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Pathology > Respiratory 1 & 2 > Flashcards

Respiratory 1 & 2 Flashcards

1
Q

What are the three routes into the respiratory system?

A

Aerogenous (inspired air), Hematogenous (blood) and Direct Extension

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2
Q

What disease agents enter the aerogenous route?

A

Infectious pathogens and toxins

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3
Q

What disease agents enter the hematogenous route?

A

Septicemia, bacteremia, parasites, neoplasia

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4
Q

What disease agents enter the direct extension route?

A

Bites, penetrating wounds, migrating foreign bodies, neoplasia.

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5
Q

Particles larger then 2um are caught in…

A

Nasal turbinates’ and at tracheal and bronchial bifurcations.

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6
Q

What is clearance? (In reference to the upper respiratory tract)

A

It is the process of destroying, neutralizing, or removing deposited particles in the respiratory system.

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7
Q

What are the methods of clearance? (In reference to the upper respiratory tract).

A

Sneezing, coughing, phagocytosis, and mucociliary transport.

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8
Q

What is mucociliary transport? Where does it extend from?

A

It extends from the bronchi to the pharynx. Sol and gel phase mucus is produced by goblet cells and serous cells by the sub mucosal glands. Mucus is transported by ciliary activity toward the pharynx (it is swallowed or coughed out).

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9
Q

What are the cell associated defenses of the nose, trachea, and bronchi?

A

Antibodies, lysozyme and mucus.

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10
Q

What are the cell associated defenses of the bronchioles?

A

Clara cells, antioxidants lysozyme and antibodies.

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11
Q

What is the special defense tissue type that is present at bronchial bifurcations?

A

BALT (bronchial-associated lymphoid tissue).

Antigen presenting cells in these regions phagocytose and transport inhaled particles.

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12
Q

What is the function of the Clara cell? What part of the lungs is it found? Is it ciliated or non ciliated?

A

Non-ciliated cell located in the bronchioles.
Has a role as a cytokine inhibitor, producer of antibacterial and antioxidant molecules, produces surfactant.
Secretes mixed function oxidase-containing granules into the lumen of the bronchioles.

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13
Q

What are the dangers of having Clara cells?

A

They are implicated in a number of pathogenic processes. They can create toxic metabolites and damage bronchiolar epithelium.

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14
Q

What are the viral infections that are known to predispose Cows to bacterial colonization and pneumonia?

A

BHV-1
PI-3
BRSV

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15
Q

What are the viral infections that are known to predispose Canines to bacterial colonization and pneumonia?

A

Canine distemper virus

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16
Q

What are the viral infections that are known to predispose Felines to bacterial colonization and pneumonia?

A

Feline herpesvirus

Feline calcivirus

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17
Q

How do toxic gases like ammonia and hydrogen sulfide impair respiratory defense systems?

A

They increase host vulnerability to bacterial colonization and pneumonia.

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18
Q

How does immunodeficiency impair respiratory defense systems?

A

Allows commensals and normally non-pathogenic microbes to become pathogens.

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19
Q

What are factors that may impair pulmonary defenses?

A 
Viral-bacterial synergism in the lungs (BHV-1, PI-3, BRSV, Canine distemper, Feline herpesvirus & Calicivirus) 
Toxic gases (ammonia and hydrogen sulfide)
Immunodeficiency
*Uremia, endotoxima, dehydration, starvation, hypoxia, acidosis, pulmonary edema, anesthesia, ciliary dyskinesia and stress.
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20
Q

What is rhinitis/sinusitis?

A

Inflammation of the nasal mucosae and/or sinuses.

Normal flora help to out-compete pathogenic microbial colonization.

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21
Q

What are the potential sequela (consequences) of Rhinitis and Sinusitis?

A

Septal deviation, osteomyelitis, meningitis (cribiform plate), otitis media or interna infections (ear).

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22
Q

What are the exudate types that can be produced with rhinitis/sinusitis infections?
*What is the special descriptive term reserved for exudate of the respiratory tract mucosa?

A

*Catarrhal (exudate that forms on surfaces as an irregular layer of tan, viscous and necrotic material that is often mucopurulent).
Serous, fibrinous, catarrhal, purulent, caseous, and granulomatous.

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23
Q

What is Oestrus Ovis?

What species does it effect?

A

It is a nasal infestation. (URI)
Larvae of this fly develop in the nostrils of sheep (myiasis: larvae infestation); other hosts are rare.
Migration of the maggots in sinuses causes irritation and inflammation.
Mucopurulent rhinitis and sinusitis and obstruction.

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24
Q

What is cuterebra spp?

What species does it effect?

