Equine 3 Flashcards
1
Q
What are the 3 ways a muscle can respond to an injury
A
Necrosis
Atrophy
Hypertrophy
2
Q
AST is released from muscle and ______
A
Liver
3
Q
Which half life is longer? AST or CK
A
AST
CK goes up first
4
Q
Is myglobin harmful to kidneys
A
Yes
If CK above 10k needs fluids
5
Q
Is CK doubles or goes above 10K after exercise then
A
Muscle dz
6
Q
Where do we take muscle biopsy
A
Gluteal
7
Q
What is not a clinical sign of muscle disease A. Hind limb cramping B. Lose gait C. Reluctant to move D. Anxious E. Sweating E. Tachycardia F. Painful muscle palpation and firm muscles G. Myoglobinuria
A
B- stiff gait
8
Q
Why would increased potassium occur with muscle dz
A
Muscle breakdown
AST LDH also go up with CK
9
Q
A dark brown urine with no red blood cells indicates
A
Myoglobin
10
Q
Exertional ehabdomylysis myopathies occur (acutely, chronically)
A
Acutely
Emergency therapy required
11
Q
A shortened stride may be a sign of
A
Muscle pain
12
Q
How is ER treated
A
Rest NSAID Fluid Pain control - flunixin phenylbutazone Muscle relaxants- methocarbamol dantrolene sodium Acepromazine Vitamin E
13
Q
Why types of horses do we normally see exhausted horse syndrome
A
Prolonged submaximal exercise
Endurance horses
Race horses
14
Q
What is not a sign of exhausted horse syndrome A. Muscle cramp B. High blood pressure C. Depresses D. Profuse sweating E. Colic
A
B- poor perfusion
15
Q
How much fluid can be lost from sweating
A
1 gallon/hr
Severe na k cl depletion
Moderate loss of Ca and mg
16
Q
What is the acid base status of exhausted horse? A. Metabolic alkalosis B. Metabolic acidosis C. Respiratory alkalosis D. Respiratory acidosis
A
A- decreased Cl decreased binding of Ca
17
Q
What is the cardiovascular response to exhausted horse
A
Higher HR
Colic in endurance horse
Decreased blood volume
18
Q
What is the respiratory response of a exhausted horse
A
Panting
19
Q
What do fluid and electrolyte abnormalities lead to in horses with exhaustion
A
Obtundatiin
Muscle cramps and spasms
Synchronous diaphragmatic flutter- Ca abnormality causes this
20
Q
T/F metabolic acidosis is often a feature of exercise induced myopathies
A
False. IS NOT
21
Q
What are risk factors for post anesthetic myopathy
A
Duration of procedure Hypotension Hypoxia Acidosis Poor perfusion Insufficient padding Weight
22
Q
How is post anaesthesia myopathy treated
A
Fluids. Especially if low Ca Dilute myoglobin in kidney Acepromazine Methocarbamol Rest Sling High fat low carb diet
23
Q
What are causes of recurrent rhabdomyolysis
A
Polysaccharide storage myopathy (type 1 quarter horses) and type 2 (quarter horse warm blood draft Arabians) Recurrent exertional rhabdomyolysis (RER) ( thoroughbred and standard bred) Mitochondrial myopathy (Arabians)
24
Q
What are some blood abnormalities of horses with recurrent rhabdomyolysis
A
CK AST creatinine with myoglobinuria
No inflammation
25
How is recurrent rhabdomyolysis dx
Exercise test
| Muscle biopsy
26
What are presenting signs for PSSM (type 1 and 2)
Decreased performance
Mild or none rhabdomyolysis
Muscle wasting
27
Type 1 PSSM is caused by a mutation in_____
Glycogen synthase 1 (GYS1)
| PAS positive inclusion on biopsy
28
In type one PSSM muscles cannot generate adequate energy Which does not occur
A. Enhanced insulin sensitivity and uptake of glucose
B. Enzyme imbalances
C. Decreased synthesis of less branches glycogen
C- increased
29
How is PSSM definitively diagnosed
