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389 Cards in this Set
- Front
- Back
Horses are what type of breeders?
|
Long day breeders, seasonal estrus
|
|
What is the average gestation period for horses?
|
340 days
|
|
In the mare, what are the signs for readiness of birth?
|
-relaxation of the perineum
-mammary gland engorges -waxing of teats -monitor milk electrolytes (decr Na, incr Ca..calcium spike more realiable) -fetal heart rate 60-90 bpm late gestation |
|
How long is stage 1 of parturition?
|
24-48 hours
|
|
How long is stage 2 of parturition?
|
20 mins max
|
|
How is stage 2 defined?
|
Time from the rupture of chorioallantois until foal is delivered
|
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What is stage 3 of parturition?
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Delivery of the placenta
|
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Why is the equine placenta different?
|
It is epithelial microcotelyndondary placentation (like velcro)
|
|
Which side of the placenta is normally presented at partuitition?
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The fetal side
|
|
When examining the placenta, what should you pay close attention to?
|
Tips of the gravid and non-gravid horns
|
|
Placentitis is usually a result of what type of infection?
|
-ascending
-hematogenous is possible |
|
What are the most common pathogens of placentitis?
|
-bacterial (staph, kelbsiella)
-fungal -nocardioform-like dz |
|
What is the serious potential side effect of placentitis?
|
Can slough the mucus plug
|
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What are the clinical signs of placentitis?
|
+/- vaginal discharge
+/- early mammary development +/- premature dripping of milk |
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If placentitis is suspected, an U/S exam to measure CTUP is performed. What is CTUP?
|
Combined Thickness of the Uteroplacental Unit
|
|
What should a normal CTUP be?
|
12 mm at term
an increase suggests edema, inflammation |
|
What other measurement is taken to dx placentitis?
|
Maternal serum progestins
|
|
His is placentitis tx?
|
-systemic abx
-Nsaids -progesterone |
|
Why is progesterone used in the tx of placentitis?
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Promotes uterine quiescence
|
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What are the potential consequences of placentitis?
|
-abortion
-still birth -premature foaling -retained fetal membranes |
|
How many hours post delivery should the fetal membranes be passed?
|
within 3 hours
(considered retained if > 3 hours) |
|
What are the potential complications of retained placenta?
|
-endotoxemia
-laminitis -metritis |
|
How is a retained placenta dx?
|
-examine placenta once passed
-palpate caudal repro tract |
|
What is the tx for retained placenta?
|
-uterine lavage
-weight the placenta -abx -cryotx ? |
|
Additional causes of equine abortion include what?
|
-viral (EHV1, EVA)
-parasitic causes -chlamydia -mycoplasma |
|
During which part of gestation does uterine torsion occur in the mare?
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Mid to late gestation
|
|
What are the signs of uterine torsion?
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Variable colic signs
mild to severe |
|
In relation to the cervix, where does uterine torsion occur in the mare?
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Cranial to the cervix
|
|
How do you dx uterine torsion?
|
Rectal exam
|
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If a uterine torsion occurs when the foal is < 10 months of gestation, what approach to tx should you take?
|
Standing, flank laporotomy
|
|
A complete examination of the uterus and GI tract can be made with a ventral midline celiotomy. What are the drawbacka to this approach?
|
-C-section requires general anesthesia
-cost |
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What is the 3rd way to correct a uterine torsion?
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Roll the mare
|
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What are the drawback to rolling the mare?
|
-requires general anesthesia
-unable to visualize the uterus -unable to examine the GIT |
|
What are the complication associated with uterine torsion?
|
-uterine rupture
-uterine ischemia -complicating GU lesions -Abortion -failure to return to repro soundness -survival of mare vs survival of foal |
|
When does large colon volvulus tend to occur in periparturient mares?
|
30 days prior
60 days post foaling |
|
What are the clinical signs of large colon volvulus?
|
-sudden onset of colic
-severe pain--> no response to analgesia -rapid deterioration of CV parameters -abdominal compartment syndrome -gastric reflux may also be present if abdominal distention is severe enough to prevent gastric emptying |
|
How can large colon volvulus be repaired?
|
-colopexy
-colonic resection |
|
Peri-Parturient hemorrhage is due to a rupture of which artery?
|
Middle uterine artery
bleed into broad ligament=hematoma bleed into peritoneum=hemoabdomen |
|
What are the clinical signs of PPH?
|
-lethargy, colic signs may be severe
-anxious/frantic -may die acutely |
|
How is PPH diagnosed?
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-anamnesis
-clincial signs (blood loss) -U/S |
|
How is PPH treated?
|
-quiet environment
-controlled hypotension -monitor vitals/bloodwork -pro-thrombotics -antifibrinolytics survival is 84% 49% return to repro soundness |
|
What are the 3 P's of fetal position?
|
-presentation
-position -posture |
|
What are the potential complication of dystocia for the mare?
|
-potential loss of foal/mare
-retained placenta -laminitis -metritis -risk of future repro soundness |
|
What are the potential complications of dystocia for the foal?
|
-HIE
-PAS -NE -dummy |
|
What are the risk factors/causes of dystocia?
|
-fetal malpositioning
-congenital malformation of the foal -gestational compromise (placentitis, systemic illness of the mare) |
|
How is dystocia diagnosed?
|
-anamnesis (has stage 2 labor begun)
-sterile vaginal/uterine palpation |
|
What can you use to pre-med the mare for tx of dystocia?
|
-xyalzine
-buscopan -lidocaine epidural |
|
How do you determine if the foal is alive?
|
-pinch
-U/S |
|
How would you first try to tx a dystocia?
|
-correct vaginally, deliver foal
|
|
What is involved in a controlled vaginal delivery?
|
-general anesthesia (O2 is important)
-lift hind legs of mare on hoist -retropuslion of foal/uterus into abdomen -deliver foal |
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What is the step you take in treating dystocia if controlled vaginal delivery fails?
|
C-section
|
|
How would you describe the intrauterine environment of the mare?
|
Hypoxic
|
|
How does the fetus adapt to this environment?
