Respiratory Pathology - lecture 1 Flashcards

1
Q

What are the three parts of the respiratory tract?

A
  1. conducting system
  2. transitional system
  3. exchange system
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2
Q

What are the differences in mucosal lining of the 3 systems of the resp tract?

A

conducting is lined by ciliated epithelium and goblet cells

transitional is lined by ciliated and secretory cells, no goblet cells

exchange is lined by pneuomocytes (type 1 and type 2)

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3
Q

what’s the difference between type 1 and 2 pneymocytes?

A

type 1 = membranous; thin cells that make up blood-air barrier with capillary endothelium + basement membrane

type 2 = cuboidal cells, make surfactant

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4
Q

how is the nasal cavity divided?

A

turbinates or conchae which are curled shelves of bone covered in mucous membrane

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5
Q

which species gets clinical sinus problems more than others?

A

horse

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6
Q

what are the five main functions of the respiratory system?

A
  1. air conduction (move air)
  2. air conditioning (heat + moisture)
  3. air filtration and immune defense
  4. smell
  5. vocalization
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7
Q

name three non-specific defense mechanisms of the resp system

A
  1. air filtration
  2. mucociliary clearance system
  3. coughing & sneezing
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8
Q

name three specific defense mechanisms of the resp system

A
  1. pulmonary alveolar macrophages & intravascular monocytes in lung
  2. antibodies
  3. mucus lining absorption of soluble gases
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9
Q

what’s choanal atresia?

A

failure of formation of the communication between nasal cavity and nasopharynx

  • is usually bilateral
  • common in camelids
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10
Q

what are congenital components of brachycephalic airway syndrome (BAS)?

A
  1. stenotic nares
  2. elongated soft palate (beyond epiglottis and into larynx)
  3. tracheal/laryngeal hypoplasia
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11
Q

how do the congenital components of BAS lead to airway obstruction?

A

any congenital component –> increased respiratory effort –> secondary malformations –> further narrow and compromise upper resp tract –> noisy breathing, inspiratory dyspnea –> airway obstruction

  • laryngeal saccules, everted tonsils, hypertrophied and folded pharyngeal mucosa, laryngeal edema and collapse, or tracheal collapse
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12
Q

what happens in tracheal collapse?

A

abnormal tracheal cartilage –> dorsoventral flattening of trachea –> abnormal tracheal rings (D instead of C) and dorsal tracheal muscle is wide & floppy –> honking cough and exercise intolerance

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13
Q

what kind of problems can happen with epiglottic hypoplasia in horses?

A

epiglottic entrapment (aryepiglottal folds are above dorsal epiglottic surface)

dorsal displacement of the soft palate (caudal free margin of soft palate is dorsal to epiglottis = obstructed airway)

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14
Q

progressive ethmoid hematomas: who gets them and from where do they arise?

A

older horses, thoroughbred and arabians are predisposed

arise from ethmoid turbinates

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15
Q

nasopharyngeal polyps: who gets them and from where do they arise?

A

common in young cats and can occur in horses

in cats: from middle ear or auditory tube or mucosal lining of turbinates

in horses: from nasal mucosa

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16
Q

what do you see grossly and histologically with equine laryngeal paralysis?

A

gross: left sided denervation atrophy of cricoarytenoid muscles

histo: progessive loss of fibres and demyelination

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17
Q

what side do we usually see laryngeal paralysis in horses?

A

left side

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18
Q

when can we see bilateral laryngeal paralysis?

A
  • anesthesia
  • hepatic encephalopathy
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19
Q

what are 2 big differences between equine and canine laryngeal paralysis?

A
  1. dogs usually have bilateral paralysis
  2. dogs have associated generalized neuromuscular disorder
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20
Q

can laryngeal & tracheal edema happen in any domestic species?

A

YES! but secondary to acute inflammatory process like anaphylaxis, atypical interstitial pneumonia (cattle), or edema disease (pigs)

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21
Q

what’s honker syndrome?

A

tracheal edema and hemorrhage syndrome in cattle

rapid breathing + increased pressure in trachea during inspiration –> mechanical injury to tracheal mucosa –> inflammation, hemorrhage, edema –> tissue protrudes into airway –> repeat

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22
Q

list the 5 types of inflammation in the upper resp tract

A
  1. serous rhinitis
  2. catarrhal
  3. purulent / suppurative
  4. fibrinous
  5. granulomatous
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23
Q

what do we get in purulent/suppurative inflammation?

