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256 Cards in this Set
- Front
- Back
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Define lameness |
alteration of the normal stance or gait pattern caused by a structural or mechanical disorder of the locomotor system
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Stages of the clinical investigation of a lame horse
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1. detailed history |
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Grades of lameness
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grade 0- sound |
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most commonly used LAs for locating lameness
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mepivicaine, prilocaine
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most common equine endocrinopahty and its names
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Equine cushings syndrome
pituitary pars intermedia dysfunction pituitary adinoma pituitary hyperplasia pituitary dependant hyperadrenocorticism in horses and ponise |
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epidemiology of ECS
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older equids- mean age 20 years |
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pathogenesis of ECD
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loss of inhibitory dopaminergic innervation of the par intermedia-->abnormal hrmone production - lose normla circadian pattern of production->- excess GCS - excess production with loss of negative feedback mechanism on the hypothalamus and pituitary |
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Clinical sign of ECD
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1. hirsutim, abnormal coat cshedding- only pathognomonic CS- initially localised then generalised in advanced cases 9. hyperlipaemia 10. neurologic abnormaliteis- narcolepsy, central blindness |
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diagnostic tests for ECD |
Hx CS
gold standard is post mortem examination of pituitary- gross enlargement, histopath, +/- adrenal cortical hyperplasia - ECD will not suppress special handling (false ngs if not handled right and transported asap), some labs dont have the assay, - seasonal variations in baseline
Serum insulin concentration- insulin insensitivity in ECD horses, not sepcific (also metabolic syndrome) but could be a prognostic factor
Future tests: domperidone response test- dopamine antagonist- causes elevation in plasma ACTH +4hrs in ECD |
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Management of ECD
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Can be managed, not cured IMPROVE OVERALL HEALTH - nutrition- calorie dense if emaciated |
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what does staight hindlimb predispose to? |
upward fixation of the patella or proximal suspensory ligament desmitits |
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when can you eel bounding digital pulses
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acute laminitis
subsolar abscesses bruising pedal bone fracture |
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Diagnostic nerve blocks
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1. palmar digital nerve
2. abaxial sesamoid 3. low 4 point/6pt high 4 point coffin joint- dorsal, palmarolateral fetlock- dorsal, palmar pouch, lateral collateral |
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preparation for intraarticulr block
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clip hair
5min alcohol and povidone iodine scrub sterile gloves new bottle adequate restraint good techique |
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overall goal of lameness exam
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find sources of pain
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lameness hx
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why are conformation faults concerning?`
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Causes ‘abnormal’ biomechanical loading on the musculoskeletal structures resulting in musculoskeletal structures resulting in overload overload that may result in:
- DJD tendon/ligament problems - hoof growth problems |
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hoof- pastern angle
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should be equal
hoof angle too sharp- broken back hoof too steep- broken forward |
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sway back, roach back
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deep curve in back, roach- hunched.
hard to find a saddle- back problems |
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risk factors for upward fixation of patella
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Young big horses
Straight hindlimb Straight hindlimb conformation Inadequate conditioning |
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things to focu on when examining forelimb
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Neck and back examination
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muscle atrophy |
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how do felxions tests help dx disadvantages
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exacerbate baseline lameness |
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disadvantages of radiographs for investigating lameness |
superimpostition |
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indications for rads to investigate lameness
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- localised by palpateion
- localised area causing lameness through blocks - prepurchase exam, yearling sales - suspected fracture |
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vital signs in the horse
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Adult |
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ddx liver failure
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theileriosis |
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how do pyrrolizidine alkaloids cause hepatotox
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PA cause mitotic arrest of hepatocyte, leading to delayed progressive liver damage. Pyrrole binf to hepatic proteins and nucleic acids- grow but dont divide, producing megalocytes
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sources of mycotoxicitie |
fusarium (fumonins) - field fungi |
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syndromes associated with Theillers disease |
Fever |
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tx chronic active hepatitis
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liver culture- rule out bacterial invovlement
then steroids (dex) + supportive therapies |
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presentation of bile stones
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fever of unknown origin
recurrent colic icterus |
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management of cholelithiasis
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often unrewarding
diet- low fat diet surgical removal should be preceded by broad spec AB |
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most common biliary obstruction in the horse
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cholangitis/ cholangiohepatitis
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casues of cholangitis, cholangiohepatitis
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fbs- grain sand stick
secondary to choleliths, intestinal inflamm/obstruction, parasitism, neoplasia, toxins often present in active chronic hepatitis |
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mx cholangitis
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ABs until GGT within normal range |
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tx fatty liver
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1. address underlying cause |
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liver u/s abnormalities
