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Respiratory System Screenshot 2025-09-26 at 12.06.25 PM - Coggle Diagram
Respiratory System
Conducting
Component
Nostrils, nasal cavity, paranasal sinus, nasopharynx, larynx, trachea, bronchi
Bronchitis: epithelial injury becomes chronic, mucus is
increased via goblet cell hyperplasia
Bronchiectasis: sequel to bronchi injury =
permanent
dilation of bronchus w/ rupture of bronchial wall. Macroscopic: lumps in lungs, cut surface filled w/ purulent exudate
Psuedostratified, ciliated, columnar cells
lines most of nasal cavity, nasopharynx, part of larynx, all of trachea, bronchi:
very sensitive to injury
Goblet cells: mucus
Cell damage sequence: degeneration, exfoliation, ulceration, mitosis, and repair: commonly found in bovine herpesvirus 1, felid herpesvirus 1, CAdV2, CPIV 2
Transitional
Component
Bronchioles
: between conducting component and air exchange
Bronchioles LACK goblet cells
Bronchioles secretory cells: 2 kind
Club cells:
Detox xenobiotics
Secrete: collectins, surfactant
Neuroendocrine cells
Epithelial
lining of bronchiolar region
very susceptible to injury
Resp viruses (canine distemper, bovine rep synctial virus), oxidative gases (NO2, SO2), toxic things
Why prone to injury (possible reasons): 1. highly vulnerable to oxidants and free rads 2. prescence of club cells rich in mixed fxn oxidases, locally generate toxic metabolites 3. tendency of pulmon alveolar macrophages and leukocytes to accum in region of lungs
Once damage is
irreversible
: cells degenerate and exfoliate into bronchiolar region. Recruited phago cells remove exudate and cell debris from lumina of affected bronchioles prepare basement to be repopulated w/ new cells pool of club cells and pluripotent stem cells. Then several days later the prolif cells fully differ into normal bronchiolar cells
Bronchiolitis obliterans
: sever energy exudate attaches and can't be removed from basement of bronchioles. Exudate becomes infliltrated by fibroblasts and form small nodular masses of fibrovasculuar tissue that develop into well organized polyps inside bronchiolar lumen. External surface of exudate becomes covered by ciliated cells. Can cause airflow impairement if large enough
Chronic bronchiolar injury
: goblet cells can be produced (bc goblets not normally in bronchioles). Profound alteration in bronch secretions: 1. normally serous bronchiolar is serous 2. additional goblets mucus makes it more tenacoious 3. increased viscoelasticity of mucus, bronch secreted can't be removed good by ciiliary action = plug and obstrux of distal airways = COPD (emphysema & atelectaiss)
Air
Exchange
Component
: :
Formed by
alveoli
: 2 types epithelium cells = 2000 m^2
Type 1
(membranous): cover majority of alveolar wall, fxn gas exchange
Type II
(granular): produce surfactant
Alveoli walls: thin delicate network
Interstitium
: supports epithelium and capillary endothelium
Interstium: Supports blood, lymphatic vessels, nerves, bronchi, bronchioles, alveoli
3 Types of Interstitium
Bronchovascular
interstitium : main bronchi and pulmonary vessels are situated
2
.
Interlobular
interstium: seperates pulmonary lobules and supporting small blood and lymph vessels
Alveolar
intersitum: supports alveolar walls that contain pulmonary capillaries and alveolar epithelial cells
Blood air barrier
Vascular endothelium, basement membrane, alveolar epithelium lining cells
Delicate structure makes alveoli vulnerable to injury: thin wall w/ 3 layers. 1. vascular endothelium 2. basal lamina 3. alveolar epithelium
Epithelial side of alveolus primarily lines by thin type 1 pneumocytes. Suscpetible to noxious agenets that reach alveolar region either
aerogenously or hematogenously
. When irreversible type 1 cells detach causing denudation of basement, increased alveolar permeability, alveolar edema, leakage of fibrin
Alveolar Repair is
possible
as long as
basement is intact
W/in 3 days, cuboidal type 2 pneumocytes, club cells, stems cells undergo mitosis and provide large pool of new undiff cells. New cells repave the denuded alveolar basement and differ into type 1 pneymocytes
Type 1 pneumocytes increase in alveolar capillary permeability, transient leakage of plasma fluid, proteins and fibrin into the alveoli. Fluids usually cleared via alveolar and lymphatic absorption, and necrotic pneumocytes (type1) and fibrin strands are phago and removed by pulmon alveolar macro's. Alveolar fibrosis can have marked impact on lung fxn due to loss of type 1 that help facil gas exchange
