resp notes good 1

Question 1

airway cells, and what they do

Answer 1

• trachea and bronchii: mainly of pseudostratified ciliated epithelium
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• Non-ciliated cells (named “club cells”) become more numerous than ciliated cells in the smaller airways
  > progenitor cells: replace demaged epithelium and
  > metabolize and detoxify chemicals and drugs in some species
  > secrete proteins that help to regulate the inflammatory response
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• no goblet cells or mucosal glands in the smaller bronchioles
• mucus secreting cells also secrete lysozyme, defensins, cathelicidins, and others

Question 2

what is BALT

Answer 2

Bronchus-associated lymphoid tissue (BALT) acts in the surveillance of inhaled antigens, as well as the effector responses of antibody production and cell-mediated mucosal immune responses

Question 3

type 1 and 2 pneumocytes - structure and function

Answer 3

Type I
- thin cells that cover 95% of the alveolar surface
- allow gas exchange and pump fluid out of the alveolus
- few defences against injury
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Type 2
- cuboidal cells at the corners of the alveolus
- progenitor cells: differentiate to type 1
- secrete surfactant lipids and proteins > reduces surface tension to allow dilation of the alveolus
- biotransform xenobiotics (including toxins) in some species (this can lead to toxic metabolites)

Question 4

alveolar macrophages
- functions
- where they come from? related cells and issues with inflammation?

Answer 4

• Self-perpetuating population of cells residing in the lung
• ingest and remove inhaled particulates
• recycle or degrade surfactant
• produce inflammatory mediators that generate a rapid response to infectious agents
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  But, infection in the lung causes neutrophils and monocytes to be recruited from the blood, and these monocyte-derived macrophages are more pro-inflammatory and capable of causing lung damage

Question 5

pulmonary function
- what it depends on

Answer 5

• gas exchange: O2 absorption and CO2 excretion.
• depends on:
• ventilation
• gas exchange
• perfusion

Question 6

factors affecting proper alveolar gas exchange

Answer 6

• Gases are exchanged across a barrier formed by type I pneumocytes, alveolar interstitium consisting of a fusion of the 2 basement membranes, and endothelium.
• This barrier can be thickened by:
• exudate in the alveolus
• “hyaline membranes” (cell and protein debris)
• thick cuboidal type II pneumocytes that have replaced damaged membranous type I pneumocytes,
• thickening of the alveolar septum with fibrous tissue

Question 7

lung perfusion - how is it affected by oxygen tension? consequences?

Answer 7

• Low oxygen tension in the alveoli triggers local pulmonary vasoconstriction, which serves to match blood flow to ventilation within individual acini
• By reducing blood flow to non-ventilated areas of lung, it prevents non-oxygenated blood from reaching the systemic circulation
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• However, widespread hypoxia—for example, due to high altitude or bronchiolar obstruction—may induce widespread vasoconstriction leading to increased resistance to blood flow through the lung, and consequent right heart failure.

Question 8

Endocrine functions of the lung

Answer 8

angiotensin metabolism and prostaglandin production

Question 9

Biotransformation of some toxins occurs in the lung. How?

Answer 9

Club cells and type II pneumocytes convert some chemicals and drugs to reactive intermediates, which are then detoxified to compounds that can be more easily excreted
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However, if these reactive intermediates cannot be adequately detoxified, they may react with membrane lipids and injure resident cells of the
lung.

Question 10

things that increase airway resistance

Answer 10

bronchoconstriction, exudates in the airway lumen, or edema and inflammation of airway wall

Question 11

Causes of hypoxemia

Answer 11

• Hypoventilation
• Impaired diffusion (alveolar septum affected)
• Ventilation-perfusion mismatching (non-oxygenated blood flows past the non-ventilated alveoli to reach the systemic circulation)
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• shunts

Question 12

lung multi-layered system of defence against infectious agents - components

Answer 12

• mucociliary clearance
• antibodies and innate defence proteins
• alveolar macrophages
• neutrophils

Question 13

result of infection that overwhelms mucociliary clearance and defence proteins in the lungs

Answer 13

• inflammation is triggered
• alveolar macrophages produce inflammatory mediators that recruit neutrophils and more macrophages to the site of invasion, and increase the production of antibacterial proteins by airway epithelial cells
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• his response has the potential to do harm:
• inflammatory exudates impair gas exchange
• leukocyte-derived enzymes and oxygen radicals cause injury to lung tissue
• repair processes organize alveolar exudates into fibrous tissue > permanently decreases lung compliance and thickens the blood-gas barrier

Question 14

Airway mucus contains many protective substances:

Answer 14

• Defensins, cathelicidins, lysozyme, complement, and lactoperoxidase cause direct damage to microbes.
• Immunoglobulin A blocks attachment of bacteria to mucosal surfaces.
• Immunoglobulin G, complement C3b, and surfactant proteins A & D opsonize bacteria and make them tastier for macrophages.
• Lactoferrin binds iron and makes it unavailable for pathogens.