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1. shouldnt be more echogenic than spleen
2. rounded edges 3, shouldnt reach costochondral arch RHS 4. masses 5. small- end stage |
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nutritional support liver dz
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breach chain AAs- mollasses
Vit B- neuro enteral best parenteral- 50% dex, 15%AAs |
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where to liver biopsy
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RHS, below line drawn from tuber coxae to below line drawn from tuber coxae to
point of shoulder, between 8th– 14th ICS |
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histology of PA toxicosis
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Megalocytes |
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lab abnormalities- hyperlipaemia |
increased
triglycerides GGT ALP GLDH azotaemia acidosis |
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Equine urinary dzs
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Acute & Chronic Renal failure |
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definition of ARF |
sustained decrease in GFR leading to azotaemia, fluid and acid base derangements |
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Causes of ARF
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1. hypoperfusion
2. nephrotoxici drugs- aminoglycosides, NSAIDS, oxytetracycline 3. myoglobinaemia 4. heavy metals 5. vitamin D or K tox 6. plant toxins- onion, red maple glomerulonephritis interstitial nephritis microvascular thrombosis postrenal failure |
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presentation of renal disease |
anorexia
PUPD dehydration colic pigmenturia uraemia encephalopathy laminities primary or secondary |
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tx renal failure |
Acute & Chronic
Renal Failure ▫ Increase GFR ▫ H yp ( ertonic saline ( 4 g/ g m g/ k g IV bolus ) ▫ Furosemide ( 1-2mg/kg IV or IM BID; 0.12mg/kg loading dose then 0.12mg/kg/hr ) ▫ Mannitol ( 0.25g – 1g/kg IV over 30 min ) ▫ Dopamine ( 3-5 g/kg/min ) ▫ N h t i d ! N o nep h ro t ox i c d rugs! ▫ Diuresis, Glucose, Bicarbonate & Insulin for hyperkalemia |
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predispostions for uroliths
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male
high urine ph infectiou nidu chrystalluria mucoprotein ca CO3 high mineral diet urine stasis decreae water intake cystitis |
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causes urinary incontience
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EHV1
cystitis sabulous urolithiasis cauda equina syndrome sorghum ataxia- cystitis syndrome ectopic ureter |
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sabulous urolithiasis tx |
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osteochondrosis |
3-20 limb joints and cervial spine |
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physitis |
4-12m distal limbs and stifles
or during early training at 20-24 months
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angular limb deformities |
1-6m distal fore and hind limbs |
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flexural deformities |
1-4m distal forelimbs |
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tarsal collapse |
1-18m |
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Wobbler disease |
6-24m cervical spine |
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vertebral abnormalities |
6-9m thoracolumbar spine |
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2 main syndromes seen with osteochondrosis and considerations for dx |
~3-9 months - - lies down a lot; -has difficulty keeping up with dam/other foals;
- usually assoc with exercise/training; - lameness + poor performance; - swollen, stiff joints - often insidious onset but can see acute lameness
older animals may exhibit signs clinical signs vary depending on the sites involved - positive flexion response, joints blockable |
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treatment and management of OC in young foals |
resrtict diet and exercise to limit growth and prevent progression of early lesions |
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treatment and management of OC in older animals |
conservative approach with some rest and progressive exercise program |
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medical and surgical treatment osteochondrosis |
intraarticular corticosteroids, hyaluronic acid
arthroscopy is tx of choice |
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where does OC occur and what are the lesions |
1. hock 2. stifle 3. shoulder 4. fetlock 5. cervical spine
cartilage thickening, loose fragments, wear lines, erosions, synovitis, cavitation and secondary arthritis |
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confirmation of diagnosis of OC |
Clinical signs ad hx radiography- characteristic signs ultrasound- early stifle lesions arthroscopy scintigraphy- if significant subchondral bone damage clin path- synovial fluid changes MRI - good for early lesions |
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Causes of OC |
1. growth and body size 2. nutrition- overfeeding(excess DE), mineral imbalance (Ca:P imbalance, excess Zn,Cd, cu def) toxicity 3. endocrinological involvement- hyperglycaemia, insulinaemia- overfeeding 4. hereditary/ genetic 5. exercise/ biomechanics |
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what is the probable cause of OC |
disruption of the blood supply to growth cartilage (cartilage canals) from the perichondrium and subchondral bone - earliest lesions are chondronecrosis - disrupted as they cross the ossification front - focal failure of endochondrial ossifications+ mechanical factors and trauma lead to dyschondroplasia--> OC |
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Pathophysiology of Physitis, aetiology & common sites |
abnormality of endochondrial ossification in metaphyseal growth plate - weakening of integrity of g/p - microfracture and pain at exercise - flaring of the growth plate
nutrition, rapid growth, trauma, genetics
tibia, radius, ulna, 3rd MC/MT, prox P1 |
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Clinical signs of physitis |
variable lameness and conformational defects, usually self limiting, common in TBs
may have other forms of DSP |
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Angular limb deformities signs and aetiology |
distal limb deviation in lateral (valgus) or medial (varus) direction
problems at birth usually corrected spontaneously with good management. Sx is common/ controversial
Ax= joint laxity, defective e/o of carpal and tarsal bones, growth rate and conformation skeeltal immaturity, growth imbalance at the ends of long bones, asymmetric rpessure across the g/p |
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Flexural deformities |
congenital contracture- not a DSP acquired flexion of the distal limbs in first few months= DSP mainly affects forelimbs causing contracture of the DDFT and SDPT
aetiology thought to be overfeeding, nutrient imbalance, rapid growtth with limited exercise- failure of ligaments and tendons to develop at the same rate as boens
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management of flexural deformities |
diet reduction and exercise recommened wiht farriery +/- surg |
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Presentation of tarsal collapse |
can be present in young foals <1m but missed if CS missed main sign is flexural deformity of hock caused by collapse of the central and 3rd tarsal bones- usually bilateral
may be swelling, local pain & lameness, most comm sign is stiffness with poor impulsion (bunny hopping)
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Sequelae of tibial collapse |
if not recodnised as foal may progress to DJD and ankylosis |
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aetiology/ management of Wobblers dz |
Characterised by vertebral stenosis or instability resulting in ataxia
