Respiratory Path Anatomy Flashcards

1
Q

Congenital anomalies of the nasal cavity and sinuses

A

Cystic nasal conchae
Cysts of maxillary sinus
Nasal septum deviations
Cleft upper lip (cheiloschisis)
Cleft palate (palatoschisis)

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2
Q

Describe a condition of the nasal cavity and sinuses that is a result of metabolic disturbance

A

Amyloidosis - in equines
Primary or secondary to chronic purulent infection / tumours
Nodular or diffuse
May cause obstruction of nasal passages
Gross appearance = smooth, waxy, opaque
Histology = deposited extracellularly near vessels, in basement membranes and connective tissue.

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3
Q

Describe epistaxis

A

Bleeding from the nose, origin of bleed is a site other than the nasal mucosa.
Sudden large amounts of blood = pulmonary haemorrhage fatal in eq/bovine
Other causes: local trauma, neoplasm, aneurysm. Coagulopathies such as vitamin k deficiency, or warfarin poisoning.

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4
Q

Inflammation of the nasal passages is called …… and we know these types ………..

A

Rhinitis

Types:
1. Catarrhal - outpouring of mucus
2. Purulent / suppurative- severe inflammation with large number of NEU
3. Fibrinous - presence of FIBRIN outside plasma = vascular damage (fibrinogen becomes fibrin in tissue)
4. Pseudomembranous / pseudodiphteritic = mucus lays on membrane that is not fully ulcerated
5. Haemorrhagic - blood present
6. Ulcerative - ulcers present
7. Granulomatous - chronic type with mononuclear cells predominate and nodules/masses form (actinobacillus/ TB)

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5
Q

What type of inflammation is common in mycobacterial infections? Describe what it may look like

A

Granulomatous chronic inflammation is common in infections of actinobacillus or TB.

Chronic specific Inflamed tissues are infiltrated by mononuclear cells such as lymphocytes and fibrous tissues replace original tissue cell structure. Fibrous tissue forms nodules or masses around bacteria. At the periphery fribroblasts and fibrocytes can be found.

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6
Q

What is IBR

A

Infectious bovine rhinotracheitis / red nose

Caused by: BHV 1 bovine herpes virus
Clinical signs: abortion, generalised calf disease, enteritis in calves, conjunctivitis, infertility, encephalitis, skin lesions of udder, inflammation and necrosis of the ovaries.

Gross findings: focal necrotising changes

Days 1-3 acidophillic intranuclear inclusion bodies expected in epithelial cells (rarely seen at necropsy).

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7
Q

Describe atrophic rhinitis

A

Inflammatory disease of pigs caused by PASTEURELLA MULTOCIDA & BORDATELLA BRONCHOSEPTICA / HAMEOPHILUS PARASUIS

Predisposing factors: genetic susceptibility, bad environment , viral infections (cytomegalovirus).

Acute stage: sneezing, coughing, serous muco-purulent nasal discharge. Dried dirt, lacrimal secretions in medial can this due to blocked nasolacrimal duct.

  • atrophic lesions of turbinates caused by toxins that have an adverse effect on OSTEOBLASTS in some areas.
  • secondary irregular hypertrophy of some areas.

Asymmetric atrophy and growth of nasal area and sinuses causes DEVIATION and median septum distortion.

DDX - cut transverse cross section of snout between premolars 1 & 2

Histology: hypoplasia of cancellous bone, exudate and epithelial destruction. Hyperactivity and distension of submucosal glands. Chronic mononuclear cell infiltration of lamina propria.

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8
Q

Characterise strangles

A

Equines stressed in transit or overcrowding, other situations.
Multiple bouts in lifetime possible as immunity is short lived.

Cause: STREOPTOCOCCUS EQUINES

Clinical signs: fever, coughing, conjunctivitis, nasal discharge that is bilateral starts as serous then becomes catarrhal followed by purulent.
LN swelling, rupture and alopecia: submandibular and retro pharyngeal.

Gross picture: nasal exudate, ulceration and embolism of bacteria to other organs liver, kidney, joints, brain LNs (rarely fatal).

Histology: abcessation

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9
Q

Characterise Glanders as an inflammatory disease of the nasal passages and sinuses

A

Serious notifiable diseas caused by PSEUDOMONAS MALLEI

cutaneous form - FARCY- purulent superficial lymphangitis, ulcerative nodules on ventral abdomen and lower limbs)

Respiratory form manifests as catarrhal to purulent exudate in nasal passages, nodules that are 1cm in diameter on nasal submucosa, ulcers resulting in STELLATE SCARS.