A
  • neutrophilic exudate
  • boston creme donut
  • mucosal necrosis
  • associated bacterial (or fungal) infection
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24
Q

what do we get in fibrinous inflammation?

A
  • suppurative + increased vascular permeability
  • runny scrambled eggs
  • may form fibrinonecrotic membranes (= necrotic debris, fibrin, suppurative inflammation forming pseudomembrane that adheres to the underlying ulcerated surface)
  • bacterial or fungal infection
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25
Q

what do we get in granulomatous inflammation?

A
  • usually chronic inflammation
  • cottage cheese or stiff cream cheese
  • fungal infection or mycobacteria
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26
Q

what are three examples of rhinitis (include species)?

A
  1. inclusion body rhinitis (pigs; suid herpesvirus 2) = catarrhal rhinitis
  2. infectious bovine rhinotracheitis (cattle; bovine herpesvirus 1)
  3. feline viral rhinotracheitis (cats; feline herpesvirus 1)
27
Q

What gross lesions are characteristic of infectious bovine rhinotracheitis?

A

hyperemia with petechial hemorrhage and pustules first, then… fibrinonectrotic membrane forms later (= sloughing of necrotic epithelial cells and leakage of serum from inflamed capillaries)

28
Q

what are your differential diagnoses to consider with IBR lesions?

A
  • aspiration of chemical irritants like stomach acid
  • infection with other viral agents
29
Q

what clinical signs and gross lesions do you see in feline viral rhinotracheitis?

A

Ocular involvement, fever, sneeze/cough, oculonasal discharge

grossly: crusting around eye and nose and erosion of nasal mucosa

30
Q

where does felines herpesvirus go latent?

A

trigeminal ganglion - you can never get rid of herpes :)

31
Q

how can you tell between feline herpes, feline calicivirus and feline chlamydia?

A

herpes – ocular involvement
calicivirus – oral ulcers (herpes doesn’t have this)
chlamydia – chlamydiosis/chlamydial conjunctivitis

32
Q

give me cause, clinical sign and herd health significance of non-progressive atrophic rhinitis

A
  • cause: Bordetella bronchiseptica
  • signs: mild transient sneezing, nasal discharge
  • min-no herd health significance (maybe decrease in weight gain
33
Q

why is progressive atrophic rhinitis (PAR) more important than non-progressive?

A
  • infection by Pasteurella multocida (Type D&raquo_space; A)
  • these strains produce potent cytotoxins that inhibit bone formation, leading to bone resorption and deformation of turbinates and snout
  • co-infection with B. bronchiseptica is common = makes dermonecrotic toxin
34
Q

how does B. bronchiseptica help out P. multocida infection?

A

P. multocida can’t colonize nasal mucosa unless it’s been breached/ulcerated by B. bronchiseptica strains who produce toxins

35
Q

best ways to diagnose atrophic rhinitis?

A
  1. gross: can see malformed turbinates behind 1st or 2nd premolar
  2. histology: hypoplasia of osteoclasts, bone resorption
  3. nasal swab: can get Pasteurella and Bordetella from culture, but need to detect toxins via PCR/ELISA
36
Q

give an example of bacterial rhinitis

A

equine strangles - Streptococcus equi spp. equi
* not a commensal but similar to another so make sure!
* clinical sign: lymph node abscesses

37
Q

what complications can come out of equine strangles-infected horses?

A
  1. guttural pouch empyema - inflammation = damage nerves in pouch causing Horner’s syndrome, facial or laryngeal paralysis (roarer)
  2. pneumonia
  3. bastard strangles - infected mediastinal & mesenteric LNs
  4. purpura hemorrhagica // vasculitis
38
Q

Give three examples of fungal rhinitis

A
  1. Aspergillus fumigatus –> suppurative, caseous, hemorrhagic rhinitis (dogs, horses)
  2. Cryptococcus neoformans or gattii –> nasal discharge, facial swelling (cats and can be zoonotic!)
  3. Rhinoporidiosis seeberi –> single unilateral nasal ‘polyp’ (dogs
39
Q

Give three examples of parasitic rhinitis

A
  1. Oestrus ovis - sheep bot fly (usually subclinical)
  2. Oslerus osleri - in dogs (rare) but usually minimal unless infected young
  3. guttural pouch disease - can by mycosis, empyema or tympany; happens in horses
40
Q

what is the most common type of epithelial tumor in dogs?

