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Semester 2 > respiratory 5 > Flashcards

respiratory 5 Flashcards

1
Q

What radiographic features are consistent with feline bronchiolar disease

A
  • Tram tracks and donuts present - bronchiolar - bronchioles and small bronchi - inflamed
  • Hyper inflated lungs - larger darker areas - unable to get the air out of the lungs - obstruction
  • Suggests thickened bronchioles
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2
Q

What are some clinical signs for feline asthma and what are some other causes and how to rule out

A
  • wheeze on expiration
  • coughing - could be feline lungworm (also close airways and eosinophils), bacterial bronchitis and neoplasia - rule out with Broncho-alveolar lavage
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3
Q

List the two main treatment options in terms of drugs for feline asthma

A

1) Bronchodilations - relievers
- beta-2 adrenoceptor agonists
2) Anti-inflammatory - prevents
- Long-term administration - problem with immune systems
More effective together - give both - synergistic

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4
Q

What would you administer to a patient that was having an emergency asthma attack

A

1) Oxygen - hoping that some will go in
2) Beta-2 adrenoceptor agonist
Corticosteroids - more long-term not really in emergency

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5
Q

What cells produce surfactant and when does surfactant production commence

A

Type II pneumocytes and some surfactant lipids may be produced by Clara cells of the distal bronchi
- production commences late in foetal life

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6
Q

What happens to surfactant to prevent its accumulation in the lungs

A

surfactant can be recycled by type II pneumocytes or degraded by alveolar macrophages

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7
Q

What is the major function of surfactant and its other functions

A

1) Lower the surface tension of fluid lining alveoli to prevent complete collapse
2) opsonise infectious agents
3) bind endotoxin and have anti-oxidant activity

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8
Q

What impairs surfactant function or secretion

A
  • function of surfactant may be impaired by the presence of fibrinogen, oedema fluid or (in neonates) aspirated amniotic fluid within the alveoli
  • decreased secretion of surfactant may also develop if there is prolonged shallow respiration
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9
Q

What domestic animals have grossly obvious lobulation of the lung and what is the functional significance of this

A

Grossly obvious in cattle and pigs
- as a result species have poor collateral ventilation (movement through pores of Kohn) in health
Benefit - inflammation may be restricted to individual lobules in disease

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10
Q

In which species is congenital melanosis of the lung seen and significance

A

piglets and young ruminants

- incidental and fade over time

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11
Q

What is foetal pneumonia and what are some causes

A
  • foetal hypoxia in late gestation or during parturition -> relaxation of the anal sphincter -> defaecation into the amniotic cavity -> yellow-green staining of the amnion and foetal skin +/- aspiration of meconium into the lungs
    1) foetal hypoxia
    2) bacterial or fungal infections
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12
Q

What is neonatal hyaline membrane disease

A

1) failure of type II penumocytes to secrete surfactant
2) increase surface tension so collapse of alveoli
3) sheer stress during inspiration
4) damage to type I pneumocytes and clara cells
5) decrease surfactant
6) diffuse pulmonary atelectasis
7) alveolar odeme and fibrin - hyaline membranes form
8) dyspnoea from birth

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13
Q

What are the major mechanisms responsible for atelectasis in domestic animals

A

1) congential ateletctasis
2) compression atelectasis
3) Obstructive atelectasis
4) Hypostatic (Dependent) Atelectasis - downside of lung recumbent for prolonged periods

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14
Q

What happens to atelectatic lung if the cause is not removed

A

may become permanent due to reduced
vascular perfusion of the collapsed lung -> local hypoxia, increased vascular permeability and oedema, and eventually fibrosis

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15
Q

What causes alveolar emphysema, why it is common in humans and is it common in animals

A

caused by exposure to other lung irritants (e.g. in coal miners), chronic bronchitis, bronchiolitis or bronchopneumonia, inherited α1-protease inhibitor deficiency, or pancreatic necrosis with release of activated proteases into circulation
Common in humans due to cigarette smoking
Rare in domestic animals, prominent in horses with heaves

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16
Q

What does alveolar emphysema look like grossly and what is the effect on respiratory function

A

appear crepitant, pale pink, bubbly or puffy and are raised above adjacent normal parenchyma
○ when severe, the air bubbles in damaged alveoli may coalesce to form large bullae (bullous emphysema)
○ spontaneous rupture of bullae -> pneumothorax
- emphysematous lung parenchyma is dysfunctional

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17
Q

What is the difference between alveolar emphysema and hyperinflation of alveoli

A

in hyperinflated lungs, there is no accompanying damage to alveolar walls (c.f. alveolar emphysema)
- hyperinflated lungs are just post mortum change due to gas trapping

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18
Q

interstitial emphysema which species most often seen and why, where can air in pulmonary interstitium track

A

most often seen in cattle, probably due to their well-developed interlobular septa and poor collateral ventilation
-○ the air tracks up the interlobular septa to beneath the visceral pleura
it may also track along lymphatics to bronchial and mediastinal lymph nodes

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19
Q

What are the normal functions of pulmonary alveolar macrophages, how are they replaced over time and what factors can compromise their phagocytic function?

