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72 Cards in this Set
- Front
- Back
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what are the 5 differentials for equine neonatal lower respiratory tract disorders?
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neonatal pneumonia
prepartum EHV 1 infection fractured ribs meconium aspiration prematurity/dysmaturity |
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what is the normal resp rate of a neonate? hat is it 1 hour post partum?
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60-80 and after 1 hour 30/min
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why are foals breath sounds not reliable?
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because significant consolidation or interstitial disease can occur without abnormal sounds on auscultation
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what is the cause of neonatal pneumonia and how do you treat it?
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it is a common sequel to bacteraemia and septicaemia. treat with ABs (C&S ideally) but pen/gent, ceftiofur, and cefquinome good empirital choices
supplement IgG as ill be concurrent FPT intense nursing, oxygen, fluids and turning of recumbent foals |
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how do you confirm prepartum EHV1 infection in a weak foal that dies despite treatment?
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PCR or histo of liver, lungs, thymus - can submit fresh foal carcase, placenta and mare blood
mind most stud mares vaccinated against EHV1 and 4 but protection is incomplete |
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what tool is useful for diagnosing neonatal rib fracture?
how do you treat it? |
ultrasonography and careful palpation
stabilise with adhesive bandage and confine foal to stable for a few weeks - surgery if flail chest |
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how do you treat meconium aspiration?
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nursing and broad spectrum antibiotics - aspirate from airways can be attempted
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what does prematurity/dysmaturity involve? how is it treated and when is prognosis poor?
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inadequate lung maturation --> severe respiratory effort and lung dysfunction.
provide surfactant (expensive), respiratory support and antibiotics - prognosis poor if under 300 days gestation |
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what are 2 differentials of respiratory disease in growing foals?
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rhodococcus equine
pneumonia strep equi var zooepidemicus |
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how long after infection of rhodococcus do foals present with signs?
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probably infected as neonates (inhale/ingest) but do not develop clinical signs until 2-6 months old
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what are the clinical signs of rhodococcus equi infection?
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ill thrift
debility progressive dyspnoea less commonly coughing and nasal discharge can spread to mediastinal and mesenteric lymph nodes, joints, physes and GIT --> diarrhoea and immune mediated polysunovitis. |
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what is seen on H&B of rhodococcus equi infection?
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hyperfibrinogenaemia, neutrophilia and thrombocytopaenia
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how do you treat R equi?
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6-8 weeks of rifampin and erythromycinc, clarithromycin or azithromycine
- hyperimmune serum available also screen other in contact foals - likely to be infected: serological test available but not 100% accurate |
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what prophylactic measures can you take against R equi?
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- improve management by reducing stock density, collect faeces from paddocks, rotate paddocks and move water and feed areas around to prevent dust build up
administer appropriate prophylactic antibiotics or hyperimmune serum to neonates vaccine under development |
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what are the clinical signs of strep equi var zooepidemicus?
how is it treated? |
nuisance rather than concern
cough, nasal discharge, slight SM LN enlargement, intermitent mild pyrexia but animals not sick give penicillin and turn out or ignore - may ax and ane for eeks |
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list the differentials for acute infectious respiratory disease in adults (5 viral, 7 bacteria)
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influenza
EHV1 and 4 rhinovirus EVA strangles M. felis and equirhinis B. bronchiseptica Strep pneumonia pasteurella actinobacillus |
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what are the most common clinical signs of acute respiratory disease in adults?
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pyrexia
dullness anorexia coughing mucoid to mucopurulent nasal discharge bilateral SM LN enlargement influenza likely if spreads very quickly |
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what should you do when faced with an acute respiratory disease outbreak?
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always test for strangles as method of control differs as does its treatment
- nasopharyngeal swab or guttural pouch wash |
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what do you submit for virus screen?
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nasopharyngeal swab, tracheal aspirate, BALF, serum or heparinised blood
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how is influenza detected and how long does it take?
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ELISA via secretions - takes 4 hours
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why isn't culture of influenza and EHV not used for clinical diagnosis?
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because it takes several weeks - more useful for epidemiology
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how long does paired serology take?
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2-3 weeks
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what samples do you take for bacterial infections and how long does culture take?
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nasopharyngeal swab (strangles) or tracheal aspirate
takes 3-4 days |
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how do you manage an acute respiratory outbreak?
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maintain horses in clean air environment that is ell ventilated with shaving bedding and haylage fed from ground (gravitational drainage)
antibiotics if horse remains febrils for more than 4-5 days or if respiratory secretions purulent or marked respiratory signs occur - particularly in young and very old horses CLENBUTEROL may aid mucociliary clearance |
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what is the commonest cause of equine repiratory infection?
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EHV 4
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what does EHV 1 cause
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abortion and encephalomyelopathy. can occasionally cause respiratory disease
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how is EHV contracted and hat is its pathogenesis?
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early in life - and probably all become asymptomatic carriers of latent virus that may recrudesce with intercurrent disease or stress - immunity short lived and get repeatedly infected especially following mixing of horses at sales or rases
causes immunosuppression and vaccines not very effective but may afford some protection in younger race horses |
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what does rhinovirus cause?
