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Flashcards in Respiratory Deck (110):

What five defence mechanisms are utilised in the airway?

  1. Aerodynamic filtration
  2. Mucociliary escalator
  3. Antibacterials
  4. IgA
  5. Protective reflexes


Describe the two mechanisms of aerodynamic filtration in the airways.

  1. Coiled turbinates cause particles >10nm to impact with airway mucosa
  2. Branched and tortuous bronchi filter out particles >3um (any less than this are deposited in bronchioles and alveoli.


What is the mucociliary escalator?

The epithelium of the respiratory tract contains ciliated epi cells and goblet cells. Mucous produced by goblet cells is swept in an oral direction by the cilia and is reswallowed by the animal. 


What is the function of mucus in the respiratory tract?

  • Mucociliary escalator (traps and transports particles to the pharynx)
  • Physical barrier
  • Prevents dehydration of mucosal epi
  • Dilutes soluble gases
  • Contains anti-bacterials


Name and describe the antimicrobial substances present in the mucous.

  1. Lactoferrin - Fe binding protein synthesized by neutrophils and epi cells - causes retardation of bact and fungal growth
  2. Lysozyme - Hydrolyses peptioglycan and key cell wall protein of g+ve bacteria


Which two factors affect the mucociliary carpet function?

What causes them?

  1. Changes in mucus viscosity - due to temperature, dehydration and inflammation.
  2. Epithelial injury - due to trauma, infection and chronic irritation (causes epi metaplasia)


What does this picture depict?


Epithelial metaplasia. An abnormal change in the nature of a tissue (ie cell type to a stratified squamous appearance) in response to a stimuli (here chronic irritation)

This is a reversible change, once the stimuli is removed and the cells turned over the native cells return.


Which Ig is the main type found in the airways?



What protective reflexes are airway motivated?

Why are they vital?

Cough and sneeze

These are the reserve clearance mechanisms and are particularly vital during situations such as those when the ciliated cells are lost (becomes only mechanism)


Describe the alveolar defences found in the LRT.

Macrophages: Three types

  1. Alveolar
  2. Interstitial
  3. Intravascular

These phagocytose particles and agents, recruit neutrophils, co-ordinate inflammation and ascend the mucociliary escalator


Describe the mechanisms of action of the of macrophages found in the alveoli.

  1. Alveolar - ingest pathogens and particles, then MO move to the bronchi and are removed by the mucrociliary escalator. Also secrete chemokines which attract neutrophils during inflammation.
  2. Interstitial - Reside within alveolar interstitial tissue and act to phagocytose particles that have traversed alveolar cells. They enter the bronchiolar/bronchial lymphatics and move to pulmonary or tracheobronchial lymph nodes.
  3. Intravascular - Only found in some species (ruminants, pig, cat) and attach to the lumenal surface of capillary endothelial cells & act like Kupffer cells in the liver to clear particulate matter from the blood (e.g. small emboli).


Describe this lesion.

A cleft palate

Failure to close the palatine shelves (primary or secondary palate) causes aspiration of food at weaning and beyond


What is seen here? What problems can this pathology cause?

GP tympany (air build up)

A defect of the nasopharyngeal opening causes (unilateral) trapping of air and mucus in the GP. 

Oesophageal pressure can lead to dysphagia and dyspnoea.

Can lead to aspiration of food and pneumonia and predisposes horses to GP bacterial infection


Describe the problems associated with Brachiocephalic airways.

  • Stenotic nares
  • Everted laryngeal saccules
  • Elongated soft palate

Leads to airway obstruction, cyanosis and syncope



Bleeding from the nose


What can cause bleeding from the URT?

  • Inflm
  • Infection
  • Trauma
  • Neoplasia
  • Clotting defects


What is the difference between active and passive congestion of the URT?

  1. Active is caused by inflammation 
  2. Passive is caused by reduced blood outflow 


What are the cardinal signs of inflammation?

  1. Redness 
  2. Swelling
  3. Loss of function 
  4. Pain 
  5. Heat


What stages of acute inflammation characterise types of nasal discharge?

Describe each stage

  1. Serous - clear, watery
    1. mucosal hyperaemia and oedema, increased fluid production
  2. Catarrhal - thick - mucoid/ creamy white
    1. Increased mucoserous secretions, some inflammatory cells
  3. +/- Fibrinous - tacky yellow red deposits
    1. Increased vascular permeability +/- necrosis
  4. Purulent - thick, white, green, brown
    1. Filled with degenerating neutrophils


What are the common pathological changes in the URT with chronic inflammation?