Lungs contain pyogranulomatous lesions that may coalesce into a diffuse pneumonic process.

Histology: nodules in upper and lower respiratory tract are pyogranulomas with NEU and necrosis at the centre. Surrounding is epithelioid macrophages, giant cells, lymphocytes and fibrous tissue.

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10
Q

Describe some inflammatory diseases of the respiratory tract in canines

A
  1. ACUTE RHINITIS

Cause: distemper virus, adenovirus 1 & 2, k9 parainfluenza virus, reovirus, herpes virus.

  1. BACTERIAL RHINITIS

Uncommon usually secondary to viral infection.

Causes: streptococci, staphylococci, E.coli, Bordatella bronchoseptica, mycoplasma’s.

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11
Q

What is MYIASIS? Describe the inflammation of respiratory tract in sheep infected with OESTRUS OVIS.

A

Fly strike - infestation of tissues by fly larvae.

Oestrus Ovis can be found in nasal cavity of sheep, goats rarely humans.

Larvae are deposited at the nares and undergo TWO MOULTS. Most drop to the ground but some may remain trapped in turbinates/sinuses where they grow rapidly and become stuck.

Physical irritation = catarrhal to mucopurulent rhinitis, erosion of the mucosa, hypertrophy of sinusoidal mucosa and occasionally meningitis caused by penetration of larvae via ethmoidal region or bacterial infection through olfactory tracts.

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12
Q

Species commonly affected by nasal tumours

A

Dogs - dolichocephalic breeds such as greyhound and GSD
Cats nasal vestibule
Horses maxillary sinus

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13
Q

Types of nasal tumours

A

Sarcomas - fibrosarcoma, chondrosarcoma, osteosarcoma

Most common are Epithelial tumours - squamous cell carcinoma, adenoma, papilloma, adenocarcinoma

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14
Q

Characterise nasal polyps

A

Non neoplastic masses that resemble tumours

They develop following chronic inflammation in equines, cats and sheep.

Macroscopically - firm nodules or masses varying in size, may be ulcerated, haemorrhagic or infected secondarily.

Histology - similar to fibromas but have GOOD VASCULARISATION an inflamed core and covered by epithelium.

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15
Q

Causes of circulatory disorders in pharynx, larynx and trachea ? Describe what it may look like

A

Haemorrhages occur as petechial bruising often seen in the larynx and trachea of cattle and pigs at slaughter.

The speckling seen is caused by small extravasation in submucosal lymph follicles. If cattle die with severe dyspnoea these haemorrhages spread in a linear form.

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16
Q

Characterise tracheitis

A

Inflammation of the trachea that often arises, due to its location, in the process of inflammatory diseases of the upper or lower respiratory tract.

It often accompanies bronchitis, occasionally pneumonias.

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17
Q

Characterise laryngitis

A

Laryngitis is the inflammation of the larynx.

Laryngitis may also arise as a result of upper and lower respiratory inflammatory diseases, however it may also occur on its own.

Laryngitis may occur due to:
- oral necrobacillosis caused by FUSOBACTERIUM NECROPHORUM in calves and swine

  • laryngeal ulcers or scarred sites are found in slaughtered feedlot cattle, caused by repeated trauma of laryngeal closure during disease.
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18
Q

Describe calf diphtheria / necrotic laryngitis

A

Common disease of feedlot cattle

Predisposition: intercurrent diseases, nutritional deficiencies, unsanitary housing facilities.

Cause: fusobacterium necrophorum

Infection occurs alongside orolaryngeal necrobacillosis. Bacteria produce various exotoxins and endotoxins which they secrete following entry to the organism following viral infection or a traumatic injury.

Clinical signs: lesions of tongue, gums, cheeks, palate and pharynx.

Macroscopic picture:

Early - lesions consist of yellow-grey necrotic areas, surrounded by a zone of hyperaemia.

Later - deep ulceration, healing by granulation

Histology: lesions which may extend deep into the submucosa have large foci of necrosis bordered by hyperaemia which is surrounded by a band of leukocytes and then granulation tissue/ fibrosis.

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19
Q

describe KENNEL COUGH / canine infectious tracheobronchitis

A

A contagious respiratory disease of dogs - the term is non specific and describes any disease that has paroxysmal coughing and canine distemper which affects lower respiratory tract.