Question 15

How are respiratory defences overcome?

Answer 15

• Aspiration pneumonia: exposure to an overwhleming number of bacteria.
• Viruses predispose to bacterial pneumonia by damaging the airway epithelium and reducing mucociliary clearance by reducing the secretion of antimicrobial peptides and by impairing the function of alveolar macrophages.
• Mycoplasma and Bordetella adhere to cilia and impair mucociliary clearance.
• Stresses and adverse climatic conditions are important causes of reduced lung defence. Stress reduces alveolar macrophage function and pulmonary immune responses, and inhibits production of antimicrobial peptides. Cold-stressed animals have reduced mucociliary function.
• Immunosuppressive drugs reduce pulmonary immune responses.
• Neutropenia deprives the lung of a major defence mechanism: neutrophils.
• Pollutants and toxic gases, for example in poorly ventilated or overcrowded barns, may reduce the ciliary function in airway epithelial cells.
• Genetic disorders are a rare cause of impaired lung defences. Ciliary dyskinesis: affected cilia lack the normal dynein arms, so ciliary beating is abnormal. Cystic fibrosis in children: altered ion exchange results in viscous airway mucus which cannot be adequately propelled to the pharynx.

Question 16

hyperemia of the lung - cause

Answer 16

• increased blood flow, leading to red discoloration
• occurs in inflammation

Question 17

lung congestion
- causes
- considerations
- vs hemorrhage and hyperemia?

Answer 17

• diffuse congestion: After death, venous blood often redistributes to the lungs. Interpret with caution!
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• localized area of red-purple lung: also firm? probably ante-mortem
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• Left heart failure > look at heart
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• hemorrhage is usually multifocal or patchy, rather than diffuse.
• Hyperemia and congestion cannot be distinguished in dead tissues.

Question 18

histologic sign of severe lung congestion:

Answer 18

• microscopic alveolar hemorrhage, with formation of hemosiderin-laden macrophages in the alveoli (“heart failure cells”)

Question 19

There are 4 general mechanisms of edema in the lungs (and any tissue):

Answer 19

• Increased permeability of the blood-air barrier.
  > As in other tissues, increased vascular permeability causes edema
  > Unique to the lung, the type I pneumocytes are also an important barrier to fluid movement from blood to alveolus. So in the lung, damage to either type I pneumocytes or to endothelial cells can both cause pulmonary edema
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• Increased venous pressure: left heart failure, or excessive administration of intravenous fluids.
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• Lymphatic obstruction: masses/tumours, etc. This is an uncommon mechanism of pulmonary edema.
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• Reduced oncotic pressure caused by hypoproteinemia (glomerular or intestinal disease). Although this is an important mechanism of edema in other organs, it usually does not cause edema in the lung

Question 20

impact of edema in the lungs

Answer 20

• fills alveoli and bronchioles, preventing ventilation of alveoli as well as gas diffusion
• disrupts the surfactant layer in the alveoli, increasing the surface tension, and reducing lung compliance

Question 21

lung hemorrhage gross lesion appearance

Answer 21

• foci or “splashes” of dark red-purple lung tissue (generally not a diffusely red-purple lung, vs congestion)

Question 22

Common causes of pulmonary hemorrhage

Answer 22

• exercise-induced pulmonary hemorrhage in racing horses
• lung trauma, lacerated vessels
• abscesses or tumours that bleed after they erode pulmonary blood vessels
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• Petechial or ecchymotic hemorrhages in the lung can result from thrombocytopenia, sepsis, or disseminated intravascular coagulation

Question 23

coagulation disorders - what type of hemorrhages do they generally cause?

Answer 23

eg. anticoagulant rodenticide toxicity
- usually cause body-cavity hemorrhages (eg hemothorax), subcutaneous hematomas, or intra-articular hemorrhage, but not petechial hemorrhages.

Question 24

consequences of pulmonary hemorrhage relate mostly to what?

Answer 24

relate more to blood loss, rather than compromised lung function

Question 25

thrombi vs emboli in the lungs - gross differentiation?

Answer 25

Thrombi that form in situ in the lung are usually not grossly visible, whereas emboli may be grossly visible

Question 26

when do thrombi form in the lungs?