  • Mucosal hyperplasia of epithelium and seromucous glands
  • Epithelial metaplasia from ciliated columnar to stratified squamous
  • Chronic inflammatory cells infiltrate - mo, l, plasma cells
  • Fibroplasia


Polipoid thickening

Abnormal thickening/ growth of tissue projecting from a mucous membrane .

It is pedunculated if attached to the mucosa by an elongated stalk. If no stalk is present it is sessile.


Polypoid thickening is characteristic of chronic nasal inflammation particularly in which species and where?

Horses - they arise in the ethmoid region

Cats - they arise from the auditory tubes or tympanic bulla (may extend into the pharynx or external auditory tubes


Causes of URT inflammation.

  1. Irritants/ allergens eg pollen
  2. FB/ trauma
  3. Parasites - oestrus ovis
  4. Dental disease
  5. Infectious agents - viral, bacterial and fungal


Name three examples of viral agents associated with URT infections

  • Infectious bovine rhinotracheitis virus (IBR) - HV1
  • Equine herpes virus 1 + 4
  • Equine influenza virus
  • Feline herpes virus 1  Flu
  • Feline calicivirus   Flu
  • Canine distemper virus
  • Canine adenovirus 2 
  • Canine parainfluenza virus 


IBR is an example of which type of herpes virus?



What environmental factors lead to increased susceptibility to IBR?



Stress and overcrowding



Describe the transmission and pathogenesis of IBR

Aerosol transmission

  1. Nasal mucosa and conjunctiva are infected
  2. Viral replication in epithelial cells +/- dissemination throughout respiratory tree
  3. Inflammatory response leads to conjunctival and nasal hyperaemia and a serous/catarrhal exudate
  4.  Damages mucociliary escalator impairs immune response = secondary bacterial infection = purulent nasal discharge


Describe this lesion and suggest a viral cause.

A tacky yellow-red substance is adhered to the nasal cavity wall throughout the nasal cavity. Underneath the mucosa is diffusely redened. 

Diffuse acute fibrinonecrotising inflammation of the nasal cavity.



After how many days are antibodies produced in an IBR infection?

10-14 days


Describe the pathogenesis of S, equi var equi in the horse.

Aerosol/ fomite transmission

  1. Colonisation of the NP mucosa
  2. Serous -> purulent nasal discharge 
  3. Lymphatic spread of the bacteria causes lymphatic abscessation
  4. Gutteral pouch empyema caused by in-bursting of abscesses  


Describe the pathogenic features of Pasteurella multocida in pigs.

Seen around 4-12 weeks

Preinfection with BB necessary, environmental and nutritional factors also instigate

Moderate to severe atrophy of nasal turbinates associated with distortion/ shortening of the snout


What structures contained within the GP can be damaged in guttural pouch mycosis?

What clinical signs can be signs?

Cranial nerve damage (VII) - Facial muscle, tongue, pharynx and larynx paralysis

Internal carotid atery - Potentially fatal haemorrhage


What is the common aetiological agent in Guttural Pouch mycosis in the horse?

This fungi is also implicated in which type of aspergillosis in the dog? Describe.

Apergillus fumigatus

  • Severe fibrinonecrotic inflammation
  • Usually unilateral

Nasal aspergillosis 

  • Forms visible fungal plaques on nasal mucosa causing fibrinonecrotic to granulomatous inflammatory response 
  • mucopurulent to haemorrhagic nasal discharge.
  • Can lead to turbinate destruction.


Upper airway neoplasia is most common in which categories of dog? 

Are they usually malignant or benign?

Middle-aged to elderly animals. Breeds with increased risk include; airedales, bassets, OESD, german SH pointers

They are usually malinant (>80%)


Describe this lesion

Multifocal round to oval raised tacky white nodules present in the guttural pouch of this horse. Varying in size from 0.5x0.5 cm to 1-0.5cm. The rim of the nodules is focally redened.

Moderate, multifocal fibrinonecrotising ginflammation of the guttural pouch mucosa. Associated with guttural pouch mycosis caused by Aspergillus fumigatis


Describe this lesion

A large (30x20 cm) focal pale red infiltrating mass is found in the nasal cavity of this horse. Externally it distorts the normal anatomy of the face and extends from the upper eyeline to about 10cm below the eyeline on the left of the face. Externally three ulcerated raised masses are seen (3x3cm)

Severe chronic? squamous cell carcinoma


In which breeds is tracheal hypoplasia likely to be seen?

