Week 6 Respiratory Flashcards
What is pulmonary surfactant made of? Who produces it?
30% protein; 70% lipid- produced by type II granular pneumocytes of the alveoli
What does surfactant do?
Lower the surface tension of the fluid lining the alveoli to prevent complete collapse of the alveoli on exhalation. Without surfactant, increased pressure would be required to inflate the alveoli at the next breath.
What impairs surfactant functions?
Presence of fibrinogen, oedema fluid, or aspirated amniotic fluid within the alveoli. Decreased secretion of surfactant may also develop if there is prolonged shallow respiration
How is lobulation in cattle and pigs?
Grossly obvious dividing of connective tissue septa of the lung into lobules. Well developed interlobular septa almost completely surround individual bronchopulmonary segments (the are of lung parenchyma ventilated by a tertiary bronchus)- these species have poor collateral ventilation– movement of air between adjacent lobules via the pores of Kohn= pores between adjacent alveoli. However, in disease, restricted movement of fluid, cells, molecules, and microbes between adjacent lobules. Inflammation may be restricted.
How is lobulation in cats and dogs?
Essentially no lobulation
How is lobulation in horses and small ruminants?
Intermediate lobulation
What are the pores of Kohn?
pores between adjacent alveoli
What can cause malformations of the lungs?
In utero infection with teratogenic agents (viruses like BVD)
What is Congenital Melanosis?
Multiple black foci of variable size randomly distributed throughout the lungs, liver, meninges, urterine caruncles. Incidental finding.
What is Foetal Pneumonia?
Foetal hypoxia in late gestation or during parturition–> relaxation of the anal sphincter–> defaecation into the amniotic cavity–> aspiration of meconium into the lungs–> IDed microscopically sometimes dark, red firm, lesions may be grossly visible, severe bronchitis or bronchiolitis may be present
What is Neonatal Hyaline Membrane Disease?
Hypothyroidsim or hypoarenocorticism can cause this in utero–> failure of type II pneumocytes to secrete functional surfactant–> increased surface tension–>collapse of alveoli and small bronchioles during expiration–> shear stresses during inspiration–> damage to type I pneumocytes and bronchiolar Clara cells (function of surfactant may also be impaired by presence of fibrinogen, oedema fluid, or aspirated amniotic fluid within the alveolar lumina)
Inaqequate surfactant–> diffuse pulmonary atelectasis, alveolar oedema, and intra-alveolar coagulation of fibrin to form hyaline membranes that line the collapse alveoli +/- small bronchioles–> dyspnoea from birth and hypoxaemia and sometimes cor pulmonale and right-sided heart failure
What is Pulmonary Atectasis?
Collapses or incompletely expanded lung parenchyma. Appears dark red to plum-coloured- depressed below aerated areas and has a fleshy or rubbery, non-spongy texture.
What is Congenital (Foetal) Atelectasis?
Partial or complete failure of the lungs to expand after birth e.g. stillborn animals, premature neonates with inadequate surfactant, neonates with brain stem injury, obstruction in the airways of neonates
What is Compression Atelectasis?
Collapse of previously aerated lung due to external compression. By pleural effusion, pneumothorax, diaphragmatic hernia, bloat, gastric dilation volvulus, severe ascites, masses (tumour, abscess)–> with pleural effusions atelectasis normally affects ventral potions of lung lobes due to gravitational pooling of the fluid.
What is Obstructive (Resorptive) Atelectasis?
Collapse of previously aerated lung due to complete airway obstruction (e.g. by exudate, parasites, aspirated foreign material, tumours, etc.). Air trapped within alveoli distal to the airway obstruction is gradually resorbed into the alveolar capillaries–> collapse of lung parenchyma–>persists then becomes permanent due to reduced vascular perfusion of collapsed lung–> local hypoxia, increased vascular permeability and oedema and eventually fibrosis. Most often seen in cattle and pigs because of their poor collateral ventilation- so blockage of a bronchiole could cause this) but not dogs and cats because complete blockage of a lobar would be necessary for them.
