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ACVIM SAIM (2023) > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is surfactant?

A

Used to greatly reduce surface tension, is produced by Type II alveolar epithelial cells (pneumocytes).

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2
Q

What is tidal breathing?

A

Tidal volume → volume inspired or expired with each normal breath

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3
Q

What is inspiratory reserve volume?

A

Inspiratory reserve volume → extra volume of air that can be inspired over and above the normal tidal volume

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4
Q

What is expiratory reserve volume?

A

Expiratory reserve volume → extra amount of air that can be expired by forceful expiration after the end of a normal tidal expiration

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5
Q

What is residual volume?

A

Residual volume → volume of air remaining in the lungs after the most forceful expiration

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6
Q

What is inspiratory capacity?

A

Inspiratory capacity → equals the tidal volume + inspiratory reserve volume
• The amount of air a person can breathe beginning at the normal expiratory level and distending the lungs to the maximum amount.

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7
Q

What is functional residual capacity?

A

Functional residual capacity → expiratory reserve volume + residual volume
• This is the amount of air that remains after normal expiration.

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8
Q

What is vital capacity?

A

Vital capacity → inspiratory reserve volume + tidal volume + expiratory reserve volume
• This is the maximum amount of air a person can expel from the lungs after first filling the lungs to their maximal extent and then expiring to their maximal extent

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9
Q

What is total lung capacity?

A

Total lung capacity →Equals the vital capacity + residual volume
• Maximal volume to which the lungs can be expanded with the greatest possible inspiratory effort

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10
Q

How does alveolar ventilation occur?

A

• Alveolar ventilation: rate at which air reaches the gas-exchange regions
o The gas in the air really only goes down to the terminal bronchioles and not into the alveoli during normal inspiration. It makes it the rest of the way by simple diffusion.

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11
Q

What is the difference between anatomic and physiologic dead space?

A
  • Physiological dead space → equal to the number of alveoli not participating in gas exchange
  • Anatomic dead space → refers solely to those airways not participating in gas exchange whereas physiologic dead space is equal to the anatomic dead space plus the non-functional alveoli (anatomic and physiologic dead space or nearly equal in healthy patients)
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12
Q

What is the rate of alveolar ventilation?

A

Alveolar ventilation per minute is the total amount of new air entering the alveoli per minute. It is equal to the amount of new air that enters the alveoli X the respiratory rate (Va=RR X (Vt-Vd))
• Vd = dead space
• Vt = tidal volume

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13
Q

What is the greatest resistance to passage of air in a normal patient?

A

The resistance of the large airways

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14
Q

Sympathetic stimulation to airways leads to…..

A

Bronchodilation (B2 adrenergic)

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15
Q

Parasympathetic stimulation to airways leads to ….

A

Bronchoconstriction via acetylcholine release (muscarinic)

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16
Q

What is the result of histamine in the airways?

A

Bronchiole constrictions (works locally)

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17
Q

Describe the cough reflex.

A

Bronchi and trachea are very sensitive to light touch (larynx and carina especially sensitive)
Afferent signals pass from the respiratory passageways to the medulla by way of the vagus nerve. The initiates an influx of air and subsequent closure of the epiglottis and vocal folds to trap the air in the lungs. The abdominal muscles contract and forcefully expel the air.

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18
Q

Describe the sneeze reflex.

A

Irritants in the nose send afferent signals to the medulla by way of CN V

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19
Q

What is the function of the nose?

A

Air is warmed, humidified, and filtered. Turbulent filtration occurs as the air hits the turbinates and must change direction

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20
Q

What occurs in automatic control of pulmonary blood flow distribution?

A

Decreased oxygen concentration in the alveoli (less than 73 mmHg PO2) results in vasoconstriction of the surrounding vessels →shunting blood away from the hypoxic alveoli.
• This is the opposite of what occurs in the other vascular beds

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21
Q

What is the normal direction of fluid flow in the pulmonary capillaries?

A

The normal outward forces of the capillary are just slightly greater than the inward force and so fluid constantly leaks into the interstitium (pumped back into circulation through lymphatics through slight negative interstitial pressure)

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22
Q

What are the layers of the respiratory membrane?

A

o Layer of fluid lining alveolus (containing surfactant: surface tension of alveolar fluid)
o Alveolar epithelium composed of thin epithelial cells
o Epithelial basement membrane
o Thin interstitial space btwn alveolar epithelium and capillary membrane
o Capillary basement membrane (fuses with alveolar epithelial basement membrane)
o Capillary endothelial membrane

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23
Q

What are factors that affect the diffusion of gas through the respiratory membrane?

