Respiratory Flashcards

1
Q

What is VO2max

A

Maximal aerobic metabolic rate.

VO2 is the oxygen uptake.

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2
Q

Give 4 reasons why there may be a decrease in pulmonary gas exchange in the lungs.

A

o Increase in pulmonary resistance: URT, hyper secretions, inflammation
o Decreased alveolar/ pulmonary compliance: oedema, hypertension, fibrosis, interstitial disease
o Dynamic airway collapse: inflammatory airway disease, tracheal collapse
o Respiratory muscle/ chest wall disease
o Decreased cardiac output- lung or tissue perfusion, VQ inequality
o Decreased haemoglobin
o RARE: limitation in muscle metabolism eg with mitochondria

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3
Q

Give the aetiology and pathology of EIPH

A

Aet: Many - High pulmonary vascular pressures (intense exercise), inflammation, locomotory shock waves.

SP/br:
Strong heritability
Race horses, Eventers (not dressage/ ponies etc)
Large proportion (>90%)

Path: progressive disease, blood in airways –>slow to be removed–> chronic macrophage activity –> alveolar septal thickening

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4
Q

How would you diagnose EIPH?

a) straight after exercise
b) several days/ weeks post intense exercise

A

A) post exercise endoscopy - check for blood in trachea and grade.
B) bronchoalveolar lavage- looking for haemosiderophages (free erythrocytes and haemosiderin in macrophages, present for several weeks post episode)

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5
Q

How would you grade EIPH on endoscopy?

A

o Grade 1: Flecks of blood or a single short stream of blood extending less than a quarter of the tracheal length. Flecks of blood within the trachea.

o Grade 2: One continuous stream of blood extending at least one half the length of the trachea or multiple streams of blood covering less than one third of the tracheal surface. More than flecks, but less than a continuous stream.

o Grade 3: Multiple streams of blood covering more than one third of the tracheal surface. Continuous stream less than half the tracheal width.

o Grade 4: Abundant blood in the trachea, completely covering the tracheal surface and pooling at the thoracic inlet. Continuous stream greater than half the tracheal width.

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6
Q

Describe EIPH findings on PME

A
  • blue discolouration of the lungs is a result of the accumulation of haemosiderin (an iron pigment) within the damaged areas of lung
  • The lesions start caudally and progress craniodorsally
  • Histologically the damaged lung has peribronchial inflammation and fibrosis
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7
Q

Tx of EIPH?

  • why is furosemide not used in UK and Australia?
A

Goal is to reduce severity (fibrosis and progression), no single treatment

  • Needs time to recover after severe bleed
  • Anti-inflammatories indicated during inflammation stage (by day 3)
  • Furosemide: only medication to effect EIPH HOWEVER IS PERFORMANCE AFFECTING DRUG
    o Moa: bronchodilator for 5 hours, drops pulmonary blood pressure via hypovolaemia. Makes horses run faster by altering power to weight ratio, alkanises blood and alters drug excretion rates.
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8
Q

Equine Influenza- what is the aet + most common subtype, and how does this cause pathology

A

Equine influenza Virus H3N5–> strips ciliated epithelium of RT

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9
Q

Equine Influenza clinical signs

A

SIMILAR TO HUMAN INFLUENZA
Fever up to 41 degrees C
cough- dry and hacking progressing to moist
oedema and hyperaemia of URT trachea
Nasal discharge: serous mucopurulent
Lethargy, inappetence +/- muscle soreness

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10
Q

Equine influenza

  • how would you diagnose and treat
  • if you did not treat, what would happen
  • are there any control measures
A

PCR nasopharyngeal swab > paired serology> haematology
supportive care, hydration, NSAIDs. ABs only for secondary infection
sequalae: chronic cough, persistent pharyngitis and tracheitis

vaccines: 3 ones, proteqflu currently best (most protective of current strains)

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11
Q

Equine herpes virus

  • which strain causes respiratory signs?
  • when might clinical signs develop
  • what are the clinical signs?
A

EHV1+4
mild, dull +/- cough, serous ND (+ abortion storms and neuro disease)
develops under times of stress

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12
Q

EHV1+4: how would you diagnose and treat resp signs

A

Nasal pharyngeal swab PCR

symtomatic tx, NSAIDs, rest and fluids

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13
Q

Rattles

  • aet?
  • what age is mostly affected
  • clinical signs
A

rhodoccocus equi
foals 3 weeks- 6 months
pneumonia, cough, nasal discharge, pyrexia

(pyogranulomatous nodules in lung –> pyogranulomatous pneumonia)

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14
Q

how would you treat rattles in foals

A

macrolides or rifampin ABs long course

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15
Q

Strangles

  • aet
  • which part of the respiratory tract mostly affected?
  • incubation period - how long and are the horses infectious at this point?
A

Streptococcus equi var equi
URT and lymph nodes
3-14 days and not usually infectious if not pyrexic

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16
Q

Strangles clinical signs

  • early signs
  • progressed signs –> how does nasal discharge change + which lymph nodes become affected
A

Early clinical signs: depression, fever, mucoid nasal discharge slight cough, anorexia/difficulty swallowing, mild swelling pharngyeal/ intermandibular area

nasal discharge changes from mucoid to purulent

submandibular lymph nodes + retropharyngeal lymph nodes

17
Q

Strangles: what happens if retropharyngeal lymph node bursts?

