Respiratory System Flashcards

1
Q

What is the division between the upper and lower respiratory tracts?

A

thoracic cavity —> cranial to thoracic inlet = URT

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2
Q

What makes up the conducting system? What does it do?

A

nasal cavity, paranasal sinuses, larynx, trachea, and bronchi lined by pseudostratified columnar ciliated epithelium and goblet cells

nasal conchae and turbinates increase surface area to increase the humidity and temperature of inhaled air

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3
Q

What makes up the transitional system?

A

bronchioles lined by non-ciliated secretory cells, club (Clara) cells, important for the detoxification of xenobiotics

club cells contain CYP450

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4
Q

What do healthy bronchioles lack?

A

goblet cells

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5
Q

What makes up the exchange system?

A

alveolar ducts and alveoli enveloped by rich network of pulmonary capillaries and lined by epithelial type I (membranous) and type II (granular) pneumocytes

I = thin single squamous, O2 and CO2 exchange
II = thick cuboidal, secretes surfactant and replaces type I upon injury

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6
Q

What is the dual blood supply of the lungs?

A
  • pulmonary arteries that conduct deoxygenated blood from the right side of the heart
  • bronchial arteries that carry oxygenated blood
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7
Q

What are some other functions of the respiratory system other than gas exchange?

A
  • phonation
  • olfaction
  • temperature regulation
  • acid-base balance
  • pressure regulation

all functions can be affected by respiratory disease

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8
Q

How does the oral and respiratory epithelium compare?

A

ORAL = pseudostratified columnar

RESPIRATORY = columnar ciliated

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9
Q

What does the mucociliary escalator do?

A

traps foreign pathogens in mucous and uses cilia to move them out of the respiratory system

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10
Q

Where is the normal flora found in the respiratory system?

A

most proximal region of the conductive system: nasal cavity, nasopharynx, larynx, and tracheal

  • distal portions are considered sterile
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11
Q

What are the 2 types of defense mechanisms that keep the distal portion of the respiratory system sterile?

A
  1. NON-SPECIFIC (non-immune-mediated): mucous trapping, mucociliary clearance, phagocytosis, air turbulence generated by coughing and sneezing
  2. SPECIFIC (immune-mediated): antibody production, antibody-mediated phagocytosis, cell-mediated immunity
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12
Q

What macrophages are found in all species’ respiratory systems? What 2 are species-specific?

A

alveolar macrophages (PAMs) - engulf pathogens and are moved out by the mucociliary aparatus

  1. intravascular macrophages (PIMs) - present in ruminants, cats, pigs, and horses, and attach to alveolar capillaries and filter out pneumotoxins/pathogens in the blood
  2. Kupfer cells/splenic macrophages - present in dogs, humans, and lab rodents and remove bacteria and other particles from blood
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13
Q

How do alveolar macrophages (PAMs) protect from pathogens?

A

use pseudopodia to move and engulf pathogens, then form a phagolysosome to degrade it with proteolytic enzymes

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14
Q

What factors predispose animals to bacterial pneumonia?

A
  • viral infections
  • stress (BRDC)
  • dehydration
  • pulmonary edema
  • uremia
  • ammonia (poorly ventilated farms)
  • immunosuppression/deficiency
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15
Q

Normal lungs, pig:

A
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16
Q

How is the nasal cavity viewed upon necropsy? How should it look?

A

sagittal section of the head

pink mucous membrane covering turbinates, lacking exudate

  • normal gray discoloration of lymphoid tissue
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17
Q

What is a common cause of unilateral epistaxis in older horses? How is it typically diagnosed?

A

ethmoidal hematoma found in the back of the nasal cavity near nasal turbinates - pedunculated tumor-like lesion

endoscopy

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18
Q

Ethmoidal hematoma:

A

common in older horses and causes unilateral epistaxis

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19
Q

How does infectious bovine rhinotracheitis affect the nasal cavity?

A

causes fibrinous rhinitis, forming a diphtheritic membrane

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20
Q

Infectious bovine rhinotracheitis:

A

not as severe - mucosuppurative exudate, congested and hemorrhagic mucous membrane

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21
Q

What species of bot commonly infects sheep nasal cavity? What does it cause?

A

Oestrus ovis - nasal bot

rhinitis —> fly deposits egg in nares and irritates; upon hatching, bots can reach the sinus

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22
Q

What is a rare sequel of Oestrus ovis infection?

A

aberrant migration of larvae —> penetrates cribriform plate and reaches the brain, causing meningoencephalitis

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23
Q

What is thought to cause atrophic rhinitis? What are some common signs?

