processes: List the problems you can get in the guttural pouch
- Same pathogens as pharynx
- Guttural pouch mycosis (Aspergillus)
- Empyema (sequel to strangles - S. equi ss equi)
- drainage problems similar to those of sinuses
List the defence mechanisms of the LRT.
- Mucociliary clearance, sneezing, coughing, swallowing. Entraps molecules >2um
- Bronchial-associated lymphoid tissue (BALT)
- Alveolar macrophages
- Pulmonary intravascular macrophages
- Oxygen & free radical scavengers
Describe the reactive changes that occur when there is injury to bronchi.
- Exfoliation of ciliated cells
- Ulceration
- Rapid dividing cells regenerate as ciliated cells
PERSISTENT INJURY: - Goblet cell hyperplasia > excess mucus > reduced mucocilliary clearance
- Damage to basal membrane > scarring (fibrosis)> squamous metaplasia (reduced mucociliary clearance)
Describe the reactive changes when there is injury to bronchioles.
- Acute and mild injury > exfoliation of bronchiolar ciliated cells> ulceration>mitotic divisions of Clara cells> regeneration
- Acute and severe injury: exudate is infiltrated by fibroblasts > nodules of fibrovascular tissue> polyp formation> obstruction
- Persistent injury> exfoliation of bronchiolar ciliated cels > ulceration > goblet cell metaplasia (usually NO goblet cells in bronchioles) > catarrhal exudate
Describe the reactive changes when there is injury to alveoli.
- alveolar injury
- pneumocytes 1 detach
- Increased permeability
- Leakage of plasma fluid
- Proliferation of pneumocytes 2
- Differentiation into pneumocytes 1 (to regenerate surface of alveolar space)
*NOTE: pneumocyte= alveolar cells. Pneumocyte 1 = gas exchange (sqaumous). Pneumocyte 2 = surfactant production (cuboidal)
5 pathological processes: List the circulatory disturbances you can get in your lungs
- Congestion (blood gets stuck in lungs usually related to HF) /hyperemia (inflammation)
- Oedema
- Cardiogenic: increased hydrostatic P
- Non-cardiogenic: inflammation or direct damage to pneumocytes type 1 (viral and toxic)
- Concentration of protein - haemorrhage
- trauma, DIC, coagulopathies, vasculitis, sepsis - 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 - 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
Pathological processes: List the INFLATION disturbances you can get in your lungs
- 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. - 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
5 pathological processes: List the types of inflammation you can get in lungs.
- 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.
- 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)
5 pathological processes: List the pigments and tissue deposits you can get in your lungs
Anthracosis
- heavy black carbon deposits
- Common incidental PM finding in city animals
5 pathological processes: List the DoG you can get in your lungs
- Primary neoplasias: uncommon, adenocarcinomas most common
- 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
5 pathological processes: List the circulatory disturbances you can get in your pleura.
- 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
5 pathological processes: List the types of inflammation you can get in your pleura.
- 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 - Pyothorax
5 pathological processes: List the DoG you can get in your pleura.
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
5 pathological processes: List OTHER disorders you can get in your pleura.
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)