|
-greater oxygen affinity for fetal Hbg
-enhanced fetal oxygen extraction by tissues -increased resistance of tissue to acidosis |
|
Oxygenated blood flows from the mare to the placenta through which vessel?
|
Umbilical vein
|
|
During stage 2 of labor, placental separation begins, what is the affect?
|
Transient asphyxia
-increased resistance in umbilical circulation-->increased systemic vascular resistance -triggers gasping reflex in foal, clears airway expands chest |
|
What happens to the foal as it moves through the pelvic canal?
|
-chest compression and evacuation/absorption of fluid from lungs
-inflation of lungs |
|
As the foal is born the lungs inflate, what else happens in the circulation?
|
-increased alveolar O2 tension
-decr pulmonary vascular resistance -decr right atrial pressure -function closure of foramen ovale and ductus venosus |
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The establishment of adult cardiopulmonary circulation requires what?
|
Direct CO to lungs for gas exchange
|
|
In the foal, pulmonary hypertension, due to hypoxemia, can cause what change to circulation?
|
Can revert back to fetal right to left shunting of blood
|
|
What is the normal body temp of a foal?
|
99-102 F
|
|
What can cause an elevated temp in a foal?
|
-exertion
-infection |
|
What can cause a lower temp in foals?
|
-environmental
-sepsis |
|
What is a normal foal heartrate?
|
80-100 bpm first 30 days
60-70 bpm by 2-3 months |
|
When would you be concerned about a murmur in a foal?
|
If the murmur lasts more than 3 days
|
|
What can be the cause of braycardia in a foal?
|
-uroabdomen
-hyperkalemia (>5.5 mEq/dl) |
|
What are the normal respiratory rates of foals?
|
-at birth 60-80 bpm (moist lungs sounds immediately post foaling)
-30-40 bpm later |
|
Ruib fxs are common with delivery, how do you dx rib fx?
|
-palpation
-U/S |
|
What are the clinical signs of a rib fx in a foal?
|
-elevated respiratory rate
|
|
How could a rib fx cause a fatal hemorrhage?
|
mid shaft fx can severe a vessel
|
|
Examination of the foal GIT should include what?
|
-auscultation
-percussion -palpation of abd, umbilicus, inguinal rings -U/S |
|
What conditions do you check for when examining a new born foals oral cavity and nasal passages?
|
-dental malocclusions (maxiallry prognathism)
-cleft palate -campylorrhinus (wry nose) -soft palate displacement |
|
When examining the eyes of a new born foal, which reflex is not yet developed?
|
No menace response
|
|
What other eye problems should you look for?
|
-entropion (lower lid usually)
-corneal ulceration -hypopyon/foibrin |
|
Premature breakage of the umbilicus can result in what?
|
Hemorrhage
|
|
When examining the umilbicus you can use U/S to help determine what possible conditions?
|
-umbilical hernia
-testicles within the inguinal canal |
|
What is the most common angular limb deformity of foals?
|
Carpal valgus
|
|
Why would you expect to see an increased ALP in neonatal foal bloodwork?
|
Increased osteoblastic activity
|
|
What other chem values will be elevated in a neonate?
|
-GGT
-Cretatinine |
|
When observing foal behavior it is imperative that you confirm that the foal is doing what?
|
Nursing
|
|
What is a hippomane?
|
thick triangular shaped tissue present within the placenta
|
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What is the term for a foal's first feces?
|
Meconium
|
|
What is meant by the term angel slippers?
|
Epinuchium
|
|
How quickly after birth should a foal stand?
|
within 1 hours
suckle w/in 30 mins |
|
It is considered abnormal behavior if the foal does not stand within what timeframe?
|
3 hours
|
|
Foals receive which antibody from colostrum?
|
IgG
|
|
How are the colostral antibodies created?
|
vaccination of mare throughout gestation
|
|
Why is the ingestion of colostrum so important?
|
There is complete separation of the foal from the mare's circulatory system in utero, virtually no transfer of antibody
|
|
How do the antibodies enter the foal's system?
|
The GIT is line with special cells that pinocytose the maternal Ab. These cells are replaced by enterocytes within 24 hours
|
|
What conditions can lead to insufficient antibody within the colostrum?
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-dripping milk prior to foaling
-high risk mare, sick during pregnancy -old/very young mare/inadequate production -breed associated (arab>qh>tb/stb) -agalactia= fescue toxicity |
|
In considering the foal, what causes can lead to lack of colosturm?
|
-sick/weak foal unable to stand and nurse
-very premature (special enterocytes may not be present) -musculoskeletal abnormalities may not allow the foal to stand and nurse |
|
Ingestion of what can cause pre-mature closure of the specialized enterocytes?
|
Anything other than colostrum
-dirty foaling environment -dirty mare (foal ingests pathogens) |
|
How much IgG should a foal ingest?
|
1 gram/ bwt kg
|
|
Specific gravity of colostrum is checked to determine the content of igG, what is a good specific gravity value?
|
1.060 = 30 g/l IgG
|
|
For a 50 kg foal, how much colostrum should be ingested?
|
1.5 -2 liters
|
|
What tool is used to test colostrum?
|
Colostrometer
|
|
What are the sources available for colostrum?
|
-mare (can be donor or banked)
-bovine -commercial supplements (don't work) |
|
What is the proper way to feed a foal with a bottle?
|
head extended forward, not up
risks of aspiration pneumonia |
|
Foals born to high risk mares are at risk for failure of passive transfer What conditions are considered high risk in mares?
|
-placentitis
-possible dystocia -prematurity/dysmaturity -previously ill |
|
When do you test a foal for IgG levels?
|
as early as 12 hours, as last eas 24-48 hours
|
|
What level of IgG is considered adequate? What level is considered partial FPT?
|
adequate = >400 mg/dl
partial FPT = 200-400 mg/dl complete FPT = 200 mg/dl |
|
What is the gold standard test to determine IgG levels?
|
Radioummunodiffusion assay
|
|
Foals with < 400 mg/dl of IgG should receive immunoglobulin from what sources?
|
-plasma transfusion
use a blood administration set |
|
How long does passive transfer last?