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largely affects URT - not that big of a deal - infection occurs in conjunction with other infectious agents
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what are the clinical signs of equine viral arteritis?
how is it spread, and how is it prevented? |
general signs of respiratory disease
severe conjunctivitis profound depression periorbital oedema venerally spread. prevent via vaccine (effective) |
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how long is strep equi var equi viable in environment for?
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weeks to months
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what is atypical strangles?
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cases that have no lymph node abscessation and may be misclassified as viral respiratory disease unless culture or PCR is done
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how do you confirm strangles infection?
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culture or PCR of bacteria in nasal, nasopharyngeal or guttural pouch swabs/washes.
need to differential from strep zooepidmicus var zooepidemicus - common commensal |
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how is strangles treated?
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can treat with penicillin early in disease course to stop clinical progression, but unclear if develop immunity: so isolate
do NOT administer antibiotics with lymph node abscesses |
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what are 3 possible sequels of strangles?
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bastard strangles: lymph nodes, physes -weight loss, malaise, etc
purpura haemorrhagica - type 3 immune mediated vasculitis 1-3 months after infection - oedema, petchiae, multiorgan failure guttural pouch empyema |
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how do you treat purpura haemorrhagica?
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immunosupp dex, penicillin, supportive care
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list 13 causes of pulmonary/chest wall disorders that only affect individual horses
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recurrent airway obstruction
summer pasture associated obstructive pulmonary disease inflammatory airway disease lungworm idiopathic pulmonary eosinophilia interstitial (restrictive) lung disease pulmonary oedema thoracic neoplasia pulmonary abscesses and pleuropneumonia pleural effusion pneumothorax diaphragmatic hernia exercise induced pulmonary haemorrhage |
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what does recurrent airway obstruction result from? what occurs in response to the aetiological agent?
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inflammatory response to pro inflammatory agents inhaled in dust - moulds, endotoxin, particulates, ammonia, from poorly conserved hay and straw
--> bronchospasm, thickening of airway walls and oedema with leucocyte (neutrophil) infiltration, mucus plugging and epithelial deciliation |
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what may aid diagnosis of RAO?
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controlled exposure of hay or straw
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what are the risk factors associated with RAO?
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over 5yo
poor stable hygiene genetics respiratory infection exposure to hay/straw early life |
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hat are the clinical signs of RAO?
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coughing - 85%: exacerbated by exercise, poor exercise tolerance
bilateral mucopurulent nasal discharge in 55% - others sallo it tachypnoea (>12/min) heave line if severe - wheeze/crackle |
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how is RAO diagnosed?
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endoscopy: mucopus
tracheal aspirate: over 20% neutrophils BALF over 5% neutrophils (lavaged distal airways with 250-300ml saline via endoscope or BAL tube under heavy sedation |
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how do you manage and treat RAO
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- eliminate organic dust: keep at pasture
- shallow shavings or paper bedding: remove all wet bedding daily - complete cubed diet with alfalfa or silage (soaking hay does not work) - adequate ventilation - turn out in dust free environment bronchodilator - clenbuterol or salbutamol or atropine as rescue drug - inhaled beclomethasone or oral pred - maintain hydration to avoid tenacious secretions |
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what is the presenting sign of summer pasture associated obstructive pulmonary disease?
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dyspnoea
crackles and wheezes heard on auscultation |
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what is inflammatory airway disease charaterised by?
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coughing, exercise intolerance, increased volumes of neutrophilic mucopus in lower airways and occasionally nasal discharge - not depressed or pyrexic and do not have overt airway obstruction that characerises RAO
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which horses may develop IAD? what is aetiology thought to be?
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any horse- commonly identified at start of training (2yo flat horses, 4-8yo national hunt= with syndrome self resolving in a few wks or persisting for months to years
think multifactorial: S. zooepidemicus, pasteurella, actinobacillus, S. pneumoniae, B. bronchiseptica, mycoplasma, dust/endotoxin |
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how do you treat IAD?
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provide dust free environment and reset
antibiotics C&S - oxytet, ceftiofur, cefquinome, enroflox, TMPS inhaled glucocorticoids if chronic |
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what time of year dose lungworm occur? how do you diagnose it?
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summer or autumn
eosinophila in tracheal mucus or BALF confirms diagnosis, or via positive response anthelmintics. infection non patent to can't use Baermann flotation treat in contact horses and donkeys with avermectin or benzimidazole and move to clean pasture |
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what are 3 idiopathic pulmonary eosinophilic diseases and how do you treat them?
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acute alveolitis, chronic small airway disease, chronic interstitial disease - respond to corticosteroids
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explain the pathogenesis of interstitial lung disease
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- acute/chronic inflammatory alveolitis --> injury to type I epithelial and endothelial cells
- serum protein leak into alvoeli --> pulmonary oedema acutely - inflammatory cells infiltrate alveoli and interstitium if survive: get interstitial fibrosis and granuloma devlopment over weeks to years --> decreased compliance, predominantly inspiratory dyspnoea |
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what can be heard on auscultation in interstitial lung disease?
how is it treated? |
wheezes and crackles, especially end inspiratory
immunosuppressive glucocorticoids and frusemide |
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what are 8 causes of pulmonary oedema?
