YR3 9 R HO1 Flashcards
Respiratory diseases common in
Production animals, less common in horses and companion animals
Upper Resp Tract components
Nasal cavity, sinuses, larynx, trachea, extra pulmonary bronchus, intrapulmonary bronchus
Lower Resp Tract components
Primary, secondary & tertiary bronchioles, resp. bronchiole, alveolar duct, atrium, alveolar sac, alveolus
Infection enter the lungs via
Inhales air or haematogenous route
Pulmonary Defence Mech
1)Nasal Turbinates - Turbulence, Particle deposition 2)Mucociliary apparatus 3)Inflammatory cells - Alveolar macrophages, BALT (Bronchial-associated Lymphoid Tissue), Inflammatory cells via bloodstream
Mucociliary Escalator funct & makeup
To remove trapped particles. Ciliated, pseudostratified columnar epithelium and goblet cells are found in the nasal cavity, trachea, and bronchi of lungs
Mucociliary Escalator process
Mucus, produced by Goblet cells, traps particles > Cilia moves trapped particulate matter: Out of nasal cavity towards nostrils or pharynx, Out of lung, up the trachea towards larynx to be swallowed. Mucus also contains IgA and lysozyme
Diseases which affect the cilia function
Immotile Cilia Syndrome (Cilia Dyskinesis) & Bronchiectasis
Immotile Cilia Syndrome (Cilia Dyskinesis)
Rare disease of humans and dogs caused by ultrastructural defects in cilia all over the body.
Results in rhinitis, bronchopneumonia, bronchiectasis
Bronchiectasis
Lack of cilia leads to retention of mucus + bacteria
Leads to inflammation which damages and weakens wall of bronchi > Dilation (ectasia) of bronchi
Alveolar macrophages properties
1)Front-line of defence 2)Phagocytose & kill microoraganism 3)Secret a variety of cytokines & enzymes 4)Repopulated from monocytes 5)Migrate to bronchioles & removed by mucociliary apparatus
Bronchial associated lympoid tissue
Alveolar macrophages, T cells and B cells
General lung disorders
1) Congestion and edema
2) Thrombosis and embolism
3) Infarction
4) Atelectasis
5) Emphysema
Pulmonary hyperaemia and congestion
Reddening of lungs due to increased blood in capillaries and larger vessels
Hyperaemia is an
Active process - part of acute inflammation
Congestion is
Passive - associated with reduced venous drainage (e.g. heart failure, barbiturate euthanasia)
Pulmonary hyperaemia and congestion is often combines with
Pulmonary Oedema
What is Hypostatic congestion
Accumulation of blood on one side of the lungs, due to gravity
Pulmonary oedema is
Wet, heavy, lungs due to fluid loss into airways
Causes of Pulmonary oedema
1) Increased hydrostatic pressure (e.g. left-sided heart failure > congestion of blood vessels)
2) Vascular endothelial injury > increased permeability (e.g. enterotoxaemia)
3) Injury to Type I alveolar epithelial cells (e.g. certain toxins and viruses)
4) Fluid overload
5) Barbiturate euthanasia
6) Decreased plasma oncotic pressure 7)Lymphatic obstruction
Pulmonary oedema clinical signs
Frothy fluid exuding from the nostrils, the trachea will be full of similar foam and the lungs will be wet and heavy.
Explain how Endocarditis of mitral valve cause congestion and oedema
Valves can’t close properly > during systole blood leaks back into the atrium & large pulmonary veins > eventually back up into alveolar capillaries > Congestion & Oedema
Damage to alveolar-capillary lining sequelae
1) Minor damage: fluid from leaks from vascular space into alveolar space
2) Moderate damage: fluid accompanied by protein (including fibrin)
3) Severe damage: fluid, protein, red blood cells (hemorrhage)
4) Acute Respiratory Distress Syndrome (ARDS)
Causes of decreased plasma oncotic pressure
1)Chronic nephritis - loss of albumin through damaged glomeruli 2)Liver cirrhosis - decreased production of albumin
Causes of Lymphatic obstruction
Metastatic melanoma of the lungs
Cause of Endothelial Injury
Heartworm aka Dirofilaria immitis. Adult worms irritate and obstruct branches of pulmonary artery
Pulmonary Embolism types
1) Thrombo-embolus originating elsewhere in vasculature
2) Septic (bacterial) embolus
3) Tumour cell embolus
4) Fat (bone marrow) embolus
Outcome of embolus
Infarcts, usually at the tip of the lobe (can ba avoided due to dual blood suppy to the lung) > (major blockage) acute onset of dyspnea secondary to massive hypoxia > death
Abnormalities of Inflation
1)Atelectasis vs. 2)Emphysema
Atelectasis definition
Incomplete expansion of pulmonary airways. Affected areas are dark red/purple and fleshy
Atelectasis types
1) Congenital - fetal lungs that have never been inflated
2) Acquired (alveolar collapse) - due to airway obstruction or compression of lungs
Causes of congenital atelectasis
1)Fetal stillbirth; no respiration, no lung inflation 2)Dystocia - Fetal hypoxia > Depression of Respiratory centers in CNS > Hypoinflation 3)Premature birth; lack of production of surfactant
Acquired obstructive atelectasis
Obstruction of distal airways due to 1)Inflammation 2)Parasites e.g. Aelurostrongylus
Acquired compressive atelectasis is due to
Pyothorax or Chylothorax
Pyothorax is
An accumulation of pus in the pleural cavity that can develop when bacteria invade the pleural space, usually in the context of a pneumonia.
Chylothorax is
Lymphatic fluid accumulating in the pleural cavity
Emphysema is
Permanent excess air accumulation in the lung
Emphysema types
1)Alveolar Emphysema - humans
Enzymatic destruction of alveolar walls results in excessive accumulation of air in the lungs
2)Interstitial Emphysema - ruminants
Forced expiration causes bronchiolar collapse resulting in alveolar rupture & leakage of air into interlobular septae
Interstial emphysema pathogenesis
Bronchopneumonia, acute interstitial pneumonia > Forced expiration > Bronchioles collapse > Air trapped distally in alveoli > Air filled alveoli rupture & air leaks into interlobular septae