A

1) rapid phagocytosis - inhaled particles, bacteria, prevent accumulation of surfactant
2) regulatory cell by releasing cytokines and other molecules
Replaced (short lifespan) by recruitment of monocytes from circulation or mitotic division of interstitial macrophages
Impaired via viral infections, hypoxia and pulmonary oedema

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20
Q

What are the characteristic gross general features of pneumonia

A

characterised by increased firmness of the affected lung parenchyma on gentle palpation
§ this change in texture is referred to as consolidation of the parenchyma and is due to replacement of air by exudate +/- scar tissue (fibrosis)
- may also have rubbery texture

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21
Q

Outline the difference between the acute red phase and chronic grey phase of pneumonia

A

Acute red phase - dominated by hyperaemia, oedema, exudation of neutrophils, and degeneration and necrosis of type I pneumocytes
Chronic grey phase - during this phase, exudate is slowly cleared by phagocytosis, epithelial repair continues and fibrosis may develop
○ atelectasis contributes to the gross pale grey “fish-flesh” appearance of the lung

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22
Q

What is meant by the term bronchopneumonia (lobular pneumonia) and what are its typical gross features?

A
  • inflammation is centred on the junction of the distal bronchioles and alveoli
  • cranioventral parts of the lungs due to the short and abrupt branching patterns of the distal airways in that location and the drop in air velocity in the distal airways -> gravitational settling of small aerosolised pathogens and gravitational pooling of exudate
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23
Q

List 3 causes of bronchopneumonia and exception to gross appearance rule

A

Mainly inhalation of bacteria

1) E.coli
2) Strep and Staph
3) nematode (lungworm) - cranioventral distribution

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24
Q

What is meant by the term lobar pneumonia (fibrinous pneumonia) and what are its typical gross features?

A
  • essentially fulminant (severe and rapidly progressive) bronchopneumonias -> consolidation of large areas of lung parenchyma (one or more entire lobes)
  • commences at the junction of distal bronchioles and alveoli, especially in cranioventral parts of the lungs
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25
Q

List 3 causes of lobar pneumonia (fibrinous pneumonia)

A

1) Mycoplasma - cattle
2) APP - dorsocaudal lesions
3) pasteurella multocida

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26
Q

Why do many animals affected by a lobar pneumonia often die despite the fact that the inflammatory process may only involve less than 50% of the lung parenchyma

A

toxaemia (i.e. absorption of bacterial toxins into the general circulation)

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27
Q

What is meant by the term bronchointerstitial pneumonia, what are its typical gross features and how is this type of pneumonia distinguished from a bronchopneumonia

A

resemble classical suppurative bronchopneumonias in that inflammation is typically restricted to cranioventral areas of the lungs and is induced by inhalation of pathogens that localise to the junction of the distal bronchioles and alveoli
microscopically, however, there is extensive injury not only to the distal bronchioles but also to the alveolar walls

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28
Q

List 3 causes of bronchointerstitial pneumonia

A

1) parainfluenza viruses
2) coronavirus
3) mycoplasma - most common

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29
Q

What is enzootic pneumonia of calves, lambs and pigs and what are the characteristic features of chronic enzootic pneumonia

A

enzootic - endemic

  • typically develops at waning of maternal immunity
  • a bronchointerstitial pneumonia with homogeneous grey consolidation and atelectasis of cranioventral areas of the lungs (“fish flesh” appearance)
  • usually caused by viral infection
30
Q

What is meant by the term interstitial pneumonia and which cells in the lungs may be targeted in an interstitial pneumonia and what is the most common route of injury?

