Lecture 3: Diseases of the nervous system Flashcards

1
Q

What is the mechanism of action for clostridium tetani

A
  1. Tetanospasmin binds to renshaw cells within the central nervous system
  2. Irreversible blockade of GABA/glycine
  3. Leads to continued stimulation of the action potential
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2
Q

What are some clinical signs of tetanus

A

Third eyelid prolapse, lockjaw, sawhorse stance, elevated tail head, hyperesthesia, muscular spasms, recumbency, convulsions, death by respiratory failure

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3
Q

How do you dx tetanus

A

Clinical signs and finding anaerobic site of infection

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4
Q

How long does it take to develop and replace new synapses with tetanus infection

A

6-8 weeks

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5
Q

What is treatment for tetanus

A
  1. Antibiotics- metro, penicillin
  2. Drain abscess
  3. Antitoxin- Colorado serum company
  4. Sedatives/ muscle relaxants
  5. Vaccinate
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6
Q

How long is passive immunity from tetanus antitoxin

A

7-14 days

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7
Q

What is a rare side effect of tetanus antitoxin that could contain parvovirus

A

Acute fatal hepatic necrosis (Theiler’s disease)

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8
Q

What symptoms is more common in non-survivors of tetanus

A

Dysphasia, dyspnea and recumbency

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9
Q

Survivors of tetanus will stabilize in __-__ days

A

5-7 days

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10
Q

What are the 3 ways horses can get exposed to clostridium botulinum

A
  1. Preformed toxin eaten
    - type B- decomposing vegetation
    - type C- decomposing carcasses in feed
  2. Grows in intestine- type B- shaker foal
  3. Grows in anaerobic wound- type B
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11
Q

What is the pathogenesis/ MOA of botulinum

A

Blocks acetylcholine release at NMJ resulting in descending symmetrical progressively flaccid paralysis

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12
Q

How can you dx botulinum

A
  1. Identify toxin in feed, serum, GI contents, feces, debris
  2. Grain test- should consume 8oz grain in under 2 minutes
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13
Q

What are some clinical signs of botulism

A

Dysphasia, poor tongue and lip tone, weakness, lethargy, head carriage, muscle tremors, recumbency, death from respiratory failure

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14
Q

What is tx for botulism

A
  1. Antitoxin
  2. Supportive care
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15
Q

Botulism antitoxin is not effective after botulinum toxin has been ___

A

Translocated into the cells

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16
Q

What is the prognosis for botulinum

A

70-99% mortality, 48% survival

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17
Q

T or F: horses with botulinum in which treatment is started after they are already down usually die

A

True

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18
Q

How do you prevent botulinum

A

Type B vaccine

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19
Q

What is the pathogenesis/ MOA of rabies

A

Virus travels to CNS via neurons and reaches salivary glands via associated cranial nerves

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20
Q

What are the reservoir hosts for rabies

A

Skunks, raccoons, bats, and red fox

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21
Q

What is the incubation period for rabies

A

9 days- 1year

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22
Q

What is the most common clinical sign of rabies in horses

23
Q

What is the furious form of rabies

A

Aggressive behavior, photophobia, hydrophobia, tremors, hyperesthesia, convulsions

24
Q

What is the dumb form of rabies

A

Depression, anorexia, head tilt, salivation, circling, ataxia, dementia

25
What is the paralytic form of rabies
Ascending paralysis, ataxia
26
How do you dx rabies and what is standard
1. Immunofluorescence of brain- standard 2. Histo of Negri bodies 3. CSF may be normal or pleocytosis
27
What is the first thing you do for suspected rabies case
Contact state vet
28
After contacting state vet what are the next steps in rabies treatment/biosecurity
1. Quarantine 6 months 2. Aggressive wound care- scrub and clean for 15 mins 3. Unvaccinated can’t be vaccinated for 6 months 4. Vaccinated horses should be boostered immediately
29
What is prognosis for rabies
100% fatal
30
What is metabolic encephalopathy characterized by
Abnormal mental status and elevation of ammonia in blood
31
What is the pathogenesis of metabolic encephalopathy
1. Glutamine and urea broken down to ammonia 2. Ammonia overwhelms hepatocytes and crosses into circulation and crosses BBB 3. Ammonia is converted to glutamine which has an osmotic effect resulting in cerebral edema
32
What cell is indicative of metabolic encephalopathy
Type II astrocytes
33
What are some clinical signs of metabolic encephalopathy
Behavior changes, depression, head pressing, circling, mild ataxia
34
What can cause hyperammonemia
1. Hepatic dysfunction: liver failure or PSS 2. Excessive ammonia produced in intestinal tract
35
What can cause renal (uremic) encephalopathy
Accumulation of metabolic wastes in the brain
36
How do you dx metabolic encephalopathy
1. Blood-ammonia levels 2. Liver enzymes may or may not be elevated
37
What is tx for metabolic encephalopathy
Lactulose
38
What does a true seizure look like
Repetitive and rhythmic muscle movements, premonitory signs and aura, postictal signs, not aware or responsive, rapid eye movement
39
What is affected in partial seizure
Discrete area of cerebrum affected
40
What is affected in generalized seizure
Arises from both cerebral hemispheres simultaneously
41
What is a status epilepticus
Succession of seizures without regaining consciousness or continual seizures for 5 minutes
42
What cardiovascular events mimic seizures
Syncopal episode from arrhythmia, ruptured chordae tendinae, myocardial infarction
43
What circulatory shock events mimic seizures
Hemorrhage, volume depletion
44
What electrolyte disorders mimic seizures
Hypocalcemia, hypo magnesium
45
What muscle diseases mimic seizures
HYPP, recumbency myopathy, exertional rhabdomylosis
46
What development abnormality can be a differential for seizures
Hydrocephalus
47
What metabolic abnormalities are differentials for seizures
Hyperammonemia, hypo/hyperosmolality, electrolyte disorders
48
What neoplasms can be differentials for seizures
Cholesterol granuloma, PPID
49
What are some iatrogenic differentials for seizures
Air embolism, intracarotid injection, fluphenazine
50
What is a differential dx for idiopathic seizures
Epilepsy
51
What are some differential dx for infectious seizures
Encephalitis, meningitis
52
What are some toxic differential dx for toxic
Locoism, moldy corn
53
What is used for immediate control of seizures
Diazepam- increase GABA
54
What drugs can be used for prevention of seizures
Phenobarbital, potassium bromide, phenytoin