A. Genetic test from hair or whole blood (75% sensitivity)
B. Muscle biopsy (type 2 only 100% sensitive)
A
| B
30
How is PSSM treated and managed
```
No cure
Acute episodes
Consistent exercise
Decreased soluble carbs
Grass hay
Add fat
```
31
When is recurrent exertional rhabdomyolysis seen
```
Thoroughbreds
Standardbred
Lameness
In cold weather
Stressful events
```
32
What mineral is changed by recurrent exertional rhabdomyolysis
Defect in intracellular Ca regulation in sarcoplasnjx reticulum - no test
Look at CK and AST
33
RER is managed by
```
No stress
Regular exercise
Low carb diet
Balances electrolytes
Dantrolene (alters Ca release in muscle) before exercise
```
34
```
Which is false about shivers
A. Gradually progressive
B. Chronic neuromuscular disease
C. Gait abnormalities when backing up
D. Occurs in front limbs primarily
```
D- pelvic region limbs and rail (jerky and trembling tenseness
35
What is pathogenomic for shivers
Raised tail head
36
```
Stringhalt is
A. Hocks flex violently toward abdomen
B. Medial patellar ligament momentarily caught
C. Scar tissue formation due to injury
D. Symmetrical muscle wasting
```
A
37
Treatment of shivers includes
```
No good treatment
Vitamin e
Selenium
Massage
Consistent exercise
Acupuncture
```
38
Mitochondrial myopathy makes it very hard to
Exercise longer than 6 minutes
39
Mitochondrial myopathy occurs when there are spontaneous mutations in _____. This is inherited from the (mother/ father). Defective oxidative phosphorylation results in a rise in _______
MtDNA
Mother
Lactate- greater emphasis on anaerobic glycolysis for energy production
40
How is mitochondrial myopathy
Muscle biopsy
Normal CK
marked plasma lactate values
EMG- dive bomber sounds
Poor prognosis (unlikely to be athletic)
41
_______ is an important energy source for fetus and neonate
Glycogen
42
Glycogen branching enzyme deficiency (GBED) causes there to be no measurable _________ activity
GBE- enzyme
Unable to form normally branches glycogen -no glucose homeostasis
Always fatal before 8 weeks old (quarter horses pain Appaloosa)
43
Hyperkalemia periodic paralysis affects mainly what breed
Quarter horses
| Mutation in voltage gated Na channels=hyperexcitable muscles
44
What are the 2 differentials of prolapse of the 3rd eyelid in horses
HYPP
| Tetanus
45
What are some clinical signs of HYPP
```
Weakness muscle fasciulations
Anxious
Stridor
Dyspnea. Tachypnea
Recumbancy
```
46
How is HYPP diagnosed
Plasma K
| DNA of blood or hair
47
How is HYPP treated
```
Karo syrup
Grain
(NOT MOLASSES)
Bicarbonate- severe
Dextrose- severe
Calcium gluconate
Insulin- try not to use
```
48
What cannot be fed to horses with HYPP
Low K
No alfalfa bran or molasses
Avoid rapid feed changes
Acetazolamide reduces K
49
Immune mediated myositis (non exertional rhabdomyolitis) affects what gene of what breeds
E321G myosin heavy chain 1 MYH1 gene in quarter horses
50
What are clinical signs of immune mediated myositis
```
Symmetrical muscle atrophy
Stiff gait
Fever
Concurrent infection or vxn
Increased muscle enzymes, WBC and fibrinogen
```
51
What are treatments for immune mediated myositis
Corticosteroids. Dexamethasone then prednisolone
52
Nutritional mouse generation is also known commonly as
White muscle disease
| Nutrional muscular dystrophy
53
What is the nutrional deficiency of horses with white muscle disease
Selenium and or vitamin e
54
The cardiac form of WMD affects (very young foals/ weanlings).
