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Semester 2 > respiratory 4 > Flashcards

respiratory 4 Flashcards

1
Q

What are the various functions of the mesothelial cells that line the pleural cavity

A

activated mesothelial cells are capable of:

1) phagocytosis (akin to macrophages)
2) they participate in pleural inflammation via production of cytokines
3) produce collagen and other proteins
4) activation of plasminogen to plasmin - fibrinolysis (and therefore protection against adhesion formation
5) also produce procoagulants that promote fibrin - less extent

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2
Q

What are the consequences of fibrin exudation into the pleural cavity

A

1) removed by phagocytosis - macrophages and activated mesothelial cells
2) 3-4 days post-injury, granulation tissue growing from the subserosal connective tissues will bridge between the parietal and visceral pleura
- adhesions may restrict movement of the lungs and chest wall but there is usually only minor interference with gas exchange and this diminishes over time as the adhesions stretch with continuous respiratory movements

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3
Q

what accumulates in the pleural cavity post mortem

A
  • serosanguineous (blood-stained watery) fluid that does not clot accumulates after death in the pleural cavity (and the peritoneal cavity and pericardial sac)
  • diffusion of haemoglobin from lysing red blood cells - red staining of the serosa and viscera
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4
Q

What are the clinical signs that might be observed in an animal with pleural disease

A

1) dyspnoea with laboured inspiration and a short effortless expiratory phase
2) auscultation and there may be dullness on percussion of the chest
3) compression of the cardiac atria - impaired venous return to the right heart and an obvious jugular pulse of increased amplitude
4) pleuritis - coughing, nasal discharge, rapid shallow guarded breathing
5) pleural pain - reluctance to move or lie down, uncomfortable

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5
Q

what are the possible causes of pneumothorax

A

1) rib fracture with tearing of the visceral pleura and lung parenchyma
2) blunt trauma to the chest
3) spontaneous pneumothorax - spontaneous rupture of lung lesion such as alveolar bullae

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6
Q

what does pneumothorax lead to

A
  • the positive intra-pleural pressure causes compression atelectasis (collapse) of the lungs -> dyspnoea and tachypnoea
  • severe bilateral pneumothorax can be life-threatening within minutes of onset
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7
Q

from where can air enter the mediastinum

A

1) tears in the trachea, bronchi, alveoli, oesophagus
2) bite wounds in neck in small animals
3) sudden change in intra-thoracic pressure caused by blunt chest trauma
4) coughing or excessive respiratory effort
5) rough placement of endotracheal tubes

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8
Q

what are the consequences of effusion into the pleural cavity

A
  • The longer the fluid is present the more likely the lung won’t recover to normal function
  • irrespective of the type of effusion, the excess fluid raises the intra-thoracic pressure and causes compression atelectasis of the lung parenchyma
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9
Q

What tests are usually performed on thoracocentesis samples

A
  • the aspirated fluid is subdivided into an EDTA tube (for total nucleated cell count, packed cell volume, total protein concentration and cytological examination) and a sterile plain tube (for aerobic and anaerobic culture)
    Characterises into transudate, exudate and modified transudate
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10
Q

what can cause haemothorax in domestic animals

A

1) most commonly chest trauma
2) bleeding intra-thoracic tumours (haemoangiosarcoma)
3) lungs lobe torsion
4) rodenticide anticoagulant poisoning

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11
Q

What does hydrothorax look like grossly and what would the fluid in hydrothorax be classified as on laboratory analysis?

A
  • the fluid may be watery or faintly cloudy or blood-stained (serosanguineous)
  • trasnduate - clear, colourless, odourless, non-degenerative neutrophils
  • modifies transudate - slightly turbid grossly and may vary in colour from yellow to white to pink-red
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12
Q

list 6 causes of hydrothorax in domestic animals

A

1) trasnudate most often severe hypoalbuminaemia OR
2) overhydrated animals - intravenous fluid therapy
3) right-sided congestive heart failure (all species)
4) left-sided congestive heart failure (small animals especially cats)
5) lymphatic or venous obstruction
6) lung lobe torsion

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13
Q

chylothorax is which species is it often diagnosed and what does it look like grossly

A

cats and dogs
- white or straw-coloured or pink-tinged, may form surface cream layer if allowed to sit, typically odourless unlike puss

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14
Q

list 5 causes of chylothorax

A

usually results from physical or functional obstruction of intra-thoracic lymphatics