A

diffuse or patchy injury to the walls of the alveoli

  • the primary insult may be to the vascular endothelium of alveolar capillaries, to type I pneumocytes or (occasionally) to type II pneumocytes
  • most interstitial pneumonias are haematogenous in origin but some can be aerogenous
31
Q

what are the typical gross features of an interstitial pneumonia

A
  • heavy, wet and rubbery due to pulmonary oedema rather than firmly consolidated
  • usually the entire lungs are involved to some extent, although lesions may be more pronounced in dorsocaudal areas
  • may be pronounced interstitial emphysema (especially in cattle)
32
Q

List 4 causes of acute interstitial pneumonia in domestic animals and why do many animals die in the acute phase of interstitial pneumonia

A

1) infectious agents in circulation - Hendra virus
2) parasites - toxoplasma gondii
3) inhalaed toxins - smoke, ammonia fumes, nitrogen dioxide
4) aspiration of gastric acid in monogastric animals
- many animals die due to (acute respiratory distress syndrome (ARDS)) due to pulmonary oedema and hypoxaemia

33
Q

List 3 causes of chronic interstitial pneumonia in domestic animals

A

1) infectious agents - bacteria myoplasma
2) parasites - heartworm, lungworm (cat)
3) ingested plant-associated toxins or precursors - pyrrolizidine alkaloids in horses

34
Q

What is fog fever (acute interstitial pneumonia) of cattle? Briefly outline its aetiopathogenesis

A
  • also known as acute bovine pulmonary oedema and emphysema
  • sudden onset of severe dyspnoea within 4-10 days of pasture access
  • metabolism of L-tryptophan in rumen, spread to lungs, metabolised type II to toxic metabolite - necrosis of bronchiolar epithelium
35
Q

List 3 causes of multifocal pneumonia in domestic animals and how do the causal agents reach the lungs

A

1) suppurative - strep
2) granulomatous - inhalation of fungi or bacteria - aspergillus, mycobacterium
3) haemotogenous parasitism - cestodes (tapeworms - Echinococcus granulosus
- enter via bloodstream (embolic pneumonia) or inhalation

36
Q

What is meant by the term aspiration pneumonia and what are some conditions that can predispose to aspiration pneumonia?

A
  • inflammation caused by inhalation of foreign material mainly liquid
  • predisposed to by force feeding, pail feeding of milk, vomiting, regurgitation, dysphagia, anaesthesia, cleft palate or laryngeal dysfunction/paralysis
37
Q

What are the possible adverse consequences of aspiration of gastric contents in a monogastric animal

A

sudden death due to laryngeal spasm, acute diffuse pulmonary oedema, or a vagal reflex that causes bradycardia or asystole

38
Q

What is the likely outcome in a herbivore of inhalation of ingesta (or aspiration of a drench intended for the stomach/rumen)?

A

a severe and usually fatal gangrenous lobar pneumonia because of the presence of putrefactive bacteria

  • affected gangrenous areas of lung are discoloured blue-green-black, malodorous, crepitant with gas bubbles
  • accompanying fibrinosuppurative to haemorrhagic pleuritis
39
Q

What is endogenous lipid pneumonia and what is the source of the lipid?

A
  • resembles exogenous lipid pneumonia grossly and microscopically but the lipid is derived from surfactant and is always intra-cellular
  • usually idiopathic but can sometimes be due to impaired clearance of surfactant because of airway obstruction
40
Q

What is exogenous lipid pneumonia and in what circumstances is it likely to develop?

A
  • aspiration of oil
  • often white-yellow grossly
    ○ free extra-cellular globules of lipid can usually be found microscopically and may sometimes be obvious grossly in the lumina of the trachea and bronchi
    ○ the oil is gradually resorbed over time
    ○ vegetable oils (e.g. olive oil) are largely non-irritant -> almost no inflammation or fibrosis
  • animal and mineral oils cause inflammation
41
Q

What are some examples of pneumonoconioses in domestic animals and what lesions do they provoke?

A

1) carbon - pulmonary interstitial fibrosis and alveolar emphysema, and predisposition to secondary pulmonary infections
2) silica - accumulation in tissues (silicosis)

42
Q

What occurs with acids within the body

A 
1) metabolic processes produce acid 	
○ H+ from protein/phospholipid metabolism
○ CO2 from carbohydrate metabolism
2) Acid is buffered by
○ HCO3-, haemoglobin, plasma proteins
3) Acid is excreted
Via lungs and kidneys
43
Q

Give two examples of when acid base balance can go wrong in the body

A
  • Diabetic animals can become acidotic if they need to use fatty acids for energy rather than glucose. These acids can lead to a significant drop in the serum pH of a patient.
    ○ This is known as diabetic ketoacidosis.
  • In chronic renal failure the kidney is no longer able to retain bicarbonate (HCO3 -), which is a base
    ○ Increased loss of HCO3- in the urine causes an acidosis in the body
    ○ Also may be increase in uric acid retention - uraemic
44
Q