common in well grown TBs <3 over nutrition and exercise excess- necrosis at cartilage/ bone junction--> growth of cartilage without ossification--> stenosis and spinal cord compression may be osteochondrosis of cervical articulations
reduced feeding and exercise restriction can be beneficial antiinflamms antioedema |
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lesions seen in Wobblers, progression |
1. cervial vertebral displacement 2. abnormalities of vertebral development 3. functional stenosis of vertebral canal 4. arthropathy of articular processes 5. synovial cyst at C5-T1- interneural articulations
can be static or dynamic acute or gradual symmetrical normal mentation |
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Acquried vertebral deformities- aetiology and management |
most congenital- not DSP kyphosis /(roach back) occurs post weaning in rapidly growing foals (6-9m) may be assoc with other DSPs (OC)
cut back growth rate and exercise |
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what needs to be done to better unerstand DSPs |
1. epidemiological studies= assess prevalence, overall problem- understand nutrition and stud management factors 2. evidence based field studies- evaluate effects of introducing improved nutritional regimes on studs 3. further research into endochondrial ossification- underlying process in all DSPs 4. role of copper, other minerals 5. role of high energy feeding 6. role of biomechanics and exercise 7. better understanding of genetic basis of DSPs |
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How to prevent DSPs |
1. ensure balanced nutrutuin and a steady growth pattern of foals 2. avoid excess carb and energy 3. adequate exercise after weaning- avoid excess 4. avoid breeding from genetic carriers
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tests of liomited value for ECD |
serum cortisol conc routine bloods blood glucose conc ACTH stim test UCCR |
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principles of medical management for ECD |
all drugs are lifelong no drug wqill completely halt progression need to tx 203m before assessing efficacy of any drug therapy monitor improvement wh CS or with DST and/or ACTH concentrations |
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Pharmacology of pergolide mesylate for ECD |
dopamine agonist Permax tabs/ ranvet pergolide luquid decreases ACTH concs and ameliorated CSs starting dose 0.001-0.002mg/kg PO SID side effects: anorexia, depression, diarrhoea, colic
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Cyproheptadine pharmacology for ECD |
serotonin antagonist- serotonin stimulates secretion of ACTH from PI Periactin tablets less efficacious than pergolide mesylate but cheaper, over he counter starting dose 0.25-0.5mg/kg SID adverse effects: drowsiness ataxia |
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trilostane for ECD |
competitive inhibitor of adrenal cortisol production vetoryl tablets ameliorates clinical signs with exception of hirsutism start 1mg/kg SID no reported side effects |
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Prognosis for ECD |
may be successfully managed for years in some cases- routine health care +/- meds require close monitoring and attention to rougtine care QOL and lifespan improved by meds |
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What is equine metabolic syndrome? |
- associated with the development of laminitis in overweight or obese middle aed horses and ponies. Often less severe than the laminitis that follows severe systemic dz - only common thread- no other CS or ABns typical od EMS - aka peripheral cushings disease no gender predilection very common in ponies used to think it was hypoT |
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clinical signs of EMS |
- generalised excessive s/c fat deposition- neck rump prepuce described as 'easy keepers'- difficult to lose weight by dietary restriction, weight gain with relatively small intake |
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pathogenesis of EMS |
insulin resistance and hyperglyc, secondary to feeding diets with high glucaemic index (eg grain) leading to high fat accumulation --> chronic glucotoxicity, oxidative stress on vesels in hoof lamellae, decreased NO synthesis leading to vasoconstriction, activation of matrix metalloproteinases - local tissue hypercortisolaemia due to conversion fo cortisone to cortisol, especially in omental fat |
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EMS management and prevention |
1. increased exercise 2. dietary change- induce weight loss, improve indulin sensiticity (low GI), avoid aggressive dietary restriction in ponies due to hyperlipidaemia 3. manage laminitis
Dont feed grain to inactive horse or ponies |
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common equine ocular diseases |
trauma keratitis uveitis- 1` or 2`
corneal stromal abcessation neoplasia- scc, sarcoids cataracts glaucoma |
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Beginning an opthalmic exam |
Distance exam- symmetry, globe position, size, movement Quiet area that can be darkened inspect area before sedation thorough Hx palpebral, menace and PLR reflexes obstacle course to test vison Sedation- a2 agonist/ opioid agonist or ag/antag Nerve blocks - auriculopalpebral - supraorbital Diagnostic miadtriasis- tropicamide |
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steps (After meds) of an opthalmic exam |
1. transillumination and retroillumination- penlight 2. direct/ indirect opthalmoscopy (cheaper equipment) 3. examination for foreign bodies 4. fluorescein staining 5. culture and/or cytology of corneal swabs or scrapings (+/- topical anaesthesia- proparacine)
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other opthalmic tests to consider |
tonometry STT slit lamp biomicroscopy- binocular magnified view ultrasonography if fundus cant be seen due to opacity |
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aetiology of ulcerative keratitis |
mechanical trauma +- secondary infection primary infectious decreased tear production ( VII paresis) irritants GCS associated infiltrative keratopathies- uncommon- Ca, WBCs etc |
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signs of ulcerative keratitis |
blepharospasm (closed) and epiphora (tearing) focal corneal opacity +- adjacent corneal oedema (mositure enters via ulcer) +- keratomalacia fluorescein positive unless descmetocoele- eroded down to descmentocoele membrane/ no stroma left +/- neovascularisation +- concurrent anterior uveitis
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ancillary diagnostics for ulcerative keratitis |
- look for causes of trauma eg Fb corneal swab / scrape for cyto and culture - fundic exam - +- STT, slip lamp exam or tonometry |
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Management ulcerative keratitis |
1. topical AMs (+- antifungal +- antiviral) - direct application - subpalpebral or nasolacrimal lavage - subconjunctival injections
2. topical atropine- mydriasis and cycloplegia- remove ciliary spasm- painful, increased aqueus drainage
3. systemic NSAIDs- analgesia, AI, PO, IV
4. tpical anticollagenase therapy to prevent keratomalacia- plasma/serum, EDTA, tetracyclines
5. Surgical intervention Get apposition with mucosa for enhanced blood supply/ healing- - tarorrhapy- suture eyelids together (horizontal mattress) - nictitans/ conjunctival flap salvage- enucleation
ADDITIONAL - eye mask- solid hard cup - systemic ABs- poor delivery if no vessels - systemic tetras for anticollagenase activity - ocular lubricants - therapeutic contact lens- initiate high drug dose |
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oinment vs solution for eye tx |
ointments- stay in tear film (oily) fatty nature may delay healing cant put through lavage system
solutions- more frequent admin required, can be lavaged, wont delay healing |
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prognosis for corneal ulcer |
superficial- heal with no scar deep- neovasc, granulation, fibrosis scar formation- permanent visual defects px poor for fungal infections, ulcers with significant keratomalacia and descmetocoeles may get concurrent uveitis- cause visual defects or become recurrent duration of therapy can be days to weeks |