A

Thickness of membrane (edema, fibrosis), surface area of membrane (↓ by lung removal, emphysema), diffusion coefficient of gas in membrane (CO2 20x faster than O2), partial pressure difference of gas btwn 2 sides of membrane (PP> alveoli than in blood (O2), net diffusion from alveoli into blood; PP> blood (CO2), net diffusion from blood to alveoli)

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24
Q

What are the two extremes of V/Q mismatches?

A

Ventilation-perfusion ratio (V/Q): Respiratory exchange when imbalance btwn alveolar ventilation and alveolar blood flow
o No exchange f gases
V/Q = 0 → Ventilation zero, yet there is still perfusion
V/Q = infinity →Ventilation adequate, but zero perfusion

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25
Q

What determines tissue PO2?

A

Tissue PO2 determined by rate of O2 transport to tissue in blood and rate at which O2 is used by tissues

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26
Q

What is the role of hemogloblin in oxygen transport?

A
  • 97% O2 carried on hemoglobin in RBCs

* 3% O2 dissolved in water in plasma and blood cells

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27
Q

How does oxygen reversible bind to hemoglobin?

A

O2 combines loosely/reversibly with heme portion of hemoglobin
o PO2 high = O2 binds to hemoglobulin (pulmonary caps)
o PO2 low = O2 is released (tissue caps)

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28
Q

What is the oxygen-hemoglobin dissociation curve?

A

↑ % Hemoglobin bound as PO2 ↑ = percent saturation of hemoglobin
o When PO2 = 95 mmHg → 97% bound to Hgb
o When PO2 = 40 mmHg (tissues) → 75% bound to Hgb

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29
Q

Name the factors that can affect the oxygen-hemoglobin dissociation curve?

A

• pH Changes:
o Acidic (7.4 → 7.2): Shifts curve to right (about 15%)
o Basic (7.4 → 7.6): Shifts curve to left
• ↑ CO2 concentration → Shifts curve to right
• ↑ Blood Temperature → Shifts curve to right
• ↑ 2,3-biphosphoglycerate (BPG) → Shifts curve to right
o Phosphate compound in blood

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30
Q

What is the Bohr Effect in regards to the oxygen-hemoglobin dissociation curve?

A

Shift of curve to right (due to ↑ CO2 or ↑ Hydrogen ions)→ Significant enhancement of release of O2 from blood into tissues, enhancing oxygenation of blood in lungs → Bohr Effect
o Blood passes through tissue: CO2 diffuses from tissue cells to blood → ↑ blood PCO2 → ↑ blood H2CO3 (carbonic acid) and hydrogen ions → Shifts curve to right and downward → forcing O2 away from Hgb and thus delivering ↑ O2 to tissues
o Lungs: CO2 diffuses from blood into alveoli → ¯ blood PCO2 → ¯ hydrogen ions → Shifts curve to left and upward → Greater binding of O2 to Hgb at any given alveolar PO2

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31
Q

Explain the dissociation of carbonic acids into bicarbonate and hydrogen ions.

A

Carbonic acid (in RBC, H2CO3) dissociates into hydrogen and bicarbonate ions (H+ and HCO3-) = Faster with carbonic anhydrase
o About 70% CO2 transported to lungs from tissue
• H+ combine with Hgb (powerful acid-base buffer)

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32
Q

What is the chloride shift in RBCs?

A

• Many ions diffuse from RBCs into plasma (Cl takes their place in RBCs = bicarbonate-chloride carrier protein → 2 ions in opposite directions
o Cl content of RBCs greater in venous than arterial RBCs → Chloride Shift (phenomenon)

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33
Q

What are the main forms that CO2 travels in the body?

A
  1. Dissolved in solution
  2. Bicarbonate (Major form)
  3. Combined with hemogloblin (o CO2 reacts with water, amine radicals of Hgb → carbaminohemoglobin (CO2Hgb)
    o Reversible rxn – slow!!
    o Only small amount of CO2 reacts this way (1/4th quantity of Hgb)
    o Carbamino + Hgb and plasma protein: 30% total amount transported
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34
Q

What is the Haldane Effect?

A

o ↑ CO2 in blood causes O2 to be displaced from Hgb (Bohr effect)
o Important factor for ↑ O2 transport
o Opposite true: Binding of O2 with Hgb tends to displace CO2 from blood (Haldane effect)
More important at promoting CO2 transport than the Borh effect is at promoting O2 transport Combination of O2 with Hgb in lungs causes Hgb to become a stronger acid
• Displaced CO2 from blood into alveoli:
1. More highly acidic Hgb has less tendency to combine with CO2 to form carbaminohemoglobin (displacing more CO2 that is present in carbamino form in blood)
2. ↑ Acidity of Hgb causes release of excess Hydrogen ions and binds with bicarbonate to form carbonic acid (dissociated in water and CO2 and CO2 is releases from blood into alveoli into air)

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35
Q

Describe what occurs with control of normal breathing (nervous control).

