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Respiratory
System
ISHTIAQ 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 200 𝑚2
 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 THE
EXCHANGE 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

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Physiological, anatomical barriers of the respiratory system

  • 2. Structure & Function  Conducting system  Transitional system  Exchange system
  • 3.
  • 4.
  • 5.  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
  • 6.  Normal tracheal mucosa of dog
  • 7. 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
  • 8.  Alveolar area of human lung 200 𝑚2  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
  • 9.
  • 10. 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
  • 11. Portals of entry for injurious agents  Aerogenous  Hematogenous  Direct extension
  • 12.
  • 13. 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
  • 14.
  • 15.  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
  • 16.  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 
  • 17.
  • 18. 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
  • 19.  Rhodococcus equi can infect the intestines after being swallowed from the respiratory tract
  • 20.
  • 21. DEFENSE MECHANISMS OF THE EXCHANGE 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
  • 22.
  • 23.
  • 24. 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,
  • 25.  If liver kupffer cells are abnormally reduced then pulmonary intravascular macrophages are increased
  • 26.  Pulmonary alveolar macrophages
  • 27. 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
  • 28. 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
  • 29.
  • 30. TOXIC GASES  Hydrogen sulfide and ammonia
  • 31. Immunodeficiency  In humans AIDS, in pigs PRRS , Secondary pneumonia by Pneumocystis carinii  Steroids and alkylating agents cause immunosuppression
  • 32. Other cause of secondary infection  Uremia, endotoxemia, dehydration,· starvation, hypoxia, acidosis, pulmonary edema, anesthesia, ciliary dyskinesia, and stress.
  • 33.  Source: Pathological basis of the veterinary diseases by James F. Zachary and M Donald Mcgavin

Editor's Notes

  1. 1.Clara cells important for detoxification of xenobiotic 2. For human beings alveolar areas is equivalent to a tennis court
  2. These macrophages are present in the alveolar capillaries. In pigs 16 % of the alveolar capillaries are lined by macrophages and in ruminants 95 % of the intravenously injected particles are rapidly engulfed by these cells
  3. Porcine reproductive and Porcine reproductive and respiratory syndrome (PRRS) virus
  4. hypoxia and pulmonary edema decrease phagocytic function of pulmonary alveolar macrophages and alter the production of surfactant by type II pneumonocytes. Dehydration is thought to increase the viscosity of mucus, reducing or stopping mucociliary movement. Anesthesia induces ciliostasis with concurrent loss of mucociliary function. Ciliary dyskinesia, an inherited defect in cilia, causes abnormal mucus transport; starvation, hypothermia, and stress can reduce humoral and cellular immune responses.