Cause: a complex of bordatella bronchiseptica, and several viruses

Macroscopic picture: lesions may be completely absent or catarrhal/mucopurulent tracheobronchitis, with enlargement of tonsils and regional LNs.

Histology: exudate rich in NEU, necrosis of the epithelium.

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20
Q

What is the histological picture of vitamin A deficiency and iodide toxicosis

A

Squamous metaplasia of the tracheal epithelium

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21
Q

What is the most common tumour found in the larynx and pharynx of canines

A

Squamous cell carcinoma

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22
Q

Congenital anomalies of the lungs

A

Accessory lungs - located in thorax, abdomen or subcutaneous tissues on the trunk.

Bronchiol hyperplasia and dilation - occur as abnormal lung components (also called congenital cystic disease, congenital adenomatoid malformation)

Agenesis

Abnormal lobulation

Pulmonary duplication

Congenital brinchoectasis

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23
Q

Characterise atelectasis

A

Atelectasis is the partial or complete collapse of lung/ or its failure to extend - the tissue is airless.

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24
Q

What is foetal atelectasis

A

When a foetus is still born and fails to make a respiratory effort, the pulmonary tissue is not expanded and remains airless.

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25
Q

What is neonatal atelectasis

A

A congenital cause of pulmonary failure to expand - animal was able to breath but not to expand enough parenchyma to meet its needs. Atelectasis is patchy in distribution, and is caused by airway obstructions of mucus or birth fluids, or anoxic damage to the respiratory centres in the brain during dystocia.

  • neonatal distress syndrome
  • hyaline membrane disease
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26
Q

Describe the ways in which acquired atelectasis may occur

A
  1. COMPRESSIVE - presence of fluid or a mass, transferred pressure compresses parenchyma stopping it from inflating. Pneumothorax, hydrothorax, chylothorax, haemothorax, empyema, tumours.
  2. OBSTRUCTIVE - airway is blocked by exudates, aspirated foreign materials, parasites or tumours.
  3. CONGESTIVE / SHOCK LUNG - severe infection, trauma, blood loss.
  4. HYPOSTATIC - when large animals are kept recumbent for a long time ie. During surgery, downer cows.
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27
Q

What is the histological picture of atelectasis

A

Atelectasis of any type appears as DARK and COLLAPSED parenchyma. It may be flabby or firm, if there is oedema or other processes ie. Shock lung.

Histology: alveoli are collapsed completely, or slit like if partial atelectasis.

Bronchioles have a cubic epithelium

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28
Q

What is emphysema

A

Emphysema is the abnormal, permanent enlargement of air spaces within the parenchyma accompanied by destruction of alveolar walls due to over distension.

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29
Q

Alveolar emphysema vs interstitial

A

Alveolar: over distension of alveoli and rupture of walls

Interstitial: lack of collateral ventilation (air into lungs but not out) forces alveolar rupture and migration of air into the interstitial tissues. (Cattle mainly)

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30
Q

Which diseases does emphysema occur in

A

COPD chronic obstructive pulmonary disease in horses

Bovine atypical interstitial pneumonia

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31
Q

Describe the histopathological picture of emphysema

A

Macroscopically: emphysematous lungs are pale, enlarged sometimes with rib imprints.

Alveolar form - small air bubbles
Interstitial form - bubbles of various sizes in connective tissues

Histology: large accumulations of air called BULLAE or BULLOUS EMPHYSEMA.

All three types alveolar, bullous and interstitial can coexist

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32
Q

Describe metabolic disturbances that may affect the lungs

A

Amyloidosis - can occur in lung tissues and calcify

Melanosis maculosa - black pigmentation in a lobular fashion occurs in ruminants

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33
Q

Vicarious emphysema

A

Emphysema occurs secondary to and around areas of atelectasis - it is a compensatory mechanism.

Lungs are patchy with areas of dark firm tissue and areas of pale puffy tissue with air bubbles that can be felt.

34
Q

Characterise pulmonary ischemia

A

Occurs following attenuation of alveolar capillaries (reduction of their ability to deliver blood) by
1. Emphysema
2. Fibrotic processes
3. Severe reduction in blood volume

35
Q

Why is arterial obstruction NOT a cause of pulmonary ischemia?

A

Because there is DUAL blood supply from both pulmonary and bronchial arteries , there is also an extensive collateral circulation therefore CONGESTION rather than ischemia is likely to occur.