A

Normal quiet breathing is controlled by repetitive inspiratory signals from dorsal respiratory group transmitted to diaphragm; expiration is passive elastic recoil of lungs and thorax

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36
Q

What is the Hering-Breuer inflation reflex?

A

o Lung inflation signals limit inspiration (Hering-Breuer inflation reflex)
Stretch receptors in the lungs transmit signals via the vagus nerve to the dorsal respiratory group to limit inspiration when the lungs are full of air
Similar to the pneumotaxic center in that it switches off the inspiratory ramp = inhibits inspiration (but increases the respiratory rate) when the lungs are full

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37
Q

What is the role of CO2 in controlling respiration?

A

Excess carbon dioxide or H+ ions → stimulate the respiratory center directly to increase strength of inspiration and expiration
• Hydrogen ions are the only important stimulus for the chemosensitive area
• However, H+ do not readily cross the BBB or Blood-CHSF barrier; thus CO2 ends up being more important

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38
Q

What is the role of O2 in controlling respiration?

A

Oxygen → no direct effect on respiratory center; acts on peripheral chemoreceptors in carotid and aortic bodies → signals to respiratory center

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39
Q

Explain what occurs at the BBB with H+ and CO2 to stimulate respiration.

A

Effect of blood PCO2 in stimulating the chemosensitive area
• CO2 + H2O → carbonic acid → HCO3- + H+ → H+ after CO2 has diffused across BBB
• Chemosensitive region is stimulated much more rapidly if the CO2 enters via the CSF rather than the brain interstitial water (less protein buffers for the hydrogen in the CSF)
• The excitation of the respiratory center to the increased CO2 is great within the first few days but subsequently declines over the next 1-2 days
o Dt renal compensation for acidosis by retaining bicarb, AND bicarb diffusing across BBB to buffer H+ there

40
Q

Explain the role of peripheral chemoreceptors in respiration. What are they are more responsive to?

A

o More responsive to changes in the oxygen content of blood but also respond to changes in pH and carbon dioxide.
o Carotid bodies: bilaterally @ bifurcation of common carotids; pass from Hering’s nerves to the glossopharyngeal nerves and onto the dorsal respiratory group
o Aortic bodies: @ aortic arch; pass from the vagus nerve to the dorsal respiratory group
o These bodies are constantly exposed to only arterial blood

41
Q

What happens in the peripheral chemoreceptors when O2 falls below 60 mmHg?

A

When the pO2 falls below 60 mm Hg, nerve impulses from the carotid body increase rapidly and respiration increases

  1. Stimulation by low PO2 may occur via glomus cells in bodies → synapse with nerve endings (or may be direct sensitivity of nerve endings to O2)
  2. Increased CO2 and H+ also activate chemoreceptors; this effect is much less in magnitude than their direct effect, but occurs more rapidly
42
Q

What stimulates ventilation during exercise?

A

Chemical signals ARE NOT the stimulus for increased respiration during exercise (they are normal!)
1, Instead, brain higher functions send collateral messages to the respiratory centers (while they are sending messages to muscles to stimulate contraction)
2. Movements of the limbs stimulates joint and muscles proprioceptive receptors that transmit impulses to the DRG to stimulate ventilation

43
Q

What is Cheyne-Stokes breathing?

A

o Characterized by slowly waxing and waning respiration, occurring over and over again about every 40-60 secs
o The basic cause is due to transient overbreathing:
1. Blow off too much CO2 → delay before changed pulmonary blood can be transported to brain and inhibit excess ventilation
2. When overventilated blood eventually reaches the brain, the center becomes depressed an excessive amount → CO2 increases in alveoli → again takes brain delay before it catches up

44
Q

Name 5 major categories of hypoxemia?

A 
Extrinsic problems
• 1. Low FIO2 (high altitude)
• 2. Hypoventilation (neuromuscular disease)
 Pulmonary disease 
• 2. Hypoventilation (increased airway resistance, decreased lung compliance)
• 3. Diffusion impairment
• 4. V/Q mismatch 
o High V/Q: physiologic dead space
o Low V/Q: physiologic R-L shunt
Anatomic shunts
• 5. Right-to-left cardiac shunts 
 Inadequate O2 transport to tissues
• 6. Anemia or abnormal Hgb
• 7. Hypovolemic shock
Inadequate capability of the cells to use oxygen (uncoupling of oxidative phosphorylation)
• 8. Metabolic abnormalities, cyanide toxicity
45
Q

Describe when oxygen therapy will be effective in hypoxemia.