1) chest trauma
2) severe coughing or vomiting
3) right-sided congestive heart failure
4) idiopathic
5) lung lobe torsion

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15
Q

what is the most common cause of pleuritis in the domestic animals, what route of entry and what cell type dominant

A

septic pleuritis

  • bacteria reach the cavity via the bloodstream or via direct extension from inflammatory foci in the lungs, penetrating injuries to chest wall and penetrating foreign bodies - hardwire disease
  • degenerative shift neutrophils (caused by bacterial toxins)
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16
Q

what are 4 causes of non-septic pleutritis in domestic animals

A

1) lobe torsion
2) feline infectious peritonitis (FIP) virus
3) chylothorax
4) sterile foreign bodies

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17
Q

what are the possible cdonsequences of pleuritis

A
  • accumulation of exudate in the cavity -> pulmonary atelectasis (especially ventrally) and, over time, pleural fibrosis
  • fibrous adhesions may form between the lobes of the lungs and/or between the lungs and the chest wall and between the lungs and the pericardial sac
  • severe fibrous adhesions may partially or completely obliterate the pleural space
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18
Q

what is the only neoplasm that arises from pleura and how is it expected to behave

A

mesothelioma - tends to implant over the serosal surface of the cavity (-> persistent effusion) rather than metastasising via blood

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19
Q

what other tumours can implant over the pleura and what class of pleural effusion is associated with intra-thoracic neoplasia

A
  • carcinomas, sarcomas involving lungs, mediastimun, chest wall
  • pure transudate but is more commonly a modified transudate or non-septic exudate
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20
Q

are tumours in the lungs more likely to be primary or secondary (metastases)

A
  • most are metastases from other sites

- the high prevalence of lung metastases reflects the rich pulmonary blood supply

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21
Q

What is the typical gross appearance of metastases to the lungs and what are common tumours that
metastasise to the lungs in domestic animals?

A
  • multiple nodules of comparable size randomly scattered throughout the lungs
    1) lymphoma - all
    2) haemangiosarcoma - dogs and cats
    3) malignant melanoma - horse
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22
Q

What are the two most common primary pulmonary tumours in domestic animals, what is their expected behaviour and which animals are most likely to develop one of these tumours?

A

1) bronchioloalveolar carcinoma, tend to arise out of periphery of the lung lobes and metastasise throughout the lung
2) bronchogenic carcinoma - tends to arise towards hilus of lung commonly metastasise to at least tracheobronchial lymph nodes
- dogs and cats

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23
Q

What is pulmonary adenomatosis (jaagsiekte) in sheep

A

pulmonary adenomatosis due to infection with oncogenic retrovirus, not in Australia or New Zealand

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24
Q

what are the two main reasons for increase respiratory effect and the 3 for no lungs sounds

A
  • Increase respiratory effect and rate
    1) Disease of pulmonary parenchyma
    2) Disease within the pleural space - fluid, air, blood
  • No lung sounds
    1) Fluid
    2) Air
    3) Displaced organ
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25
Q

what are some differentials that suggest septic pleuritis

A

○ Presence of neutrophils, macrophages, bacteria on the blood smear - septic
○ Also foul smelling and creamy coloured from thoracocentesis (between 7-8th intercostal space)
○ Fever - suggest inflammation
Radiograph - fluid in the pleural cavity - hypoechoic around the lungs not within the lungs

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26
Q

what made puss in boots in a critical condition and how to examine

A
  • Has in critical condition - increased respiratory effect and rate - cyanotic and oxygen saturation of 80%
  • Therefore we need to avoid struggling as only just maintaining at rest - decrease stress
    ○ Use sedation to calm
    ○ Also leave on the belly - if put on the side get one lung push against the other resulting in collapse of alveoli
  • Need to stabilise with oxygen delivery through the nose
  • Use ultrasound instead of radiograph and thoracocentesis to determine whether fluid, air etc.
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27
Q

what would cause an increase in urea, creatinine, total protein, albumin, globulin, USG, increase PCV without renal or liver problems and what may cause increase in glucose that is sustained

A

1) dehydration
2) Increase in glucose
- Pancreas produce insulin when increase glucose therefore in dehydration glucose up but pancreas should normalise it
- Actually related to the stress of the cat not the dehydration

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28
Q

List the 4 treatment for cat with dehydration and septic pleuritis

A

1) intravenous fluids
2) chest drainage
3) antibiotics
4) oesophagostomy tube

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29
Q

chest drainage where place, how often drain and what do you need to give

A
  • Give general anaesthetic
    Placement - towards 7-8th intercostal space - to avoid the heart
    ○ Pull skin tighter before place in so when let go the hole is further down creating tunnel under skin
    ○ Create tunnel and so no entrance of air into the chest if the tube is pulled out
  • Chest drain every 4 hours for 48 hours then every 8 hours
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30
Q

What is the normal rate of formation of pleural fluid in ml/kg body weight/day?