36
Q

Causes of generalised pulmonary congestion include

A

Congestive heart failure (left sided) failure to pump blood to the body leads to pulmonary congestion followed by pulmonary oedema.

37
Q

Pulmonary haemorrhages are caused by

A

Ruptured aneurysm
Haemorrhagic diathesis
Toxins
Exercise induced ie. Race horses

38
Q

Histopathological picture of congestive heart failure in the lungs

A
  1. Hyperaemia and congestion

Seen as colour changes - the shade of red depends on oxygen saturation of the blood and whether there is oedema and fibrin.

Histological lesions may contain one or all of these components. Most commonly seen is capillaries engorged with erythrocytes.

  1. RBCs that bleed into alveoli are ingested by alveolar macrophages = HEART FAILURE CELLS

SIDEROPHAGES macrophages contain hemosiderin dark granules

39
Q

Characterise pulmonary oedema

A

A common lesion of the lung with multiple causes:

Congestive LS heart failure, iatrogenic fluid overload, brain injury, shock lung, endotoxemia, type 1 HS allergy reactions (cattle and horses), noxious gases, pulmonary embolism, acute pancreatitis, neoplastic obstruction of lymphatic system, any inflammatory process in the lungs.

Macroscopically: lung is wet and heavy various colours - depending on concurrent congestion or haemorrhage.

*** very difficult to differentiate from peracute pneumonia.

Histology: alveolar spaces are filled with a protein rich transducer fluid that is eosinophilic (pink) with congested alveolar septa.

40
Q

In what situation may an infarction develope in the lungs following an embolism or thrombosis?

Describe infarction from a histological perspective

A

Only when the pulmonary circulation is compromised. Usually in lungs with generalised passive congestion.

Why? Because there is duel supply from the pulmonary and bronchial arteries + extensive collateral circulation (excellent blood supply from multiple sources)

Macroscopically: occur frequently in causal lobes, extend into the pleura, prone to effect costophrenic borders.

41
Q

Types of exudate in acute bronchitis

A

Catarrhal, mucopurulent, Fibrinous, fibrinopurulent, purulent

42
Q

Characterise purulent acute bronchitis

A

Exudate in bronchi is is yellow and viscous, rich in NEU with concurrent epithelial necrosis.

43
Q

Characterise acute ulcerative bronchitis

A

Occurs in severe viral or bacterial infections - large areas of epithelium are necrotised with ulcers and catarrhal to purulent exudate.

44
Q

Which type of acute bronchitis is seen in IBR infectious bovine rhinotracheitis

A

Fibrino-necrotic bronchitis

Fibrinous exudate with epithelial necrosis

45
Q

In which situation may severe necrotising bronchitis occur?

A

In cases of bronchiectasis or as a result of a foreign body aspiration.

46
Q

Characterise chronic bronchitis

A

Usually of viral, bacterial or allergic causes.

Catarrhal, mucopurulent bronchitis common in K9s - irritation and hypersecretion of mucus causes a chronic intractable cough.

Suppuraative/purulent bronchitis occurs in cattle that have had bronchopneumonia and bronchiectasis. Bacteria can be isolated: ARCANOBACTERIUM PYOGENES, PASTURELLA ETC.

47
Q

What is bronchiectasis

A

Chronic dilation of bronchi and bronchioles leading to secondary infections.

Destruction of walls, purulent luminal content.

Causes ATELECTASIS in parenchyma that it is connected to.

48
Q

What are the two main anatomical varieties of brinchiectasis

A
  1. SACCULAR thin walled outpouchings of the bronchi and bronchial walls leading to focal necrotising bronchitis and bronchiolitis (usually in sheep / cattle)
  2. CYLINDRICAL occurs in part of bronchi or along entire length. In cattle always secondary to chronic superlative bronchitis / bronchopneumonia.
49
Q

Which categories of dogs are mainly affected by chronic bronchitis

A

Small toy breeds that are obese and over 5y of age.

Aetiology: previous KC infections, air pollutants, allergies, hereditary predisposition.

Macroscopic: viscous mucopurulent exudate in lumen, mucous membranes are thickened and edematous, hyperemic, rough with polyp like projections.

Histology: mixed cellular infiltration of mucosa (why it is thickened) hyperplasia of goblet cells and mucosal glands (hypersecretion of mucin)

50
Q

What is different about feline chronic bronchitis histological picture?

A

Similar to canine however there is a prominent infiltration of eosinophils in the luminal walls of bronchi and bronchioles.