A
  1. 100% effective with decreased atmospheric oxygen
  2. Pretty effective (5x O2 delivery) with hypoventilation hypoxia
  3. Pretty effective with a decreased alveolar membrane diffusion because the increased PaO2 facilitates diffusion at a higher partial pressure
  4. Minimally effective in hypoxia caused by anemia, abnormal hemoglobin transport of oxygen, circulatory deficiency, or physiologic shunt
    • Normal amounts of oxygen are already available to the alveoli
    • Small amount of increased O2 transport in the dissolved state may make a difference
    5, Not effective in hypoxia caused by inadequate tissue use of oxygen
46
Q

What graph is used to assess the compliance of the lungs?

A

Pressure-volume loops - The slope of each line is the compliance of the lung itself

47
Q

What are the effects of emphysema and pulmonary fibrosis on lung compliance?

A

Emphysema = Increased lung compliance (loss of elastic fibers)
Pulmonary Fibrosis = Decreased lung compliance (increased stiffness of the lungs)

48
Q

What is the most important component of surfactant?

A

DPPC (dipalmitoyl phosphatidylcholine) - based on amphipathic nature of phospholipid (hydrophobic on one end and hydrophilic on the other end) - Reduces surface tension depsite small radius on alveoli

49
Q

What is the intrapleural pressure?

A

It is negative pressure (opposing forces of the lung trying to collapse and the chest wall trying to expand

50
Q

Based on the oxygen-hemoglobin dissoication curve, what is the PO2 when 50% of Hb is saturated?

A

PO2 at 25 mmHg when Hb 50% saturated

51
Q

Name the 4 major factors that will shift the oxygen-hemogloblin dissociation curve to the right.

A

Situations when there is a decreased affinity of Hb to oxygen → Unloading of O2 (great in tissue)

  1. Increased PCO2
  2. Decreased pH (more acidic)
  3. Increased temp
  4. Increased 2,3-DPG (byporduct of glycolysis)
52
Q

What happens when there is left shift in the oxygen-hemogloblin dissociation curve?

A

There is an increased affinity of Hb to oxygen → Harder to unload O2 (great in lungs)

53
Q

Where is carbonic anyhdrase found in high concentrations?

A

In RBCs

Aids in transport of CO2 in blood

54
Q

What is the equation for forming bicarbonate from CO2?

A

CO2 + H2O → (carbonic anhydrase) H2CO3 → H+ + HCO3-

55
Q

What controls the mechanism of hypoxic vasconstriction?

A

Direct action of alveolar PO2 on the vascular smooth muscle of pulmonary arterioles

56
Q

Where is the inspiratory center in brain?

A

Dorsal respiratory center

57
Q

Where is the expiratory center in brain?

A

Ventral respiratory center

58
Q

What Law governs the diffsuion of O2 and CO2 across membranes?

A

Fick’s Law of Diffusion (driven by partial pressures difference of the gas)

59
Q

How many molecules of oxygen can be bound by 1 Hemoglobin?

A

4 molecules of Oxygen per 1 Hb

60
Q

What does the sigmoidal shape of the oxygen-hemoglobin curve reflect?

A

Increased affinity for each successive molecule of O2 that is bound

61
Q

What are the cut-offs for pulmonary arterial (PA) systolic and mean pressures that define pulmonary hypertension (PH)?

A

PA systolic > 30mmHg, PA mean >20mmHg

62
Q

List the 5 disease classes which can lead to pulmonary hypertension.

A

ACVIM consensus
Group 1 (pulmonary arterial hypertension) – primary diseases of the vasculature. E.g. idiopathic, familial, drugs/toxins, congenital heart disease (systemic-to-pulmonary shunts), HWD, veno-occlusive disease, persistent PH of newborns.

Group 2 (pulmonary venous hypertension) – left-sided heart disease & chronic increases in LA pressure. Valvular or myocardial dz. MOST COMMON in dogs.

Group 3 (PH associated with lung diseases or hypoxemia) – obstructive pulmonary disease, interstitial lung disease, alveolar hypoventilation, sleep apnea, chronic exposure to high altitude, developmental abnormalities.

Group 4 (PH associated with chronic thrombotic or embolic) – obstruction of proximal or distal PAs, non-thrombotic embolism (HWD or other parasites, neoplasia, foreign material – catheter or coil)

Group 5 (systemic & other disorders) – compression of pulmonary vessels, lymphadenopathy, neoplasia, fibrosing mediastinitis, granulomatous disease, others (histiocytosis, sarcoidosis, lymphangiomatosis)

63
Q

Bronchial collapse occurs most commonly in which regions?

A

L cranial & R middle bronchi

64
Q

Bronchial collapse occurs most commonly in which regions?

