Physiological, anatomical barriers of the respiratory system
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Transcript of Physiological, anatomical barriers of the respiratory system
Conducting system: Nasal cavity, paranasal sinuses, pharynx, larynx, trachea, bronchi
All lined by Pseudostratified ciliated columnar epithelium. Goblet cell and serous cells present.
Transition system: Bronchioles. Gradually ciliated epithelium disappears. Clara cells and neuroendocrine cells present.
Exchange: Alveolar ducts & alveoli. Lined by type-1(membranous)& type-2 (granular) pneumocytes
Why Respiratory system
vulnerable to injury
The extensive area of the alveoli, which
are the interface between the respiratory
system and inspired air
The large volume of air passing
continuously into the lungs
The high concentration of noxious
elements that can be present in the air
Alveolar area of human lung 200𝑚2
9000 L air inhaled daily
Alveolar area of equine lung 2000𝑚2
Susceptibility to blood borne insults
Entire output of right ventricle in the lungs
9 % of the total blood volume in pulmonary vasculature
Pulmonary capillary bed is 2400 km long in adult human being
Normal flora
Mannheimia (Pasteurella) haemolytica in
cattle
Pasteurella multocida in cats, cattle, and pigs
Bordetella bronchiseptica in dogs and pigs
Restricted to the most proximal (rostral) region
of the conducting system (upto larynx).
Thoracic region is sterile
Pulmonary defense sneezing, coughing, mucociliary transport,
and phagocytosis
Specific anatomy of nasal passage does not allow particles more than 10 µ to pass
Particles between 2-10 µ are trapped at tracheo-bronchial bifurcation.
Infective aerosols containing bacteria and viruses are within the size ranges (0.01 to
2 µm) that gain access to the bronchiolo-alveolar junction
Shape, length, electrical charge, and
humidity are important in retention and
pathogenecity of particles
Mucociliary mechanism is very important
for clearnce
A healthy human being produces around
100 ml of mucus per day
Each ciliated cell has around 250 cilia
Mucociliary transport in proximal (rostral)
airways is physiologically faster than that
of the distal (caudal) ones.
In impairment of ciliary movement or
excess mucous production coughing
become important for clearance
Cellular components
M cell : Modified epithelial cells lining the BALT
Macrophages, dendritic cell etc transport trapped antigen to BALT
Cellular and humoral response.
Antibodies produced by mucosal plasma cells (IgA, IgG, IgM) are important
BALT hyperplasia in chronic airway diseases
DEFENSE MECHANISMS OF THEEXCHANGE SYSTEM (ALVEOLI)
Phagocytosis provided by the pulmonary alveolar macrophages
Blood monocyte shift from glycolytic to oxidative aerobic metabolism in interstitium of lungs
Life span of alveolar macrophages in the alveoli is notably short, few days
Alveolar macrophages can kill most of the bacteria without inflammation except facultative pathogens e.g. Mycobacterium
Defense Mechanism
against blood borne
pathogens
In dogs, laboratory rodents, and human
beings, the hepatic (Kupffer cells), and
splenic macrophages remove circulating
pathogens.
While in ruminants, cats, pigs, and horses,
is mainly the pulmonary intravascular
macrophage,
If liver kupffer cells are abnormally
reduced then pulmonary intravascular
macrophages are increased
Defense against oxidative
stress
Damage is caused by inhaled oxidant gases e.g.,nitrogen dioxide, ozone, sulfur dioxide, tobacco smoke
Xenobiotic toxic metabolites e.g. 3-methylindole and paraquat
Free radicals released by phagocytic cells during inflammation.
Catalase, superoxide dismutase, and vitamin E protect against peroxidation
IMPAIRMENT OF DEFENSE MECHANISMS Viral agents: Secondary Pneumonia (viral-
bacterial synergism.)
Mechanism: viral infection impairs the phagocytic function of alveolar macrophages (5-7 day P.I.)
Examples of viruses predisposing to pneumonia: influenza virus in pigs and horses,bovine herpesvirus1,parainfluenza-3 ,and bovine respiratory syncytial virus in cattle and canine distemper virus in dogs
Immunodeficiency
In humans AIDS, in pigs PRRS , Secondary
pneumonia by Pneumocystis carinii
Steroids and alkylating agents cause
immunosuppression
Other cause of secondary
infection
Uremia, endotoxemia, dehydration,·
starvation, hypoxia, acidosis, pulmonary
edema, anesthesia, ciliary dyskinesia, and
stress.