51
Q

Characterise bronchiolitis

A

Inflammation of bronchioles which commonly occurs secondary to bronchitis and pneumonia caused by virus, bacteria, parasites or inhalation of noxious gases.

Accumulation of exudate within bronchioles and delayed epithelial repair commonly leads to destruction of bronchioles by fibrous connective tissue (chronic NON SPECIFIC inflammatory response). BRONCHIOLITIS FIBROSA OBLITERANS.

Mild bronchiolitis, if it develops lesions diffusely can cause significant obstruction and increase in respiratory resistance.

Bronchioles are easily obstructed due to their small luminal size and readily collapse, they are easily blocked by exudate.

52
Q

Characterize chronic small airway disease / chronic bronchiolitis- emphysema complex of horses

A

Adult horses of any breed, multiple different factors cause airway hypersensitivity with the same signs and symptoms.

Macroscopic: lungs unremarkable … over inflated if severe case. Evident emphysema is uncommon!

Generalized chronic bronchiolitis of airways < 2 mm in diameter epithelial, goblet cell and lymphoid hyperplasia. Excess mucus obstructs lumen in severe cases, may be peribronchiolar fibrosis with NEU and EOS present.

53
Q

Define pneumonia and it’s types / categories

A

Inflammation of the lung classified according to:
Time - acute, subacute or chronic
Etiology - causative agent ie. viral or bacterial
Morphology a) character of inflammation - exudative or proliferative
B) site of involvement - bronchopneumonia, lobar pneumonia, interstitial pneumonia, focal pneumonia

54
Q

What types of exudative pneumonia do we know

A

Alveoli filled by exudate rich in …

Catarrhal, Fibrinous, suppurative/ purrulent, hemorrhagic or necrotising

Potential for a mixed type

55
Q

According to the site of involvement which types of pneumonia can we categorize

A

Bronchopneumonia
Interstitial pneumonia
Focal pneumonia
Lobar pneumonia

56
Q

Characterize bronchopneumonia

A

Inflammation of the bronchi, bronchioles ( bronchitis and bronchiolitis) that has extended education into the alveoli.

Cause: bacterial infection following a virus, stress or other factors causing a depression of immune defenses in the respiratory system.

Viruses, mycobacterium and chlamydiae can also cause it

Pasturella spp
Actinobacillus pleuropneumoniae
Haemophillus spp
Bordatella bronchiseptica
Salmonella cholaraesuis

Characteristics: suppurative/purulent pneumonia

Macroscopically: irregular consolidation in cranioventral lobes, dark red to grey coloration, palpable firmness. Pattern, and homogeneity of consolidation depends on severity of the infection.

  • multiple areas of spaced raised grey-white foci separated by narrow dark red zones.
  • Pleura retains smooth shiny appearance when overlying mild inflammatory areas, in areas of severe inflammation pleura is rough, reddened with yellow grey accumulation of Fibrinous to fibrinopurulent exudate = pleuritis.

Grey white = areas of exudation
Dark red = congestion, edema, atelectasis

Cut section appears moist and exudate can be squeezed out, fluid or foamy exudate may be apparent in larger airways.

Histology:

EARLY /MILD catarrhal BP

the core/start of BPneum is bronchoalveolar junctions, therefor in early cases bronchi, bronchioles and adjacent alveoli are filled with NEU, cell debris, mucus, fibrin and MACPH.

Bronchiole epithelium may be necrotic to hyperplastic with mild acute inflammation of the connective tissue: variation according to causative agent.

Alveoli are atelectatic, or may contain edema, serofibrinous exudate, erythrocytes, MACPH and other leukocytes.

Vessels are engorged - red colour of lung.

Catarhal BP may resolve in 7-10 days with return to normal 3-4 weeks. Once immune defenses have overcome causative agent, macrophages predominate and phagocytose debris, dead cells and lyse fibrin.

SEVERE BP:
- causes death by hypoxemia, toxemia. Healing with scarring causes atelectasis, chronic brnochopneumonia, bronchiectasis, abcesses, necrosis and sequestration.

CHRONIC BP:

Lesions with chronic suppuration and fibrosis - occur in airways in cattle and pigs leading to bronchiectasis and abcesses. As a result parenchyma is atelectatic and fibrotic, exudate is organized and visible - if it contains fibrin often pleural adhesion occurs.

57
Q

Characterise lobar pneumonia

A

Pneumonia that visibly involves a large portion of / or all of one lobe, multiple lobes of the lungs.

