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Equine Medicine > Unit 1 - Athsma > Flashcards

Unit 1 - Athsma Flashcards

1
Q

What is Severe Asthma (SA) also known as? What about Mild to Moderate Asthma?

A

Heaves (Recurrent Airway Obstruction (RAO), Small Airway Disease, COPD, Broken Wind, Hay Sickness, SPAOPD)
Mild to moderate: Inflammatory Airway Disease (IAD)

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2
Q

Describe the character of inflammatory respiratory conditions of the horse.

A
  1. Excessive Airway Mucus Production
  2. Airway Neutrophilia
  3. Bronchial Hyperreactivity
  4. Reversible Bronchospasm (usually)
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3
Q

What geographic locations are high prevalence of equine asthma? What feeding forms are risk factors?

A

Environment - Regions of cool and wet weather like the northeast and midwest.
Stabling and hay feeding, especially round bales in round bale feeders.

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4
Q

Following exposure to inhaled triggers, ______ ________ have upregulated gene expression of TNF-a, IL-1B, and IL-8, among other cytokines and factors.

A

alveolar macrophages

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5
Q

______ production, which attenuates neutrophil chemotaxis, is reduced in RAE affected horses and suggests an absence of an inflammatory braking system.

A

secretoglobin

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6
Q

True or false: Th17 cells are increased in equine RAO in addition to increased IL-17 at IL-8.

A

true - the roles of lymphocytes are unclear at this time

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7
Q

What do mast cells and histamine do in RAO? Do antihistamines provide therapeutic relief to RAO horses?

A

They increase vascular permeability and bronchoconstriction.

They do not provide relief to RAO horses.

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8
Q

Are NSAIDs and COX inhibitors effective in providing bronchodilation and bronchoconstriction to give relief to RAO horses?

A

Nope - there’s a lack of therapeutic response in RAO horses even though these treat prostaglandin inflammatory mediators.

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9
Q

True or false: Miniature horses and standardbreds are predisposed to RAO.

A

False - There is no gender or breed predisposition, but the average age of horses with RAO is 7 years old. There is a genetic component - horses are more likely to get it if at least one parent has RAO.

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10
Q

What seasons increase severity of asthma?

A

winter (stabling time) and summer due to the increase in airborne pollen and molds

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11
Q

What are some of the common clinical signs of equine asthma?

A

Coughing
Nasal discharge (after exercise or head lowering)
Exercise intolerance
Abnormal breathing effort/difficulty
With increased severity, tachypnea, nasal flaring, and heaving may be noted.

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12
Q

What heart condition may occur in horses with long standing RAO?

A

Cor pulmonale (RV dysfunction) with jugular distension, pulsation, ventral edema, and tachycardia. PA enlargement is likely in these cases.

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13
Q

How does pulmonary fibrosis or interstitial disease differ from RAO?

A

Cases of severe pulmonary fibrosis or interstitial disease result in restrictive pulmonary disease while RAO causes increased expiratory effort, characterized by marked inspiratory distress (obstructive).

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14
Q

What will BAL cytology find in a horse with severe asthma? What about mild asthma?

A

Severe (RAO): >20-25% neutrophils, Mild: >5% neutrophils

Normal or RAO-remission BAL should reveal >90% macrophages and lymphocytes.

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15
Q

Microscopic inspissated airway mucus and cellular debris is often identified and known as _____ _____.

A

Curschmann’s spirals

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16
Q

What might you see on CBC/Chem and Arterial blood gas in a horse with severe asthma?

A

CBC/biochem: stress leukogram +/- acute phase proteins

ABG: hypoxemia and hypercapnia (<85% PaO2)

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17
Q

True or false: intradermal skin testing has been extensively researched and allows for the identification of RAO-susceptible or affected horses.

A

FALSE

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18
Q

What are the four measurements and findings in RAO affected horses in which you perform pulmonary function testing?

A
  1. ) Dynamic lung compliance (Cdyn): Decreased (reflects changes in peripheral airways)
  2. ) Pulmonary resistance (RL): Increased (reflects changes in central/large airways)
  3. ) Maximal pleural pressure changes((delta)Pplmax): Increased (>15 cm H2O)
  4. ) Peak inspiratory and expiratory flow rates: Increased
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19
Q

Are pulmonary artery pressure and pulmonary vascular resistance increased or decreased in RAO cases?

A

Significantly increased - Airways that are narrowed, obstructed, or both result in increased pulmonary resistance and fail to participate in efficient gas exchange.

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20
Q

How do clinical RAO lungs appear on gross pathology?

A

On gross pathology, clinical RAO lungs fail to collapse and may have rib impressions (hyperinflation), however animals in remission may have normal appearing lungs.

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21
Q

How can you treat equine asthma?

A

Evironmental manafement, bronchodialators, and anti-inflammatory drugs

22
Q

How can you alter the environment to treat equine asthma?

A

Shelter outside with a well-ventilated shelter free of urine and manure.
Avoid dusty scenarios
Avoid straw and wood shavings; remove horses from the barn when cleaning
Avoid feeding hay (give complete pelleted feeds or pelleted forages) or feed wet/steamed hay. Do not tie RAO horses by a hay net and allow them to lower their heads.

23
Q

How do bronchodilators treat equine athsma?