What is Hypostatic (Dependent) Atelectasis?
Atelectasis of the downside lung is common in large animals that are recumbent for prolonged periods (general anaesthesia); shallow ventilation, inadequate production of surfactant and pooling of secretions in airways on the affected side.
What is Alveolar Emphysema?
Abnormal and permanent enlargement of air spaces distal to terminal bronchioles (i.e. respiratory bronchioles, alveolar ducts, alveolar sacs, and/or alveoli) accompanied by damage to the alveolar walls. Can be caused by lung irritants. Proteases can damage alveolar walls- healthy lung has anti-protease defences but the function can be reduced in the prsence of reactive oxygen species.
What is Interstitial Emphysema?
Air within the interstitial connective tissues and lymphatics of the lung (of the interlobular septa, beneath the visceral pleura and around major blood vessels and airways). The air is derived from ruptured alveoli situated close to terminal bronchioles- tracks up the interlobular septato beneath the visceral pleura maybe to the lymphatics. Most often seen in cattle due to their well-developed interobular septa and poor collateral ventilation.
What species have a bronchus that supplies the right cranial lobe?
Ruminants and pigs
What is the problem with this pathologically?
predisposes the right cranial lobe to inhalation of foreign material (especially liquids) and to accumulation of inflammatory exudate
Poor collateral ventilation predisposes cattle and pigs to what?
Obstructive atelectasis, interstitial emphysema, and chronic suppurative bronchopneumonia
Why are alveolar type I (membranous) pneumocytes particularly vulnerable to oxidant injury?
Large surface area and low concentration of anti-oxidants
What happens with irreversible injury to type I pneumocytes?
Sloughing–> increased permeability of blood-air-barrier–> pulmonary oedema
What do type II (granular) pneumocytes do?
Produce pulmonary surfactant, metabolize xenobiotics (via cytochrome P450 enzymes), and help prevent pulmonary oedema by resorbing sodium ions and hence water from the alveolar lumina
What are some of the surfactant proteins?
Collectins that agglutinate and opsonise infectious agents. Bind bacterial endotoxin and have anti-oxidant activity.
What are the principal defenders of the alveoli?
Pulmonary alveolar macrophages. Can be impaired by viral infection for 5-7 days therefore predisposing lungs to secondary bacterial infection. Hypoxia and pulmonary oedema also compromise their phagocytic function.
Who has pulmonary intravascular macrophages? What do they do?
Ruminants, horses, pigs, and cats have PIM. They are responsible for phagocytosis of circulating bacteria and particulates.
What are pulmonary interstitial macrophages responsible for?
Phagocytosis of any inhaled particles that pass by endocytosis across type I pneumocytes into the alveolar interstitium
What are other types of cells that are present in the lower respiratory tract for protection?
Leukocytes can be recruited from the circulation and immune cells- dendritic cells are scattered in the pulmonary interstitium. They present antigens to naive T lymphocytes to prime them to become T helper cells. plasma cells in bronchus associated lymphoid tissue (BALT) produce antibodies.
What is pneumonia?
Inflammation of the lung parenchyma. 80% would have to be inflamed before death from respiratory failure occurs. Characterized by increase firmness of affected area- due to consolidation of the parenchyma- due to replacement of air by exudate +/- scar tissue (fibrosis).
What is pneumonia often triggered by?
Inhalation of viruses and bacteria.
What is the acute phase of pneumonia dominated by (aka red phase)?
Hyperaemia, oedema, exudation of neutrophils and degeneration and necrosis of type I pneumocytes.
What happens within 3 days of onset?
Alveolar injury with necrosis of type I pneumocytes, type II pneumocytes undergo mitotic division to repave alveolar basement membrane and differentiate into type I pneumocytes. widespread hyperplasia of type II pneumocytes can impair gas exchange–> hypoxaemia
What happens within 7 days of onset?
Hyperaemia of inflammation has subsided and affected parenchyma appears grey and firm. Exudate is slowly cleared by phagocytosis, epithelial repair continues, fibrosis may develop. (fish flesh appearance)
