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24 Cards in this Set

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Define “tying-up”,
general term for muscle cramps assoicated with equine myopathies
Define HYPP
Hyperkalemic periodic paralysis
Define PSSM
polysaccharide storage myopathy
Define RER
Recurrent exerttional rhabdomyolysis
How is HYPP inherited?
Decenedents of a single Quarter Horses Stallion named "impressive". Seen in quarter horses, paints, and appaloosas. .4% of all quater horses affected. Autosomal dominant with incomplete penertrance. N/N=normal, N/H=heterozygote, H/H= homozygous affected
What are the clinical signs of an HYPP episode?
seen in heterozygotes and homozygotes but more frequent and greater intensity in homos. Episodes are periodic and are related to a drastic increase in serum potassium. results in muscle depolarization and weakness.
1.period of muscle contraction which may progress to recumbency, muscle fasciculations, respiratory stridor, and/or bradycardia.
2.episodes last for 15-60 minutes.
3.rarely horses may die episodes horses are normal
What is the mutation that results in HYPP in the horse?
point mutation in the skeletal muscle sodium channel alpha subuint. In HYPP the muscle resting potential is closer to firing. as an episode progresses, some sodium channels may fail to close resulting in efflux of potassium. during epsiodes serum K may elevate from 4 to 8mEq/L or more. death is due to cardiac stasis in the face of severe hyperkalemia
How is HYPP diagnosed?
1.Genetic History.
2.take K level during an episode
3.DNA probe and PCR on whole blood to document mutation (perfered test)
4.abnormal EMG
5.K challenge to provoke episode- dangerous and unnecessary mortem vitreous fluid K or DNA test on spleen or hair
How are horses with HYPP managed?
1.prophylaxis acetazolamide: carbonic anhydrase inhibitor (K wasting diuretic) only needed in horses with frequent and severe episodes.
2.low K and consistent diet:
a.commercial pellets exist
b.oasts, barley and corn
c.low K hay (requires hay to be analyzed)
3.avoid stress and change
4.avoid fasting
What would you do for a horse having an acute episode of HYPP?
take blood sample prior to treatment for K and muscle enzymes
For mild attack(not down but has muscle tremors)
1.exercise: stimulates adrenalin which helps replace K inside cells. careful horse can fall
2.feed grain: stimulates insulin which promotes K uptake
3.give oral acetazolamide
For severe attacks
1.IV 23% calcium gluconate (150ml in 1-2 L of 5%glucose/500kg
2.if no response, follow with 1L 5% sodium bicarbonate IV
3.if still no response, give 3L 5% dextrose IV. monitor K levels
What type of horses have been diagnosed with PSSM?
Quarter horses and related breeds (paints and appaloosas) Draft horses. Inheritance in QH's appears to be autosomal recessive
What clinical signs are associated with PSSM?
1.exercise associated cramps (ususally hind limbs)
2.cramps are painful, horse may stretch, sweat, and look colicy.
3.muscles firm and painful
4.episodes are intermittent
5.draft horses often have periodic progressive episodes of weakness
How is PSSM diagnosed?
1.repeated episodes of muscle cramping
2.serum CK and AST will be sig increased for at least 24hrs. post episode of rhabdomyolysis
3.biopsy: semimembranosus or middle gluteal. evidince of rhabdomyolysis and accumulation of abnormal polysaccharide
What is the current theory for the etiology of PSSM, and for what breed?
QH's: abnormal glucose transporter, resulting in long chains of glucose without normal branching points.
How are PSSM affected horses managed?
1.low carbohydrate diets, if supplemental calories are needed use fat.
2.regular exercise
PSSM treatment of acute episodes
episodes last 15-60 mins and should be treated depending on their severity.
1.keep stationary and quiet, use a blanket to keep muscles warm
3.if mild give acepromazine, if severe give robaxin (efficacy is questionable
In what breed is RER seen?
Thoroughbreds, autosomal dominant trait. young female horses, and enviromental influences increase incidence
What is the likely etiology of RER?
abnormal Ca regulation that is similar but not identical to malignant hyperthermia of swine. becuase the exact defect is unkown no genetic test exists
what are the clinical signs of RER?
1.episodes are intermittent
2.muscle cramps develop during exercise
3.painful and affected horses are anxious and sweat profusely
4.episodes last from a few mins. to 1 + hrs. if very severe horses may become recumbent.
How is RER diagnosis made?
1.history of mulitple episodes of muscle cramping in the face of normal serum electrolytes
2.increased serum CK and AST for at least 24hrs. after episode
3.biopsy: chronic muscle damage and absence of abnormal polysaccharide
Treatment of RER
1.identical to PSSM treatment
management of RER
1.regular routines
2.minimal amounts of grain and fat supplementation
What activities are associated with episodes of RER?
1.high grain diets
4.nervous or very nervous temperament
What is glycogen branching enzyme deficiency?
emerging dz of quarter horses
inborn error of metabolism
seen in foals, present during the first hrs or weeks of life with clinical signs similar to sepsis and may have some or all the following: increased CK, AST, sepsis, congenital limb deformities, hypoglycemia.
Fatal and likely inherited as a recessive dz