A

3ml/kg/d

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31
Q

What is the most common source of the bacteria seen in the pleural fluid from cats with pleural effusions

A

Parapneumonic extension of a respiratory tract infection

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32
Q

What clinical signs are suggestive of laryngeal disease

A 
inspiratory stridor (a high-pitched wheezing sound) or roaring caused by air turbulence through the narrowed laryngeal opening) and a change in the voice or loss of voice
○ stridor may be audible at rest or only during exercise or on laryngeal auscultation
- may gag or cough while eating
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33
Q

what clinical signs would be suggestive of tracheal disease

A

1) narrowing of extra-thoracic trachea - occurs during inspiration, inspiratory stridor
2) obstruction intra-thoracic thrachea - wheezing is usually loudest during early expiration
3) productive coughs sound moist and result in delivery of mucus, inflammatory exudate, oedema fluid or blood into the pharynx, followed usually by swallowing
4)

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34
Q

what clinical signs expect with bronchitis and bronchiolotis

A
  • in bronchitis and/or bronchiolitis, wheezes (due to airway narrowing) and crackles (akin to bubbles popping or paper being crumpled) due to oedema or exudate in the airways may be heard on chest auscultation
  • bronchiolotis often clinically silent
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35
Q

what are the possible consequences of a small epiglottis

A

Main issue in horses

1) predisposes to epiglottic entrapment, with the anterior margin of the epiglottis trapped below the aryepiglottic fold - exercise intolerance and chiefly expiratory obstruction to laryngeal air flow
2) intermittent dorsal displacement of the soft palate

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36
Q

In which animals is tracheal hypoplasia most often seen and what is characteristic of a hypoplastic trachea?

A

brachycephalic airway syndrome in dogs - English Bulldogs and Boston terriers
- the cartilage rings are smaller than normal and typically round in profile rather than C-shaped -> diffuse reduction in tracheal diameter and decreased air flow

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37
Q

what is a scabbard trachea

A
  • lateral flattening of the trachea into a narrow vertical slit -> decreased air flow
    • most common in dogs and horses
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38
Q

To what conditions does hypoplasia/dysplasia of bronchial cartilage predispose

A

predisposition to bronchiectasis (permanent dilation of the bronchi), alveolar emphysema and lung lobe torsion

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39
Q

What are possible causes of acute laryngeal oedema in domestic animals, why is this condition potentially life-threatening and where in the larynx is oedema most likely to be obvious grossly?

A

causes
1) acute laryngitis
2) acute phases of many systemic infections
3) prolonged barking
4) severe dyspnoea
Potentially life-threatening due to obstruction of air flow
Most prominent over the epiglottis and in the aryepiglottic folds and laryngeal ventricles

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40
Q

what is meant by the term layngeal collapse and which animals most likely to be affected

A

Obstruction of the laryngeal lumen

Component of brachycephalic airway syndrome in dogs and is a poor prognostic indicator in affected dogs

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41
Q

What is laryngeal hemiplegia in horses, what clinical signs do affected horses display and what is the aetiopathogenesis of this condition?

A
  • unilateral laryngeal paralysis (laryngeal hemiplegia
  • denervation atrophy of intrinsic laryngeal muscles, especially the left dorsal cricoarytenoid muscle -> inability to abduct the left arytenoid cartilage and vocal fold -> partial airway obstruction -> inspiratory stridor (“roaring”)
  • most cases are idiopathic - suspect genetic predisposition
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42
Q

which other species is laryngeal paralysis a common diagnosis and what are possible causes in this species

A 
Dogs 
- usually bilateral 
causes 
1) inherited forms - dalmatians 
2)  manifestation of a polyneuropathy or polymyopathy (disease affecting multiple muscles) such as hyperadrenocorticism
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43
Q