A

L cranial & R middle bronchi

65
Q

Thoracic radiographs most sensitive for the diagnosis of airway collapse in which regions of the lungs?

A

Sn for the detection of bronchoscopically identified collapse was highest for radiography at the trachea, left lobar bronchi & right middle bronchus. But relatively low Sp.

66
Q

What clinical sign can epiglottic entrapment of the soft palate cause?

A

Reverse sneezing

67
Q

How to calculate estimated systolic PA pressure from echo?

A

Measure TRV max
Modified Bernoulli equation:
Pressure gradient (aka estimated systolic PAP) = 4 x (TRVmax)^2 in mmHg

68
Q

ACVIM consensus panel’s definition (cut-offs) for pulmonary hypertension in dogs?

A

TR PG cut-off of >46 mmHg (TRVmax >3.4 m/s)
Defined as moderate PH historically

69
Q

Specific treatment for PH targets which 3 pathways?

A

ACVIM consensus.
NO, endothelin & prostacyclin pathways
These mediate pulmonary arterial/arteriolar vasoconstriction (secondary to endothelial injury).

70
Q

What is a rare disease to be suspected if a dog with pulmonary hypertension develops pulmonary oedema after sildanefil treatment? How does this occur?

A

ACVIM consensus
Pulmonary veno-occlusive disease or pulmonary capillary hemangiomatosis.
Also caution when administering PDE5-i in dogs with LHD & congenital shunts.

Reactive” or “responsive” pulmonary arteries (or arterioles) have an unpredictable response to tx. Increased right sided CO, acutely increases pulmonary VR to the LA&raquo_space; subsequently increase LA & thus pulmonary venous and capillary pressures&raquo_space; pulmonary oedema.

71
Q

What anti-neoplastic drug may be considered as an adjunct treatment for refractory PH in dogs & MOA? What evidence is there to support its efficacy?

A

ACVIM consensus
TKIs (e.g. toceranib, imatinib) - cause PA vasodilation by inhibiting action of PDGF (by inhibiting phosphorylation of PDGF-receptor TK). Used in people, little data in dogs, but imatinib reduced PAP in dogs with PH 2’ to LHD in 1 study.

72
Q

List the broad clinical signs of respiratory disease in dogs and cats

A
  1. Sneezing
  2. Reverse sneezing
  3. Nasal discharge
  4. Open mouth / postural breathing
  5. Audible respiratory sounds
    • Stridor
    • Stertor
    • Wheezes?
    • Crackles?
  6. Coughing
73
Q

List the various abnormal respiratory sounds and describe how they help localise respiratory disease

A
  1. Stertor - soft palate / nasopharynx
  2. Stridor - inspiratory noise, continuous - larynx
  3. Wheeze
    • low pitched versus high pitched
      • large airway versus small airway
    • Monophonic versus polyphonic
      • large airways vs smaller/multiple airways
  4. Crackles
    • Loudest end inspiratory
    • Indicate alveolar or bronchiolar disease
  5. Decrease / absent sounds
    • Pleural space
      • Dorsally reduced sounds - air
      • Ventral reduced sounds - fluid
74
Q

List the various imaging modalities to assess the respiratory tract.

Together with their major indication and limitation

A
  1. Radiography
    • General assessment of heart size and lung/airway changes. Assess symmetry of the nose.
    • Nasal studies limited by complexity of the structure and difficulty identifying early lesions
  2. Computed tomography
    • Indicated for nasal and thoracic imaging - Ideal for thoracic studies due to spatial definition, contrast and speed of acquisition
    • The need for sedation / general anaesthesia is the biggest limitation in thoracic investigations
  3. MRI
    • Primarily indicated for assessment of nasal disease and other fixed soft tissue changes
    • Thoracic investigation limited by movement and bony change may be underestimated
  4. Fluoroscopy
    • Dynamic airway disease and swallowing studies (pharyngeal and oesophageal function)
    • Limited by patient compliance primarily
  5. Ultrasonography
    • Assessment of extra-luminal soft tissue structures. Descriptions of changes have been reported for laryngeal paralysis (insensitive for laryngeal collapse)
    • Limited by tissue/air interface and tissue/bone interface artefacts
  6. Nuclear Imaging
    • Global assessment of lung perfusion and lung ventilation (IV versus nebulized technetium) including V/Q scans
    • Most sensitive for identifying PTE
    • CAn be used for assessment of mucocilliary clearance
    • Cumbersome and requires patient isolation
    • Poor spatial resolution
75
Q

List the options for sampling of the respiratory tract

Nose, large airways and lower airways

A
  1. Nasal swab
  2. Nasal flush
  3. Nasal biopsy
  4. Transtracheal wash
  5. Bronchial brushing
  6. Bronchoalveolar lavage
  7. Transthoracic needle aspirate or biopsy
  8. Surgical biopsy
76
Q