Species Differences
LEFT lung of domestic species
Cranial lobe
Caudal lobe
RIGHT lung: depends species
Cranial lobe
Middle (NOT horses)
Caudal lobe
Accessory lobe
Degree of lobulation: depends on air movement between lobules
Pigs, Cattle: movement basically
ABSENT
bc thick connective tissue of interlobular septa
Collateral ventilation: movement of air between lobules and between adjacent alveoli
Cattle & Pigs: POOR
Dogs: GOOD
Thoracic Cavity, Mediastinum, Pleura
Pleurae
: single layer of mesothelial cells overlying many layers of connective tissue
Surface of lungs: lined by
visceral pleura
Thoracic wall, diaphragm, mediastinum: lined by
parietal pleura
Plueral space
: between parietal and visceral pleura: separated into L/R via mediastinum. Contains traces of clear fluid and few exfoliated cells
Cattle, goats, pigs: mediastinum is
complete
: allows no communication between R/L
Horses, sheep:
fenestrations
allow communication
Cats, dogs: controversial if mediastinum is complete/fenesterated
Mesothelial
cells: most
numerous
cells in pleural space
Metabolically active and capable of secreting variety of pro/anti inflam mediators in response to injury (bact, foreign material, trauma)
Mesothel cells play a role in repair and fibrosis through growth factors
Chronic stim. they bcome reactive and proliferate and may form plaque like or vilious like proliferations that can be hard to differ from neoplasia (mesothelioma)
Portals of Entry
Aerogenous
(inhale)
Deposition: particles of vary sizes/shapes are trapped w/in specific regions of resp system (asbestos)
Clearance: particles destroyed, neutralized, or removed from mucosal surfaces
Abnormal retention via increased deposition, decreased clearance or combo = patho mech of vary pulmon dz
particles longer than 200 um: can reach lower resp system if diameter <1um
Vulnerability to insult
(aerogenous)
extensive area of alveoli (reach blood quick). 2. large volume of air passing constantly into lungs 3. high conc. of noxious elements that can be present in the air
Hematogenous
(blood)
Common occurence bc it's well vascularized: lungs
large vascular bed
Size/Deposition
greater 10 um: lodge in nasal passage
<10um: can progress to tracheal and bronchial bifurcation
<2um: can progress to bronchiole and alveoli
pulmonary intravascular macrophag
e
:
removes circ. particles, bacteria, endotoxin from ruminants (95%), cats, pigs (16%) , horses
Vulnerability to insult
(hematogenous)
entire CO of R ventricle goes into lungs 2. 9% total blood volume is w/in pulmonary vasculature 3. pulmonary capillary bed is LARGEST in body
Direct
extension
Direct through thoracic body wall
Rupture of caudal esophagus
Perforation of diaphragm
Parapneumonic spread of infex agents as sequel to bronchopnemonia or lung abscess rupture
Defense System/Barrier
Conduction/Transitional Components
mucociliary
clearance
: physical unidirectional movement/removal of deposited particles and gasses dissolved in mucus
provided by mucociliary blanket
main defense
mucus= barrier and vehicle. Water, glycoproteins, IG's, lipids, electrolytes. Produced by goblet cells, submucosal glands,
Air Exchange Component
phagocytosis from pulmonary alveolar macrophages
lack ciliated and mucus producing cells so mucociliary apparatus NOT available
alveoli main defense: phago via pulmonary alveolar macrophages, antimic molecules of alveolar lining fluid
pulmon alveoli macro's highly phagocytic
pneumoconiosis lung dz caused by deposition of dust: carbon (anthracosis)
commonly found in dogs: black dots on lung
rapidly attach and phago bacteria or other that reach alveolar lumens
lifespan short: few days -> continously replaced by new migrated blood monocytes
Oxidants/Free Radicals
ROS induce extensive pulmon injury; found in alveolar/bronchiolar epithelial cells/interstitium
Oxygen/FR scavengers = superoxide dismutase, Vitamins E/C: protect pulmon cells against damage
Damage caused by: inhaled oxidant gas (nitrogen dioxide), xenobiotic toxic metabolites (3 methyloide), free rads (ROS) rls by phago cells during inflam
Impaired defense leading to pnemonia
Viral Infections
5-7 days after viral infex, phago fxn of pulmon alveolar macro's and mucociliary clearance are impaired
Viruses known to predispose to secondary bacterial infex
Pigs/horses: influenza virus
Cattle: BRSV
Dogs: canine distemper
Feline: FeHV-1, FCV
Toxic Gases
Immunodeficiencies
Arabian foals w/ combined immunodeficiency dz easily succomb to infex dz (adenoviral pnemonia)
Corticosteroids, chemotherapies