A

Infestation in rabbits, rodents and cats.

Migrations in the nasal cavity. (rarely the brain).

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25
Q

Equine influenza
What is the pathogenesis?
What are the symptoms?
*Is this a reportable disease?`

A

Viral infection, highly contagious, type A strain, self-limiting.
Serous nasal discharge, fever, conjunctivitis.
Infections with pneumonia suggest immunocompromised; bronchointerstial pneumonia complicated by ARDS on rare occasion.
*OIE notifiable disease, low morbidity and mortality but important in racing industry.

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26
Q 
Equine viral rhinopneumonitis
What is another name for this disease?
What are the three common presentations?
What is the source of infection?
How is it spread (what transmission type?)
A

Equine herpes virus 1 and 4 (EHV 1,4)
1)Mild respiratory disease in foals (4-8 months)
2)Myeloencephalopathy (degenerative disease of the brain/spinal cord)
3)Mare abortions
Persistent carriers, both virus types can remain latent in trigeminal ganglia (a ganglion on the sensory root of the fifth cranial nerve), reoccur, and shed.
It is shed via aerogenous transmission.

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27
Q

Strangles

1) What is the causative agent?
2) What is the most common age group it effects?
3) Is it in normal nasal flora?
4) How is it spread initially (and what transmission type?)
5) What are the symptoms?

A

1) Streptococcus equi spp. equi
2) Young horses.
3) Not in normal nasal flora.
4) Aerogenous infection of the nasopharynx mucosa > lymphatic vessels > mandibular and retropharyngeal LN > superlative rhinitis and lymphadenitis. Some horses become carriers and continue to shed bacteria.
5) Cough, nasal discharge, conjunctivitis and swollen lymph nodes (heamtogenous spread is possible from here). Abscess formation in disseminated organs is potentially fatal (Bastard strangles).

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28
Q

What are the sequela (consequences) of an equine Strangles infection?

A

Bronchopneumonia.
Nerve compression (recurrent laryngeal/laryngeal hemiplegia; sympathetic nerve-facial paralysis and Horner syndrome (miosis (constricted pupil), partial ptosis (drooping upper eyelid) and loss of hemifacial sweating (anhidrosis).
Purpura hemorrhagica: strep equi antigen-ab complexes form in small vessels of the skin and mucosa.
Guttural pouch empyema (pus/fluid collection)
Abscess ruptures and fistulous (abnormal connections between two organs) tracts.

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29
Q

Infectious bovine rhinotracheitis (IBR)

1) Causative agent

A

1) Bovine herpesvirus 1 (BoHV-1)

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30
Q

Porcine atrophic rhinitis

1) Causative agents (4)
2) Pathogenesis/symptoms?

A

Multi-pathogen lesion
Infectious
Bordetella bronchiseptica, pasturella multocidia, haemophilus parasuis, and porcine cytomegalovirus.
2) Infection causes sneezing and coughing, nasal discharge > increased osteoplastic activity and osteopenia > atrophy and loss of nasal conchae > septal deviation and facial deformity.

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31
Q

Bovine necrotic laryngitis

1) Causative agent?
2) Predisposing agents?
3) What are symptoms?
4) Possible outcomes?

A

Fusobacterium necrophorum
Infectious
2) Predisposing conditions: unsanitary housing, underlying disease or trauma, oral ulceration, nutritional deficiency, being on a feedlot.
3) Bilateral laryngeal ulcerations and necrotizing lesions. Promotion of extensive bacterial growth and release of endotoxins and exotoxins.
4) Endotoxemia/bacteremia > endotoxic/septic shock.
Laryngeal obstruction > asphyxiation
Aspiration > bronchopneumonia

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32
Q 
Infectious laryngotrachetis (ILT) of Chickens
1)Pathogenesis
A

1) Stressed latent carriers shed herpes virus > aerosolized in environment > inhalation by naïve chickens > mild laryngitis to thick diphtheritic membranes and necrotic plugs > severe dyspnea, gasping, coughing.
* In photo the laryngeal lumen is occluded by fibrinonecrotic exudate.

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33
Q 
Nasal polyp
Description?
Composition?
Most common in..?
Associated with chronic..?
A

Non-infectious
Benign, smooth, pedunculated.
Composed of inflammatory vascular stroma covered by squamous or psudostratified epithelium.
Cats (nasopharynx and Eustachian tube) - ear
Also seen in horses (ethmoid)
*Associated with chronic rhinitis and sinusitis.

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34
Q

Equine ethmoid hematoma
Neoplastic? Description?
Presentation/symptoms?
Pathogenesis?