A

combined infection of Bordetella bronchiseptica and Pasteurella multocida types D and A

  • upper respiratory disease
  • nasal discharge
  • lateral deviation of snout/nasal septum near the first and second premolars
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24
Q

Atrophic rhinitis, pig:

A
  • lateral deviation of nasal septum
  • atrophied turbinates
  • more suscpetible to respiratory disease, leading to pneumonia (turbinates usually warm and humidify air)
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25
Q

How does infection cause atrophic rhinitis? Where is affected most?

A

toxigenic strains of Pasteurella multocida produce cytotoxins that inhibit osteoblastic activity and promote osteoclastic reabsorption of the nasal turbinates

ventral scroll of the ventral nasal tubrinate

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26
Q

What causes inclusion body rhinitis? What animals are most affected?

A

porcine cytomegalovirus and herpesvirus 2 (SHV-2)

usually pigs 3-5 weeks, but can cause fatal systemic infection in younger suckling pigs under 3 weeks

  • increased cell size and nuclei with large basophilic inclusions
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27
Q

How does feline herpesvirus 1 typically affect the respiratory system?

A

rhinitis and conjunctivitis —> usually transient, but kittens in poor body condition can develop severe disease

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28
Q

How does feline calicivirus typically affect the respiratory system?

A

oculonasal discharge with vesicular and ulcerative stomatitis and interstitial pneumonia

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29
Q

Feline calicivirus:

A
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30
Q

How can ulcerative stomatitis from feline calicivirus infection be differentiated from uremic glossitis?

A

NOT ventral or marginal —> results from burst vesicles

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31
Q

Feline calicivirus, pneumonia:

A

diffuse, INTERSTITIAL

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32
Q

What is the cause of granulomatous rhinitis in dogs? When is it common for dogs to become infected?

A

Rhinosporidum seeberi, a rare aquatic protistan parasite

dogs in the Midwest and Southern US that have been in contact with stagnant water

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33
Q

Granulomatous rhinitis, dog:

A
  • Rhinosporidum seeberi
  • proliferative, tumor-like
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34
Q

What typically causes guttural pouch tympany in foals?

A

congenital problem with Eustachian tube causing entrapment of air within the guttural pouch

  • typically no pain upon touch, seems inflammed
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35
Q

What causes Strangles in horses? What does this cause?

A

Streptococcus equi

lymph node and guttural pouch involvement, resulting in suppurative accumulation within the guttural pouch and eustachitis
+ fistulous tracts

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36
Q

Strangles, horse:

A
  • Streptococcus equi
  • fistulous tracts
  • raise and lower head and guttural pouch contents will come out
37
Q

What is a common sequel to Strangles?

A

guttural pouch inflammation (empyema) causes puss to accumulate, and movement while eating and mastication causes dry (inspissated) exudate to accumulate —> chondroids

  • chronic suppurative eustachitis
38
Q

Why are horses kept inside more likely to develop mycotic eustachitis? What does this result in?

A

decreased ventilation allows for the humid environment that fungi can proliferate in

infection in the guttural pouch —> damage to carotid artery

39
Q

What is the most common cause of guttural pouch mycosis? What are 2 common involvements?

A

Aspergillus fumigatus or other Aspergillus spp.

  1. cranial nerves (VII, IX, X, XI, XII)
  2. erosion of the wall of the carotid leading to epistaxis or fatal hemorrhage
40
Q

Guttural pouch mycosis, horse:

A
  • multifocal, ulcerative and necrotizing eustachitis
  • vasculitis and thrombosis = ischemia
  • moldy, green
41
Q

Guttural pouch mycosis, horse:

A

internal carotid artery —> lumen filled with thrombus containing fungi

42
Q

Guttural pouch mycosis:

A

fibrinonecrotic exudate

43
Q

Guttural pouch mycosis:

A

carotid artery involvement —> filled with blood

44
Q

What 2 special stains can be used to visualize fungi in tissue sections?

A
  1. Gomori’s methenamine silver
  2. periodic acid schiff
  • guttural pouch mycosis
45
Q

What causes nasal squamous cell carcinoma? How does this cancer act? In what animals is this most common?

A

solar exposure in unpigmented areas, typically the tip of the nose and ears

slow to metastasize, but is locally aggressive and invasive (more destructive than proliferative)

white cats

46
Q

Nasal squamous cell carcinoma, cat:

A
  • DESTRUCTIVE —> necrosis and ulceration with breakdown of the cranial portion of the nose
  • collapsed eyelid suggestive of invasion into the orbit
47
Q

Nasal SCC, cat:

A
  • necrotizing and ulcerative
  • secondary bacterial infection with inflammation
  • prolapsed 3rd eyelid
48
Q

What nasal neoplasia is most common in older dogs? Where does it commonly arise from? Clinical signs?