Lobar distribution suggests ACUTE SEVERE inflammation especially in pigs and ruminants.

Lobar pneumonia may be: Hemorrhagic, Fibrinous, fibrinopurulent, necrotising and occasionally gangrenous (aspiration of foreign materials.)

MOST are Fibrinous so lobar pneumonia = Fibrinous pneumonia

Macroscopically: located in cranioventral regions, it often has Fibrinous exudate within the parenchyma and on the pleural surface.

Depending on lesion age it may appear red/black, reddish brown to grey.

It starts in the same way as bronchopneumonia (bronchitis/bronchiolitis) but spreads so rapidly that no typical marble pattern is observed.

Changes = 4 phases that overlap
1. Congestion - active hyperaemia, edema. Love is red, firm but still contains air - few hours.

  1. Red hepatiziation - consolidated or hepatitis same firmness as liver. Sinks in water, congestion still present and alveoli contain Fibrinous exudate and PMNLs organisms and eryth - 2 days.
  2. Grey hepatization - love is firm, dry and airless. Exudate still present but RBCs are lysed and alveolar walls are no longer congested. If progenitor bacteria are the cause exudate contains PMN Neu.
  3. Resolution - exudate is digested and liquified by leukocytes. Exudate is coughed up or drained away by veins/lymph vessels.

PUS IS NEVER FORMED AT ANY STAGE

Pleura over the pnemonic area may or may not be involved - if pleuritis occurs = pleuropneumonia!

Complete resolution is normally expected however some complications that can slow/ interfere with return to normal function are:

  1. Cardiac: right heart strain - blood is redistributed due to lobar consolidation potential for pericarditis.
  2. Septicemia: organisms gain access to blood stream leading to meningitis, suppurative arthritis or pyemic abscesses in various organs and tissues.
  3. Suppuration: a large pleural infection may lead to effusion and empyema. Occasionally alveolar walls may break down in consolidated areas = abscesses.
  4. Incomplete resolution: delayed resolution causes hyperplasia of cells lining alveolar epithelium, instead of flat become cuboidal - inefficient gas exchange.Fibrinous exudate that remains too long, fibroblasts arrange fibrin and it becomes attached to surrounding tissues = CARNIFICATION.
    Same process may occur in pleuropneumonia - pleura is adhered to parenchyma by fibrous connective tissue = ADHESIVE PLEURITIS.
58
Q

Characterize interstitial pneumonia

A

Exudative and proliferative Inflammation conditions involving alveolar walls.

Terms: Interstitial pneumonia // diffuse fribrosing alveolitis // chronic diffuse infiltrative lung disease // diffuse interstitial pulmonary fibrosis.

Causes: VIRAL pneumonias (BRSV bovine respiratory syncytial virus, Maedi in sheep, equine influenza, K9 distemper virus) it may also be caused by toxins in the blood stream.

ACUTE

variety of agents cause diffuse alveolar wall damage, intraalveolar exudate followed by proliferative and fibrotic response.

  • diffuse patchy damage to alveolar septa with no obvious orientation of lesions in or around small airways (unlike bronchopneumonia). Lesions are spread throughout lungs involving dorsocaudal regions.
  • lungs are enlarged and rubbery, pale or mottled appearance may or may not have emphysema, edema.

Histology: damage of capillaries and epithelium (alveolar blood interface). Exudate with fibrin and edema in alveolar spaces. Debris, hyaline membranes line surface of alveoli.

Day 3 - TYPE 2 alveolar cell hyperplasia, cuboidal cells replace Type 1 pneumocytes that have been destroyed by the causative agent.

Day 6-7 gradual differentiation into TYPE 1 cells. Fibroblasts appear COLLAGEN present.

Week 2 prominent collagen, fibrosis and thickening of interstitium by fribrous material and leukocytes, occasionally smooth muscle hyperplasia.

CHRONIC - granulomatous MNL infiltration.

59
Q

Characterise focal pneumonia

A

Areas of inflammation in the lung that form a single focus or multi focal pattern.

Causes/ types:

  1. Embolic pneumonia caused by bacteria - single or multiple foci, discrete lesions in various sizes distributed in one or any of the lobes. Caused by emboli of bacteria traveling in circulation gets trapped in lung capillary bed —> abscess formation.

Clinically silent unless numerous emboli arrive at once causing respiratory insufficiency or hemorrhage, exsanguination and death.