A

Ethmoid (unpaired bone in the skull that separates the nasal cavity from the brain)
Non-neoplastic, dark red, pedunculated mass extending from the mucosa of the ethmoid conchae.
Presents as unilateral nasal bleeding (epistaxis)
Pathogenesis unknown.

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35
Q

Laryngeal hemiplegia (paralysis)
What side/s does it usually effect? What muscles?
What are the causes?
Species specific causes?

A

Degenerative upper airway disease
Unilateral, usually left sided, atrophy of the muscles that abduct and adduct the arytenoid cartilages (doral and lateral cricoarytenoid muscles).
Caused by recurrent laryngeal neuropathy. Usually idiopathic, possible nerve trauma.
Dogs: Heritable in Siberian huskys and bouvier des flandres, degenerative in older dogs.
Horses: roaring may be a sequela of strangles, lymph node enlargement or abscesses compress the recurrent laryngeal nerve.

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36
Q

Canine infectious tracheobronchitis, otherwise known as…?
Pathogenesis/Causative agent?
Symptoms?

A

Kennel cough.
Mixing dogs (kennel/shelter), infection with Bordetella bronchiseptica +/- adenovirus-2 +/- canine parainfluenza virus 2, +/- poor ventilation +/- nutritional/environmental factors/stress.
Suppurative to mucopurulent rhinitis, conjunctivitis, tonsillitis, tracheobronchitis > cough that is exacerbated with exercise > can progress to severe bronchopneumonia.

37
Q

Brachycephalic airway disease.
What are the anatomic features that inhibit normal respiration in these breeds?
Sequela?

A

A constellation of anatomic features that inhibit normal breathing: long soft palate that occludes the larynx, small nares, everted laryngeal saccules, +/- narrow or collapsing trachea.
Exercise intolerance, cyanosis and collapse

38
Q

Equine guttural pouch disease

Where is the infection most prominent?

A

Infection of the large diverticula on the ventral portion of the Eustachian tubes of horses.
Prone to fungal as well as bacterial infection - aspergillus fumigatus and streptococcus sp.
Sequela related to anatomical structures in this area.

39
Q

What are the cell associated defenses in the alveoli? (4)

A

Alveolar and intravascular macrophages, opsonizing antibodies surfactant, antioxidants.

40
Q

What is the key specialized cell in the alveoli?

A

Type II pneumocyte, produces surfactant

41
Q

What are pulmonary macrophages?

A

Specialized macrophages for aerobic environment, it is the primary defense mechanism in the alveoli. Part of innate immunity, cells rapidly phagocytose particles and are removed via mucociliary transport.

42
Q

What bacteria are resistant to pulmonary macrophages?

A

Mycobacterium tuberculosis, listeria monocytogenes, brucella abortus, some salmonella species.

43
Q

Intravascular macrophage in the lungs reside in…? Function?

A

Pulmonary capillaries. They are the primary cells removing circulating pathogens.

44
Q

What is the most vulnerable portion of the respiratory system?

A

Alveoli

45
Q

What is the clearance in the alveoli?

A

Poor, no cilia or mucus producing cells.

46
Q

What shape of particles can pass through to the alveoli?

A

Long, slender particles (asbestos) are able to pass through the physical barriers of the airways and reach alveoli. This also includes bacteria and viruses due to their small size. (0.01 to 2 um)

47
Q

What is the metastatic risk in the alveoli?

A

The lower respiratory tract is highly vascularized with extensive capillary beds to maximize oxygen exchange. This is also a destination for circulating pathogens, emboli and neoplastic metastases. When primary tumors invade the venous system, tumor cells embolize to the lungs through the pulmonary or bronchial arteries. They also reach the lungs via lymphatics.

48
Q

When investigating pulmonary disease, it is important to identify patterns in what three tissue areas of the lungs?

A

Bronchi
Alveoli
Interstitum

49
Q

Atelectasis (definition)?

A

Deflation of alveoli leading to partial or complete collapse of the lung.

50
Q

Emphysema (definition)?

A

Hyperinflation of the alveoli, potentially leading to septal rupture and fusion of airspaces.

51
Q

Bullae (definition)?

A

Fusion of airspaces/ septal rupture. Caused by obstruction and increased alveolar pressure and/or alveolar septal weakness.

52
Q

Describe the radiographic change you see with a bronchial pattern.

A

Doughnuts and railroad tracks distant from the normally thick proximal bronchi; small vessel walls remain sharp and distinct.

53
Q

Describe the gross change you see with a bronchial pattern.

A

Thick, white, firm airway walls

54
Q

List a few CAUSES of a bronchial pattern on radiographs.