List major pros and cons of the various nasal sampling techniques

A
  1. Nasal swabs
    • Cell collection is often superficial inflammation and cannot aid in distinguishing the underlying cause
    • Cultures typically respresent normal flora or secondary infection and do not identify a causual organism
    • Samples can be collected for PCR to test for viral / bacterial disease with some utility
    • Highly beneficial in diagnosing nasal cryptococcosis in cats
  2. Nasal hydropropulsion
    • Large samples may be obtained
    • Minimal equipment required
    • May relieve obstruction
    • Care must be taken to avoid aspiration
  3. Biopsy (guided or blind)
    • Can be guided by endoscopy or CT for smaller lesions
    • Blind samples can be useful for larger lesions
    • Samples can be obtained for histopath or culture
    • Bleeding is the major risk.
77
Q

Discuss and compare sampling techniques from the lower airways.

Tracheal wash samples vs BAL vs endobronchial brush samples

A
  1. Tracheal wash
    • samples can be obtained via transtracheal approach or via a cuffed ET tube
    • Generally indicated for sampling from large airways or when there is diffuse disease.
    • TTW can be performed in an awake animal with preserved coughing reflex
    • TTW dogs >15 kgs
    • Sample volumes are typically small
    • Cannot be utilised if there is skin contamination
  2. Bronchoalveolar lavage
    • Requires general anaesthesia
    • +/- endoscopic guidance. Necessary for targeted sampling of lobar disease
    • Sample at least two sites if there is diffuse disease
    • Fluid can be submitted for cytology, routine culture, fungal culture, mycoplasma culture or PCR.
    • VQ mismatch and hypoxia are common and usually self-limiting and managed by oxygen supplementation
  3. Endobronchial Brush (or needle) samples
    • Requires general anaesthesia and bronchoscopy
    • Requires endoscopic brush and needle instruments
    • Can provide information on focal lesions
    • Good at detecting inflammation in larger airways
    • lymphocyte numbers may be underestimated
    • Clinical implication of the results has yet to be fully ellucidated
78
Q

Discuss the pathogenesis of Tracheal Collapse

A
  • Multifactorial and likely degenerative
  • Congenital forms do occur also
  • Primary cartilage factors causing intrinsic weakness
    • Suspected reduction in glycosaminoglycans and chondroitin sulfate
    • Tracheal cartilage weakness leads to flattening of the rings and widening of the dorsal membrane
  • Secondary factors capable of causing progression
    • Obesity, Irritant inhalation, Periodontal disease, Respiratory infection, ET intubation?
  • Chronic obstruction can contribute to the degeneration including pulmonary fibrosis in WHWT
  • Controversial if concurrent or subsequent airway inflammatory disease is relevant to the pathogenesis of airway collapse
  • Worsening collapse can lead to further oedema and inflammation which may precipitate further degeneration or at least perpetuate the cough.
79
Q

List the options for pulmonary function testing in dogs and cats

A

Mechanical function

  1. Spirometery - only for tidal volume measurement
  2. Tidal breathing flow volume loops
  3. Barometric whole body plethysmography
  4. Lung compliance
  5. Lung resistance

Pulmonary gas exchage

  1. Arterial Blood Gas Analysis
  2. Oxygen Tension based indices
  3. Pulse oximetry
  4. End tidal capnography
80
Q

Discuss the various forms of eosinophilic airways disease proposed in dogs

A
  1. Eosinophilic Bronchitis
    • Mildest form of the disease
    • Airway hyperaemia with no to mild mucus accumulation
    • Radiographs may appear normal (17/28 - 61%)
    • Peripheral eosinophilia is rare
  2. Eosinophilic Granuloma
    • Bronchiectasis and nodular masses common on rads
      • Radiographs uniformly abnormal
    • Mucus exudation and inspissated mucus expected
    • BAL eosinophilia almost universal
    • Septic suppurative inflammation uncommon
  3. Eosinophilic bronchopneumopathy
    • BAL eosinophilia is almost universal
    • 60% have peripheral leukocytosis
  4. Parasitic airway diseases that cause airway eosinophilia
    • Lung worm (Angiostrongylus Vasorum)
    • Heartworm (Dirofilaria immitis)
    • oslerus osleri, capillaria aerophila, others
81
Q

Eosinophilic airway disease

What is the proposed pathogenesis of eosinophilic airway disease?