|
8 weeks
|
|
What is the leading cause of death in foals < 7 days of age?
|
Sepsis
|
|
What are the risk factors for a foal developing sepsis?
|
-FPT
-unsanitary environment -prematurity -dystocia -unhealthy mare -lack of immunologic response from mare to environment |
|
What is the gold standard test for confirming sepsis?
|
Blood culture
|
|
Sepsis is most often a result of which gram negative organism?
|
E coli
|
|
Why is blood culture so important?
|
To ensure that the correct tx is applied
|
|
What are the typical portals of entry of infection in foal sepsis?
|
-umbilicus
-respiratory tract -GIT |
|
Sepsis can localize in what areas, causing what types of dz?
|
-respiratory tract: pneumonia
-GIT: enterocolitis, ileus -MSK: joint/physeal/umbilical -CNS: meningitis |
|
What are the 2 most common complications of sepsis in foals?
|
-septic arthritis
-septic osteomyelitis |
|
Poor prognosis for sepsis include what factors?
|
-hypoglycemia (<60 mg/dl)
-hypothermia (<100 F) -severe depression |
|
What is the survival rate of foals with sepsis?
|
40%- 70%
|
|
When does dummy foal syndrome manifest?
|
During the 1st week of life
|
|
What is confusing about dummy foal syndrome?
|
Foals appear normal at birth
|
|
What neurologic disorders do dummy foals show?
|
-respiratory depression
-altered consciousness -depressed reflexes -seizure activity |
|
What causes Hypoxic Ischemic Encephalopathy?
|
Insufficient oxygen delivery during the perinatal period
|
|
What is the most common manifestation of HIE?
|
CNS dysfunction (seizures)
|
|
What are the risk factors for developing HIE?
|
-hypoxia in utero (placentitis, twinning, fescue tox, decr bloodflow)
-hypoxia during parturition (dystocia, premature placental separation -hypoxia in the neonatal period (c-section, meconium aspiration, immature respiratory developemtn etc) |
|
Which organ system is most often affected by HIE (hypoxia)?
|
CNS
|
|
What drugs are given as anti-seizure therapy to HIE foals?
|
-diazepam
-phenobarbital |
|
What other drugs can supplement the anti-seizure drugs?
|
Anti-oxidant tx
-Vit E -magnesium sulfate -Ascorbic acid -Thiamine -DMSO |
|
HIE fooal may be in need of O2 tx (nasal or mechanical vent), what other stimulant can be used?
|
Caffeine tx
central stimulant to promote respiratory activity (give rectally) |
|
When would fluid tx be indicated in a case of HIE?
|
A "flat foal"....CV compromise
(50 kg foal needs 1L) |
|
For maintenance purposes, how milk should a foal be fed?
|
20% of BWT/day
|
|
1 liter of milk is equal to how much weight?
|
1 liter = 1 kg
so feed 20% of the foals BWT over 12 feedings 50kg foal 20% = 10L =833 ml 12 times a day |
|
When beginning enteral feeding, what volume should you start with?
|
5% of body weight
feed every 2 hours check for reflux, endure foal is standing or in sternal recumbency |
|
Nutritional supplementation can be from what sources?
|
-mares milk
-goats milk -mares milk replacer |
|
A foal must show what pysiologic function prior to enteral feeding?
|
Good GI motility
(checked by US) monitor daily weight gain |
|
Why are HIE foals at risk for sepsis?
|
-FPT
-prematurity -pulmonary dz -recumbency -IV/urinary catheter -Gi dysfunction -nosocomial infection |
|
What abx do you tx HIE foals with?
|
-broad spectrum
-beta lactams -K+ pcn -3rd gen cephalosporins |
|
Nursing care of a HIE foal include what steps?
|
-maintain in sternal recumbency
-turn q 2 hrs -keep foal clean, dry, warm -padded enivro -contact with mare -monitor body weifht |
|
Meconium is comprised of what?
|
Cellular debris, glandular secretions swallowed in utero
|
|
Why does meconium impaction occur more often in colts than in fillies?
|
Colts have a narrower pelvic brim
|
|
How does a meconeum impaction cause colic?
|
-abdominal distention
-ileus |
|
What are the clinical signs of a meconium impaction?
|
-flagging tail
-straining -constipation +/- abd distention |
|
How is a meconium impaction dx?
|
-absence of milk feces
-PE and blood work (healthy foal) -digital rectal exam -contrast rads (barium enema) |
|
How do you tx a meconium impaction?
|
-enemas
-analgesics -nsaids |
|
What type of enema is used, and what type should be used with caution?
|
-warm, soapy water
-use a Fleet enema with caution (high phosphorus content) |
|
What is the primary drug in a retention emena?.
|
Acetlycysteine
-given through a Foley catherter |
|
Which dx technique is NOT used to diagnose meconium impaction?
|
Abdominocentesis
|
|
What are the clinical signs of a urinary bladder rupture in a foal?
|
-foal is 24-72 hours old
-mild to moderate colic -posture to urinate -abdominal distention -foals are sick +/- recumbent -dehydrated |
|
What electrolyte abnormalities are seen with a ruptured bladder?
|
-hyponatremia
-hypochloremia -hyperkalemia also azotemia |
|
Why does a uroabdomen have the triad of hyponatremia, hypochloremia, hyperkalemia?
|
mare's milk is low in sodium and high in potassium, fluids equilibrate
|
|
Uroabdomen casues azotemia due to what?
|
-post renal
-low USG -high creatinine in urine |
|
What technique is the key to dx uroabdomen?
|
U/S
|
|
With U/S what procedure should you perform in a foal with uroabdomen?
|
Abdominocentesis
|
|
What values do you measure when performing an abdominocenteisis for uroabdomen?
|
Creatinine
Cr should not be in peritoneal fluid, compare with serum Cr values |
|
Prognosis of uroabdomen is dependent of stabilization of the patient. Which electrolyte level can be life threatening?
|
Hyperkalemia--> fatal arrhythmias
|
|
How do yo utx hyperkalemia?