Very young foals. Weaning is skeletal form (weakness. Stiff gait. Poor suckle. Painful muscles. Limited jaw motion and weight loss). Cardiac (edema. Recumbancy. Heart murmur. Fatal)
55
How is WMD diagnosed
```
Increased CK and AST
Myo globinuria
Selenium concentration in blood
Glutathione peroxidase activity
Muscle biopsy
```
56
Which is false about WMD’s treatment and prevention
A. Give oral shipments as IM injections can have severe reactions in adults
B. Restrict exercise
C. NSAIDS
D. Give selenium injections at birth
E. None of the above
E. It’s all of them
57
Seasonal pasture associated myopathy occurs in the mid-west in the spring and summer. It’s caused by ingestion of
Seed pods from box elder trees
| Hypoglycin A causes multiple accounts CoA dehydrogenase deficiency (MADD)
58
T/F. Seasonal pasture myopathy tends to have a good prognosis when given supportive care
False. Up to 90% mortality. Severe rhabdomyolysis of skeletal cardiac and respiratory muscles. Sudden death
59
Clostridial myonecrosis is caused by what pathogen and usually occurs with what
Clostridial perfringes ( Gram + rod)
Follows IM injection or puncture wound
May also invade GIT
Necrotizing and hemolysin toxins cause Cl Signs
60
What are clinical signs of clostridial myonecrosis
```
Death
Obtunded
Pyrexia
Tachypnea
Swelling pain
Discharge. Odorous
Rapidly progressive
```
61
How is clostridial myonecrosis treated
```
K penicillin
Debridement
Metro
Fenestration
Remove necrotic tissue to disrupt anaerobic environment
O2
AB min 7 days after wound is resolved
Corticosteroids are controversial
```
62
CN1
Olfactory
63
CN2
```
Optic
Menace
Dazzle
Obstacle course
PLR
Fundic
```
64
CN3
Oculomotor
PLR
Eye position
65
CN 4 and CN6
Trochlear and abducens
Eye position
Strabismus if abnormal
66
CN5
Trigeminal
Muscles of mastication
Sensory- skin and MM
67
CN7
```
Facial
Motor of muscles of facial expression
Menace blink
Prehension
Lacrimal gland
```
68
CN8
Vestibulocochlear
Balance
Hearing
69
CN 9 10 11
```
Glossopharyngeal
Vagus
Accessory
Pharynx and larynx atrophy. Slap test. Endoscopy
Swallowing, aspiration pneumonia
```
70
CN12
Hypoglosus
| Tongue motor
71
Sacral segments of damaged nerves may show what
Atrophy and sweating y
72
What is the difference between lame and neurological gait
Lame- regularly irregular
| Neuro- irregularly irregular
73
What is pacing in. A horse
Both front and back leg on one side move at the same time with a step forward
74
Gait grading- horse that stumbles and is at risk for falling
4/5
75
Gait grading- detectable during maneuvers. Hard to see I straight line
2/5
76
Gait grading. Normal gait
0/5
77
Gait grading- recumbent
5/5
78
How is juvenile epilepsy treated
Resolves 6-12 months
Diazepam iv and phenobarbital
Acepromazine. Xylazine and ketamine make it worse
79
A premature foal (premature separation of the placenta) has a nystagmus and seizures
Perinatal asphyxia syndrome
Multiple organs affected
Control seizures
Poor prognosis
80
Enrofloxacin given into the carotid would result in what clinical signs
```
Seizures
Unresponsive
Low HR
No PLR
Hypothermia
Blindness
Necrosis of brain
```
81
Severity with a carotid injection is dependent on
PH
Composition (oil worse)
Volume
82
How is a carotid injection treated
Edema- mannitol, hypertonic saline, furosemide
NSAIDS DSMO
Elevate head
Fluids diazepam
83
What is seen in blood work with a horse with hepatic encephalopathy
```
Neutrophilia
High liver enzymes
Low fibrinogen
High ammonia
Prolonged coagulation
```
84
Leukoencephalomalacia is caused by what bacteria and where is that bacteria found
Fusarium moniliforme and moldy corn disease
| In late fall or early spring
85
What are some clinical signs of leukoencephalomalacia
```
In coordination
Lethargy
Obtundation