What clinical signs can be seen?


Pekinese, english bull terrier/ bulldog.

Causes exercise intolerence and dyspnoea.

Resistence in the tube is inversely proportional to the radius (/diameter) of said tube. Therefore a small decrease in tube diameter leads to a large increase in tube resistence.


Describe the effects of a dorsoventrally flattened trachea in the dog.

DV flattening of the trachea can often lead to prolapse of the dorsal membrane of the trachea (increasing tube resistence)

This leads to dyspnoea and increase respiratory noise. May lead to separation of the dorsal ligament and mucosa from cartilage in severe cases.


True or false

Laryngeal paralysis in the dog is often bilateral.

How does this differ in the horse and why?


In the horse the paralysis is often unilateral on the left side, the large tortuous path of the left recurrent laryngeal nerve leaves it prone to damage.


What is abnormal in this picture of the larynx?

What pathology and clinical signs are associated?

Unilateral atrophy of the left cricoarytenoid muscles, associate with paralysis of the left recurrent laryngeal nerve.

Atrophy/ paralysis of these muscles leads to failure/ partial abduction of the arytenoid cartilages of the larynx at inspiration.

(Exercise intolerence) and increased respiratory noise (roaring)


What are the five common causes of laryngeal oedema?

Describe the gross path findings in this case.

  • Local trauma eg. intubation
  • Irritants eg. smoke
  • Acute respiratory infections
  • Laryngeal chondritis
  • Anaphylaxis/allergic reactions

Moderate acute diffuse laryngeal oedema. Diffuse redening and swelling of the entire larynx is seen causing constriction of the laryngeal opening.


Describe this lesion.

Multifocal redening of the tracheitis is seen here covering approximately 50-60% of the tracheal mucosa. Similar lesions also seen in the larynx (approximately 20%). The ulcerative lesions range from dark to pale red and are soft in texture.

Severe acute multifocal serous ulcerative tracheitis


What are the four main causes of laryngeal hemiplegia?

  1. Primary neuronal degeneration
  2. Congenital neuronal abnormality
  3. Neurotoxins eg lead
  4. Secondary compression of the nerve - GP disease, neoplasia, cervical trauma etc


How does laryngeal paralysis occur?

Damage to the recurrent laryngeal nerve.

This causes atrophy of the cricoarytenoid muscle

Leads to failure of the arytenoid cartilages to abduct on inspiration 


Chronic inflammation of the respiratory tract leads to which four pathological changes?

  1. Mucosal hyperplasia
  2. Epithelial metaplasia
  3. Chronic inflammatory cells
  4. Fibrosis


Describe this lesion. & MD

Suggest an aetiological agent.

What clinical signs are associated with such lesions?

The larynx shows focally extensive reddening. Two round nodules (3x3cm) protruding from the respiratory surface which are firm and creamy/brown in colour.

Sub-acute, severe, ulcerative fibrinonecrotic of the larynx.

Caused by an opportunistic infection of Fusobacterium necrophorum secondary to mucosal damage.

Death occurs due to toxaemia, asphyxiation or aspiration pneumonia.



Name a parasite which can cause laryngitis/tracheitis in dogs.

What type of pathological lesions are associated with the pathogen and describe clinical signs?


Oslerus osleri

Submucosal 1x1cm nodules 

Nodules may be assymptomatic or cause coughing in dogs usually noted between 6-18 months of age. Severe infection may cause tracheal occlusion.


Describe this lesion & MD.

A large 4x5cm nodular mass is distorting the normal laryngeal anatomy and occluding the laryngeal opening. The mass is firm and shows multifocal areas of reddening.

Laryngeal chondrosarcoma


What anatomical features of the bronchioles render them vunerable to insult?

  • Lack of supporting cartilage
  • Lack of mucus due to no goblet cells + smaller and fewer cilia = poor mucociliary defences
  • Clara cells are metabolically active and produce reactive metabolites
  • Alveolar macrophages and neutrophils accumulate at terminal bronchioles and may release free rads which cause oxidative damage 


What causes can lead to acute bronchitis and bronchiolitis?

  1. Infectious agents
    1. extension of upper airway infections
    2. lower respiratory tract infections
  2. Irritants – gases, smoke
  3. Allergens – fungal spores
  4. Foreign bodies
  5. Parasites – Oslerus osleri, lungworm, migrating ascarids.