List 6 causes of laryngitis and tracheitis in the domestic animals

A

1) viral infection - canine distemper virus
2) bacterial infection - kennel cough or calf diphtheria - fusobacterium necrophorum - nectoric laryngitis
3) inhalation of smoke during fires
4) aspiration of feed
5) contact trauma associated with increased respiratory effort - e.g. laryngeal contact ulcers
6) parasites

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44
Q

what is honker syndrome in feedlot cattle

A
  • also known as tracheal oedema and haemorrhage syndrome or tracheal stenosis
  • characterised by at least partial luminal obstruction of the trachea by severe oedema +/- haemorrhage in the distal half of the trachea
  • if severe, can cause asphyxiation and sudden death
45
Q

What is meant by the term tracheal collapse and in which animals is it most often diagnosed

A

most often in middle-aged toy and miniature dog breeds
- characterised by dorsoventral flattening of the tracheal rings with widening and flaccidity of the dorsal trachealis muscle and connective tissue

46
Q

what are potential causes of segmental tracheal collapse

A

1) external compression (e.g. by tumours or enlarged cranial mediastinal lymph nodes)
2) peritracheal inflammation

47
Q

what are possible causes of bronchitis in domestic animals

A

1) viruses
2) bacteria (e.g. Mycoplasma spp.),
3) allergens, inhaled toxic gases or other irritants,
4) parasites (lung worm) (e.g. Oslerus osleri in canids)

48
Q

What are known triggers of chronic bronchitis in dogs and cats

A

chronic viral infection or chronic exposure to cigarette smoke, sulphur dioxide or other air pollutants, or dry air

49
Q

what are the structural changes that can lead to airway obstruction in bronchitis

A

airway obstruction in bronchitis is caused by a combination of luminal exudate, wall thickening by oedema, inflammation and/or fibrosis, and reflex bronchoconstriction mediated by smooth muscle contraction

50
Q

What causes bronchiectasis, what species most often seen and what does it look like grossly

A

consequence of chronic bronchitis
- especially associated with chronic bacterial bronchitis and bronchopneumonia
- always responsible for chronic coughing
- cattle with chronic bacterial bronchopneumonia and horses with heaves
grossly - formation of protruberant lumps or bosses in the lungs, with the lumps accentuated by atelectasis of the surrounding parenchyma

51
Q

List 5 reasons why are the distal bronchioles prone to injury

A

1) vulnerability of ciliated epithelial cells of the bronchioles to oxidative injury
2) lack of mucosal goblet cells and submucosal mucus-secreting glands so no mucociliary clearance
3) the steep decline in the velocity of air flow, allowing deposition of small inhaled particles (< 5 μm
4) lack of supporting cartilage in the bronchioles so the bronchioles are thin-walled and collapsible and vulnerable to direct spread of inflammation from adjacent alveoli
5) in some species, bronchiolar Clara (non-ciliated) cells possess cytochrome P450 enzymes and may generate toxic intermediate metabolites

52
Q

what are some causes of brnchiolitis in domestic animals

A

1) viruses - canine adenovirus 2, bovine parainfluenzavirus - 3
2) bacteria - mycoplasma
3) nematodes
4) inhaled allergens - cat and horses
5) inhaled noxious gas - ammonia
6) toxin metabolised by clara cells

53
Q

What are the characteristic microscopic changes that occur in acute and chronic bronchiolitis

A

acute - necrosis and sloughing of ciliated epithelial cells with mucosal erosion or ulceration and accumulation of exudate and debris in the lumina of the bronchioles
chronic - hypertrophy, hyperplasia and/or mucoid metaplasia of the mucosal epithelium

54
Q

what is bronchiolitis fribrosa obliterans

A

○ necrosis of the bronchiolar mucosa and luminal fibrin exudation is followed by ingrowth of granulation tissue from the submucosa from 7 days post-injury -> bridging of the lumen -> permanent obliteration of part or all of the lumen by scar tissue

55
Q

What is heaves in horses, what is its aetiopathogenesis and where internationally is heaves a common disease?