  1. Abscessation - secondary to pulmonic processes, bacterial infection following trauma of thorax or aspiration of foreign material.
  2. Granulomatous / pyogranulomatous pneumonias ie. TB, mycosis - actinobacillus, actinomyces, nocardia spp.

Local damage to tissue such as trauma, aspirated materials or immune deficiency - access of bacterial agents ie. Systemic nocoardosis, K9 distemper virus, foals with immunodeficiency.

TB in cattle - starts at bronchio-alveolar junction extending into the alveoli being sub-lobular then lobular. Tuberculous structure with one or more foci per lobule.

Appearance varies with age of the lesion, early lesions are non encapsulated, small and surrounded by condense alveolar tissue. Yellowish caseous centers with calcification are characteristic of bovine tubercles.

Dissemination of infection is either via the airways or intrapulmonary tuberculous lymphangitis (lymphatics). Depending on the speed the infection spreads we can see a pattern of irregular caseous bronchopneumonia or a more confluent caseous lobar pneumonia (fast severe spreading).

In chronic progressive pulmonary TB it is common to find lesions in the trachea and bronchi too.

Equine TB - different from cattle, tubercles have a uniform, fatty appearance that resembles a sarcoma. It’s usually haematogenous and can be milliary or coursely nodular.

Sheep/goats TB - similar to cattle

Swine TB - haematogenous and milliary. Infection with bovine TB causes consolidation of cranial lobes.

K9/feline TB - primary foci in dorsal part of caudal lobes - firm pale bulging nodules with a sarcoma like appearance - differential Dx important.

  1. Metastatic neoplasm
  2. Parasitic infections ie. Muellerius, paragonimus
60
Q

Characterise gangrenous pneumonia

A

Commonly a complication of other types of pneumonia where there is extensive necrosis of parenchyma. Occasionally seen in cattle following foreign body trauma from the reticulum, or aspiration of foreign material.

Cause: SAPROPHYTIC PUTREFACTIVE BACTERIA

Macroscopically: yellow to greenish black coloration and foul smell of tissues, ragged cavitation developers rapidly, if it extends to the pleura empyema results in a putrefactive pneumothorax with a foul smell.

61
Q

Aspiration pneumonia

A

Pneumonia caused by the aspiration of foreign materials into the lungs (often liquid) via the airways.

Macroscopically: lungs remain inflated, hyperaemic, small amounts of exudate in small airways.

Histology: acute bronchiolitis with acute alveolar inflammation.

Causes: inhaled milk, milk + feed in calves that are bucket fed. Aspiration of vomit and medications - risk of anaesthesia.

62
Q

Describe uremic pneumonia

A

This is a severe pneumonia that causes increased permeability of the alveolar air-blood Barrier —> pulmonary Edema

Usually forms in dogs with chronic uraemia: degeneration and calcification of smooth muscle and connective tissue, edema in the bronchiole walls and alveolar ducts.

Severe cases result in calcification of alveolar septa which can be recognised as a gritty, porous texture of lung parenchyma.

63
Q

Pneumonia caused by parasites

A

Parasitic pneumonia - lungs are site of parasitic migration, parasites cause damage. Some lesions may be severe to fatal if parasites are large in number or in size, this is particularly dangerous if the host has a hypersensitivity reaction.

Ascaris suum- migrate in large numbers and fatal in pigs

Trematoda - fasciola hepatica, gigantica invade lungs accidentally from the liver. They are large so a few parasites can cause extensive damage.

Dictyocaulus = LUNGWORMS: d.filiara in small ru, d. viviparus in cattle, d. arnfieldi in equids.

2 phases of tissue lesions:

  1. Time between arrival to tissue and maturation
  2. Time taken for mature parasite to reach bronchi

Adults cause alveolar reaction = 2-4mm nodules that are homogenously grey or grey with a green centre.

Muellerius capillaris - small ru - most common lung worm also called nodular lung worm as adults live in alveoli and cause an enveloping granulation response. Lesions present as multiofocal interstitial pneumonia, present beneath the pleura on the dorsal surface of caudal lobes.

Metastrongylus in pigs - bronchi and bronchioles lesions are multiple foci with intensive eosinophilic accumulation surrounding larvae in the alveoli. A granulomatous response occurs when to eggs and larvae, adult parasites provoke a chronic catarrhal and eosinophilia bronchitis/bronchiolitis.

