Respiratory Pathology - lecture 1 Flashcards
What are the three parts of the respiratory tract?
- conducting system
- transitional system
- exchange system
What are the differences in mucosal lining of the 3 systems of the resp tract?
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)
what’s the difference between type 1 and 2 pneymocytes?
type 1 = membranous; thin cells that make up blood-air barrier with capillary endothelium + basement membrane
type 2 = cuboidal cells, make surfactant
how is the nasal cavity divided?
turbinates or conchae which are curled shelves of bone covered in mucous membrane
which species gets clinical sinus problems more than others?
horse
what are the five main functions of the respiratory system?
- air conduction (move air)
- air conditioning (heat + moisture)
- air filtration and immune defense
- smell
- vocalization
name three non-specific defense mechanisms of the resp system
- air filtration
- mucociliary clearance system
- coughing & sneezing
name three specific defense mechanisms of the resp system
- pulmonary alveolar macrophages & intravascular monocytes in lung
- antibodies
- mucus lining absorption of soluble gases
what’s choanal atresia?
failure of formation of the communication between nasal cavity and nasopharynx
- is usually bilateral
- common in camelids
what are congenital components of brachycephalic airway syndrome (BAS)?
- stenotic nares
- elongated soft palate (beyond epiglottis and into larynx)
- tracheal/laryngeal hypoplasia
how do the congenital components of BAS lead to airway obstruction?
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
what happens in tracheal collapse?
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
what kind of problems can happen with epiglottic hypoplasia in horses?
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)
progressive ethmoid hematomas: who gets them and from where do they arise?
older horses, thoroughbred and arabians are predisposed
arise from ethmoid turbinates
nasopharyngeal polyps: who gets them and from where do they arise?
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
what do you see grossly and histologically with equine laryngeal paralysis?
gross: left sided denervation atrophy of cricoarytenoid muscles
histo: progessive loss of fibres and demyelination
what side do we usually see laryngeal paralysis in horses?
left side
when can we see bilateral laryngeal paralysis?
- anesthesia
- hepatic encephalopathy
what are 2 big differences between equine and canine laryngeal paralysis?
- dogs usually have bilateral paralysis
- dogs have associated generalized neuromuscular disorder
can laryngeal & tracheal edema happen in any domestic species?
YES! but secondary to acute inflammatory process like anaphylaxis, atypical interstitial pneumonia (cattle), or edema disease (pigs)
what’s honker syndrome?
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
list the 5 types of inflammation in the upper resp tract
- serous rhinitis
- catarrhal
- purulent / suppurative
- fibrinous
- granulomatous
what do we get in purulent/suppurative inflammation?
- neutrophilic exudate
- boston creme donut
- mucosal necrosis
- associated bacterial (or fungal) infection
what do we get in fibrinous inflammation?
- 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
what do we get in granulomatous inflammation?
- usually chronic inflammation
- cottage cheese or stiff cream cheese
- fungal infection or mycobacteria
what are three examples of rhinitis (include species)?
- inclusion body rhinitis (pigs; suid herpesvirus 2) = catarrhal rhinitis
- infectious bovine rhinotracheitis (cattle; bovine herpesvirus 1)
- feline viral rhinotracheitis (cats; feline herpesvirus 1)
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)
what are your differential diagnoses to consider with IBR lesions?
- aspiration of chemical irritants like stomach acid
- infection with other viral agents
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
where does felines herpesvirus go latent?
trigeminal ganglion - you can never get rid of herpes :)
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
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
why is progressive atrophic rhinitis (PAR) more important than non-progressive?
- infection by Pasteurella multocida (Type D»_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
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
best ways to diagnose atrophic rhinitis?
- gross: can see malformed turbinates behind 1st or 2nd premolar
- histology: hypoplasia of osteoclasts, bone resorption
- nasal swab: can get Pasteurella and Bordetella from culture, but need to detect toxins via PCR/ELISA
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
what complications can come out of equine strangles-infected horses?
- guttural pouch empyema - inflammation = damage nerves in pouch causing Horner’s syndrome, facial or laryngeal paralysis (roarer)
- pneumonia
- bastard strangles - infected mediastinal & mesenteric LNs
- purpura hemorrhagica // vasculitis
Give three examples of fungal rhinitis
- Aspergillus fumigatus –> suppurative, caseous, hemorrhagic rhinitis (dogs, horses)
- Cryptococcus neoformans or gattii –> nasal discharge, facial swelling (cats and can be zoonotic!)
- Rhinoporidiosis seeberi –> single unilateral nasal ‘polyp’ (dogs
Give three examples of parasitic rhinitis
- Oestrus ovis - sheep bot fly (usually subclinical)
- Oslerus osleri - in dogs (rare) but usually minimal unless infected young
- guttural pouch disease - can by mycosis, empyema or tympany; happens in horses
what is the most common type of epithelial tumor in dogs?
adenocarcinoma (most common carcinoma in dogs)
what is the most common type of epithelial tumor in cats and horses?
squamous cell carcinoma
what is the most common round cell tumor in cats?
lymphoma –> nasal lymphoma
* most common upper resp tract tumor in cats
* B lymphocyte origin
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
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
are there less or more ciliated cells as you progress from conducting to transitional system?
less // ciliated cells decreases
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
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
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
list the structural components of respiratory bronchioles
- cuboidal, ciliated epithelium
- wall of smooth muscle
- alveolar capillaries within wall
what are type I pneumocytes specialized for?
gas exchange
they are incapable of cell division
what are type II pneumocytes specialized for?
secrete surfactant and are progenitor cells for type I pneumocytes
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
what makes up the blood-air barrier (6 things)?
- alveolar surfactant
- type I pneumocytes
- basal lamina of type I pneumocytes
- interstitial connective tissue
- basal lamina of capillary endothelial cell
- capillary endothelial cell
why is the resp system so vulnerable to airborn injury? (3 things)
- alveoli have huge surface area = large interface between blood and air
- large volume of air passing through constantly
- high concentration of noxious element in the air
name the three main layers of the blood-air barrier
- cytoplasm of type I pneumocyte
- dual basal lamina (fused basement membranes of 1 & 3)
- cytoplasm of endothelial cell
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
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
what are the defense mechanism components of the conducting system?
- mucociliary clearance
- antibodies
- lysozymes
- mucus
- cough/sneeze
what are the defense mechanism components of the transitional system?
- club cells
- antioxidants
- lysozyme
- antibodies
what are the defense mechanism components of the exchange system?
- alveolar macrophages
- intravascular macrophages
- opsonizing antibodies
- surfactant
- antioxidants
what are the 3 portals of entry into the respiratory system?
- aerogenous (inhalation) - pathogens & toxins
- hematogenous (blood) - pathogens & toxins
- direct extension - penetrating wounds, foreign bodies, bites, ruptured esophagus or diaphragm
fill in the blank: if the pulmonary defenses are impaird, then the efficiency of the lung at eliminating bacteria is greatly ________ (increased/decreased)?
decreased
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