Head pressing
Liver failure
Seizures
Sweating
Hyperexcitability
```
86
How is leukoencephalomalacia treated
Not
Euthanasia
Grey/ brown areas of malacia on necropsy in white matter. Unilateral
87
Nigropallidal encephalomalacia is caused by what
Yellow star thistle
Russian knapweed
Prolonged ingestion (not palatable)
88
What are clinical signs of nigropallidal encephalomalacia
```
Sudden onset
Impaired prehension and mastication
Can swallow if food put in back of throat
Tongue paresis
Lethargy
Ataxia
Chewing
Hypertonicity of facial muscles
Head droop
Not treatment (bilateral symmetrical malacia necropsy)
```
89
EEE WEE VEE all cause severe encephalitis. How do the symptoms progress
Fever stiffness to
Compulsive walking depression excitability abnormal CN to
Recumbancy and death
EEE is 2-3 days until stage 3
90
EEE VEE AND WEE have what prognosis
EEE 90% mortality
VEE 40-80% mortality
WEE 50% (no cases in 50 years)
Supportive treatment
91
T/F vaccinating for EEE is highly effective and is given yearly
True. Every 6 months if year round mosquitos
92
What are other ways to prevent EEE
Mosquito control
Full body blanket- zebra stripes
Screens
93
How is EEE diagnosed
IgM capture Elisa
CSF- increased LT high protein
Necropsy- viral isolation
94
When are peak levels of west bile virus
Peak in late summer b/c mosquito
95
What are clinical signs for WNV
```
Weakness
Ataxia
Altered mentation
Muscle fasciculations
CN deficits
Recumbency
30% experience a recrudescence of cl. Signs
```
96
How is WNV diagnosed
IgM capture ELISA
CSF increased LT high protein
Necropsy - polioencephalomalacia tissue PCR
Only symptomatic treatment
97
T/F WNV has a very effective vaccine that needs to be given Q4 months
True
98
Rabies have 3 broad categories of clinical signs in horses. What are they
Furious (brain)- photophobia and aggressive
Dumb (brainstem) - obtunded anorexia circling
Paralytic (spinal)- paralysis ataxia lameness self mutilation
99
Rabies is diagnosed once euthanized How
```
Direct fluorescent Ab
Negri body (less used now due to direct fluorescent ab)
```
100
```
A IgM titer of WNV >400 indicates
A. Infection
B. Vaccinated
C. Both
D. Neither
```
A only
| Vaccine doesn’t get that high
101
Cerebellar abiotrophy is the most common cerebellar disease and causes the premature death of what cells
Purkinje cells
| Arabian foals- genetic
102
At what age is cerebellar abiotrophy typically seen
6 weeks - 4 months
| Born normal
103
What are clinical signs of a foal with cerebellar abiotrophy
```
Intention tremor
Symmetric ataxia
Hyper extension of limbs
Wide base stance
No menace
Visual and normal mentation
No sense of space or distance
Hard to coordinate and balance
```
104
How is cerebellar abiotrophy diagnosed
Test carrier status
| Histology- degeneration of purkinje cells
105
What is the prognosis of a foal with cerebellar abiotrophy
Good but there is no treatment. It doesn’t get worse but won’t get better
Can’t be safely ridden
Prone to self trauma and can be euthanized
106
A head tilt from a peripheral lesion goes (toward/away) from the lesion
Toward
107
A horizontal nystagmus fast phase from a peripheral lesion goes (toward/away) from the lesion
Fast phase away from lesion
108
A head tilt from a central lesion goes (toward/away) from the lesion
Away?
109
A head tilt from a peripheral lesion goes (toward/away/unknown) from the lesion
Unknown. Can go in any direction
110
What are seen in both central and peripheral CN 8 lesions
EPM
| Trauma
111
What are seen in central CN 8 lesions
EEE
WNV
EHM
Mass
112
What are seen in peripheral CN 8 lesions
THO
otitis interna
Idiopathic labyrinthitis
113
Are CN7 signs seen before or after CN8 in THO
After
7- keratitis and corneal ulceration
Subpalpebral lavage (enucleation?)