|
-IV fluids (isotonic saline 0.9%)
-calcium tx -HCO3- |
|
What treatment steps are taken for uroabdomen?
|
-place urinary catheter
-drain peritoneal fluid -correct e-lyte imbalances -surgical repair |
|
Where is the most common location for the bladder to rupture?
|
Dorsal bladder
|
|
How is neonatal isoerythrolysis characterized?
|
Destruction of rbc's by alloantibodies of maternal origin
|
|
Form where are the maternal Ab's absorbed?
|
Through colostrum
|
|
What is the result of NI?
|
massive intravascular hemolytic anemia
|
|
Which blood types are at risk for NI?
|
-Qa and Aa
|
|
What conditions have to be met for NI to occur?
|
-mare has to be negative for antigen
-mare has to be sensitized to antigen -foal has to acquire antigen from sire |
|
What are the clinical signs of NI?
|
-progessive weakness
-lethargy -icterus mucous membranes -evidence of hypoxemia -decreased PCV - increased T bili |
|
What is kernicterus?
|
Bilirubin toxicity--> may lead to CNS signs
|
|
What test is used to Dx NI?
|
Coomb's test
|
|
How is NI treated?
|
-improve O2 carrying capacity
-blood transfusion -fluid therapy -restrict exercise -nutrition--> feed IV if not hypoxemic |
|
Blood transfusion is given when the PCV is at what level?
|
<15%
|
|
What is the source of the blood for a transfusion?
|
Mare--wash the red cells
|
|
Which organism is a common cause of pneumonia is foals?
|
Rhodococcus equi
|
|
When are foals infected?
|
from 3weeks to 5 months of age
|
|
What type of organism is R. equi?
|
Gram positive intracellular bacteria
-resides in alveolar macrophages |
|
Where is R equi found?
|
Soil contaminant
|
|
R equi infection causes what type of pneumonia?
|
Chronic suppurative bronchopneumonia
|
|
early dx of R equi is difficult, the subacute form can lead to what?
|
Foal death
|
|
What are the presenting complaints in a foal with R equi?
|
-pneumonia
-lameness -fever -tachypnea |
|
What diagnostics are used to dx R equi?
|
-bloodwork
-rads -US -transtracheal wash |
|
What is the tx for R equi?
|
-erythromycin (keep away from mare)
-azithromycin -az + rifampin -doxycycline -good nursing care |
|
What other signs of R equi infection might you see?
|
Extrapulmonary lesions:
-GI -polysynovitis -panopthalmitis (green eyes) |
|
Diagnosis of muscle dz in horses includes what components?
|
-PE
-HX -biochem -U/A -exercise testing -U/S -electrmyography -muscle bx |
|
Creatinine kinase is released in response to what?
|
Breakdown of muscle
-short T1/2 -is specific |
|
Is AST specific to muscle dz?
|
No, supports a rise of CK
|
|
How quickly does serum CK rise?
|
Within hours or muscl insult (falls off in hours)
|
|
How do you perform an exercise test?
|
-take pre-exercise blood sample
-trot for 15 mins -check Ck 4 hours later |
|
When would you NOT perform an exercise test?
|
If there is already increased Ck, could cause more damage
|
|
U/S can help dx what conditions of the muscles?
|
-edema
-hematoma |
|
If taking a muscle bx, which muscle is the sample taken from?
|
-gluteal
-semimembranosus/tedinosus |
|
What is rhabomyolysis?
|
Syndrome of muscle cramping that occurs during physical exertion or exercise
|
|
Causes of rhabdomyolysis have been categorized into what 4 groups?
|
-exertional (recurrent exertional, PSSM)
-nutritional (myodegeneration) -Inflammatory (clostridal myonecrosis) -Traumatic (post anesthetic myoneuropathy) |
|
Recurrent Exertional Rhabdomyolysis is seen more in which breed?
|
TBs
|
|
What are the predisposing environmental triggers to RER?
|
-gender (67% female)
-temperament -diet (starch, CHO) -excitement -exercise duration and intensity -lameness |
|
What are the clinical signs of RER?
|
-severe cramping in hind musculature
-anxiety, sweating, refusal to move, incr HR/RR -most cases recover in several hours -severe cases-->recumbency |
|
What blood chem results are seen with RER?
|
-significantly elevated CK
-elevated AST -+/- azotemia (pigment nephropathy) -myglobinuria |
|
What results are seen on histopath of a muscle bx of a horse with RER?
|
-increased centrally located nucleus
-normal glycogen staining -incr sensitivity/contracture to halothane or caffeine |
|
How do you tx an acute episode of RER?
|
-IV, oral fluids (avoid ARF due to myoglobin tox)
-Nsaids w/ caution -sedative.tranqs to reduce anxiety/pain |
|
How do you prevent RER?
|
-daily exercise routine
-low CHO diet/high fat (add corn oil, rice bran for additional calories -Dantrolene: administer prior to exercise |
|
What is a common name for Polysaccharide Storage Myopathy?
|
Monday morning sickness
|
|
PSSM is a form of what dz?
|
Exertioanl rhabdomyolysis
|
|
PSSM is a glycogen storage disorder resulting in glycogen and ploysacchrides accumulating where?
|
in the myocytes
|
|
What would lead you to suspect PSSM?
|
perisistently elevated CK/AST...even at rest
-chronic muscle pain -exercise challenge results are supportive -muscle bx = definitive diagnosis |
|
On histopath, abnormal glycogen storage is seen with which stain?
|
PAS
|
|
PSSM horse have an increased ability to do what?
|
Synthesize glycogen (incr sensitivity to insulin, high CHO diets inncrease glycogen synthesis)
|
|
Glycogen in PSSM horses can't be used as energy due to what?
|
Glygogen branching synthase-1 deficiency
|
|
What does rhabdomyolysis occur from?
|
A separate dysfunction within energy metabolism
|
|
How can PSSM be treated?
|
-manage to minimize clinical signs
- prevent stall confinement > 48 hours -strict exercise routine -decrease CHO, incr fat -must combine diet with exercise |
|
Nutritional rhabdomyolysis (myodegeneration) is also known as what?