What is bronciolitis obliterans?

Describe their formation.

Fibrous polypoid nodules found in the bronchioles.

  • Severe bronchiolitis leads to loss of epithelium and attachment of exudate to exposed basement membrane
  • Exudate is infiltrated by fibroblasts during repair and forms a polyp 
  • Epithelium covers the polyp
  • This structure protrudes into the resp lumen and causing airflow obstruction


Name and describe the two main pathological signs associated with bronchitis and bronchiolitis.

Increased mucus production

  1. Gland hyperplasia
  2. Goblet cell hyperplasia
  3. Goblet cell metaplasia

Thickening of mucosa

  1. Epithelial hyperplasia / metaplasia

  2. Bronchial gland hyperplasia

  3. Smooth muscle hyperplasia

  4. Inflammatory cells and fibrosis

Overall reduction in lumen diameter and increased airway diameter


Describe the lesion.

The bronchi of this specimin is multifocally reddened and diffusely thickened and the lumen is filled with a creamy viscous fluid.

Chronic severe diffuse bronchitis


What clinical signs are associated with airway obstruction?


  1. Dyspnoea
  2. Cough
  3. Stridor
  4. Atelecasis
  5. Emphysema (due to blockage of other areas)
  6. Reduced blood oxygenation



What is it?

What is its pathogenesis?

Permanent dilation of the bronchus.

  1. Obstruction of the airway by exudate
  2. Release of proteolytic enzymes from the exudate causes necrotising inflammation of the bronchial wall
  3. Damage and destruction of the bronchial wall tissue = perm dilation



Name the parasite also known as cattle lungworm.

What stage of the parasite lifecycle causes pathology?

Dictyocaulus viviparus

  1. Larvae - migration through alveoli causes acute pneumonia and bronchiolar blockage with exudate
  2. Adult: Worms in bronchi cause irritation, increased mucus production, thickened mucosa and chronic bronchitis


Which lobes of the lung do D. viviparus generally reside in?

Obstruction of lobes can lead to what?

Caudal lung lobes



What condition is also known as heaves and COPD?

What is the aetiology of the condition?

Pathological findings?

Clinical signs?

Recurrent airway obstruction

Type 3 hypersensitivity due to inhaled allergens from mouldy hay or bedding.

  • Increased mucus production
  • Mucosal thickening
  • Peribronchial fibrosis
  • Bronchospasm

C/S: Coughing, stridor, dyspnoea, heave lines, wheeze and crackling at the end of expiration and inspiration, exercise intolerence, mucopurulent exudate


Describe the comparative anatomy of the collateral airflow in cattle, equine and carnivores.

  1. Cattle: thick complete septa = little collateral airflow
  2. Horse: incomplete thick septa
  3. Carnivores: no distinct septa


Give three examples of developmental abnormalities of the lung parynchyma.

Are these conditions generally rare or common?

  1. Congenital melanosis
  2. Agenesis of one or more lung lobes
  3. Ectopic lung tissue



What is the difference between atelectasis and emphysema?

Atelectasis - incomplete distension of the lung

Emphysema - excessive inflation of the lung


Describe this lesion

The lobules of this lung are multifocaly dark red. This covers about 90% of the tissue. Affected areas are depressed and firm and sink in water.

Severe acute multifocal atelectasis of the lung.


Why do bronchiolar obstructions cause emphysema of the lung tissue?

Air enters the lung during inspiration.

At expiration it is unable to leave and therefore the alveoli remains partially expanded.

This continues with the next respiratory effort 


What are the functional consequences of alveolar emphysema?

Rupture of alveolar walls leading to

  1. Reduced lung elasticity
    1. Early airway collapse + trapping of air (increased dead space)
  2. Loss of pulmonary capillaries
    1. Reduced alveolar perfusion
  3. Fibrosis of remaining alveolar walls (in horses)
    1. XX gas exchange
    2. Reduced compliance (greater expiratory effort)


Why does pulmonary oedema generally not occur?

Which factors lead to fluid accumulation?

Alveolar epithlium is very permeable and fluid accumulates in the intestitium and is drained by lymphatics.

Factors leading to accumulation

  • Epithelium damage
  • Increased interstitial fluid damage - overloads lymphatics


What gross pathological findings are associated with pulmonary oedema?