A

(previously known as chronic obstructive pulmonary disease
cause - stabled in poorly ventilated barns, decomposing wood shavings - inhalation -> widespread neutrophil- and mucus-rich inflammation of the distal bronchioles, possibly as a type 3 or 4 hypersensitivity reaction
common in Europe and North America, particularly in the winter or spring
- rare in Australia

56
Q

are tumours of the larynx or trachea common in domestic animals

A
  • primary tumours of the larynx or trachea are rare in the domestic animals
  • squamous cell carcinoma - the most common laryngeal tumour in dogs
  • lymphoma in cats arising in the cranial mediastinum may extend to involve the trachea
57
Q

What are the two arterial systems within the lungs, pressure, flow and what do they supply

A

1) bronchial arterial system - low flow, high pressure supply bronchi - oxygenated
2) pulmonary arterial system - high flow, low pressure - deoxygenated, alveolar capillary beds and distal bronchioles

58
Q

What are the drainage routes of blood and lymph

A

dual venous drainage routes from the lungs
○ the pulmonary veins drain the capillary beds supplied by the pulmonary artery -> left heart
○ the azygous veins drain the capillary beds supplied by the bronchial artery -> right heart
- the lungs are also drained by two sets of lymphatic vessels
1) superficial
2) deep bronchovascular

59
Q

What are the components of the blood brain barrier

A

1) monolayer of alveolar capillary endothelial cells
2) alveolar interstitium
3) attenuated mnolayer of epithelial cells - mainly type 1 pneumocytes - impeable to fluid
4) thin layer of surfactant-containing alveolar fluid

60
Q

Which cell type is capable of active resorption of sodium and hence water from the alveolar lumina, which cell type can similarly resorb water from the lumina of the bronchioles and What can impair this resorption mechanism and hence predispose to pulmonary oedema?

A

1) Type II pneumocytes as they have passive sodium channels on their luminal surfaces and Na+-K+-ATPase pumps on their basolateral surfaces
2) clara cells of distal bronchioles
3) enhanced by catecholamines and glucocorticoids but is impaired by hypoxia, reactive oxygen and nitrogen species (e.g. during inflammation), use of anaesthetics, malnutrition, and if the alveolar fluid is highly proteinaceous

61
Q

To where does the lymph formed within the lungs and visceral pleura drain and what encourages drainage of the lymph to this location (often against the force of gravity)?

A

The pressure within the interstitial tissues of the lungs is lower than the intra-alveolar pressure and becomes increasingly subatmospheric towards the hilus of the lungs
- this pressure differential promotes the rapid drainage of fluid via the deep bronchovascular interstitial lymphatics and the superficial pleural and interlobular lymphatics to the hilus of the lungs and the mediastinum

62
Q

what are the 4 main adverse effects of pulmonary oedema on respiratory function

A

1) oedema fluid flooding the alveoli and filling the lumina of terminal bronchioles prevents ventilation and gas exchange
2) reduced lung compliance so that increased effort is required to expand the lungs
3) in the presence of surfactant, the oedema fluid forms a stable foam by mixing with air; the foam further compromises ventilation
4) phagocytic function of alveolar macrophages is compromised due o alveolar hypoxia

63
Q

What are the two major mechanisms responsible for pulmonary oedema?

A

1) Increased Hydrostatic Pressure in Alveolar Capillaries

2) Increased Permeability of the Blood-Alveolar Barrier

64
Q

Increased Hydrostatic Pressure in Alveolar Capillaries what does it cause, where does it accumulate, type of protein concenration and examples that cause this

A

Pulmonary oedema
overloading of the drainage sump -> initial accumulation of oedema fluid in the bronchovascular interstitium
low protein and generally pale pink
1) left-sided congestive heart failure
2) gravitional pooling of blood in dependent areas of the lungs - large animals recumbent

65
Q

Increased Permeability of the Blood-Alveolar Barrier what does it cause, where does it accumulate, type of protein concentration and examples that cause this

A

direct movement of fluid from the alveolar capillaries into the alveolar lumina -> high risk of fatality (“acute respiratory distress syndrome” or ARDS)

  • typically high protein
    1) inflammation of lung parenchyma
    2) direct damage to alveolar capillary endothelium - ureamia, clostiridal toxins, anaphylaxis
66
Q

List 6 less common mechanisms responsible for pulmonary oedema

A

1) hypoalbuminaemia
2) lymphatic obstruction
3) neurogenic pulmonary oedema
4) acute upper airway obstruction - strangulation
5) impaired active transprt of alveolar fluid - direct damage tot type 11 pneumocytes
6) lack or inhibition of surfactant