|
White muscle disease
|
|
Does nutritional myodegeneration affect cardiac or skeletal muscle?
|
Both
|
|
nutritional myodegeneration is primarily a deficiency of what?
|
Selenium/ Vit E
affects young animals <1 year |
|
What are the 2 forms of nutritional myodegeneration ?
|
-Cardiac form: acute, sudden myocardial decompensation
-Skeletal form: muscular weakness/stiffness.recumbency |
|
What serum chem results are seen with nutritional myodegeneration ?
|
-elevated Ck and AST during acute phase
-myoglobinuria |
|
Diagnosing nutritional myodegeneration requires the measurement of Se/Vit E in tissue and whole blood. Why is GSH-Px also measured.
|
Glutathion peroaxidase is Se dependent and formed in RBCs
|
|
Which food source is usually Vit E deficient?
|
Poor quality hay
|
|
What results of nutritional myodegeneration are found on necropsy?
|
-bliateral symmetrical myodegeneration
-pale discoloration -white streaks in muscle bundles |
|
What is the prognosis of the cardiac form of nutritional myodegeneration ?
|
Poor
|
|
Is the skeletal form of nutritional myodegeneration treatable.
|
Possible: Se and Vit E supplementation
-supplement mares during gestation -allow access to green forage |
|
Inflammatory Rhabdomyolysis is also called what?
|
Clostridial myonecrosis
|
|
An infection of Clostridial myonecrosis is characterized by what?
|
-fever
-systemic toxemia -very high mortality |
|
Is Clostridial myonecrosis contagious?
|
No , it is infectious
|
|
What are the synonyms for Clostridial myonecrosis?
|
-black leg
-malignant edema -gas gangrene |
|
Most commonly, an infection with Clostridial myonecrosis occurs when?
|
Following an IM injection
(likely spores are present in the muscle in dormant form) |
|
Once inoculated into the tissues, what do the spores do?
|
Convert into vegetative, toxin-producing form
-proliferation of spores in devitalized tissues |
|
What is the tx for Clostridial myonecrosis?
|
-agressive PCN tx
-aggressive tissue debridement (fasciotomy, aerate tissue) -supportive care (IV fluids, anti-endotoxemic tx, laminitis prophylaxis) |
|
Traumatic rhabdomyolysis is also called what?
|
Post anesthetic myoneuropathy
|
|
What are the 2 categories of Post anesthetic myoneuropathy?
|
-localized
-systemic (malignant hyperthemia) |
|
Localized myopathy is a resul tof the use of what?
|
Inhalation anesthetics, elevated muscle enzymes
(ischemia from hypoperfusion) |
|
What is the tx for localized Post anesthetic myoneuropathy?
|
Supportive care
|
|
Hyperkalemic Periodic Paralysis is an autosomal dominant trait from which sire?
|
Impressive
|
|
What do episode of HYPP look like?
|
-myotonia
-proplapse of the 3rd eyelid -sweating/muscle fasiculations -muscular weakness -respiratory distress from uscular paralysis of URT |
|
In horses with HYPP, what happens to the resting membrane potential?
|
Closer to threshold
inward flux of ns outward flux of K |
|
Is HYPP a complete or incomplete prenetrance condition?
|
Incomplete
|
|
What is the definitive test for HYPP and what type of sample do you submit?
|
DNA
hair root sample |
|
What other tests could be performed?
|
-EMG
-Oral Ca++ chloride challenge (not recommended |
|
In the case of an acute episode of HYP{P what tx would you provide?
|
-karo syrup
-calcium -IV dextrose |
|
What long term tx can you give to a HYPP horse?
|
K+ wasting diuretic (acetazolamide)
Dietary management ( decr K+, avoid alfalfa/molasses -regular exercise -small frequent meals |
|
What is thumps?
|
Synchronous diaphragmtic flutter
|
|
What causes thumps?
|
E-lyte imbalance
-hypocalcemia -metabolic alkalosis |
|
How do you dx thumps?
|
Observe contracture of diaphragm in synchrony with the heart beat
|
|
Cushing's dz is a dz of what age of horse?
|
Middle age to older
|
|
What is the cause of Cushing's in horses?
|
Dysfunction of the pars intermidia of the pituitary (humans and small animals its the pars distalis)
|
|
What conditions of the pars intermedia can cause Cushing's?
|
Hyperplasia/hypertrophy
Melanotropes with excess production (innervated by the dopaminergic nT's of the hypothalamus, loss of inhibition by dopamine |
|
Loss of dopaminergic innervation leads to increased systemic release of what?
|
POMC- proopioidmelanocortin peptides
POMC--> ACTH |
|
The pars intermedia dysfunction also leads to what increased levels of what?
|
-increased alpha MSH
-increased beta endorphines -increased CLIP |
|
The action of ACTH on the adrenal cortex leads to what condition?
|
Syndrome of corticol excess
|
|
Clinical signs associated with PPID result from what?
|
A combination of compression of adjacent pituitary/hypothalamic tissues and increased circulating POMC peptides
|
|
What are the clinical signs of PPID?
|
-hirsutism
-weight loss/muscle wasting -PU/PD -chronic laminitis -suspensory ligament laxity -chronic infections -poor wound healin -coat color changes -docility/blidness/seizures -infertility/pseudolactation -abnormal fat deposition -secondary (type II) diabetes |
|
What dx test can be run for PPID?
|
Overnight dexamethsone test
|
|
How is the Overnight dexamethsone test performed?
|
-baseline blood sample
-inject dex -19 hrs later sample again -normal response is to suppress endogenous cortisol |
|
What other tests can be performed?
|
-endogenous ACTH concentration
-ACTH stim -TRH stim |
|
TRH directly stimulates what part of the pituitary?
|
Melanotropes
|
|
What drugs are used to treat PPID?
|
-Pergolide
-Cyproheptadine |
|
what effect does Pergolide have?
|
Increases Dopamine
|
|
What type of management is needed for horse with PPID?
|
-strict husbandry
-diligent foot care -good dentistry -parasite control -coat clipping during summer |
|
What is the prognosis for PPID?