  • Heavy, sinking in water
  • Lungs do not fully collapse when thorax is opened 
  • Wet, oozing on cut surface
  • Foamy fluid is present in upper airways 
  • Increased pleural fluid
  • Microscopically: eosinophiliic, +/- homogenous, granular/ foamy fluid present within lumen


What physiological failures lead to oedema?

What could be the causes of each?

  1. Increased hydrostatic pressure: 
    1. inflammation
    2. passive congestion - heart failure
    3. circulatory overload - renal failure, overtransfusion
  2. Increased capillary permeability
    1. toxic damage to endothelium
    2. shock/ anaphylaxis
    3. inflammation
  3. Reduced osmotic pressure - dilutes blood
    1. Hypoproteineamia 
    2. Overtransfusion
  4. Reduced fluid drainage
    1. Inflammation
    2. tumours


Name three substances which can become emboli.

  1. Thromboemboli
  2. Fat
  3. Air
  4. Neoplastic cells



What effects can sterile and non-sterile emboli have on the body?

What are the common sources of septic thromboemboli?

Sterile: fibrinolytic TE breakdown, infarcted tissue scaring and fibrosis

Non-sterile: vasculitis/ thrombosis at emboli site,  infection spread into adjacent tissue, abscess formation

Common sources:

  • Right heart bacterial endocarditis

  • Joint / navel infections

  • Liver abscesses 


Describe the aetiology and sequalae of pulmonary embolism in cattle.

  1. Rumenitis causes hepatic abscessation
  2. Hepatic abscess causes obstruction and erosion of the vena caval wall causing thrombosis
  3. Septic thromboemboli spreak from the vena cava to the lungs
  4. Emboli cause pulmonary arteritis, thrombosis and aneurysm formation
  5. Rupture of aneurysm causes pulmonary haemorrhage


Describe this lesion.

One of the lobes of the lung is focally deep purple to black (20% of the tissue affected), the tissue is firm and sinks in water. 

Focal severe acute necrotising pulmonary infarction secondary to pulmonary emolism.


Name five causes of pulmonary haemorrhage.

  1. Pulmonary thromboembolism
  2. Trauma
  3. Inflammation
  4. Vessel erosion - abscesses/ tumours
  5. Exercise induced (race horses)


Describe the lesion.

The mucosa of the trachea is focally reddened. The two lesions seen here are round in shape and the mucosa shows signs of haemorrhage.

Multifocal acute moderate pulmonary haemorrhage


Name the four morphological types of pneumonia.

  1. Bronchopneumonia

  2. Interstitial pneumonia

  3. Embolic pneumonia

  4. Granulomatous pneumonia


What are the common causes of Bronchopneumonia?

  1. Bacteria

  2. Aspiration of food / GI contents

  3. Mycoplasmas

  4. Viruses


Descrine the distribution of lesions in an inhalation pneumonia.

Why does such a distribution occur?


  • Gravity
  • Regional variation in defence mechanism efficiency, perfusion and ventilation


Describe the appearance and texture of a lung affected by bronchopneumonia.

  • Dark red to grey
  • Firm to hard - sinks in water
  • moist to firm cut surfaces
  • +/- exudate expression


Outline the pathogenesis of Bronchopneumonia.

  1. Inhaled agents cause inflammation at the bronchoalveolar junction
  2. Acute inflammatory response
    1. Exudation of fluid and plasma protein in bronchioles and alveoli
    2. MO and neutrophils are recruited
  3. Infection spreads through lung through pores of Kohn
    1. Along airways to other lobules, bronchioles and bronchi
    2. to adjacent alveoli through septa


What is the difference in distribution between suppurative and fibrinous Bronchopneumonia?

Which is considered more severe?

Fibrinous spreads rapidly throughout the parynchema and often found throughout lobes.

Supprative often stays within a lobe and may have a patchy distribution.


Name three aetiological agents of suppurative and fibrinous bronchopneumonia,

  1. S - Pasteurella multocida, Bordetella bronchoceptica, Distempa, PI3, Mycoplasma spp.
  2. F - Mannheimia haemolytica, irritant materials, Actinobacillus pleuropneumonia


What sequelae are associated with bronchopneumonia?


Chronic changes - fibrosis, lymphoid hyperplasia, goblet cell metaplasia

Atelectasis & emphysema

Bronchiolitis obliterans





 Interstitial pneumonia

Inflammation mainly within alveolar walls


Thickened alveolar walls with infiltrating inflammatory cells - interstitial pneumonia


What routes of transmission can lead to interstitial pneumonia?

How is infection distributed within the lung?