Why is it significant that H+ is an acid and a cation and examples of when this occurs

A
  • Because H+ has a positive charge its concentration can be significantly impacted by any changes in cation (Na+, K+, Ca++, etc) concentration in the body.
  • body ALWAYS needs to remain electroneutral
    Example
  • When vomit lose H+ and Cl- -> to maintain electroneutrality need to retain Na+ and Cl- in kidneys, when Cl- depletes retain HCO3- and therefore worsen the alkalosis
45
Q

List the 3 buffers present in the blood stream and 3 inside cells

A
  • Buffers in the blood stream
    ○ HCO3 -, lactate, albumin
  • Buffers inside cells
    ○ Haemoglobin, phosphates, proteins
46
Q

What is the other buffer important in the body, what occurs in acidosis and alkalosis

A

Bone - 40% of acute acid load can be buffered, swap H+ for Ca2+ in bone (maintain electroneutrality) which is excreted in urine

  • Chronic acidosis can lead to fragile bones and pathologic fractures
  • Alkalosis causes carbonate to be laid down in bone
47
Q

What does the isohydric principle state and how do we use it

A

behaviour of any buffer in solution can be predicted by knowledge of any one buffer pair
- In medicine, we use the carbonic acid-bicarbonate system to predict the acid base balance in the patient

48
Q

List some clinical effects of severe metabolic acidosis

A
  • Cardiac arrhythmias
  • Decreased cardiac contractility
  • Arterial vasodilation (low blood pressure)
    ○ Decreased perfusion of liver and kidney
  • Shift of oxygen-haemoglobin dissociation curve to right
    ○ Increased off-loading of oxygen in tissues
  • Insulin resistance
  • Increased intracranial pressure
  • Alterations in [K+] and [Ca++]
49
Q

What are the 4 main mechanisms of metabolic acidosis and example from each

A

1) increase production of acid - cellular hypoxia (anaerobic metabolism)
2) increased acid intake - ethylene glycol toxicity - antifreeze
3) Decreased excretion of acid - uraemia
4) increase excretion of base - chronic renal failure

50
Q

Metabolic alkalosis is it common, why or why not, what is the main cause

A
  • much less common than metabolic acidosis as kidneys able to better excrete alkali than acid
  • most common cause is low chloride concentration - vomiting, increased excretion of cholride (frusemide)
51
Q

List some clinical effects of metabolic alkalosis

A
  • Muscle twitching
  • Seizures
  • Cardiac arrhythmias
  • Shift in oxygen-haemoglobin dissociation curve to left
    ○ Haemoglobin binds more tightly to oxygen
  • Hypokalemia
  • Hypocalcemia
52
Q

Respiratory acidosis possible causes

A

any disease or injury that causes hypoventilation

1) anaesthesia - most common
2) upper airway obstruction
3) respiratory muscle weakness/paralysis - snake venom, tick paralysis, myasthenia gravis

53
Q

Respiratory alkalosis possible causes

A
  • Any disease process or injury that causes hyperventilation
    ○ Stress, pain, catecholamine release
    ○ Pulmonary disease or injury
    ○ Pleural space disease
    ○ Intracranial disease - could cause hypoventilation as well
54
Q

what is a SBE and what does it include

A
  • Standard base excess (SBE) is a measure of all the nonvolatile acids and bases in the bloodstream
    ○ Does not include CO2 (which is volatile)
    ○ Includes organic molecules as well as ions
55
Q

what are the normal ranges found on a venous blood gas analysis and what is the respiratory and metabolic component

A
  • pH 7.4: (7.35 – 7.45)
  • pCO2: 40 mmHg (35-45 mmHg)
  • SBE: 0 (–4 - +4mmol/L)
  • HCO3-: 24
    pCO2 = respiratory component
    SBE = metabolic component
56
Q

How to tell primary from compensatory process and mixed acid-base disorders

A
  • Primary process will change similarly to the pH, compensation in opposing fashion
  • mixed if normal pH as body cannot compensate back to normal pH therefore acidosis and alkalosis are occuring and cancelling each other out - still need to fix both
57
Q

Generally how to you treat respiratory acid/base and metabolic acid/base disorders

A

respiratory - treat primary disease (Severe cases may need to take control of ventilation)
metabolic - fluid therapy will resolve 90%, also may provide buffers, improve renal perfusion - diabetics will need insulin

58
Q

Why don’t you just give bicarbonate in metabolic acidosis?