A

Chronic bronchitis, feline asthma, eosinophilic pulmonary infiltrates and parasitic infestations.

55
Q

Chronic bronchial inflammation and damage induces (5) changes that can lead to inhibited pulmonary clearance.
*What (2) disease do they all contribute to?

A

1) Bronchial gland hyperplasia/goblet cell hyperplasia- excess mucus production.
2) Smooth muscle hypertrophy, hyperplasia, and fibrosis around the bronchi and bronchioles- results in firm, non-compliant airways.
3) Squamous metaplasia- replaces ciliated cells of bronchi, inhibiting mucociliary transport.
4) Bronchiectasis: permanent loss of mural integrity, results in dilation and dysfunction of bronchi.
5) Bronchiolitis obliterans: fibrotic response to bronchiolar wall damage that can occlude the airway lumen.
* All contribute to the clinical presentations of COPD and emphysema.

56
Q

Squamous metaplasia (what does it change?)

A

Replaces ciliated cells of bronchi, inhibiting mucociliary transport. Due to bronchial inflammation/damage.

57
Q

What is Bronchiectasis?

A

Permanent loss of mural integrity, results in dilation and dysfunction of bronchi. Due to bronchial inflammation/damage.

58
Q

What is Bronchiolitis obliterans?

A

Fibrotic response to bronchiolar wall damage that can occlude the airway lumen. Due to bronchial inflammation/damage.

59
Q

True or False; It is likely that most species have some form of allergic or immune mediated bronchiolar disease?

A

True

60
Q

Equine Recurrent Airway Obstruction (RAO)

1) What are the bronchiolar diseases that create this disease?
2) Clinical signs?

A

1) “Heaves”, COPD, emphysema, and chronic small airway disease. They have overlapping clinical signs and likely common or overlapping pathogenesis.
2) Recurrent respiratory distress, chronic cough, exercise intolerance.

61
Q

Equine Recurrent Airway Obstruction (RAO)

Pathogenesis?

A

Initiating bronchiolar damage (via viral infection, toxin, or other environmental irritant +/- genetic predisposition > Th2 allergic immune response to subsequent exposures > hyper-reactive airway > cytokine production > leukocyte induced bronchiolar damage (mix of lymphocytes, plasma cells, eosinophils, and neutrophils). Chronic alterations of the lower airways.

62
Q

Feline allergic bronchitis (feline asthma)

1) What age does it occur?
2) How does it present?
3) Pathogenesis?

A

1) Any age.
2) Recurrent bronchoconstriction, cough, dyspnea.
3) Inhaled allergen > type 1 hypersensitivity > peribronchial inflammation (strong eosinophilic component) > alterations in airway structure may develop over time.

63
Q

Describe the radiographic change you see with a alveolar pattern.

A

Dense (white) appearance, silhouetting with adjacent soft tissue structures such as the heart and creating air bronchograms (when dense infiltrates surround the bronchi, they highly the air (black) within them).

64
Q

Describe the gross change you see with a alveolar pattern (Bronchopneumonia).

A

Meaty to firm red to tan tissue that may exude Suppurative exudate on cut section, may contain abscesses; frequently accompanied by blood/edema.

65
Q

Describe the gross change you see with a alveolar pattern (atelectasis):

A

Firm and meaty, red, no inflammatory exudate.

66
Q

Describe the gross change you see with a alveolar pattern (edema):

A

Firm, color variable, exudes frothy fluid on cut section.

67
Q

Describe the gross change you see with a alveolar pattern (hemorrhage):

A

Dark red, exudes blood on cut section.

68
Q

Name 4 causes of an increased alveolar pattern on radiograph

A

Bronchopneumonia, pulmonary edema, hemorrhage, lobar collapse/atelectasis.

69
Q

What is bronchopneumonia?

What is the most common distribution?

A

Inflammation of the bronchi, bronchioles and alveoli.

*It is the most common form of pneumonia in animals, and cranio-ventral is the most common distribution.

70
Q

What are the contributing factors to cranioventral distribution of bronchopneumonia?

A

Gravitational: exudate and bacteria settle to dependent portions of the lung lobes.
Vascular: less perfused portions of the lung.
Short, abrupt branching of the airways and less ventilation in these regions.

71
Q

Describe the radiographic change you see with a interstitial pattern. (Structured and unstructured)

A

Diffuse opacities that obscure structures; small vessel walls are indistinct.

72
Q

Describe the gross change you see with a interstitial pattern. (unstructured)

A

Lungs fail to collapse, feel air-filled but firm, tend to associate with pure viral infections particularly in large animals.

73
Q

Describe the gross change you see with a interstitial pattern. (structured)

A

Obvious masses of varying appearance.