A
  • Unknown
  • Presumed hypersensitivity reaction to inhaled allergen
  • Increase in CD4+ T cells and decrease in CD8+ T cells in BALF
  • Activated Th2 cells may accumulate at sites of inflammation
    • Th2 cytokine expression not different from control?
  • Transcription of MCP-3, eotaxin-2, eotaxin-3 has been shown in dogs with EBP.
  • Eotaxin release is induced by IL-4 and IL-13
  • Eotaxin binds to C chemokine receptor 3 (CCR3)
  • Eotaxin stimulates recruitment of eosinophils
  • Pulmonary damage is in part mediated by increase collagenolysis and proteolysis
    • matrix metalloproteinase produced by epithelial cell and macrophages increases collagenolysis
    • markers of increased ECM turnover or collagen type III production are increase - procollagentype III amino terminal propeptide
      • PIIINP increased in EBP and pulmonary fibrosis
82
Q

Describe the aetiology and pathogenesis of primary ciliary dyskinesia

A
  1. PCD is the result of dysmotility of cilia
  2. Cilia abnormalities are ultrastructural and electron microscopy is required for diagnosis
  3. Ineffective clearance of mucus from airways is a hallmark
  4. Dysfunction of the monocilia on the embryonic node can lead to randomisation of left/right body symmetry
  5. ~40 human genetic PCD causing mutations have been identified
  6. Usually autosomal recessive inheritance
  7. Gene has been identified in Old English Sheepdog and Alaskan Malamutes
83
Q

Cilia abnormalities

Note the normal cilia structure together with the various abnormalities seen in patients with PCD

A

Motile cilia: Microtubule backbone - axonema. The axonema comprises nine microtube doublets surrounding a certal pair. Arising from the doublets are inner and outer dynein arms together with a radial spoke. There is a nexin-dynein regulatory complex (nexin link)

PCD patients can have the following cilial defects:

  • abnormal or absent inner dynein arms
  • abnormal or absent outer dynein arms
  • Defects in radial spokes
  • Defective nexin links
  • General axonemal disorganization
  • microtubule transposition
84
Q

Define Bronchiectasis

A
  • An abnormal and permanent dilatation and distortion of subsegmental airways
85
Q

List potential causes of bronchiectasis in dogs and cats

A
  1. Congenital disorders
    • Primary ciliary dyskinesia
  2. Acquired disorders
    • Bronchial foreign body
    • post-aspiration injury
    • Chronic infectious bronchitis / bronchopneumonia
      • including B. bronchoseptica and pneumocystis carinii
    • Eosinophilic bronchopneumopathy
    • Chronic bronchitis
    • Pulmonary fibrosis
    • Immune deficiency syndromes
    • bronchopulmonary aspergillosis
    • Neoplasia
86
Q

Describe the primary and secondary changes seen with bronchiectasis on radiographs or CT

A

Primary:

  • Abnormal bronchial dilatation (increased bronchoarterial ratio)
  • Lack of peripheral bronchial tapering
  • Distinct airways within 1 cm of the lung periphery (people)

Secondary:

  • Bronchial wall thickening
  • Mucus plugging
  • Peripheral air trapping (reduced pulmonary density)
  • Lobar consolidation
87
Q

Discuss the pathogenesis of Feline Inflammatory Bronchial Disease

A
  • Thought to arise secondary to previous airway insult
    • Prior infection or inhaled irritant
  • Damage to the airways causes inflammation
    • Pirmarily non-degenerate neutrophilic inflammation
  • Ongoing inflammation can cause permanent changes to the airways
    • Thickening of the bronchi
    • Secretions leading to air-trapping
  • Bronchiectasis can result from chronic disease
88
Q

Discuss the pathogenesis of feline asthma

A
  • Though to be allergic, similar to the human form disease
  • Allergens (eg. house dust mites, bermuda grass) bind to dendritic cells in the airway lumen
  • Presented via MHC II to naive TH0 cells
  • In susceptible individuls, this can trigger a Th2 response
  • T helper 2 cell mediated response
    • IL4 / IL5 mediated
    • Production of IgE
    • cytokines (detected in blood and BALF) including eotaxin drive recruitment of eosinophils, mast cells and basophils which avidly bind IgE
    • re-exposure to allergen causes cross linking of bound IgE leading to degranulation
  • Eosinophilic airway inflammation
  • Increased airway responsiveness (allergen specific)
  • Airflow obstruction / remodelling
  • Note that clinical signs can wax and wane despite persistance of airway inflammation.
  • ~50% of cats clinically improved without medication
  • Ongoing airway inflammation has been documented in cats receiving high dose oral glucocorticoids
89
Q

