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VETM 425 - Systemic Pathology > Respiratory Pathology - lecture 1 > Flashcards

Respiratory Pathology - lecture 1 Flashcards

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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
what do we get in granulomatous inflammation?
- usually chronic inflammation - **cottage cheese or stiff cream cheese** - fungal infection or mycobacteria
26
what are three examples of rhinitis (include species)?
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
What gross lesions are characteristic of infectious bovine rhinotracheitis?
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
what are your differential diagnoses to consider with IBR lesions?
- **aspiration of chemical irritants** like stomach acid - infection with other viral agents
29
what clinical signs and gross lesions do you see in feline viral rhinotracheitis?
**Ocular involvement**, fever, sneeze/cough, oculonasal discharge grossly: crusting around eye and nose and erosion of nasal mucosa
30
where does felines herpesvirus go latent?
trigeminal ganglion - you can never get rid of herpes :)
31
how can you tell between feline herpes, feline calicivirus and feline chlamydia?
herpes -- ocular involvement calicivirus -- oral ulcers (**herpes doesn't have this**) chlamydia -- chlamydiosis/chlamydial conjunctivitis
32
give me cause, clinical sign and herd health significance of **non-progressive atrophic rhinitis**
* cause: *Bordetella bronchiseptica* * signs: mild transient sneezing, nasal discharge * min-no herd health significance (maybe decrease in weight gain
33
why is **progressive atrophic rhinitis (PAR)** more important than non-progressive?
* infection by *Pasteurella multocida* (Type D >> 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
how does *B. bronchiseptica* help out *P. multocida* infection?
*P. multocida* can't colonize nasal mucosa unless it's been breached/ulcerated by *B. bronchiseptica* strains who produce toxins
35
best ways to diagnose atrophic rhinitis?
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
give an example of bacterial rhinitis
equine strangles - *Streptococcus equi spp. equi* * not a commensal but similar to another so make sure! * clinical sign: lymph node abscesses
37
what complications can come out of equine strangles-infected horses?
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
Give three examples of fungal rhinitis
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
Give three examples of parasitic rhinitis
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
what is the most common type of epithelial tumor in dogs?
**adenocarcinoma** (most common carcinoma in dogs)
41
what is the most common type of epithelial tumor in cats and horses?
squamous cell carcinoma
42
what is the most common round cell tumor in cats?
lymphoma --> nasal lymphoma * **most common upper resp tract tumor in cats** * B lymphocyte origin
43
what is **enzootic nasal tumor**?
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
what kind of epithelial cells line the mucosa of the conducting and some of the transitional system of the respiratory tract?
pseudostratified, ciliated respiratory epithelial cells goblet cells are there too, they make mucus and are non-ciliated
44
are there less or more ciliated cells as you progress from conducting to transitional system?
less // ciliated cells decreases
45
what is the relationship between diameter of airway and amount of cartilage and smooth muscle?
as diameter of airway decreases, amount of cartilage and smooth muscle gets smaller
46
what are the main differences between bronchi and bronchioles?
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
do bronchioles have good defense mechanisms overall?
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
list the structural components of respiratory bronchioles
- cuboidal, ciliated epithelium - wall of smooth muscle - alveolar capillaries within wall
49
what are **type I pneumocytes** specialized for?
gas exchange they are incapable of cell division
50
what are **type II pneumocytes** specialized for?
secrete surfactant and are progenitor cells for type I pneumocytes
51
if you notice hyperplasia of type II pneumocytes on histology, what could this indicate?
it's a marker of alveolar injury and attempted repair for both type I & II cells within alveolus
52
what makes up the blood-air barrier (6 things)?
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
why is the resp system so vulnerable to airborn injury? (3 things)
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
name the three main layers of the blood-air barrier
1. cytoplasm of type I pneumocyte 2. dual basal lamina (fused basement membranes of 1 & 3) 3. cytoplasm of endothelial cell
55
alveolar macrophages: where are they and what do they do?
* in alveolar lumen (arrive by bloodstream) * function: phagocytose inhaled dust particles and other foreign material
56
club cells: where are they and what do they do?
* found in **bronchioles** * involved in detox of foreign material, produce protective secretions (against oxidative stress and inflam), and make surfactant
57
what are the defense mechanism components of the conducting system?
* mucociliary clearance * antibodies * lysozymes * mucus * cough/sneeze
58
what are the defense mechanism components of the transitional system?
* club cells * antioxidants * lysozyme * antibodies
59
what are the defense mechanism components of the exchange system?
* alveolar macrophages * intravascular macrophages * opsonizing antibodies * surfactant * antioxidants
60
what are the 3 portals of entry into the respiratory system?
1. aerogenous (inhalation) - pathogens & toxins 2. hematogenous (blood) - pathogens & toxins 3. direct extension - penetrating wounds, foreign bodies, bites, ruptured esophagus or diaphragm
61
fill in the blank: if the pulmonary defenses are impaird, then the efficiency of the lung at eliminating bacteria is greatly ________ (increased/decreased)?
decreased
62
give an example pathogenesis showing how complex respiratory diseases are
ex. BRDC husbandry conditions --> stress --> immunosuppression --> viral infection --> damage to defense mechanisms --> secondary bacterial infection

VETM 425 - Systemic Pathology (2 decks)

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