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What is uveitis |
inflamm of iris ciliary body choroid common cause of blindness may be acute and completely resolve or become chronic/ recurrent |
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aetiology of uveitis (4) |
trauma, IM, 2` to corneal disease primary infections- lepto, onchocerisais |
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Dx of uveitis |
1. periocular swelling, blepharospasm, epiphora 2. scleral and conjunctival injection/ hyperaemia +/- chemosis (bulging) 3. aqueus flare (headlights in fog), hypopyon, hyphaemia 4. miosis 5. +/- diffuse corneal oedema (fluorescein neg unless concurrent corneal ulceration) and corneal neovascularisation
look for signs of external trauma fundic exam- scars in non tapetal investigate systemic dz or ocular infections +- slit lamp exam and or tonometry +- anterior chamber paracentesis |
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management of acute uveitis |
1. AInflamms- GCS - topical and or systemic NOT IF ULCERATION PRESENT
2. NSAIDS- systemic or topical
3. topical atropine- mydriasis, cycloplegia, prevents synechiae (iris adheres to cornea), increased aqueus drainage
4. +/- AM drugs 5. +/- cyclosporine if IM 6. +/- tx of primary ocular or systemic dz 7. Eye mask |
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management of chronic uveitis |
-GCS +/- NSAIDS - cyclosporine - chemical ablation of ciliary body - surgical vitrectomy - enucleation |
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sequelae to acute uveitis |
1. chronic or recurrent uveitis 2. glaucoma, synechiae, cataracts, choroidal/retinal degeneration, chronic corneal disease 3. chrinic ocular pain 4. blindness 5. phthisis bulbi (small globe) |
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px uveitis |
poor if acute uveitis not controlled poor if recurrent or chronic enucleation might be neccesary if eye is painful, non functional |
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atrial fibrillation |
Atrial fib- most common assoc with poor performance. normal CO at rest but compromised during exercise. predisposed if has high vagal tone, large atrium
irregularly irregular auscultated rhythm baseline flutter R to R irregularly regular normal QRST
mightwarrant KCl supp |
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Ventricular tachycardia |
most common life threatening arrythmia ectopic ventricular rhythm- unifocal or multifocal systemic illness (GI disease), bacterial/ viral myocarditis, immuno mediated, ionophores
results in resp distress, oedema, syncope, CHF, hypoxaemia,
treat underlying dz if present, antiarrythmics- lignocaine, mg sulfate, procainamide |
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ddx arythmia with long pause |
SA block- never fires 2` AV block- most common, high vagal tone |
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systemic events leading to endotoxaemia |
1. breach of defences 2. endotoxin comes into contact with macrophages - release IL1, TNF, thromboxane, IL6 - cause marginalisation, initial neutropaenia, inflammatory cascades 3. second wave- IL6/8 neutrophilia with left shift (degenerative shift in overwhelmin infection) |
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sequelae of endotoxaemia |
Endotoxic shock - severe hypotension - decreased contractility - capillary congeston - poor organ perfusion - platelet aggregation - coagulation- DIC- venous thrombosis renal failure, icteus, laminitis dehydration Acidosis, elevated blood lactate cold extremities petechiae
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treatment of endotoxaemia |
Aggressive fluids- blood volume expansion- crystalloids and colloids electrolytes maintain blood pressure- IVFT dopamine treat primary disease- antimicrobials antithrombotics- heparin, aspirin anti endotoxin therapy - flunixin meglumine - hyperimmune plasma - polymixin B |
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px endotox |
poor- can lead to renal failure, DIC, laminities, thrombophlebitis which prolong recovery or cause death
if consumptive neutrophilia- very grave px |
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approach to colic |
Get a thorough hx- duration of ownership, previous problems, recent management, other horses, defecation, worming, weight loss, dietary changes, appetite, concurrent illness, recent meds
PE- get HR RR PR, CRT, GI sounds BEFORE analgesia or sedation
NGT- gatric reflux rectal abdominocentesis PCV/TPP and biochem ultrasound
Analgesia laxative oral IV fluids (6-8L every 1-2hrs) GI rest anthelmentics (once stable)
Refer if abdo ditension, severe pain, |
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analegesics for colic |
a2 agonists- good visceral analgesia short acting
opioids- good visceral analgesia (butorphanol, GI hypomotility
NSAIDS- no decreased GI motility, no sedation, long lasting
buscopan if there are increased GI sound= think spasm i contributing to the pain |
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what NOT to give to colicy hore |
phenylbutaxone- poor visceral analgesia, slow aCP- no analgesia, hypotension repeated drugs that decrease GI motility
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Non GI causes of colic |
parturition urogenital pleuropneumonia laminitis oesophageal obstruction hepatic intraabdominal haemorrhage
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Medical colics (8/9) |
- Spasmodic - Flatulent/ gas colic - LI impaction - Meconium impaction (foal) - gastric dilation/ impaction - Gastroduodenal ulcer - peritonitis - duodenitis/ prox jejunitis - colitis - sand colic - Non GI
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signs of spasmodic colic |
usually change in diet, environment OP anthelmentics
increased gut sounds mild tachy, no reflux reponds to analgesia usually |
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flatulent/ gas colic |
priamry- ileus, abnormal fermentation secondary- intestinal obstruction moderate to severe, variable GI sounds pings may develop CV signs and resp distress analgesics, gastric decompresion +/- caecal trocharisation +/- surg |
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LI impaction |
common sites- pelvic flexure, caecum, small colon risks- poor dentition, poor nutrition (fibrous), large colon displacement, amitrax toxicity mild to mod paoin with decreased gu sounds dehydration decreased faecal production
dx rectal palp- difficult with caecal impactions tx- analgesics, laxatives, rehydration, withold feed +/-surgery for caecal impaction |
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presentation of meconium impaction |
no faeces in first 24 hours most common form of neonate colic small colon and or rectum colts more than fillys digital rectal exam warm water enema, manual extraction, laxatives wia NGT, analgesics, IVFT, +/- surgery |
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gastric dilation and impaction signs dx tx |
dietary indiscretion gastric outflow obstruction reflux from small intesting (ileus, obstruction) mild to severe with variable guy sounds +/- spontaneous reflux
tx- analgesics, decompression, gastric lavage |
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gastroduodenal ulceration signs dx tx |
common but can be aysmptomatic stress or other diseases, iatrogenic most common in squamous mucosa along margo plicatus - foals may get prox duodenal ulcers- predisposed to stricture. bruxism, ptyalism, anorexia, D+, colic, poor growth, rupture, death - adults- mild to mod colic, anorexia, poor performance, severe- anaemia and or hypoprot
dx CSs, gastroscopy, faecal occult blood, sucrose absorption test
tx remove stress grass and roughage H2 antagonist, proton pump inhibitor, sucralfate, misoprostol |
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causes of peritonitis |
primary (actinobacillus) secondary- burst abscess, penetrating wound, GI rputure, uterine rupture, surgery.