Differential diagnoses for feline asthma / inflammatory bronchial disease

A
  1. Pulmonary parasitic disease
    1. Aerulostrongylus abstrusus
    2. Eucoleus aerophilus (formerly capillaria)
    3. Troglostrongylus brevior
    4. Dirofilaria Immitis
    5. Wolbachia
  2. Infection with Toxacara Cati
  3. Bacterial / mycoplasm infection
  4. Pulmonary neoplasia
90
Q

List readily available diagnostic testing options for feline asthma

Note expected abnormalities or required changes to confirm a diagnosis

A
  1. History and clinical examination
    • chronic cough versus acute respiratory difficulty
    • wheezing (expiratory) +/- end expiratory push
    • tachypnoea
  2. CBC/biochemistry
    • peripheral eosinophilia in 17-46% (not correlated to airway eosinophilia
  • Diagnostic imaging - radiographs or CT​
    • diffuse bronchial or bronchointerstitial pattern
      • Normal radiographs in ~ 25%
    • airway hyperinflation
    • collapse of right middle lung lobe - mucus obstruction
    • bronchial wall thickening
    • pulmonary infiltrates
    • bronchiectasis
  • Bronchoscopy
    • non-specific
    • mucus accumulation, airway dilatation or stenosis, hyperaemia, mucosal abnormalities, airway collapse
  • BAL
    • Eosinophilia > 17% cells is arbitrary cut off
    • Subclinial eosinophilia in apparently healthy cats
    • eosinophilia also seen with parasitic infections
    • May be submitted for PCR (bacterial, mycoplasma, viral, parasitic)
  • Faecal test
    • Baerman technique to assess for lung worm
    • Faecal float for Toxacara cati
91
Q

Discuss adjunctive testing options for feline asthma

A
  1. Allergen testing
    • IDST or IgE blood tests
    • results may not be reliable
  2. Pulmonary function testing
    • Indirect measure of airway resistance in response to airway provocation
    • May help differentiate asthma from chronic bronchitis
  3. Biomarker testing
    • endothelin-1 - increased in cats with asthma compated to controls.
      • endothelin 1 has not been assessed in cats with other respiratory disease
    • Exhaled Breath Concentrates - hydrogen peroxide and acetone increases correlated with eosinophilia on BALF.
      • Uncertain if EBC will become clinically useful biomarker
92
Q

List the therapeutic options available for treatment of feline asthma.

Discuss the potential utility of the ‘experimental’ treatment options

A

Mainstay

  1. Glucocorticoids
  2. Bronchodilators

Experimental

  1. Allergen specific immunotherapy
    • Variable diagnostic utility of IDST and IgE ELISA
    • enzymoimmunometric assay inaccurate
    • Rush immunotherapy (RIT) has resulted in reduction in airway eosinophilia
      • Reductions have occurred even when allergens not inplicated in sensitization are used.
  2. Omega 3 fatty acid with antioxidant luteolin
    • diminished airway hyper-responsiveness, but not airway eosinophilia
  3. Inhaled lidocaine
    • decreased airway hyper-responsiveness in an experimental model
  4. Tyrosine kinase inhibitors
  5. Stem cells
    • May help reduce airway eosinophilia in the acute setting.
    • Commercially available stem cells have not been assessed
93
Q

Discuss the use of corticosteroids in the treatment of feline asthma

A
  • Ongoing inflammation is expected despite variability and flutuation in clinical signs
  • No prospective, controlled studies on oral corticosteroid use in spontaneous asthma!
    • Retrospective studies often document clincal improvement as sufficient for a positive response - not reduction in BALF eosinophilia or airway hyper-responsiveness
  • Oral prednisolone, inhaled fluticasone, inhaled budesonide have all shown positive responses
  • Inhaled budesonide - improved BWBP readings in naturally occurring asthma (Galler 2013)
    • 400 ug q 12 hour
    • 3/15 had HPPA suppression
  • Fluticasone - 44 ug, 110 ug, 220 ug doses q 12 hours - equipotent (Cohn 2010)
    • no suppression of HPAA at either dosage
94
Q

Discuss the use of bronchodilators in the management of feline asthma

A
  • Responsiveness to bronchodilators is a hallmark of the diagnosis of asthma
  • Monotherapy is not recommended as the airway inflammation that contributes to hyper-responsiveness is not controlled
  • Inhaled bronchodilators do not reduce the time to recovery from an early asthmatic reaction in an experimental model (Leemans 2009)
    • Therefore injectable terbutaline is often preferred in acute crisis and can be used long term
  • Inhaled albuterol can reduce life threatening bronchoconstriction.
    • racemic mixture of R- and S-enatiomers with the S- version promoting bronchocontriction and having a longer half life.
    • Chronic use can worsen underlying airway inflammation
  • Long acting Beta agonists are a mainstay of therapy
95
Q
A

ACVIM SAIM (2023) (19 decks)

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