|
many horses are managed for years with Pergolide and proper foot care
chronic laminits leads to euthansia in many cases |
|
Why does PPID cause laminitis?
|
Insulin resistance
hyperinsulinemia |
|
What are the signs of equine metabolic syndrome?
|
-obesity
-insulin resistance -subclinical/clincial laminitis |
|
Which breeds have genetic predisposition to EMS?
|
ponies>morgan>arabs>fjords
diet and exercise play a role |
|
What diagnostics are used to dx EMS?
|
-resting hyperinsulinemia
-combined glucose-insulin test |
|
How is the combined glucose-insulin test performed?
|
-collect baseline blood glucose
-admin 150 mg 50% dextrose IV -foloow with .10 U insulin -elevated blood glucose above baseline for >45 mins =insulin resistance |
|
What diet changes should be made to a horse with EMS?
|
-remove CHO
-feed grass hay -restrict pasture grazing |
|
Which exercise is best for EMS?
|
swimming
|
|
What is the effect of giving Levothyroxine?
|
Improves insulin sensitivity
|
|
Hypothyroidism in the mare is asscoiated with what syndromes?
|
Fescue toxicity
-enophyte alkaloids= dopamine agonists -prolonged gestation in mares -agalactia |
|
What effects of hypothyroidism can be seen in foals?
|
-incomplete ossification
-msk deformities -mandible prognathism -goiter |
|
What is the common neoplasia of the thyroid gland in horses?
|
Thyroid adenoma
|
|
Most thyroid adenomas are benign, when would tx be considered?
|
If it is a space occupying lesion
(compression of the respiratory/alimentary tracts) |
|
What is another name for Nutritional secondary hyperthyroidism
|
Bran dz
Big head dz |
|
Nutritional secondary hyperthyroidism causes what condition in the horse?
|
osteoporosis
|
|
What is the cause of Nutritional secondary hyperthyroidism?
|
Diets low in Ca++/ high in phosphorus
induces hyperparathyroid PTH inhibits Vit D synthesis, increases bone resorption/bone loss none replaced by unmineralized conn tiss |
|
What are the clinical signs of Nutritional secondary hyperthyroidism?
|
-facial bone enlargement
-difficult mastication due to bone loss -molar fxs -long bone fxs -unthriftiness -shifting lamness -physitis/limb deformities |
|
What is the tx for Nutritional secondary hyperthyroidism?
|
-eliminate grain/oxalate containing feeds
-Supplement calcium (limestone) -confinement for severe cases -nsaids |
|
What can cause hypervitiminosis D?
|
Ingestion of plants containing Vit D like compounds (cestrum)
|
|
What is the result of hypervitiminosis D?
|
-hyperphosphatemia
clin signs= wt loss, mineralization of soft tissue poor prognosis |
|
What is the goal of an equine neuro exam?
|
Establish whether a neuro problem is present and determine the anatomic location of the problem
|
|
When taking the hx for a neuro case, what info should you ask for?
|
-duration.progression of signs
-diet, changes, stresses, injuries -vaccination, herd problems |
|
What is the first part of a neuro exam?
|
Observe the animal
mentation/behavior/postures, coordination |
|
How can you test Cn 1 on a horse?
|
feed test
|
|
A CN 3 deficit will show what kind of strabismus?
|
Ventral lateral
|
|
For a Cn 7 (facial) deficit, does the muzzle deviate away or towards the affected side?
|
Away
|
|
Deficits of Cn 8 (vestibulocochlear) will show what clinical signs?
|
head tilt, nystagmus
|
|
Atrophy of the neck muscles can occure with a deficit of which CN?
|
11 spinal accessory
|
|
Yellow star thistle ingestion can lead to a deficit of which cranial nerve?
|
12- hypoglossal
can't hold tongue against presure |
|
Damage to which nerve fibers can cause Horner's?
|
-sympathetic fibers
-from brachial plexus avulsion -injury to cranial thoracic spine -cervical sympathetic trunk injury -guttural pouch dz |
|
What are the clinical signs of Horner's in a horse?
|
-ptosis
-enopthalmos -prolapse of 3rd eyelid -miosis -sweating along affected side |
|
Animals can walk without cerebral function, when are the deficits seen?
|
When performing complex motor activities
|
|
What are the requirements for a normal gait?
|
-musculature
-motor and sensory peripheral nerves -local spinal reflexes -ascending and descending pathways of spinal cord -motor centers in the brainstem |
|
What are the signs of paresis?
|
-toe dragging and wear
- bounce to stride -difficulty backing -muscle fasiculation |
|
What are the gait tests for paresis?
|
-sway test
-tail pull -incline -hopping response |
|
What are the signs of ataxia?
|
-inability to finely coordinate muscle activity during voluntary movement
-inconsistent foot placement -side to side motion |
|
What are the tests used for ataxia detection?
|
-circling
-incline -obstacles -move with head elevated -blindfold |
|
What is hypometria?
|
-ataxia characterized by under reaching
-decreased motion at joints -limb stiffness |
|
What is hypermetria
|
-over reaching
-exaggerated joint motion -high stepping gait |
|
What is the definition of a proprioceptive deficit?
|
Loss of perception of the movement of the body to the limbs
|
|
Is proprioception dependent or independent of vision?
|
Independent
|
|
What are the clinical signs of a proprioception deficit?
|
-abnormal stance
-abnormal or inconsistent foot placement -sisde to side swaying of trunk |
|
CSF collection at the AO joint requires what?
|
general anesthesia
|
|
CSF analysis of normal fluid should have what parameters?
|
-clear
-low TP <100 mg/dl -low cellularity -no rbc's |
|
What is xanthochromia?
|
Yellow fluid
|
|
xanthochromia of csf is a result of what?
|
-traumatic cord injury
-hemorrhage of cord -EHV |
|
Rabies spreads by which routes?
|
Spread in saliva, enters through broken skin, mucus membranes or respiratory tract
|
|
How does rabies migrate to the brain?
|
Up the peripheral nerve to the spinal cord
|
|
Death from rabies is due to what?