A

nasal carcinoma

respiratory and olfactory epithelium

asymmetrical swelling, mucosuppurative exudate from nose, epistaxis, dyspnea

49
Q

What nasal neoplasia is most common in younger dogs?

A

mesenchymal —> nasal fibrosarcoma

50
Q

Nasal fibrosarcoma, 3 y/o dog:

A
  • proliferative, nodular mass
  • solid, gray
  • effacement of normal nasal cavity
51
Q

What causes enzootic nasal carcinoma? How does it typically act? In what animals is this most common?

A

enzootic nasal tumor virus (ETV), an ovine beta-retrovirus

malignant, but slow to metastasize —> proliferative and grows slowly, highly compressive

sheep and goats

52
Q

What causes necrotic laryngitis (calf diphtheria)? How does it present?

A
  • secondary infection by Fusobacterium necrophorum following trauma or viral infection (IBR)
  • part of oral necrobacillosis in calves and swine

plaques of ulceration covered by caseous fibrinonecrotic exudate near the arytenoid cartilage

53
Q

What is laryngeal hemiplasia?

A

ROARING - atrophy of the left dorsal cricoarytenoid muscle due to idiopathic neuropathy affecting the left recurrent laryngeal nerve (long, more susceptible to trauma)

  • the adductor (opening) of the larynx
54
Q

Tracheal collapse is usually subclinical. What are some manifestations? What animals is it most common in?

A
  • exercise intolerance
  • chronic coughing
  • clinical signs of airway obstruction
  • susceptibility to respiratory infection

toy and miniature dogs, occasionally in miniature horses, cattle, and goats

55
Q

How does tracheal collapse look grossly? How is it treated?

A

ligament detachment causes the trachea to become stenotic and appear flat

stint replacement

56
Q

What is tracheal collapse referred to as in horses?

A

scabbard trachea —> looks like a sheath of a sword

  • dorso-ventral flattening of the trachea and concomitant widening of the dorsal tracheal membrane
  • coughing and exercise intolerance
57
Q

What causes infectious bovine rhinotracheitis? How does it look grossly in the trachea?

A

bovine herpesvirus 1 —> common in feedlot beef cattle

ulcerative and necrotizing laryngotracheitis with the formation of a diphtheric membrane

58
Q

When is it common for herpesvirus infections to become systemic? What 3 things does it cause?

A

common in neonatal calves

  1. high mortality
  2. ulcerative and necrotizing rumenitis
  3. necrotizing hepatitis with miliary foci of necrosis
59
Q

What plays the primary role in causing canine infectious tracheobronchitis (kennel cough)? What are 4 pathogens with predisposing roles?

A

Bordetella bronchiseptica

  1. canine adenovirus 2
  2. canine parainfluenza virus 2
  3. canine distemper virus
  4. Mycoplasma spp.
60
Q

What is heaves? What is suggestive of chronic bouts?

A

chronic bronhiolitis-emphysema complex, or recurrent airway obstruction (RAO), asthma-like syndrome —> formerly COPD

heave line - hypertrophy of external abdominal oblique muscles

61
Q

What causes clinical signs of recurrent airway obstruction (RAO), or heaves? When are clinical signs worst?

A

resistance to airflow in the lungs due to diffues bronchoconstriction and mucous accumulation caused by goblet cell metaplasia within bronchioles

winter - horses are housed indoors and ventilation is not optimal

62
Q

How can goblet cell metaplasia resulting in recurrent airway obstruction (RAO, heaves) be observed?

A

Alcian blue stain will visualize mucous

63
Q

What is implicated in the pathogenesis of recurrent airway obstruction (RAO, heaves)?

A

exposure to aeroallergens

64
Q

What is feline asthma?

A

feline allergic bronchitis, or hyperactive airway disease, where the airway is filled with mucous, which constricts it

  • smooth muscle atrophy
  • eosinophils
65
Q

What are the 3 components of the blood-air barrier?

A
  1. basement membrane of endothelial cells
  2. basement membrane of type I pneumocyte
  3. cytoplasm of type I pneumocyte
66
Q

In what animals is exercise-induced pulmonary hemorrhage (EIPH)? What is it caused by? How does it present?

A

race horses

increased arterial and capillary pressures during strenuous exercise

  • hemorrhage in the dors-caudal portion of the caudal lung lobes
  • epistaxis in 1-10% of affected horses
67
Q

What is a common cause of epistaxis and pulmonary hemorrhage in feedlot cattle? How does this occur?

