Respiratory Flashcards
What is VO2max
Maximal aerobic metabolic rate.
VO2 is the oxygen uptake.
Give 4 reasons why there may be a decrease in pulmonary gas exchange in the lungs.
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
Give the aetiology and pathology of EIPH
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
How would you diagnose EIPH?
a) straight after exercise
b) several days/ weeks post intense exercise
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)
How would you grade EIPH on endoscopy?
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.
Describe EIPH findings on PME
- 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
Tx of EIPH?
- why is furosemide not used in UK and Australia?
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.
Equine Influenza- what is the aet + most common subtype, and how does this cause pathology
Equine influenza Virus H3N5–> strips ciliated epithelium of RT
Equine Influenza clinical signs
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
Equine influenza
- how would you diagnose and treat
- if you did not treat, what would happen
- are there any control measures
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)
Equine herpes virus
- which strain causes respiratory signs?
- when might clinical signs develop
- what are the clinical signs?
EHV1+4
mild, dull +/- cough, serous ND (+ abortion storms and neuro disease)
develops under times of stress
EHV1+4: how would you diagnose and treat resp signs
Nasal pharyngeal swab PCR
symtomatic tx, NSAIDs, rest and fluids
Rattles
- aet?
- what age is mostly affected
- clinical signs
rhodoccocus equi
foals 3 weeks- 6 months
pneumonia, cough, nasal discharge, pyrexia
(pyogranulomatous nodules in lung –> pyogranulomatous pneumonia)
how would you treat rattles in foals
macrolides or rifampin ABs long course
Strangles
- aet
- which part of the respiratory tract mostly affected?
- incubation period - how long and are the horses infectious at this point?
Streptococcus equi var equi
URT and lymph nodes
3-14 days and not usually infectious if not pyrexic
Strangles clinical signs
- early signs
- progressed signs –> how does nasal discharge change + which lymph nodes become affected
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
Strangles: what happens if retropharyngeal lymph node bursts?
inwards–> guttural pouch empyema ( becomes chronic, chondroids- can shed bacteria for long time)
outwards–> will see externally
Diagnosis and treatment of strangles
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.
Control of strangles
- does -ve antibody = not a PI?
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
What are 3 common ddx of LRT in horses?
Heaves ( recurrent airway obstruction) –>mild asthma
Inflammatory airway disease–> severe asthma
viral/ bacterial infections
what is the cause of equine asthma?
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
What are the clinical signs of equine asthma
- mild cases
- severe cases
- v severe cases
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
how would you diagnose and treat equine asthma
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+/-
which lobes of the lung are most affected in bronchopneumonia?
mixed spp bacterial infection of right ventral lobes > other lobes