A

Anticholinergics to block smooth muscle constriction by acetylcholine(Atropine, Ipratropium, N-butylscopolammonium bromide NBB)
Beta-2 agonists to relax smooth muscle by increasing intracellular cAMP (Clenbuterol, Albuterol, Salmeterol)
Phosphodiesterase inhibitors to relax smooth muscle by inhibiting breakdown of intracellular cAMP along with being anti-inflammatory (rarely used - Aminophylline, Pentoxifylline)

24
Q

What anti-inflammatorys can be used to treat asthma?

A

not NSAIDs - prednisolone, dexamethasone, triamcinolone, isoflupredone acetate, and more. There are also inhaled corticosteroids and other therapies

25
Q

What are the major potential side effects of glucocorticoid use in horses?

A

adrenal gland atrophy, immunosuppression, precipitation of laminitis

26
Q

Where do we typically see pasture asthma?

A

Southeastern United States

27
Q

What does Endothelin-1, which is often increased in SPAOPD cases, do?

A

ET-1 induces bronchoconstriction, increases mucus secretion, increase ASM, and is pro-inflammatory. ET receptors in bronchial smooth muscle of affected horses are increased.

28
Q

How do you treat pasture asthma?

A

Move the horse from the offending pasture to another pasture or a cool, dust-free stall. All other medical management would be the same as RAO.

29
Q

____ ______ ______, or mild to moderate asthma, is characterized as a low-grade airway inflammation that leads to poor performance in young to middle-aged athletic horses.

A

inflammatory airway disease

30
Q

True or false: at rest, horses with IAD do not demonstrate any discernible evidence of respiratory dysfunction.

A

TRUE

31
Q

What is one of the most common IAD findings?

A

Exercise intolerance, with or without signs of respiratory disease at exercise.

32
Q

How may severe IAD present?

A

Severe IAD may have mild abnormalities on auscultation and endoscopy, and occasionally coughing. Tracheal mucus may be present on endoscopic exam. It’s exacerbated during hot and humid weather. Racehorses may be described as fading during the last quarter of the race.

33
Q

What is the preferred method of cytology to diagnose IAD?

A

BAL: primarily alveolar macrophages and lymphocytes in normal horses.

34
Q

What will BAL look like in IAD patients?

A

IAD horses have increased nucleated cell counts including neutrophils, eosinophils, mast cells, or lymphocytes. Airway lymphocytosis may be the predominant finding.

35
Q

What is IAD diagnosis based on?

A

Diagnosis of IAD is based on clinical signs, airway inflammation with excess mucus, abnormal lower airway cytologic evaluation, or abnormal pulmonary function.

36
Q

What condition is associated with higher airway neutrophilia on BAL cytology, RAO or IAD?

A

RAO (>20% neutrophils)

37
Q

What are your differential diagnoses for cases with signs similar to IAD?

A

EIPH, RAO and SAOPD in remission, upper respiratory tract disease, septic lower tract disease (though systemic signs of illness are seen in this case)

38
Q

How do you treat IAD?

A

Tx of IAD is similar to RAO in some ways, like managing environment and reducing pulmonary inflammation, but there isn’t a lot of evidence based support for its treatment.

39
Q

What is the most important means of treating airway inflammation and dysfunction?f

A

environmental control

40
Q

What is the mainstay of drug therapy for IAD?

A

parenteral or inhaled corticosteroids - additional options include bronchodilators, mast cell inhibitors, and aerosolized therapy

41
Q

_______ is characterized as the presence of blood in the airways during or following strenuous exercise.

A

EIPH

42
Q

What are the clinical signs of EIPH?

A

poor athletic performance and epistaxis during or shortly after exercise (in only 4%)

43
Q

Observation of blood in the trachea using ________ 30-120 minutes after racing or strenuous exercise provides a definitive diagnosis of EIPH.

A

tracheobronchoscopy

44
Q

Describe Grade 0 of the EIPH grading system.

A

No blood detected in the pharynx, larynx, trachea, or main stem bronchi

45
Q

Describe Grade 1 of the EIPH grading system.

A

presence of one or more flecks of blood or less than or equal to 2 short, narrow, streams of blood in the trachea or main stem bronchi visible from the tracheal bifurcation

46
Q

Describe Grade 2 of the EIPH grading system.

A

one long stream of blood or >2 short streams occupying less than 1/3 of the tracheal circumference

47
Q

Describe Grade 3 of the EIPH grading system.

A

multiple, distinct streams of blood covering more than 1/3 of tracheal circumference - no blood pooling at the thoracic inlet

48
Q

Describe Grade 4 of the EIPH grading system.

A

multiple, coalescing streams of blood covering >90% of the tracheal surface, with pooling of blood at the thoracic inlet

49
Q

The presence of what on pathological examination of airway secretions or lavage fluid is evidence of EIPH?

A

RBCs or macrophages containing RBC fragments.

50
Q

Describe the pathogenesis of EIPH.

A

The cause of EIPH is rupture of alveolar capillary membranes with subsequent extravasation of blood into interstitial and alveolar spaces. The source of blood in such instances is the pulmonary circulation, not bronchial circulation.
Rupture of alveolar capillaries occurs secondary to an exercise-induced increase in transmural pressure (pressure difference between the inside of the capillary and the alveolar lumen), which can occur as a result of venous remodeling and loss of distensibility of pulmonary veins.

51
Q

True or false: the amount of racing completed is a risk factor for EIPH.

A

TRUE

52
Q

What drug can you give to reduce the frequency and severity of EIPH in TB racehorses?

A

Furosemide (Lasix)

Equine Medicine (27 decks)

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