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acute URT obstruction
cardiac failure alveolitis/interstitial lung disease smoke inhalation neoplasia plant and drug toxicity immune mediated volume overload |
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what are the CS of pulmonary oedema and how is it treated?
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frothy nasal discharge 8often blood tinged), increased inspiratory effort with reduced compliance, widespread fine crackles (some may have quite chest despite obvious dyspnoea)
endoscopy - see frothy fluid in airways treat underlying cause (e.g. tracheostomy if URT obstruction), frusemide, intranasal oxygen, antibiotis and steroids where appropriate |
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what is the most common thoracic neoplasm in horses? what are some oft he clinical signs?
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lymphosarc. signs nonspecific includeing plerual effusion, ventral oedema, jugular distension
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what is the cause of pulmonary abscesses and pleuropneumonia?
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prolonged transport: pulmonary defences compromised/sequel to aspiration of saliva and food: usually mixed infection
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what are the stages of developing pleuropneumonia?
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- bac colonise lung --> pneumonia or absces: extends to pleura: get sterile effusion - ABs may be effective in this stage
- bac infection extends to pleura --> purulent effusion: need to drain - fibrin formed which lines pleural space - get significant fibrin deposition --> pleural peel which limits thoracic expansion |
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what is parapneumonic plerural effusion?
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sterile inflammatory effusion seen in first phase of pulmonary abscesses/pleuropneumonia development - responds to ABs alone
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what are the clinical signs of pulmonary abscesses and pleuropneumonia? what can it be mistaken for?
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sick - lethargy, anorexia, pyrexia
ventral oedema respiratory distress pleurodynia: reluctance to move, base narrow stance, elbow abduction soft muffled coughin fast shallow ventilation malodorous breath: suggests anaerobic infection or lung necrosis = poor prognosis can be mistaken for colic, laminitis, hypocalcaemia |
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how do you diagnose pulmonary abscesses and pleuropneumonia and how to you treat it?
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diagnose with ultrasonogrphay : essential to assess nature and extent and to select site for thoracocentis s which confirms diagnosis, C&S and is part of treatment with antibiotic therapy
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list some of the causes of pleural effusion - what do you do with sample?
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thoracic neoplasia (most common cause)
bacterial pleuropneumonia penetrating chest wall ound concurrent peritonitis CHF hypoproteinaemia chylothorax diaphragmatic hernia perform cytology, aerobic and anaerobic culture and gram smear for bac |
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what are the clinical signs of diaphragmatic hernia?
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usually asymptomatic
- GI signs due to strangulaton or incarceratino of bowl or respiratory signs due to lung compression |
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what causes exercise induced pulmonary haemorrhage and what lung lobe is affected?
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very fast exercise horses bleed from DORSOCAUDAL LUNG becuae of very high pulmonary capillary pressures, sub atmospheric inspiratory pressures and presence of other disease: Urt (RLN), IAD, cardiac, etc
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hat can marked EIPH result in? what is not a feature?
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coughing is not a feature
can cause epistaxis, poor exercise performance, pulling up and rarely death |
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how is EIPH diagnosed?
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via bronchoscopy 30 minutes post exercise:
fresh blood in trachea and bronchi for dayws following bleed haemosidering secretions visible for a wek haemosiderophages identified in tracheal aspirate and BALF for months following bleed |
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how do you treat EIPH?
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rest, treat underlying disease, NSAID to reduce interstitial lung fibrosis, nasal dilator strips, dust free environment and train at slower speeds, train on softer track to reduce concussion
pre race admin of frusemide permitted in some countries but not UK and efficacy questionable RETIRE NON RESPONSIVE HORSES TO LESS DEMANDING DISCIPLINES |
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what conditions --> neutrophilia on BALF (7)
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RAO
SPAOPD IAD bacterial bronchopneumonia lung abscess pleuropneumonia acute (under 10 days) viral airway disease |
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what conditions --> eosinophilia on BALF (4)?
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lungworm
parascaris equorum migration idiopathic pulmonary eosinophilia eosinophilic sub type of IAD |
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what may result in erythrocytes and hgaemosiderophages on BALF?
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EIPH
trauma during collection (just erythrocyte) neoplasia, abscess, coagulopathy (rare) |
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where do you collect pleural fluid from on RHS vs LHS?
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just above lateral thoracic vein
RHS: 6-8th intercostal space US guided LHS 7-9th intercostal space US guided |
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what is the pathogenesis of developing
1) transudate 2) modified transudate 3) exudate |
1) decreased colloid pressure and increased hydrostatic pressure
2) increased capillary and lymphatic hydrostatic pressure 3) increased capillary permeability and decreased lymphatic drainage |
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when is a horse considered to have recovered from strangles?
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when 3 nasopharyngeal swabs collected at weekly intervals negative for S equi var equi
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what are 3 properties of septic pleural fluid?
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low glucose (under 2mM)
low pH (under 7) PF lactate > plasma lactate |
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what is seen radiographically of pneumothorax?
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absence of aerated lung dorsally
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