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signs peritonitis,dx, tx |
mild to moderate pain may be febrile, A_, CV signs low freq D+ (cow pats) variable gut sounds dx- abdominocentesis, hyperfibrinogenaemia, abnormal leukogram, retal (gritty serosal peritoneum), transabdominal or transrectal u/s
analgesia, AB to prevent endotox, NSAIDS +/- sx for primary. Euth for GI rupture |
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significant reflux ddx |
gastric dilation and impaction small intestinal impaction duodenitis/ proximal jejunitis |
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signs colitis |
mild to moderate colic- others not painful usually have D+ except peracute dehydration, electolye imbalance, acid base disturbance, hypoprot, endotox
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causes colitis |
dietary indiscretion parasites AM theraby infectious- salmonella, clostridia NSAID tox stress many cases idiopathic |
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diagnosis of sand colic |
auscultation faecal exam |
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compliations of diarrhoea |
dehydraton electrolyte derangement endotoxaemia thrombophlebitis renal failure malabsorption |
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diagnostic approach to acute diarrhoea |
NGT abdominocentesis +/- rectal bloods incl lactate faeces for float, sand, faecal occult blood, culture, virology |
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what constitutes chronic D+. WHats the diagnostic approach |
over month abdominocentesis rectal full haem/biochem- look at liver, inflamm, renal, foecal samples mucosal biopsy transabdominal ultrasound looking for mass, thickened bowel
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therapy for acute D+ |
FLuids 50ml/kg/hr + deficit + ongoing losses plasma if hypoproteinaemia flunixin- antiendotox endotox treatments probiotics
Antimicrobials for clostridial/lawsonia only |
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Causes of acute diarrhea |
1. dietary indiscretion- - grain overload- endotox, laminitis- lavage, laxatives, endotox therapy - sand - heavy metals - rapid dietary change 2. parasitism - ascarids, small and large strongyles - mass emergence of larval smalls trongyles 3. Dysbiosis- ABs 4. Acute salmonellosis- isolate, 6 daily consecutive daily cultures, no ABs unless leukopaenic 5. CLostridiosis- perfringens or difficile similar to salmonella but D+ can be haemorrhagic demonstrate organism AND toxin in faeces metronidazole and supportive therapy |
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less common causes of acute colitis/ diarrhoea |
1. NSAIDs 2. peritonitis 3. stress 4. lawsonia 5. idiopathic (>50%) |
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causes of chronic diarrhoea (10) |
1. chronic salmonellosis 2. chronic parasitism 3. lawsonia 4. liver dz 5. peritonitis 6. sand 7. IBD (granulomatous/ eosinophilic) 8. neoplasia LS 9. sietary sensitivity IDIOPATHIC |
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approach to dysphagia |
H, CS try to pass a NGT tube- obstruction watch horse ear thorough oral exam neuro exam endo exam of URT and oesophagus u/s |
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signs of choke + tx |
rapid ingestion of feed reflux out nose distress, retching, extended neck, palpable mass in neck
sedate, muscle relaxation (oxytocin prox 2/3) keep head lowered might need GA small meals, avoid food competition |
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other cuases dysphagia |
strangles guttural pouch tympany subepiglottic cysts masses structure ME dental disease- quidding neuro disease |
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common causes of weight loss |
1. parasites 2. dental disease 3. inadequate feed/ quality less comm 4. eosinophilic/ granulomatous enteritis - xylose/glucose absorption test, hypo prot, may have skin lesions, thickened bowel wall 5. neoplasia 6 ECS liver dz chronic colic chronic resp disease renal dz dysphagia CHF |
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liver enzymes |
injury- ALT, AST stasis- GGT, GLDH fxn- bile acids, alb, glob, glucose |
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cause of cholangiohepatitis, signs |
ascending from SI
fever weight loss depression icterus |
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presentation of hyperlipidaemia |
mini horses and shetlands over represented Neg energy, increase triglycerides, accumulation in hepatocytes, overrides gluconeogenesis, no VLDLs to remvoe them, inhibits hepatic fxn |
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joints of the carpus |
radiocarpal middle carpal carpometacarpal
last two communicate |
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joints of the stifle |
lateral femorotibial
medialfemorotibial femoropatella |
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joints of the hock |
tibiotarsal proximal intertarsal
distal intertarsal
tarsometatarsal |
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main lameness ddx |
foot abscess laminitis intrasynovial/thecal sepsis periarticular cellulitis fractures |
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tx for foot abscess |
if organised- decompress, drainage, saline, flush h2o2 and iodine, 3 layered foot wrap, tetanus toxoid
disorganised- no obvious tract or discolouration- soak foot in warm water and epsoms, apply a paste of sugar and iodine or epsom salts and wrap. repeated daily |
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define laminitis. What is considered as acute lameness |
syndrome in which a series of pathophysiological events cause injury to the dermal and epidermal lamellae, weakening their attachment. Can lead to separation of the hoof capsule from the underlying tissues
acute if under 72 hours and not associated with distal phalanx displacement |
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causes of acute laminitis |
toxaemia - grain overload - endotox - renal failure mechanical overload glucocorticoid toxicity - iatrogenic - stress -ECS -EMS idiopathic |
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clinical signs of laminitis |
digital pulses boundin heat in feet shifting weight abnormal stance stiff gait reluctant to pick up foot recumbent` |
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treatment of acute laminitis |
- aggressive therapy of primary disease - NSAIDS- phenylbutazone - strict stall rest - remove the shoes - mechanical support with cuff and wedge pad- frog support, syrofoam - soft ground - good nutrition- avoid grain less accepted
- vasodilators- ACP - ice baths
- antithrombotics |
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mechanical support for laminitis |
sole and frog recruited to bear weight to take stresses off the wall. Point of breakover moved palmarly to decrease length of the lever arm as horse breaks over. heels elevated to decrease tension in DDFT
heart far shoes, silicone putty sole support
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treatment of chronic laminitis |
shoeing, sole support if therapeutic shoeing not adequate- tenotomy to reduce tension in DDFT |
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px laminitis |
poor to guarded rotation, even follwoing derotation- predisposes to recurrent lameness and poor px for return to previous workload sinking- poorer px prone to cracks, hoof deformities, sole bruising- recurrent lameness complete deparation of the hoof wall- euth
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etiology of septic synovial structures |
trauma iatrogenic haematogenous- foals, foci of infection, septic physitis, failure of passive transfer |
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most common septic arthritis islates |
adutls- staphs, strep, enterobacteriaceae pseudomonas
foal- e.coli, kelb, salmonella, actinobacillus, rhodococcus |
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qualities of a septic joint fluid |
dark yellow or red, turbid (clear yellow) WBC 30-100 (0.5) TP >30 (<2.5) >90% PMH +/- toxic changes +/- bacteria +/- pos culture |
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tx septic arthritis |