|
respiratory depression...viral efffects on medullary function
|
|
The cerebral form of rabies is also called what?
|
Furious form
|
|
What are the clinical signs of the furious form?
|
-aggression
-photophobia -convulsion -self mutilation -hyperesthesia -straining, tremors -hypersalivation |
|
What are the clinical signs of the dumb or brainstem form of rabies?
|
-lethargy
-dementia -ataxia -Cn signs |
|
What is the gold standard dx test for rabies?
|
-indirect fluoresce3nt Ab test
-need brain tissue -negri bodies in hippocampus |
|
How can rabies be prevented?
|
Vaccination
-vaccine protects after 30 days of administration -wear gloves -reportable dz |
|
Equine protozaol myeloencephalitis is caused by which protozoan parasite?
|
Sarcocytsis neurona
|
|
Which animal is the definitive host for Sarcocytsis neurona?
|
Opossum
|
|
Which animals are the intermediate host for Sarcocytsis neurona and how are they infected?
|
-amadillo, raccoon (cat, skunk?)
-eat sporocyst, develop muslce sarcocyst |
|
What are the clinical signs of EPM?
|
Cranial nerve deficits
-head tilt -facial nerve paralysis -dysphagia -sensory deficits Gait deficits -incoordination -weakness -asymmetric ataxia -may resemble lamness muscle atrophy focal sweating sensory deficits |
|
How is EPM dx antemortem?
|
-hx and cs
-CFS analysis cytology and protein normal, western blot for S. neurona antibodies rule out other diseases |
|
What does a serum postive result for S neurona anitbodies mean?
|
EPM exposure, nor necessarily disease
|
|
What indicates consistency with EPM disease?
|
CSF positive + clinical signs
|
|
What pathologic findings are seen with EPM?
|
Multifocal hemorrhage
-hemorrhage, nonsuppurative inflammation and necrosis -perivascular cuffing with mononuclear cells -fewer than 50% of cases visualization of lesions |
|
What is the older tx used for EPM?
|
Folic acid inhibitors
|
|
Whcih coccidiostat can be used to tx EPM?
What is it's MOA? |
Trizine
distupts plastid bodies of merozoite and energy metabolism of protozoa |
|
What are the side effects of using Thiazolise antiparasitic tx?
|
diarrhea
colic laminitis |
|
What other supportive tx can be used in EPM?>
|
-nsaids
-dmso -steroids -vit e, thiamin |
|
What is still unknown about EPM?
|
-clearance of parasite fro nervous system
-duration of anti-parasite antibodies in nervous system -definition of cure -optimal tx duration |
|
What is the px of EPM?
|
-60% show improvement
-fewer return to normal -early dx incr outcome -appropriate type and duration of tx |
|
How can EPM be prevented?
|
-prevent wildlife access to horse feed
-keep barn clean -limit bird dropping -EPM vacc but no efficacy data, NOT recommended |
|
What is the mechanical vector of the zoonotic togavirus?
|
Mosquito
|
|
Which animal is the amplifier host?
|
Passerine birds
|
|
Which species is the accidental host of the togavirus?
|
Horse
|
|
What are the clinical signs of an alphavirus (togavirus) ecephalitis?
|
-brain & spinal cord dysfunction
-biphasic fever spike -initial virmeic phase non-specific signs -progression to neuro signs -sleeping sickness |
|
What is the distribution of Eastern equine encephalitis?
|
East of the Mississippi
|
|
Does EEE have a viremic phase?
|
Transient viremia but not signficant
|
|
which species are the dead end hosts for EEE?
|
horse
human deer |
|
What is the px of EEE?
|
Poor, 90% mortality
|
|
Does Western EE have a viremic phase?
|
No, horse is dead end host
|
|
What animal is the reservoir for WEE?
|
Birds
mosquito is the vector |
|
What is the px of WEE?
|
fair to poor, 50% mortality
|
|
What is the viremic stage of Venezuelan EE like?
|
constant/high horse is significant amplifier
|
|
VEE is transmitted by mosquitos, what is the reservoir host?
|
rodents
|
|
What is the px of VEE?
|
poor, 50% mortality
|
|
How do you dx EEE/WEE/VEE?
|
-clinical signs
-seasonality of vector -CSF neutrophilai, xanthochormia, incr protein Def Dx: virus isolation from brain |
|
What is the tx for the alphavirsues?
|
-supportive care is the only option
-prevention is key -mosquito control -vacc in spring |
|
West Nile Virus is in what viral family?
|
Flavivirus of the togavirus family
|
|
How is WNV transmitted?
|
Culex mosquito
|
|
Which animals are the reservoir for WNV?
|
birds (crows are susceptible)
|
|
Which species are the dead end hosts for WNV?
|
Humans
HorsesLow |
|
What are the clinical signs of WNV?
|
-fever
-acute onset ataxia, weakness (rear limbs usually) -muscle fasiculations, primarily facial -somnolence |
|
How do you dx WNV?
|
-IgM capture Elisa
-viral isolation -PCR on tissue tx by supportive care |
|
How can you prevent WNV?
|
-vaccs (decr viremia and mortality)
-mosquito control |
|
EHV 1 causes what type of dz?
|
-myeloencephalitis
abortion -rhinopneumontitis |
|
What dz does EHV2 cause in foals?
|
mild respiratory and conjunctivitis
|
|
EHV 3 causes what dz?
|
coital exanthema
|
|
Rhinopenumonitis is also caused by which EHV?
|
EHV 4
|
|
What are the clinical signs of EHV myeloencephalitis?
|
-acute onset (may be epizootic)
-rear limb ataxia -bladder paresis -fecal retention -perineal hypalgesia -occasional cranial nerve deficits -pyrexia, respiratory signs |
|
EHV is a vrial infection of which cells?
|
Endothelial cells of CNS
|
|
What other rxn may play a role in EHV enceph?
|
Immune mediated type III hypersensitivy (Arthus)
|
|
What other signs of EHV infection can be seen on pathology?
|
-arteriolar vasculitis
-white matter ischemia -clinical signs from CNS infarct & necrosis |
|
How do your dx EHV myeloencephalitis?