67
Q

What are the characteristic gross features of pulmonary oedema

A
  • watery fluid oozes from the cut surface
  • subpleural and interstitial tissues of the lungs are distended
  • moderate to severe oedema, stable frothy foam (produced by admixture of oedema fluid, surfactant and air bubbles) is present in the lumina of the trachea
68
Q

What happens in the lungs if an animal survives pulmonary oedema into the chronic phase

A
  • with chronicity, pulmonary oedema leads to interstitial fibrosis so the lungs may feel firmer than normal and may not be obviously wet
69
Q

What is the most common cause of pulmonary congestion in domestic animals and what is the characteristic gross appearance of pulmonary congestion in the acute and chronic phases of this condition?

A

Left-sided congestive heart failure
Acute - congested lung parenchyma appears dark red-purple (cyanotic) and is heavier than normal
there is usually accompanying pulmonary oedema due to increase hydrostatic pressure
Chronic - fibrosis of alveolar septa and accumulation of haemosiderin pigment by alveolar macrophages, the lungs may be grossly discoloured tan brown “bronzing”

70
Q

List 3 other possible causes of pulmonary congestion

A

1) prolonged recumbency in especially cattle and horses (with gravitational pooling of venous blood in the downside lung) (hypostatic congestion)
2) lung lobe torsion
3) euthanised by intravenous injection of barbiturates and can only be distinguished from genuine ante mortem congestion and oedema by histopathology (lysed RBCs found with euthanasia)

71
Q

What causes active hyperaemia of the lungs and what does this look like grossly?

A
  • prominent during the acute to subacute phase of lung injury and inflammation
  • lungs are grossly bright red due to arteriolar vasodilation, may be some accompanying pulmonary oedema
  • usually subsides within 7 days
72
Q

List 5 possible causes of haemorrhage into the lungs of animals?

A

1) blunt chest trauma
2) penetrating injuries - rib fracture
3) bleeding lung tumours (haemangiosarcoma)
4) bacteriaemia, septicaemia
5) excercise induced pulmonary haemorrhage in horses

73
Q

Outline the aetiopathogenesis of exercise-induced pulmonary haemorrhage of horses and how
common is this condition?

A

Results from rupture of alveolar capillaries
1) stress-induced, due to an exercise-induced increase in transmural pressure (i.e. the pressure difference between the lumen of the capillary and the alveolar space)
2) strenuous exercise in horses -> a marked increase in pulmonary arterial and hence alveolar capillary pressure
Overall marked decrease in negative pleural pressure resulting in rupture
- Thoroughbred and Standardbred racehorses (> 80%) have episodes of bleeding into the lungs during vigorous exercise

74
Q

How would you know if a horse is affected with exercise-induced pulmonary haemorrhage, where in the lungs are
the lesions located and what do they look like grossly

A
  • minor, subclinical and only detectable by finding blood in the trachea and/or bronchi via endoscopy after exercise
  • more severe epistaxis after excercise
  • typically into dorsocaudal areas of the diaphragmatic lung lobes (more pulmonary blood to these areas during high excercise
    Grossly - acute - dark-red black and blood oozes from cut surface, chronic - gross tan-brown discolouration
75
Q

What are the possible consequences of obstruction of pulmonary arterial blood flow to the
lungs and Provide some examples of circumstances in which pulmonary arterial obstruction can
develop.

A

1) medium to small branch then no adverse effects healthy animal unless already compromised
2) sudden obstruction of ≥ 60% of pulmonary arterial flow, sudden death from cor pulmonale and cardiogenic shock
Causes
1) parasitism - heart worm
2) jugular vein thrombosis
3) pulmonary vasculitis - Hendra virus
4) hyperadrenocorticism - via corticosteroid-induced release of plasminogen activator inhibitors inhibition of fibrinolysis

76
Q

gross appearance of a pulmonary infarct

A
  • cute phase as red to black, swollen, firm wedges of tissue located at the periphery of the lung lobes, with a film of fibrin over their pleural surface
  • non-fatal heal via fibrosis
77
Q

In which animals is lung lobe torsion most often diagnosed, what are predisposing causes and
What are the consequences of lung lobe torsion?