1. consider referral 2. retraint- standing, IV anaesthesia, GA 3. Lavage joint- arthroscopy or through and through 4. ABs- penicillin G, Gentamicin - 10xMIC synovial infections -100xMIC orthopaedic infections intraarticular inj or impregnated beads- high dose, reduce systemic side effects, long duration 5. Phenylbutazone 6. contralateral limb support |
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local delivery of antibiotics to septic joint |
intraarticular/ intrathecal- 500-600x MIC IV resional perfusion 1/3 systemic diluted impregnated beads intraosseus continuous intra articular AB infuion device |
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what is perarticular cellulitis |
infection of ubcut tissues of the skin- normal flora or exogenous- where skin has previouslt ben broken bandage, ABs (regional), NSAID, topical nitrofurazone and DMSO (topical AB/AI) |
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DIrect AI/IT abs |
gentimicin amikacin ceftiofur |
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how does nuclear scintigraphy work |
injection of radioactive isotrope- bind to hydroxyapatite of newly formed bones- detection of uptake by gamma camera
vascular phase- immediate soft tissue phase- 10-15m bone phase 3hrs |
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indications of nuclear scintigraphy |
poor performance, no obvious lameness multiple limb lameness dangerous horse non blockable lameness |
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most common cause of HL lameness in mature horses |
osteoarthritis of the tarsometatarsal and distal intertarsal joints, and to a lesser extent the proximal intetarsal joint |
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conequences of joint inflamm |
catabolic processes lead to proteoglycan loss, decreased HA conc in the matrix change in collagen orientation and integrity loss of elasticity superficial carilage necrosis chondromalacia- decreased proteoglycans fibrillation swollen joit-- reduced ROM, pain on ROM |
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therapy for joint dz |
1REST 3IA GCS better than NSAIDS (Depo Medrol- methylpred)- low motion joints only Triamcinalone- chondroprotective 4sodium hyaluronate- no site effects +- NSAIDS 5. Pentosan- chondroprotective, inproves cartilage and synvoial joint fluid, increased proteoglycan and HA 6. Glucosamine/chondroiton- replace matrix substrates 7. interleukin 1 antagonist-young horse, early dz, poor response to GC |
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what is the peroneus tertius and where does it originate/ insert |
lateral femoral epicondyle to dorsal proximalaspect of the metatarsus. Major contributer to the reciprocal apparatus- responsible for flexion of the tarsus when the stifle is flexed
can stand normally variable lamness overextended hock at stance phase may be swelling and oedema
rest 6w then slowly introduce work over 3m px good
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types of stringholt |
sporadic (north america) usually unilateral- trauma, adhesions, protozoan myopathy? usually do not spontaneously recover
Outbreak- bilateral, summer/fall, dandelions left recurrent laryngral nerve affected in 60%- laryngoscopy to check tx- remove dandelions, can take 3-12m to resolve |
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tx of sporadic or unresolving strongholt |
lateral digital extensor tenectomy repsonse difficult to predict, often improve |
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presentation of fibrotic myopathy |
unilateral hindlimb injury to hamstrings- semitendinosis, membranosis, biceps injections, sharp turns, catching fot in halter scartissue formation
dx- gait- short cranial phase-slappd on ground palpation of scar tissue u/s |
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tx and px fibrotic myopathy |
transection of the semitendinosis insertion- GA or standing
px fair to good. More problematic in performance horse some completely resolve, post op rehab important |
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Risk factors for upward fixation of the patella |
medial PL hooks over medial trochlear
young big horse weak thigh muculature straight hindlimb conformation inadequate conditioning hereditary fit horses suddenly given box rest |
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dx upward fixation & tx |
palaption stablity of patella lameness exam- walk trot, slo mo might be necc
strengthn quads increase work on inclines- work in long grass, trotting over polls, deep soils no circle work- painful |
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surgical tx of upward patella fixation |
inject middle and medial patella ligaments with irritants- iodine in almond oil medial patella ligament splitting medial patella ligament desmoplasty- has been assoc with osteodytophy of patella, only if other methods dont work |
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classifications of ER |
sporadic- overexertion- no hx, poor warm up, lack of fitness, dehydration - too much grain - VitE, Se def - hormone imbalance - grain
recurrent (genetic)- autosomal recessive. abnormal intracellular Ca regulation, nervou behaviour, more common in fillies and young hore, usually while galloping |
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CS Erhabdo |
cramping tachycardia -pnea stiff, unwilling to move sweating anxiety discomfort lamene firm muscles myoglobinuria |
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Dx ERhab |
1. elevated CK (peak 4-6h), AST (peak 24 hrs-->weeks) 2, urinalysis- myoglobin 3. muscle bipsy if multple episodes |
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tx Erhabd |
mild- walk back to stall severe- dont move cover to prevent chill IVFT flunixin- wait till horse has had 10-20L of fluid first ACP- not in hypovolaemix |
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check ligamens |
superior- disal radius to SDFT limits MCP hyperextenson, prevents overstretching of SDF belly, stay apparatus
Inferior- carpal ligaments to prox DDFT. Prevents overstetching of DDF muscle belly, stay apparatus |
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suspensory lig |
proximal cannon bone to proximal sesamoid bones and CDET support fetlock and stay apparatus |
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different breeds and their usual tendon injuries |
standardbreds- loads on the SL aprox 2x the flexor tendons- susp branch lesions
thoroughbreds- high tensile load on the SDF at the gallop, DDFT lesions uncommon
Jumpers and dressage- prox suspensory desmitis |
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etiology of tendon and ligament injuries |
ageing and exercise cumulative microtrauma exercise indued hyperthermia risk factors- breed, work compensatory injury acute single event trauma (not common) |
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Risk factors for ligament and tendon injuries |
horse age >5 foot imbalance conformation presence of toe grabs exercise characteristics racetrack surface distance |
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tendinitis and desmitits dx px |
H, CS, local analgesia (mainly prox suspensory), u/s +/- rads +/- scintigraphy
px poor to fair slow metabolic rate meaning slow/ inadequate healing 8-14 months to return to maximal strength after damage scar tissue formation- weaker 85% original predisposed to reinjury 30-50% |
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factors improving px of desmitis, tendinitis |
- early dx client compliance repeated clinial and u/s exams controlled exercise program expectations- future career svereity chronicity conformation |
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therapy for acute tendinitis, desmitis
plan for rehab |
NSAIDS 2-3w cold therapy 2-3w BID good heel support- egg bar shoes stall confinement bandaging- decrease oedema topical AI- DSMO
stall rest until working at previous level reckeck u/s every 3m before increaing exercise level start exercise at 5m and increase by 5m
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theory behind tendon splitting |
decrease size of lesion, increase vascularity may be beneficial early, not late |
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how do fasciotomy and demoplasty improve chronic tendon/ligament injury? |
faciotomy- relieve compartmental pressure desmoplasty- introduce blood supply |
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cause of annular ligament syndrome tx |
primary desmitits, tendonitits, infectiou tenosynovitis