64
Q

Which type of primary neoplastic tumours are more common in the lungs

A

Primary tumours of epithelial origin

Examples: papilloma, adenoma, carcinoma (epidermoid), adenocarcinoma, anaplastic carcinoma

65
Q

Which type of primary mesenchymal neoplastic tumours may we find in the lungs

A

Haemangioma and haemangiosarcoma

Often presented as single nodules, they have the ability to metastasise within the lung and beyond.

66
Q

General distribution of secondary neoplastic tumours in the lungs may be?

A

Usually multiple nodules, that vary in size.

67
Q

Which species are most commonly inflicted with primary pulmonary tumours and of which kinds?

A

Cats and dogs - carcinomas more common in canines than cats > 10 years old.

68
Q

Name some anomalies of the pleura and thoracic cavity

A

Canine mediastinal cysts - may grow large enough to impact pulmonary function

Thoracic duct anomalies leading to chylothorax

69
Q

Characterise some degenerative disturbances that occur in the pleura and thoracic cavity

A
  1. Pleural mineralisation

Secondary to renal failure - mineralisation of alveolar ducts and arterioles, and on the parietal pleura between the ribs Uraemia causes horizontal pale thickening.

  1. Vitamin D toxicity

Causes mineralisation/ calcification and pleural lesions

  1. Pneumothorax

Air in the thoracic cavity where their should be negative pressure to facilitate inspiration, leads to collapse of lungs. Caused by trauma, rupture of emphysematous bullae, and rupture of parasitic cysts that communicate with airways.

Signs: respiratory distress and atelectatic lungs

70
Q

Hydrothorax

A

Accumulation of serous fluid in the thoracic cavity.

Severity of respiratory distress is determined by volume of fluid compressing the lungs.

Causes = lesions, left sided congestive heart failure, hypoproteinemia, neoplasia, toxicity, pancreatitis.

71
Q

Chronic hydro thorax causes what?

A

Pleural opacity due to reactive hyperplasia of mesothelial cells and fibrous thickening of pleural connective tissue.

72
Q

Haemothorax

A

Blood in the thoracic cavity

Causes: trauma, erosion of BVs by malignant tumours and inflammation, clotting defects, ruptured aneurysms.

73
Q

What is the consequence of chronic hydro thorax that may imitate haemothorax

A

Development of well vascularised papillae on pleura that rupture and cause effusion which resembles blood.

74
Q

What is a chylothorax

A

Accumulation of milky lymph in the thoracic cavity

Causes: neoplasia, trauma, congenital abnormalities of the thoracic duct, iatrogenic following surgery

75
Q

Pleuritis

A

Inflammation of visceral or parietal pleura

Inflammatory process may or may not spread to the lungs

Lesions may be: fibrinous, purulent, granulomatous, necrotising, haemorrhagic, depending on the disease process.

Purulent exudate in the cavity = pyothorax or empyema

Causes: pyogenic organisms reaching the pleura - traumatic injury, ruptured pulmonary abscess, extension of disease form elsewhere in the body ie. Traumatic reticuloperitonitis.

Consequences= fibrinous restriction of pleural expansion and contraction. Adhesions may be diffuse or between parietal and visceral layers. Atelectasis may occur as a result of lesions and or pleural effusion.

76
Q

Characterise pleural TB

A

Nodular, caseous or intermediate type. Both visceral and parietal layers if affected are thickened by fibrous granulation tissue - the TB process DOES NOT invade the underlying tissues (birds only). Nodules tend to occur in clusters, heavy calcification may follow = PEARL DISEASE.

Caseous tuberculous pleuritic. = plaques of caseous exudate lie on top of thickened pleura, fibrin deposited between plaques.

Generalisation of the disease (spread to other organs) can occur both early (post primary ) or late in the course of disease.

77
Q

The pleural surface of the lungs is often involved with which type of tumours

A

Tumours that have metastasised from other organs

78
Q

Which type of primary tumour may we see in the pleura of the lungs

A

Mesothelioma - only tumour, rare usually seen in calves (congenital).

79
Q

Describe the appearance of pleural mesothelioma

A

Multiple discrete nodules or tree like spreading growths on pleural surface. Histologically, they have a mesothelial covering of cells or the connective tissue may be the predominant malignant component.

Tumours can appear to be carcinoma or fibrosarcoma

80
Q

Which kind of secondary tumours may we see in the pleura of the lungs

A

Transpleural dissemination of carcinomas and sarcomas may occur occasionally