A
  • most often diagnosed in dogs, especially deep-chested breeds
  • often idiopathic but predisposing causes include neoplasia, pneumonia or atelectasis
  • congestion and oedema -> ultimately venous infarction
78
Q

List 5 causes of pulmonary hypertension

A

1) heart worm in pulmonary arterial bracnhes
2) congenital cardiac anomalies such as PDA, large atrial or ventricular septal defects
3) severe pulmonary arterial thrombosis
4) severe pulmonary atelectasis
5) metabolic acidosis via vasoconstrction of pulmonary arterioles

79
Q

What is high altitude disease of cattle? Briefly outline its aetiopathogenesis.

A

“brisket disease”

  • caused by failure of the cardiorespiratory system of cattle to adjust to hypoxia of high altitudes
  • ○ hypoxaemia -> sustained vasoconstriction of the small pulmonary arteries and arterioles -> chronic smooth muscle hypertrophy and increased pulmonary vascular resistance -> pulmonary hypertension -> cor pulmonale +/- right-sided congestive heart failure
80
Q

What are possible causes of inspiratory effect, expiratory effect and both

A

Inspiratory effort
- Resistance to air-filling of lungs
• Upper airway (also stridor)
• Fibrosis - alveoli themselves - lungs cannot expand
• Pleural space disease
Expiratory effort
- Resistance to expulsion of air from constricted bronchi
• Asthma - mainly in cats, chronic obstructive pulmonary disease in horses
Inspiratory and expiratory effort
- Wet, heavy lungs
• Oedema, pneumonia etc.

81
Q

What non-thorax disease may result in dyspnoea

A 
Pyrexia
– Anaemia
– Acid-base imbalance
– Fear/anxiety
– Pain
– Abdominal disease
82
Q

Vesicular sounds where best to hear

A
  • over large airway (trachea)
    Expiratory = Inspiratory normally
    Inspiratory sounds softer towards periphery
    Lower airways - can only hear sound travelling towards stethoscope
83
Q

What occurs with vesicular sounds if have fluid filled bronchioles and when else may this occur

A
  • Just have one large lung, area not attenuated so sounds louder towards periphery
  • If overweight or heavy coat can lead to problems with hearing breath
84
Q

When are wheezes and crackles normally heard and cause

A

Wheezes
- Loudest during expiration - caudo-dorsally generally
- Often loudest ventral as compressed airways sink to the bottom - diffusing with asthma
• Crackles
- Loudest during inspiration
Pneumonia and oedema

85
Q

Trans-tracheal aspirate what animals use on, potential issue, where introduce and how

A
  • Medium to large dogs
  • Often contaminated by pharyngeal flora
  • Palpate cricothyroid ligament
  • First depression above cricoid cartilage (there is a notch)
    1) Stabilise trachea when pushing needle through, then thread catheter down
  • Do not do for small dog or cat as needle likely to hit something else
    2) Catheter will induce coughing
    3) Inject 2-3 warm saline boluses and aspirate back
    4) Submit for cytology and culture
86
Q

Endotracheal tube what animals use on, what require, what good for and what not good for

A

cats and small dogs
required GA and sterile ET tube
- good for localised disease however may not get small bronchi or alveoli sample

87
Q

Bronchoalveolar lavage what involve, what need, what good for

A
  • endoscopic
  • need pre-oxygen and monitoring afterwards
  • great for localised disease processes and visually assess airways
88
Q

What are the 2 more invasive tests of the respiratory system

A 
Trans-thoracic needle aspirate/biopsy
- Good for exfoliative lesions
- Good for masses close to chest wall
- Blind or US guided
• Thoracotomy
- Cut out of the mass and tumour 
- Good if possibly curative as well
89
Q

Thoracocentesis what use and where put in

A

Butterfly catheter with 3- way tap and local anaesthetic
- Prevent air being put back into chest as emptying the needle
• Cranial border of ribs
- Costal artery runs along the caudal border, don’t want to haemorrhage

90
Q

How get lateral view for Dyspneoic patients

A
  • May not be able to be placed safely on its side
  • Therefore take a horizontal bean lateral view
    ○ shift X-ray machine to the side of the patient so animal still in sternal rucumbency
    ○ prop cassette up aside the patient
    quality is decreased a little
91
Q

Describe the correct positioning of a patient in lateral and VD view

A

lateral view
- Stretch forelimbs forward
○ Weigh down with sandbags if need be
- Form wedge used to lift up dog - allowing sagittal plane of dog to be parallel with the table ensuring easy and accurate interpretation
VD view
-Use form wedges on both sides of the patient to restrain
○ Avoid manually retraining dogs when possible as staff will be more exposed to radiation
- Palpate the sternum - ensure the dog isn’t rotated to ensure correct lining of the dog