transect annular ligament. good px if no tendonitis |
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therapies to help tendon and ligament healing |
bone marrow intralesionally shockwave therapy stem cell therapy |
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analgesia for wolf teeth extraction |
Regional anaesthesia useful for teeth extraction: |
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communication of tooth roots with sinuses |
Roots of 108, 109, 208 and 209 are in the rostral maxillary sinus, whilst those |
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investigating sinus disease |
1. hx, CS 2. percussion 3. endoscopy- nassomaxiliary aperature- find the source of DC 4. radiographs/ CT very useful |
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tx strangles |
supportive - NSAIDs - ABs only if life threatening - tracheostomy - FLuids - NG feeding - surgically drain abscesses if needed - GP lavage - steroids (purpura haemorrhagica) |
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control of strangeles outbreak |
cease movement of all horses on and off property isolate horses test all in contact an d recoverign horses. Can gie penicillin to those with positive NP swabbut no CS endoscopy of potentail carriers
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pathogeneisi of rhodococcus equi |
pleomorphic gram pos rod, facultatively intracellular endemic on many farms life threatening resp disease- rattles- in fials 1-5 m dry dust conditions organ replicates, sheds, in faeces.. resp disease from inhalation, likely within first 2 weeks of life |
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CLINICAL signs rhoddococcus |
fever crackles, wheezes suppurative pleuropneumonia lymphadenitis D+ IM polysynovitis, uveitis, anaemia, thrombocytopaenia septic osteomyelitis, physitis colic, weight loss |
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treatment of rattles |
rimfapin, erythromycin 4-9 weeks- expensive!! AIs minimise stress, sunlight
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Herpesvirus syndromes |
EHV1 respiratory abortion neuro (rare) EHV4 resp in weaner age foals- biphasic fever, ethargy, serous nasal DC, pharyngitis, cough, secondary bacterial, latency |
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EHV1 respiratory disease dx tx |
viral isolation or PCR from NP swab citrated blod aborted foetys CN tissue 4 fold increase in titre Tx- rest 4-6w, nursing care, NSAIDs, tx secondary bacteria |
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incubationand signs of EI |
1-5 days
harsh cough high fever lethary, inappetance mucoid ND\recovery in 10 days but takes 3-4 weeks for RT to recover shed 14 dyas |
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Hendra virus |
natural host of HeV is the fruit bat rare but potentially fatal disease of horse and humans horse to human spread via body fluids- requires close contact not considered highly ocntagious
Clinical signs Respiratory: peractue, high fever, tachycardia, dyspnoea, pulm oedema, frothy nasal discharge, facial oedema, bloody dc, fatal 1-3days Neurological signs • wobbly gait,
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site of frontal sinus trephination |
frontal 60% from midline and midal canthus, 0.5 caudal |
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stie of caudal maxillary trephination |
under eye 2 cm rostal, 2 cm ventral to medial canthus
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site of cranial maxiliary trephination |
halway beterrn medial canthus and frontal crest, below line drawn from medial canthus and infraorbital foramen |
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Sinu probelms |
1infections 2cysts- young horses 3dental problems- smells bad, older horse, referral 4neoplasia- SCC, HS, LS, dental- most malignant 5. ethmoid haematoma- not a tumour, originates for ethmoid labyrinth, hormal respiratory epi, giant cells, |
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Cause of dental sinusitis and work up |
apical tooth root infections patent infundibulum fracture tooth periodontal disease.
Oral exam, rads, sinuscopy, scintigraphy identify affending tooth, tooth removal, antibiotics, sinus flap and repulsion ($$) |
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diagnosis and tx of ethmoid haematom |
CS- epistaxis, rads (can look like sinus cyst), endoscopy, sinuscopy (green mass), biopsy (but H+++)
intralesional formalin via endoscope, surgical resection
recurrence high |
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Guttural pouch disease and workup |
1. empyema 2. chondroids 3. mycosis 4. temporohyoid arthropathy
Endoscopy, radiographs, wash
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anatomy of the guttural pouches |
stylohyoid divides into lat/med
medial compartment bigger- contains cervical symp trunk, cranial cervical ganglion, CN9, 10, 12 internal carotid
lateral compartment contains CN7, external carotid, maxillary artery (dorsally)
retropharyngeal lnn visible through floor communicated with eustachian tube (NP to middle ear) |
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tx of GP empyema, chondroids, mycosis |
empyema- GP lavage, long term antibiotics chondroids- surgical removal- viborg triangle approach, difficult mycosi- ligate artery, baloon occlution, med therapy usually futile |
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GP mycosis |
fungal plaques attach to vessels in GP and live off nitrients of the vessel. Begins to invade lumen
severe epistaxis mycotic plaques- aspergillus usually important to determine which artery affected |
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what is temporohyoid osteoarthropathy |
bony proliferation and paiin associated with the temporohyoid articulation. Has a highly varialbe presentation depending on the structures affected
head tilt, ataxia, corneal ulcers, ear droop, oral dyphagia (CN9), pain when mandibles are squeezed together |
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causes of temporohyoid osteoarthropathy |
OM/OE ascending GP infection haematogenous DJD ankylosis- fx petrous temporal bone fx stylohyoid |
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treatment temporohyoid osteoarthropathy |
ABs NSAIDS remove ceratohyoid reduce prssure off articulation- reduce load |
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pathophys of ILLH |
paralysis of left arytenoid cartilage progessive atrophy of the cricoarytenoideus dorsalis m leeft recurret laryngeal nerve longest in the body inspirtory nosie exercise intolerance |
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grading ILLH |
grade 1- symmetric abduction grade 2- asymmetric, achieves full abduction grade 3- at rest not fully abducted during exercise Afull abduction Bnot full C collapes acreoss midline |
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workup of ILLH + Tx |
endoscopy without sedation - nasal occlusion - slap test rads- masses palpate CAD m- check for scars treadmill- all G3, some G2s
Tie back- prosthetic suture + ventriculocoredectomy/ sacculectomy
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presentation, tx arytenoid chondritis |
inflammation/ infection of arytenoid- uni or bi resp noise, poor performace, often deformed rad helpful med tx often fails- NSAIDS abs rest
surgical tx- laser assisted debridement
high risk of infection of prosthesis placed- need to differentiate for ILLH |
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common epiglottis/ laryngeal problems |
entrapment- aryepiglottic fold subepiglottic masses epiglotitis- can be idiopathic deformities subepiglottis cysts- young horse vocal fold collapse rostral displacement of palatopharyngeal arch (no tx) axial deviation of aryeppiglottic fold- laser folds |
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presentation fo dorsal displacement of soft palate, cause |
2 forms persistent- seen at rest, may be dysphagic, uncommon
intermittent- exercise, een with fatigue expiratory gurgle, v poor performance
neuromusclular dysfunction, epiglottic hypoplasia, GP inflamm (CNX) rest, NSAIDS
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tx of dorsal displacement of the soft palate |
figure 8 collar, tongue tie to keep mouth closed
sx 1. myectomy, tenectomy of sternothyrohyoideus 2. staphylectomy/ laser 3. tie forward (COMMON)- permanently move the position of the laryx forward using prosthetic sutures mimick action of thyrohyoid mm |