74
Q

List a few causes of a interstitial pattern on radiograph (unstructured)

A

Fibrosis, interstitial pneumonia (pneumonitis), pulmonary lymphoma, early or resolving edema.

75
Q

List a few causes of a interstitial pattern on radiograph (structured)

A

Pulmonary masses due to neoplasia or granulomas.

76
Q

Embolic pneumonia.
Cause?
Pattern in the lungs?

A

Bacteria reach the lungs via the vascular system. Initially lesions form in the interstitium.
Embolic (multifocal) pattern in the lungs.
Abscesses form around pulmonary blood vessels.

77
Q

What are the bacteria associated with Embolic Pneumonia?

Bovine

A

a. pyogenes, f. necrophorum, and to a lesser extent e. rhusiopathiae.

78
Q

What are the bacteria associated with Embolic Pneumonia?

Swine

A

f. necrophorum, e. rhusiopathiae, streptococcus suis Type II

79
Q

What are the bacteria associated with Embolic Pneumonia?

Poultry

A

e. rhusiopathiae

80
Q

What are the bacteria associated with Embolic Pneumonia?

Equine

A

Streptococcus equi

81
Q

What are the bacteria associated with Embolic Pneumonia?

Canine

A

staphylococcus aureus and to a lesser extent e. rhusiopathiae

82
Q 
Endogenous lipid pneumonia of cats.
Cause?
Gross appearance?
Histo?
Etiology?
A

Lipids from surfactant and degenerate cells accumulate in alveolar macrophages.
Multifocal, white nodules
Alveoli contains vacuolated macrophages with variable degrees of mononuclear inflammation and fibrosis.
Unknown etiology (maybe associated with degenerate neoplastic cells).

83
Q

Aspiration pneumonia

1) What is the degree of inflammation related to?
2) Conditions that predispose?
3) What lung lobe is most likely infected?
4) Sequela?

A

1) Aspiration of food or other foreign materials will cause bronchopneumonia, the severity of alveolar damage and degree of inflammation are related to the nature of the aspirated material.
2) Cleft palate, megaesophagus, vomiting, regurgitation, dysphagia, anesthesia, collapse (large animal), force feeding or oral medication, use of contrast media for imaging studies.
3) Right cranial lung lobe.
4) Septic shock and ARDS.

84
Q

Describe the appearance of pulmonary edema and hemorrhage.

A

Always consider findings with the rest of the body.
Pulmonary edema: copious frothy fluid exudes from airways of cut section. *Can be secondary to heart failure or pneumonia.
Embolic pattern (hemorrhage): Petechial pulmonary hemorrhages, hemorrhagic disease (Calicivirus) and pulmonary hemorrhage (anthrax).

85
Q

Acute respiratory distress syndrome: (ARDS)
Symptoms: (3)
Triggers:

A

Diffuse alveolar damage, pulmonary hypertension, and aggregation of neutrophils in capillaries with extensive leakage of fluid.
There are a number of systemic ARDS triggers; sepsis, major trauma, aspiration of gastric content, extensive burns and pancreatitis.

86
Q

Pulmonary emboli and infarction

1) What does this help prevent?
2) Types of emboli:
3) Source:
4) Route
5) Causes:

A

1) The pulmonary capillary bed helps to prevent emboli from reaching critical tissues like the brain.
2) Fat, tumor, thrombosis and bacterial.
3) Venous- deep vein thrombi, hepatic abscesses, valvular endocarditis, jugular thrombi, venous invasion of malignant neoplasia.
4) Pulmonary artery
5) Parasitic, neoplastic metastasis, coagulation problems, endocrine and glomerular diseases that predispose to thrombosis.

87
Q

What is Bovine venal caval thrombosis and metastatic pneumonia?

A

It is a sudden death syndrome seen in cattle with characteristic presentation of acute, bright red hemorrhage from the nose (hemoptysis)

88
Q

What is the pathogenesis of Bovine venal caval thrombosis and metastatic pneumonia?
*An important differential for..?

A

Hepatic abscess ruptures into either hepatic veins or directly into the vena cava.
Thrombus formation within the vena cava > septic emboli reach the pulmonary artery and arterioles.
Secondary abscesses may form within the lung parenchyma.
Necrosis of vascular walls and eventual rupture > intra-pulmonary hemorrhage.
Further erosion into adjacent airways leads to hemorrhage from blood vessels into airways (hemoptysis and death) .
*Anthrax
**(Thromboembolism travels from the pulmonary vein, artery then to the bronchus); the pulmonary artery was the last vessel to erode prior to necrosis of the bronchial wall).

Pathology (5 decks)

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