114
Where are THO typically seen
West side of US for unknown reasons
| Fractured hyoid inner ear infection trauma
115
In THO it is usually (unilateral/ bilateral)
Bilateral. But 1 usually happens first
116
Cervical vertebral stenotic myelopathy (CVSM) occurs primarily in what types of breeds
Large fast growing breeds
| Malformed vertebrae
117
What are some components of CVSM
Stenosis of vert canal
Compression of the spinal cord
Persistent or dynamic
118
What are the clinical signs of CVSM
```
Weakness
Symmetrical Ataxia
Spasticity and paresis
All limbs= c1-5 (hind limbs worse)
C6-7 (same or front limb worse)
```
119
How is CVSM diagnosed
Radiographs (looking for any fracture or arthritis site)
Don’t correlate with compression site
Narrow- likelihood of CVSM
Indication for myelogram- ataxia with no neck lesion diagnostic if malformation
120
How should the horse be placed for a myelogram
Elevate the head to prevent contrast from getting to the brain (b/c seizure)
121
How is CVSM treated
Corticosteroids (intra articular)
NSAIDS (phenylbutazone)
Surgery - cervical stabilization (80% improve 1 degree of ataxia, 40% improve 2) but takes 1 year to recover r
122
Equine degenerative myeloencephalopathy is also known as
Equine neuroaxonal dystrophy (NAD)
| Is a non-compressive diffuse symmetric degeneration seen 1minth-3 years
123
What can predispose a horse to. EDM
Low vitamin E in diet
| Dry lot= higher risk
124
What are clinical signs of EDM
```
Symmetrical ataxia
Weakness
No menace (40%) but visual
Pigment rentinopathy
Behavioral issues- aggression
DOES NOT affect CN, anal tone or atrophy!!
```
125
How is EDM diagnosed
Rule out other dz
Plasma/serum alpha-tocopherol levels (not difinitive)
Opththalmic exam
Histo of brain and spinal cord
126
How is EDMA prevented/treated
Green pasture with vitamin E in mares and foals
Natural RRR for vitamin E supplement
Poor prognosis- usually stabilize signs but don’t improve. Wasting of muscle
127
EMP 3 A’s are
Asymmetric
Ataxia
Atrophy
128
CVSM and EDM both have what type of ataxia
Symmetric and less atrophy
129
Equine protozoal myeloencephalopathy is caused by what pathogens
Sarcocystis neurona- 1
Neospora caninum/ hughesi
Western Hemisphere
All breeds all ages
130
Ataxia in a horse with EPM will be
Asymmetric
| Focal muscle atrophy LMN
131
T/F EPM clinical signs tend to be acute
F
Onset gradual
Multi focal or diffuse lesions
Gray and white matter- brain brainstem or spinal cord
132
How is EPM diagnosed
None are good
Serum/ CSF ratio- <100= dz
Serology - rules it out if negative
133
EPM treatment will allow what percent to improve
60-75%
| 15-30% relapse
134
How is EPM treated
```
Pyrimethamin and sulfadiazine
4-6months but cheaper than:
Ponazuril 28day
Diclazuril 28day
Supportive- NSAIDS Vitamin E thiamine
```
135
Equine herpes myeloencephalomalacia causes what in young horses
Respiratory dz
Abortion in last 1/3 of pregnancy
Myeloencephalopathy - uncommon (neuropathic strain)
136
What are clinical signs with EHM
```
Fever
Ataxia
Tetraparesis (weakness, hind limbs are worse)
Hypotonia- anus and tail
Urinary incontinence
```
137
How is EHM diagnosed
Contact state vet
Quarantine
Nasal swab and blood PCR
CSF- Canthochromia and high pt and monocytes
138
How is EHM treated
```
Heparin
Antiviral (acyclovir valacyclovir)
NSAID
Only 50% survival. If down much less
Vaccine doesn’t work
```
139
Acquired neuro degenerative disease known as equine motor neuron disease affects the ventral horns of the ____ matter
Grey. Spinal cord (brainstem nuclei). Horses are older than 2 and vitamin E deficiency
140
```
Which is not a sign of Equine motor neuron disease
A. Sweating
B. Ataxia
C. Muscle trembling
D. Weight shifting
E. Weak and muscle wasting
F. Elevated tailhead and low head
G. Sluggish PLR
H. Honeycomb pattern (non-tapetal)
```
B- no ataxia
141
How is equine motor neuron disease treated
Vitamin E (RRR)
20- unchanged
40%- deteriorate (6 weeks)
40%- recover
142
What biopsy is taken for equine motor neuron disease
Sacrocaudalis dorsalis (tailhead)
To dx - low serum/ plasma alpha tocopherol, increased CK AST, abnormal EMG or accessory nerve biopsy
143
Suprascapular nerve injury can be caused from trauma of the cranial shoulder What muscles does it innervate
Supraspinatus and infraspinatus muscles. See atrophy over a few weeks and outward rotation of the shoulder
144