92
Q

At what point during respiration due you want to take radiograph, why and how to tell and where want lesion taken

A

on maximal inspiration
- lungs well aerated providing contrast for lung pathology
Well inflated lungs cura intesect vertebrae at T13, underinflated lungs at T9
- lesion on lateral projection in uppermost corner - contrast, Left lobe easier to see on Right view

93
Q

Mediastinal shift what view best seen and what occurs

A

best seen on VD/DV view

1) Atelectasis
- reduced lung volume
- causes a mediastinal shift TOWARD the affected side
2) Mass
- increased volume
- causes a mediastinal shift AWAY from affected side

94
Q

What are the 3 compartment of the lung

A

1) alveolar
2) Interstitial - connective tissue and blood vessels between the alveoli
3) bronchial

95
Q

Trachea position and opacity

A

Position
- Should deviate away from spine as move towards lung
Opacity
- Radiolucent, margins seen should deviate away from spine

96
Q

Distribution approach to assessing pulmonary parenchyma and examples

A
  • Cranioventral
    • Caudodorsal
    • Diffuse
    • Focal
    • Multifocal
      Aspiration pneumonia usually cranioventral
      Cardiogenic pulmonary oedema is usually caudodorsal and perihilar
97
Q

Interstital pattern within lungs

A
  • Hazy increase in opacity
  • Can see vessels but not as clearly
    Usually in conjunction with other patterns
98
Q

Alveolar pattern within lungs

A
  • Increase in opacity
  • Cannot see vessels
  • More severe lobar boundary - clear distinction between affected and unaffected lobule
99
Q

Bronchial pattern within lungs and vascular pattern

A
  • Increase thickness of bronchial wall
  • Tram tracks and doughnuts
    Vascular
  • Normal artery and vein similar diameter
  • VD view: width caudal lobar vessel = 9th rib
    If larger suggest pulmonary arterial dilation
100
Q

List some radiographic characteristics of pleural effusions

A
  • Interlobar fissures - soft tissue opacity
  • Leafing of lung lobes - curved margin of lung that floats back from thoracic wall due to accumulation of fluid
  • Border effacement
  • Rounding of costophrenic angle
  • Best seen on VD view
101
Q

List some radiographic characteristics of pneumothorax

A
  • Retraction of the lung lobes
  • Separation of the heart from sternum
  • Interlobar fissures of gas
102
Q

What are the different codes for CPR when patient admitted

A

1) DNAR - Do Not Attempt Resuscitation - red
2) External CPCR - orange
3) Open Chest CPCR - green

103
Q

Compressions CPR for dogs what is important

A
  • Chest compressions must be continuous, uninterrupted for at least 2 min with interruption of less than 10 seconds.
  • performed with the patient in right lateral recumbency, on a firm surface at a rate of 100 to 120 compressions per minute.
104
Q

What are two mechanism used in compression for CPR, what weight each used and mechanism

A

1) Heart Pump:
- Smaller animals ( <10 Kg)
- Compression of the ventricles causes blood to flow
- Backward flow prevented by AV valves
2) Thoracic pump:
- Dogs ( >10-15 Kg)
- Increase in thoracic pressure causes blood to flow
- Backward flow prevented by collapse of the great veins and presence of valves

105
Q

CPR - what to do with airway

A
  • Cuffed endo-tracheal tube should be placed to maintain the airway open.
106
Q

CPR - breathing how, at what rate

A
  • Intermittent positive pressure ventilation (IPPV)
  • deliver 100% oxygen
    Rate of 10-12 breaths per minute
107
Q

When use CPR and when use defibrillatory

A

CPR - Asystole - myocardium stops contracting

Defibrillaion - ventircular fibrillation - not coordination between cells

108
Q

What is the major problem with patients who return with CPR

A

care should be continued after the return to a normal cardiac rhythm as still 50% of the patients will be likely die from a sepsis-like syndrome (including coagulopathy, immunologic dysfunction and multiple organ failure) due to reperfusion injury.

109
Q

What IV fluid therapy is important for after CPR

A

1) crystalloids
2) hypertonic slaine
3) epinephrine
4) vasopression
5) atropine

Semester 2 (17 decks)

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