A

inwards–> guttural pouch empyema ( becomes chronic, chondroids- can shed bacteria for long time)

outwards–> will see externally

18
Q

Diagnosis and treatment of strangles

A

PCR (+/- culture) from
o Nasopharyngeal swabs/lavage
o Guttural pouch washes/ aspirates
o Aspirate from abscess- FNA or swab

To confirm a horse is free of infection
Nasal swabs 3X negative swab 1 per week for 3 weeks 85% sure of no infection

Guttural pouch wash: 1 negative to be 88% sure

Tx: monitor, symptomatic. only give AB if outbreak–> prevention. if abscess formed in lymph node ABs will only prolong issue.

19
Q

Control of strangles

- does -ve antibody = not a PI?

A

quarantine new animals for 3 weeks
modified live vaccine= Equilis strep E (3 month immunity)
PI can have low levels of antibodies which are undetectable on ELISA

20
Q

What are 3 common ddx of LRT in horses?

A

Heaves ( recurrent airway obstruction) –>mild asthma
Inflammatory airway disease–> severe asthma
viral/ bacterial infections

21
Q

what is the cause of equine asthma?

A

Dust/ primary insult> lands in airway > inflammation> bronchoconstriction

Mucosal hyperplasia/ inflammatory infiltrate/ oedema
Goblet cells + mucus production

Chronic> fibrosis > progressive impairment of function
Decreased mucocilliary escalator
Increased inflammatory cells

22
Q

What are the clinical signs of equine asthma

  • mild cases
  • severe cases
  • v severe cases
A

mild- non at rest, mild exercise intolerance
severe- expiratory wheeze (+/- insp wheeze), tachypnoea, cough, nostril flare, nasal discharge. forced expiration> HEAVE LINE
v severe- resp distress and weight loss

middle age onset

23
Q

how would you diagnose and treat equine asthma

A

airway endoscopy: increased mucus in trachea, graded 0-5
lung function test: resistance
BAL: count 200 cells, neut> 25%, mast eosinophils>1%, curschmans spiral (plugs mucus)

Short term flare ups: bronchodilators: clenbuterol, atropine, nuscopan
mid term: corticosteroids systemic= predisolone,
inhaled: better action
• Ciclesonide,
• Beclomethasone dipronpionate,
• fluticasone propionate,
• nebulised dexamethasone fluticasone
Long term: management, soaked hay, bedding rubber mat etc
mucolytics+/-

24
Q

which lobes of the lung are most affected in bronchopneumonia?

A

mixed spp bacterial infection of right ventral lobes > other lobes

25
Q

when does pleuropneumonia develop and what are its clinical signs

what procedure might need to be done

A

when bacteria in bronchioles cross into pleural space

reduced lung sounds ventrally, dull on percussion, US, thoracentesis + bronchopneumonia signs

thoracic drainage as part of tx (+ broad spectrum ABs)

26
Q

what are the stages of pleuropneumonia

A

Stages of Pleuropneumonia
1. Acute exudative stage: Inflammation of the lung and pleura – sterile protein rich pleural exudate

  1. Fibrinopurulent stage: Bacteria invade and multiply in the pleural fluid. Fibrin deposits on pleural surfaces. Lymphatic obstruction.
  2. Organisational Stage- mature fibrin tags connecting lung to wall.
27
Q

clinical signs of bronchopneumonia

A

Bronchopneumonia: dyspnoea, tachypnoea, systemic illness, adventitious lung sounds,

  • DX: cough, tracheal aspirate and culture. May US lungs.
  • Tx: penicillin, gentamicin, metronidazole, (broad spec abs) Antiinflamms
28
Q

cause of equine lungworm?

how would you diagnose this

A

Dictylocaulus arnfieldi - donkeys asymptomatic carrier

Dx: identification of worms in tracheal wash or BAL
!NB eosinophils in TW or BAL DO NOT INDICATE lungworm!

Tx: ivermectins
- Horses grazed with donkeys should receive ivermectin regularly

29
Q

Equine Multinodular pulmonary fibrosis

- which common infectious LRT condition is this associated with

A

Associated with Equine Herpes Virus -5 (EHV-5)
Dx: Inclusion bodies may be detected on BAL or on lung biopsy tissues - EHV-5 can also be isolated from normal horses
Cx: Often weight loss / pyrexia
Ddx: RAO
Px Guarded - poor

30
Q

how common is thoracic neoplasia in horses?

A

rare