|
-clin signs
-hx of abortion, fever or resap dz on farm -virus isolation from nasal swab or buffy coat -CSf antibody titer or PCR for virus -CSF xanthochromia, high protein, low cells |
|
How is EHV myeloencephalitis? treated?
|
-supportive care
-anti-inflammatory -manage rectal impaction and urine retention -Valcylovar may decr viremia -prognosis worse if recumbent |
|
How can EHV myeloencephalitis be prevented?
|
-pregnant mares are susceptible
-isolate affected animals, rapid spread -vaccinate for respiratory and abortion forms of disease, not protective against neuro form |
|
What is the cause of leukoencephalomalcia in horses?
|
Fumonsin B1 toxin of Fusarium moniliforme found in corn, corn screening sometimes oats and pellets
|
|
How does fumonsin affect the brain?
|
Interfers with sphingolipid production, build up of metabolic products results in neuronal damage
|
|
What are the clinical signs of leukoencephalomalcia?
|
-dementia, blindenss, convulsion, death, toxic hepatopathy (less common in horse)
|
|
How do you dx leukoencephalomalcia?
|
-identify toxin (not just mold) in feed
-CSF leukocytosis and high protein -clin signs in corn fed animals |
|
How do you tx leukoencephalomalcia?
|
-supportive
-remove contaminated feed -usual fatal in 48-72 hours |
|
What is the causative agent of botulism?
|
clostridum botulinum
|
|
What is the MOS of botulism?
|
Nwuromuscular blockade- blocks release of Ach at neuromuscular junction
|
|
Forage poisoning botulism usually occurs from what?
|
Carcass contamination of large bales (type C, rare in horses)
|
|
What are the signs of forage poisoning
|
-dysphagia
-muscle tremor -hyometria, weakness -ileus, bladder atony -death from respiratory paralysis -herd outbreaks may occur |
|
Toxins produced in the GIT in foals causes what syndrome?
|
Shakers (c botulimun type B)
dysphagia, weakness, tires easily -poor PLR, poor tone eyelid,tail (dysphagia in foals = milk from nose) |
|
How is botulism dx?
|
-isolation of C botulinum
-tongue stress test -toxin rarely isolated -mouse assay |
|
How do you tx botulism?
|
K+ or Na+ PCN (procain pcn potentiates NM blockade)
-polyvalent antiserum -may need to ventilate -prevent w/ toxoid in hi risk areas -exercise restriction --> depletes Ach |
|
Tetanus is an infection with what agent?
|
Clostridium tetani
|
|
Where are C tetani spores found?
|
soil and feces
resistant to high temps and common disinfectants |
|
Tetanus favors what type of environment?
|
Low O2...wounds/punctures
necrotic tissues |
|
What is the key to tetanus prevention in horses?
|
vaccination
|
|
How does tetanospasmin work?
|
Toxin inhibits the neurotransmitters GABA and glycine
-irreversibly binds inhibitory neuron (inhibits the inhibitor) causes muscle spasm, interruption of autonomic control |
|
What are the clinical signs of tetanus?
|
-extreme muscle rigidity
-saw horse stance -normal conscious proprioception -CN deficits |
|
What are the goals for tetanus tx?
|
-neutralize unbound.circulating toxin
-debridement of wound -abx targeting C tetani (PCN) -sedatives for muscle spasms -supportive/symptomatic care |
|
What is the mortality rate of tetanus?
|
80%
|
|
What is the purpose of giving tetanus toxoid?
|
-inactivated intact toxin from C tetani
-stimulates active immunity |
|
What is the purpose of giving tetanus antitoxin?
|
-serum contains antibody to tetanus
-confers passive immunity -will bind circulating toxin |
|
Cervical stenotic myelopathy is also called what?
|
Wobbler's dz
|
|
In which breed does wobblers occur more often?
|
TB
males > females |
|
What type of compression occurs in foals 6-18 months?
|
Dynamic compression
(static in 2-4 y/o) |
|
What are the dietary factors that contribute to wobbler's?
|
-decreased copper
-increased zinc -increased CHO (cartilage doesn't form properly) |
|
What are the clinical signs of cervical stenotic myelopathy?
|
-spinal ataxia
-weakness -dysmetria -symmetrical -rear limbs usually worse than front |
|
Cervical verterbral instability causes dynamic compression of the cord when?
|
During flexion and extentsion
|
|
What are the common sites of compression?
|
C3-C4 and C4-C5
|
|
Cervical vertebral malformation causes static compression the cord at what levels?
|
C5-C6 and C6-C7
|
|
What narrowing is seen from the malformation?
|
Ventral-dorsal narrowing
also Wallerian degeneration of neurons |
|
How do you calculate the saggital ratio of the c spine?
|
Ratio of widest part : narrowest part of the cord
|
|
How do you dx Wobbler's?
|
-signalment, hx, pe
-lameness and neuro exams -cervical rads -CSF analysis -myelography |
|
What is the tx for cervical stenotic myelopathy?
|
-minimize spinal cord injury and inflammation
-stall confinement -anti-inflammatory drugs -restricted diets -sx: ventral stabilization of malarticulation, basket sx |
|
Cauda equina syndrome is also known as what?
|
Polyneuritis equi
|
|
What is the suspected etiology of Polyneuritis equi?
|
Immune mediated or inflammatory syndrome (antibodies to P2 myelin protein)
|
|
How does the acute form of Polyneuritis equi manifest?
|
Hyperastesia or perineal and/or head region
|
|
How does the chronic form of Polyneuritis equi manifest?
|
Paralysis of tail, anus and rectum with fecal retention +/- incontinence
-muscle atrophy & ataxia of hind limbs -Cn dysfunction |
|
How do you dx Polyneuritis equi?
|
-chronic active inflammation on blood work (fibrinogen)
-CSF elevated total protien, incr WBC -presence of P2 myelin antibody supportive but not definitive Post mortem: granulomatous inflammation at nerve roots |
|
How do you tx Polyneuritis equi?
|
-corticosteroids
-supportive care |