Exam 1: Pulmonary Flashcards
Function of respiratory system
ventilation
gas exchange
What tissue type is the nasal mucosa
respiratory epithelium
ciliated, pseudostratified columnar epithelium with goblet cells
Where does tissue change from squamous –> transitional –> respiratory epithelium
nares
Diffusibility of CO2
20x more diffusible than oxygen
Aerogenous
most common route of entry into lungs
get cranioventral dz (bronchopneumonia)
Pathogens that utilize aerogenous entry
bacteria mycoplasma viruses toxic gasses foreign particles
Hematogenous
common route of entry into lungs for septicemia and viremia
get diffuse, non-collapsing lung (interstitial pneumonia)
Pathogens that utillize hematogenous entry
viruses
bacteria
parasites
What do respiratory clinical signs indicate about level of disease?
not much
small affected area may cause severe signs, large affected area may have no/mild signs
Irritation of URT = what clinical sign?
sneezing
Irritation of trachea and/or bronchi = what clinical sign?
coughing
3 causes of mucociliary dysfunction
- congenital (dogs with immotile cilia syndrome)
- environmental (e.g. smoke, pollution)
- infectious (e.g. mycoplasma, bordatella, viral)
Primary ciliary dyskinesia (PCD)
genetic defect makes ciliary movement defective –> reduced clearance –> predisposition to infection
Early URT damage
decreased cilia, increased goblet cells + inflammation –> hyperemia, edema, neutrophils = impaired mucociliary clearance
Can early URT damage be fixed?
Yes, resp epithelium will repair if basement membrane is intact
(if damaged –> scarring)
Chronic URT damage
If basement membrane lost: goblet cell hyperplasia, fibrosis
If basement membrane intact: squamous metaplasia
reptile with URT squamous metaplasia
hypervitaminosis A
Defense at level of alveoli
- no cilia or goblet cells
- fluid covering alveoli
- resident alveolar macrophages (80-90% of immune cell pop in alveolus)
what antimicrobial agents are in fluid that covers airways?
transferrin (iron sequestration)
opsonins
surfactant
Common bacteria that cause respiratory disease
Mycobacterium bovis
Listeria
Rhodococcus
Most predominant response of bronchiole mucosa to chronic injury
epithelial hyperplasia (cuboidal)
+/- development of polyps
+/- smooth m. hyperplasia
= increased resistance
Pathogenesis for type II pneumocyte hyperplasia
- type I alveolar cells highly vulnerable to damage
- if damaged, necrosis then replaced by type II hyperplastic alveolar cells
- increased, poor quality surfactant produced that forms hyaline membranes (block gas exchange)
- damaged tissue may be replaced by fibrosis
= impaired gas exchange, decreased compliance, congestion, edema
Defense against blood borne pathogens
Dogs, rodents, humans
primarily Kupffer cells and splenic macrophages phagocytose pathogens
Defense against blood borne pathogens
Cats, Rum, EQ, Pig
primarily pulmonary intravascular macrophages phagocytose pathogens
Distribution pattern of bronchopneumonia
- cranial (b/c URT cause)
- ventral (b/c gravity)
Distribution pattern of interstitial or verminous pneumonia
dorsocaudal, diffuse patchy damage to alveolar septa
Acute pneumonia alveolar septal response
edema, leukocytes in interstitium
chronic pneumonia alveolar septal response
squamous metaplasia, fibrosis, non-suppurative inflammation
Distribution of embolic pneumonia
random multifocal distribution (hallmark)
Distribution of granulomatous pneumonia
random multifocal, but variably sized (mebe mineralized) firm nodules that are well circumscribed