A

adenocarcinoma (most common carcinoma in dogs)

41
Q

what is the most common type of epithelial tumor in cats and horses?

A

squamous cell carcinoma

42
Q

what is the most common round cell tumor in cats?

A

lymphoma –> nasal lymphoma
* most common upper resp tract tumor in cats
* B lymphocyte origin

43
Q

what is enzootic nasal tumor?

A

this is a virally induced tumor found in sheep (ENTV-1) and goats (ENTV-2)

found growing in ethmoid turbinates, usually too small to cause severe clinical symptoms

43
Q

what kind of epithelial cells line the mucosa of the conducting and some of the transitional system of the respiratory tract?

A

pseudostratified, ciliated respiratory epithelial cells

goblet cells are there too, they make mucus and are non-ciliated

44
Q

are there less or more ciliated cells as you progress from conducting to transitional system?

A

less // ciliated cells decreases

45
Q

what is the relationship between diameter of airway and amount of cartilage and smooth muscle?

A

as diameter of airway decreases, amount of cartilage and smooth muscle gets smaller

46
Q

what are the main differences between bronchi and bronchioles?

A

bronchi have cartilage, glands,** goblet cells** and a mucociliary apparatus – bronchioles don’t

broncioles have club cells and wayyyy fewer ciliated cells copmared to bronchi

47
Q

do bronchioles have good defense mechanisms overall?

A

no, they have fewer (no mucociliary apparatus, no mucus-producing goblet cells and few ciliated cells) so broncioles are more susceptible to collapse and infection

48
Q

list the structural components of respiratory bronchioles

A
  • cuboidal, ciliated epithelium
  • wall of smooth muscle
  • alveolar capillaries within wall
49
Q

what are type I pneumocytes specialized for?

A

gas exchange

they are incapable of cell division

50
Q

what are type II pneumocytes specialized for?

A

secrete surfactant and are progenitor cells for type I pneumocytes

51
Q

if you notice hyperplasia of type II pneumocytes on histology, what could this indicate?

A

it’s a marker of alveolar injury and attempted repair for both type I & II cells within alveolus

52
Q

what makes up the blood-air barrier (6 things)?

A
  1. alveolar surfactant
  2. type I pneumocytes
  3. basal lamina of type I pneumocytes
  4. interstitial connective tissue
  5. basal lamina of capillary endothelial cell
  6. capillary endothelial cell
53
Q

why is the resp system so vulnerable to airborn injury? (3 things)

A
  1. alveoli have huge surface area = large interface between blood and air
  2. large volume of air passing through constantly
  3. high concentration of noxious element in the air
54
Q

name the three main layers of the blood-air barrier

A
  1. cytoplasm of type I pneumocyte
  2. dual basal lamina (fused basement membranes of 1 & 3)
  3. cytoplasm of endothelial cell
55
Q

alveolar macrophages: where are they and what do they do?

A
  • in alveolar lumen (arrive by bloodstream)
  • function: phagocytose inhaled dust particles and other foreign material
56
Q

club cells: where are they and what do they do?

A
  • found in bronchioles
  • involved in detox of foreign material, produce protective secretions (against oxidative stress and inflam), and make surfactant
57
Q

what are the defense mechanism components of the conducting system?

A
  • mucociliary clearance
  • antibodies
  • lysozymes
  • mucus
  • cough/sneeze
58
Q

what are the defense mechanism components of the transitional system?

A
  • club cells
  • antioxidants
  • lysozyme
  • antibodies
59
Q

what are the defense mechanism components of the exchange system?

A
  • alveolar macrophages
  • intravascular macrophages
  • opsonizing antibodies
  • surfactant
  • antioxidants
60
Q

what are the 3 portals of entry into the respiratory system?

A
  1. aerogenous (inhalation) - pathogens & toxins
  2. hematogenous (blood) - pathogens & toxins
  3. direct extension - penetrating wounds, foreign bodies, bites, ruptured esophagus or diaphragm
61
Q

fill in the blank: if the pulmonary defenses are impaird, then the efficiency of the lung at eliminating bacteria is greatly ________ (increased/decreased)?

A

decreased

62
Q

give an example pathogenesis showing how complex respiratory diseases are

A

ex. BRDC
husbandry conditions –> stress –> immunosuppression –> viral infection –> damage to defense mechanisms –> secondary bacterial infection