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Respiratory System ISHTIAQ AHMED

Physiological, anatomical barriers of the respiratory system

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Respiratory

SystemISHTIAQ AHMED

Structure & Function

Conducting system

Transitional system

Exchange 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

Normal tracheal mucosa of dog

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

Portals of entry for injurious

agents

Aerogenous

Hematogenous

Direct extension

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

Rhodococcus equi can infect the

intestines after being swallowed from

the respiratory tract

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

Pulmonary alveolar macrophages

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

TOXIC GASES

Hydrogen sulfide and ammonia

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.

Source: Pathological basis of the

veterinary diseases by James F. Zachary

and M Donald Mcgavin