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aetioogy, dx and tx/px dynamic pharyngeal collapse |
treadmill endiscopy diagnosis- ECG at the same time as cardiac issues 2nd most comm cause poor performance
much more common in young horses, linked to inflammation - phangeal lymphoid hyperplasia - generalised inflamm of throat- nervous dysfxn tx- young horse treated with 4-6m rest has good prognosis
old horse, no inflamm- guarded px- no sx options |
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signs, dx Exercie induceed pulm haemorrhage |
epistaxis, cough after exercise, poor performance up to 80% racehorses high pulm arterial pressure
1endoscopy to see fi theres blood in trachea 2BAL- caudodorsal lung- erythrophagocytosis, haemosiderophages (previous bleeds) 3rads |
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treatment of EIPH` |
difficult improve ventilation - IAD concurrent inflamm predisposing to bleeds- investigate and treat diuretics- furosemide- bt not while training. reduce presur of capillaries in lung - nasal strips to open nostils to improve air flow
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neuro dieases |
viral encephalomyelitis CNS trauma cervical stenotic myelopathy tetanus hepatic enceph |
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wahat kind of virus is hendra, non neuro signs |
paramyxovirus
rapid onset illness fever and depression tachycardia rapid deterioration with either resp and or neuro signs |
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neuro signs hendra
|
ataxia blinfness aimless walking head tilt and circling muscle twitching recumbency urinary incontinence
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WHat to do with suspect case of hendra |
Alert LHPA or DPI inspector
dont examine without adequate PPE |
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viral encephalomyelitis |
hendra herpes EHV1 kunjin |
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What is Kunjin virus |
Kunjin virus is an Arbovirus in the Flavivirus group. It is carried by mosquitoes. Waterbirds, especially herons and ibis act as a natural reservoir for Kunjin virus. Has been present in northern australia for some time but not known to cause disease. It has been associated with an increase in neurological cases since 2011 in NSW and Vic |
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signs of Kunjin viru |
Neurologic signs included depression, ataxia, |
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dx tx kunjin virus |
sewrology +/- virus isolation
antiinflammatories antioedema supportive interferon- not usually used no hyperimmune plasma in aus no vacc
usually resolve uneventfully over a few days to a few weeks. 10% severe disease and mortality otherwise good px |
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Hendra vs Kunjin |
Kunjin slow progression, klacks high fever |
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Herpes myeloenceph |
can occur subsquent or concurrent to resp dz direct viral infetion of CN endothelial cells- casculitis, thrombosis, ischaemia acute onset symmetrical ataxia and weakness signs predom FLs sacral nerve signs common- U incontinence, bladdor atony, penile prolapse, F incont, decreased tail tone, perineal sensation loss may see CN deficits |
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dx herpes myeloencephalo |
H, CS, CSF- elevated TP but NCC normal or slightly up virus isolate from blood or NP viral tires in CSF increasing Ab titre |
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therapy herpes myeloenceph+ tx |
suportive- bladder catheriation, evacuate rectum, sling dex and/or NSAIDs acyclovir ($$$$$)
good px if ambulatory |
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dx CNS trauma |
hx of trauma acute onset neuro exam- locate lesion rads/ CT/MRI CSF- haemorrhage/xanthochromia |
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tx CNS trauma |
treat if in shock- IV fluids anti inflamms- dex, NSAIDS, DSMO anti oedema therapy- mannitol, hypertonis saline, furosemise seiure control- benzodiazepines, phenobarb aggressive ABs if open fracture stall rest |
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aetiology tetanus, incubation |
2` to anaerobic wound site- cl/ tetani incubation 1-4w
muscular tetany as the toxin ascends the peripheral NS, binds to CNS receptor sites and blocks release of inhibitory neurotransmitters GABBA and glycine. continuous, painful mucular contraction |
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CS tetanus |
stiff gait/ tetany (+- recumbency) lock jaw muscle tremors trismus elevated tail head anxious expression hyperaesthesia death due to respiratory tetanu |
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|
treatment tetanus |
dfebride wound site high dose parenteral penicillin antitoxin supportive care- sedation, muscle relaxants, IV fluids, nutrition, decrease stimuli (dark stall, wool in ears) |
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|
preventon tetanus |
toxoid 2x 1 m apart then yearly antitoxin for unvaccd horse
receovery does not convey resistance
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pruritic parasitic diseases |
1pediculosis- lice- tape impression 2chorioptes- well feathered fetlocks- superficial scrape 3. environmental mite 4. endoparasites- onchocerca, oxurids, helmonths, onchocerca 5. pin worm 6. helmonths- strongyloides westeri/ pelodera- larvae invade skin
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tx of pediculosis |
treat beyond 3w lifecycle as eggs resistant tx all in contact animals 1-2 weekly OPs, permethrin or ivermectin |
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|
tx of chorioptes |
1. topical pour on- part hair and apply to skin- moxidectin, doramecin 2. fipronil spray 3. injectable ivermectin not reliable
all in contact animals 2wklyx3 2-4wkly prophylaxis at high risk time- winter, intensive housing |
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main categories of equine dermatitis |
1. pruritic - HS, parasitic 2. non pruritic - alopecia/ scaling/ crusting Infectious- parasitic, bacterial, fungi, viral (RARE) immuno mediated photosensitisation 3. nodular - sarcoid - SCC - melanoma - papiloma - proud flesh - eosinophilic granuloma - deep bacterial + abnormal bacterial - habronemiasis - pythiosis |
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infectious non pruritic |
1. parasitic- demodex- very rare 2. bacterial- dermatophilus, bacterial folliculitis 3. fungal - dermatophyte |
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presentations of dermatophilus |
dorsal midline- rain scald muzzle, distal limbs- mud fever |
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|
dx dermatophilys + tx |
hghly suggestive lesions and CS cytology- impression smear, minced , saline soaked crusts gram positive branching bacteria in train track confiuration- parralel rows of zoospores
shelter, soak rusts in chlorhex and remove chlorhex spray daily, +/- pyohex daily- twice weekly Penicillin IM if svere |
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|
dx dermatophytes + tx |
trichogram, tape prep,
woods lamp- M. equinum and 50% m.canis posiotive
often self limiting 1-3 m malaseb shampoo topically, thoroughtly clean bedding, combs, rugs, tacks using bleach treat 2-3 w beyond resolution
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tx of bacterial pyoderma |
topical chlorhex BID initially then daily toweekly as preventative
Adress primary prob TS 3 w min |
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viral dermatoses |
horse pox viral coital exanthema |
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pemphigus presentations
ddx |
young horse- 2-12 m good px adult- guarded
papules, vesicles, crusting, scaling, oedema ventrum, limbs (50%), lethargy )50%)
generalised, localised to coronary band (rare)
dermatophilosis dermatophytes SBP |
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IM alopecic diseas |
PF alopecia areata |
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pastern dermatitis ddx |
1. infectious- bacterial (staph, dermatophilus), fungal (dermatophytes), Parasitic (chorioptes, envionmental mites, nematodes) 2. Allergic- contact? plants, topical treatments 3. immune mesiated- PF (rare form), vasculitis- purpura, photoactivated |