Inhalation and haematogenous

Dorsocaudal/ diffuse


Describe the three phases of an acute interstitial pneumonia.

  1. Injury
  2. Exudation
  3. Proliferation

What are the clinical outcomes for the patient?

  1. Injury to T1 pneumocytes or capillary endothelium
  2. Exudation of proteins and inflammatory cells into the interstitium, this expands into the alveolar space
  3. Macrophages mop up the exudate and regenerative proliferation of T2 pneumocytes occurs

Hypoxia and pulmonary oedema



Describe the changes which occur with chronic interstitial pneumonia.

What clinical consequences would be associated?

  • Interstitial fibrosis
  • Chronic inflammatory cells - macrophages and lymphoplasmacytic inflammation
  • Persistent T2 cells
  • Smooth muscle hyperplasia

Decreased lung compliance and increased respiratory effort, hypoxia, hypertension (VC)



Name three causes of chronic and acute interstitial pneumonia.

Acute - PI3, hypersensitivity, parasitic migration

Chronic - OPA, paraquat toxicity


Which infectious causes can cause Bronchointerstitial pneumonia?





Embolic pneumonia - disseminated appearance due to haematogenous spread


Cranioventral distribution of bronchopneumonia - gravitational effects of inhalation


Suppurative bronchopneumonia


Proteinaceous exudate found within the alveolar spaces - Fibrinous bronchopneumonia


Diffuse (or dorsoventral) distribution of interstitial pneumonia


Describe this lesion

Diffusely affected lung. Shows cream to grey mottling, is heavy and firm to touch (atelectasis).

Chronic severe diffuse interstitial fibrosing pneumonia


T1 pneumocytes have been replaced with T2

Proteinaceous exudate and macrophages found within the alveolar space


Thickening of the alveolar wall - contains fibroblasts (collagen) and macrophages

Small amount of proteinacous fluid - fibrin - within the alveolar space

Type 2 pneumocytes have replace T1


Inflammatory cells are found within both the alveolar space and interstitium

Bronchopneumonia - BRSV, PI3


Describe this lesion.

Focal raised firm nodule present on the surface and cut surface of the lung. 3.5x3.5cm creamy white centrally with a ring of cream to red surrounding it.

Acute focal severe suppurative embolic pneumonia

Cause: Hepatic abscess, right valve endocarditis, joint/navel ill - haematogenous spread

Aetiology: A pyogenes, Staph aureus, Strep equi, F necrophorum


Disseminated, firm creamy white-yellow multifocal lesion 2x2cm or smaller. Lung tissue in these areas is consolodated. Disrupts to normal smooth surface of the lung.

Chronic multifocal severe granulomatous pneumonia

Agents: Migrating parasites (DV, AV, DI), bacterial (mycobacterium, actinomyces), FIP


Describe this lesion

Multifocal to coelescing white-red nodular lesions (up to 3x3cm). Raised from the lung surface with poorly demarcated edges.

Pulmonary papillary adenocarcinoma


Why might the lung be sucsceptible to secondary neoplasia metastasis?

Good blood supply

Developed capillary network


What can cause pleural mineralisation?

Vitamin D toxicity

Uraemia - chronic kidney disease


Describe these radiographic findings.

Pneumothorax - extra pulmonary air present in the thorax - decreased radio-opacity of the pleural cavity - AIR


  • Spontaneous - abscessation, paracytic cysts, emphasematous bulla
  • Traumatic - rupture, penetrating wounds




Fluid accumulation within the thoracic cavity.

Hydrothorax - oedema/ transudate


  • Heart failure
  • Tumour
  • Hypoproteinaema



Causes of haemothorax

BV rupture, inflammation, neoplasia, clotting disorders



Pale red fluid build up within the thoracic cavity.



  • Rupture of the thoracic duct - traumatic, neoplasia, congenital
  • Heart disease




Purulent brown fluid present within the thoracic cavity


Causes: Abscess rupture

  • E.coli
  • A. pyogenes
  • Streps
  • Nocardia



Describe this lesion

The pleural membrane of this pig shows a focally irregular area of creamy white friable exudate. 5x5cm.

Acute focally extensive moderate fibrinous pleuritis

Glassers disease - Haemophilus parasuis


Pleural adhesions due to chronic pleuritis


Neoplasia of the pleural membrane can originate from what cell types?

  • Primary
    • Mesothelioma
  • Mediastinal tumours
    • Thymoma
    • Lymphoma
  • Metastases