Answer 26

in hypercoagulable states:
- glomerular disease with loss of antithrombin
- corticosteroid treatment or hyperadrenocorticism
- disseminated intravascular coagulation
- sepsis
- disseminated neoplasia.

Question 27

Pulmonary embolism may originate from:

Answer 27

• endocarditis of the right heart valves
• liver abscesses in cattle
• jugular thrombi as a complication of intravenous injection
• occasionally other unusual primary sites

Question 28

The functional importance of pulmonary thrombosis or embolism:

Answer 28

depends on the extent of vascular obstruction
- Minor thrombosis or embolism may result in pulmonary hemorrhages that are of no functional consequence
- Ischemia and infarction of the lung are more likely if thrombosis or embolism occurs at the periphery of the lung, or if the bronchial or systemic circulation is also impaired
- Emboli that obstruct a large proportion of the branches of the pulmonary artery may cause right heart failure or sudden death because of obstruction to flow

Question 29

atelectasis - what is it? gross appearance?

Answer 29

• failure of the lung (alveoli) to expand / inflate
• Gross appearance: The entire lung, or the affected lobules, are collapsed compared to normal, is reddened because capillaries are more closely spaced, and is rubbery and lacks the spongy texture of normal lung because of the absence of air.

Question 30

atelectasis causes

Answer 30

• Airway obstruction: air cannot enter alveoli, and trapped air is gradually absorbed. For example, in bronchiolar inflammation, neutrophils fill and obstruct the bronchioles, causing a lobular pattern of alveolar collapse.
• Compression of the lung: pleural effusions, pneumothorax, rumen tympany/bloat, diaphragmatic hernia.
• Surfactant dysfunction. Surfactant reduces surface tension in the lung and permits expansion of the alveoli. Animals that are born prematurely may not have produced surfactant yet, and their lungs may fail to inflate.
• Congenital atelectasis: lung inflates after birth, so atelectasis in aborted or stillborn animals is normal.

Question 31

overinflation vs emphysema of the lungs?
types of emphysema?

Answer 31

• Overinflation: excessive air distending alveoli. This is reversible if the cause can be corrected.
• Alveolar emphysema: enlargement of alveolar airspaces due to destruction of alveolar walls.
• Interlobular and bullous emphysema: air bubbles within the interlobular septa or subpleural connective tissue.

Question 32

Over-inflation or air trapping in the lungs, cause:

Answer 32

• partial airway obstruction
  > gas can enter the lung when the airways are expanded during inhalation, but the gas is trapped in the alveoli when the airways collapse during exhalation
• bronchiolitis, masses are common causes

Question 33

Interlobular and bullous emphysema cause

Answer 33

• destruction of alveolar septa with subsequent loss of gas into the interlobular tissue
• often the result of severe dyspnea due to interstitial lung disease (or other diseases, incl. non-resp)
• barometric trauma

Question 34

Alveolar emphysema - what is it? cause?
- related condition?

Answer 34

• rare in animals
• enlargement of airspaces results from destruction of alveolar septa, which is a permanent change
• unknown casues. Common in human smokers.
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  A related condition in dogs is the formation of bulla (large air bubbles due to destruction of alveolar septa), which can rupture and cause spontaneous pneumothorax and severe dyspnea

Question 35

pulmonary neoplasia - origin of most tumors

Answer 35

• mostly metastases from a distant site
• primary lung tumors uncommon in domestic animals
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  Metastatic lung tumours form multiple small nodules throughout the lung. In contrast, primary lung tumours usually cause one or a few larger masses. Note that primary lung tumors may metastasize within the lung before venturing to more distant sites, and such cases typically have a large primary mass and multiple small metastases.

Question 36

pulmonary carcinoma in cats, presentation

Answer 36

• the metastases, not the lung tumour, are frequently responsible for the presenting clinical signs
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• metastasizes to unusual places—footpad, skeletal muscle, bone, eye, or brain—and frequently invades through the pleura to cause pleural effusion

Question 37

The clinical manifestations of lung tumours result from:

Answer 37

• Lung failure from occupying space within the lung tissue
• Compressing an important structure such as the bronchus
• Invasion into the pleura, causing pleural effusion that leads to dyspnea
• Rupture leading to blood loss (hemangiosarcoma is a typical example)
• Metastasis (e.g. feline pulmonary carcinoma to the digit, described above)
• Systemic effects of malignancy: malaise, anorexia, weight loss
• Paraneoplastic syndrome: hypertrophic osteopathy, manifesting as periosteal new bone formation in the long bones