A horse that is not weight bearing of the front right leg with the dorsum hoof in the ground and a flexed elbow what is a likely cause
Radial nerve paralysis. Also can’t flex shoulder or extend limb. Elbow trauma is the cause
145
Bilateral damage of the brachial plexus could result in
Inability to stand on front legs. Trying to get up
| Can be torn nerve or just swollen
146
Severe pruritus of perineum followed by a lack of tail tone or anal tone may indicate an issue with what nerves
Polyneuritus equi
| EHV- also differential
147
Polyneuritis equi is a immune mediated disease with no sex, breed or age predisposition that forms what on nerve roots
Granulomatous lesions
148
What is the toxin of tetanus
Tetanopasmin that inhibits inhibitory neurons of the spine
149
What types of wounds cause tetanus
Low o2 (deep. Necrosis)
Impaired blood supply
Puncture would castration metritis abscess
Umbilical infection- foals
150
What is a common clinical sign of both vaccinated and non vaccinated horses that were infected with tetanus
Third eyelid prolapse
151
How is tetanus treated
```
Wound debridement
AN- penicillin
Tetanus antitoxin (TAT)
Toxoid
Theiler’s dz
```
152
What usually kills a tetanus horse
Paralysis of respiratory muscles
153
T/F the vaccine for tetanus is 100% effective
True. According to sanz
154
What type of botulism is most common
B. - from wound. Shaker foal
A(west)
C (FI). These are from feed
155
What are clinical signs of botulism
```
Weak
Dysphasia
Poor muscle tone
No PLR
Muscle fasciculations
```
156
What are treatments for botulism
Antitoxin (bind to free toxin) not effective if down
| Supportive - wait until new receptors are made
157
When should a mare be vaccinated for botulism when bred
I month pre foaling
| No vxn for A or C (no cross protection)
158
What is the prognosis of botulism
Poor if down
| Guarded to good if standing with antitoxin
159
Wound for toxin testing for botulism tests for what types
PCR for A B C
160
What should be immediately addressed when a outbreak is thought to have occurred
```
Minimize exposure
Contain spread
Treat affected horses
Stop movement
Isolate
Don’t be a fomite
```
161
What oxidizing agents are used in foot mats to prevent spread of dz
Virkon accel
| Broad spectrum and safe but corrosive to metal
162
How long should new arrivals be quarantined
28 days/ > 2 weeks
Test for EIA S. equi
163
If a horse has diarrhea leukopenia and fever what should it be tested for
Salmonella
Target testing ( no whole herd if they don’t have symptoms)
164
What is the best way to ensure streptococcus free status in an outbreak
Nasopharyngeal washes on all horses every other week until 3 negatives consecutively
165
What biosecurity resource helps with vaccination guidelines and infectious dz control guidelines
AAEP
166
For a substance to be considered antigenic it’s must have a molecular weight above
8000
Also depends on spirited on cell surface
167
T/F Vaccines are considered a passive immunization process
False. Is active
Passive- Ab go unimmunized individual
168
Killed vaccines rely on _______ to create an immune response
Adjuvants
169
T/F a vaccine must be demonstrated to be safe and effective before marketing
False. Only safe
170
What are the core vaccines in horses
Tetanus toxoid
EEE WEE Venezuelan EE
WNV
Rabies
171
T/F administration of MLV and killed vaccine is discouraged as adjuvants may inactivate MLV
True
172
Horses greater than 3 years old are more susceptible to parasite infection
False
Younger than 3
173
Currently _____ are considered the primary equine parasitic pathogen
Cyathostomin. Small strongyle
Anaploceohala perfoliata can be a major cause of colic in horses
174
```
Which is false regarding cyathostomin
A. In environment
B. All grazing horses are infected
C. Only disease at very high levels
D. Frequent anthelmintic needed
```
D- not needed
175
What are the main anthelmintics
Ivermectin
Moxidectin
Pyrantel
Fenbendazole
Deworming every 2-3 months is not recommended
176
What is the only test currently available for detecting parasite resistance in horses
Fecal egg count reduction test
177
Low egg shedders should be dewormed how often
2 times a year
178
Resistance is considered to be less than ___% of egg reduction
80
Deworm if above 200 (moderate to high shedders)
179
1st deworming is at _____ months of age with fenbendazole/oxibendzole
2-3 months
Fecal float then at 5-6 months