A
  • The acidosis is an indication that there is decreased oxygen supply to cells
  • If cells are deprived of oxygen for too long, they will die
  • We will not stop cells dying by giving bicarbonate
    ○ (and there are side effects to bicarbonate administration)
    ○ Not treating the primary problem
  • Sometimes give if severe and in renal failure however not first treatment on the list
59
Q

How to humans hold breath (static apnoea) for long periods of times

A 
inducing the diving reflex, cold water on the face and bradycardia slow hearty rate and redirecting blood to the brain and essential organs and away from peripheral tissues etc
- Free diving responses 
○ Apnoea
○ Hypertension
○ Bradycardia
○ Splenic contraction
60
Q

What causes an increase risk of death while diving

A
  • Increase due to hyperventilation before the snorkelling, reducing signal for need for ventilation - lead to asphyxia
    ○ Levels of CO2 go down due to hyperventilation, no big stimulus to breath, O2 levels then decrease to the point at which you black out because you didn’t breath when you are meant to. This can be fatal when underwater as try to breath but cant
61
Q

What are the 2 bad conditions that can occur due to deep diving and characteristics

A

1) barotrauma - burred vision, retina detachments, ruptured eardrums, collapsed lung, drowning
2) Decompression sickness (bends) - condition arising from dissolved gases coming out of solution (from the lungs) into bubbles inside the body on depressurisation (into the blood)
○ Nitrogen (inert) is the biggest problem when go into blood however problem when come out too quickly bubbles out into the blood
- Treated decompression chamber (hyperbaric chamber)

62
Q

List some non-respiratory and respiratory adaptations sperm whales have to deep sea dive

A

non-respiratory
- tissue metabolism conserve O2, O2 directed to brain, more circulation than in lungs, splenic contraction release more RBCs more oxygen carrying in blood, hgih blood to body ratio
respiratory - breath out when dive, highly compressible lungs and thorax, lung anatomy allows explusion of air out of gas exchange regions

63
Q

What occurs during respiration at high altitudes

A

Hypoxic responses

  • High altitude sickness
  • High altitude pulmonary oedema
  • High altitude cerebral oedema
  • Cor pulmonale
64
Q

list some adaptations bar-headed geese have

A
  • Skeletal and cardiac muscles better supplied with O2
  • More homogeneous capillary spacing
  • higher proportion of mitochondria
  • More oxidative fibres than water fowl
  • Hb more efficient O2 loading
  • Larger lungs
  • Hyperventilate in response to severe hypoxia
65
Q

what occurs to V/Q with microgravity and macrogravity environments

A

Microgravity environments (weightlessness)
- Improves V/Q matching
Macrogravity environments
- Worsens V/Q matching

66
Q

What is a major adaptation for all animals living at high altitudes

A

left shift of haemoglobin saturation curve - higher saturation of oxygen at lower partial pressures

67
Q

What occurs within horses that allows them to undergo elite excercise

A
  • Horses become hypoxaemic with intense exercise
  • Horses have maximal O2 uptake /kg 2.5 fold greater than similar weight steers
  • Horses have lungs that are twice as large as those of cattle, with gas exchange surface area 1.6 times that of cattle
68
Q

What are two haemotology results with acute haemorrhage and why

A
  • Doesn’t cause concentration of red blood cells or protein to drop however when fluid moves into interstitium then PCV and protein drops
    ○ Splenic contraction responds to the decrease PCV therefore increases the RBC for a while - no anaemia acutely
    ○ There is no acute response to decrease in protein - so hypoproteinaemia
69
Q

P:F ratio what does it stand for and what should the ratio be

A

Pa02:FiO2 (21% in air)
PaO2(P) should be 5 times F
So Pa02 should equal 105 when Fi02 = 21%

70
Q

What fluid treatment is most commonly used and what are the others and benefits and negatives

A

1) balance isotonic (lactated ringer solution) - balance salts within vascular space - buffered with lactate so good for acidosis
2) whole blood - best to replace RBC and platelets however expensive and short shelf life - not assessable
3) hypertonic saline solution - draws in interstitial fluid rapidly - rapid increase in blood volume but only lasts 30-40mins before diffuse back into tissues
4) colloid - not really used, causes sustained increase in blood volume as stay within vascular space, may cause renal failure

Semester 2 (17 decks)

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