A

pulmonary abscesses as a complication of vena cava thrombosis

  • hepatic abscess secondary to chemical rumenitis due to increased carbohydrates
  • abscess close to the vena cava can erode the wall and rupture into it and lead to septic shock OR…
  • slow leakage of abscess into the vena cava, forming septic emboli that will attach to the right valve and cause valvular endocarditis and travel from the pulmonary artery into the lungs
68
Q

Pulmonary edema, pig:

A
  • takes up a lot of space in the thoracic cavity
  • will not collapse
  • moist, shiny, heavy
69
Q

What is a unique manifestation of pulmonary edema in pigs?

A

swine lungs have an increased amount of interstitial connective tissue —> upon edema, it will become yellow and distended

70
Q

What are the 3 main pathogenic mechanisms of pulmonary edema?

A
  1. left-sided CHF causes a back up of blood into the pulmonary artery, leading to increased hydrostatic pressure (cardiogenic edema)
  2. increased vascular permeability caused by damage to the blood-air barrier (inflammation)
  3. obstruction to lymphatic drainage caused by neoplasia involving thoracic LN or vessels
71
Q

Chronic pulmonary congestion and edema, horse:

A
  • frothy, wet
  • heavy
  • hypertension —> observable pulmonary vessels
72
Q

Chronic pulmonary edema:

A

gray lesions

73
Q

How does chronic pulmonary edema present histologically?

A
  • increased cellularity
  • presence of heart failure cells —> siderophages
74
Q

Chronic pulmonary edema, heart failure cells:

A

dark brown pigment within cytoplasm of alveolar macrophages (siderophores)

  • alveoli filled with low protein fluid that does not stain pink like inflammatory edema
75
Q

How can heart failure cells be visualized? When are they typically present?

A

iron (Perl’s) stain —> visualized hemosiderin-laden macrophages (siderophages)

chronic survival with left-sided CHF - not common in animals

76
Q

What causes pulmonary anthracosis?

A

deposition of carbon particles in parenchyma —> pinpoint foci

usually subclinical - common in high-population cities with smog

77
Q

Pulmonary anthracosis, histology:

A

pneumoconiosis - deposition of dust or minerals

bronchiole macrophages with carbon particles

78
Q

What is atelectasis? How does it appear grossly?

A

incomplete expansion of the lungs or portions of the lungs

dark red and sunken in comparison to aerated lungs with a fleshy consistency and inability for the tissue to float

79
Q

What are the 3 types of acquired atelectasis?

A
  1. COMPRESSIVE - caused by space-occupying lesions, like hydrothorax, hemothorax, or pleuritis
  2. MASSIVE - caused by pneumothorax that causes the loss of negative pressure in the thorax
  3. OBSTRUCTIVE - inflammatory exudate, edema
80
Q

When is atelectasis normal or congenital?

A

fetus/stillborn before the first breath is taken

  • dark red
  • increased consistency, firm
  • no loner pliable
  • sinks in fluid
81
Q

When is it common for a fetus to aspirate amniotic fluid and meconium?

A

dystocia - hypoxia in uterus relaxes anal sphincter and allows the release of meconium, the dark green mucilaginous material of the intestine of full-term fetuses

  • hang neonate by legs to drain amniotic fluid to stimulate breathing
82
Q

Meconium aspiration syndrome (MAS):

A
  • meconium stining kitten fetus
  • kitten was stuck in birth canal
  • cat in septic shock
83
Q

How does pulmonary atelectasis look grossly?

A
  • patchy due to compression
  • secondary to aspiration of meconium and amniotic fluid
  • meconium = irritant —> inflammation, pneumonia
84
Q

What is pulmonary emphysema? How does it affect the lungs?

A

permanent enlargement of air spaces distal to terminal bronchiole accompanied by destruction of alveolar walls

no septa = decreased surface area available for gas exchange

85
Q

What is thought to cause pulmonary emphysema?

A
  • imbalance between protease and anti-proteases (α1 antitrypsin)
  • neutrophil-derived serine proteases (elastase, matrix metalloprotease) concentration enhanced by neutrophil and macrophage activation induced in chronic bronchitis
86
Q

What are 2 causes pulmonary emphysema in animals?

A
  1. obstruction to outflow of air or agonal at slaughter
  2. bronchopneumonia causes an airflow imbalance where the volume of air entering the lungs exceeds the volume exiting during expiration
  • interstitial is most common in cattle
87
Q

What is bullous emphysema?

A

large focal air-filled spaces rupture, which can lead to fatal pneumothorax, losing negative pressure

88
Q

Interstitial pulmonary emphysema, bovine:

A

air bubbles in interstitial septa