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Equine Med and Surgery II > Lecture 3: Diseases of the nervous system > Flashcards

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

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

A

Colic

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
Q

What is the paralytic form of rabies

A

Ascending paralysis, ataxia

26
Q

How do you dx rabies and what is standard

A
  1. Immunofluorescence of brain- standard
  2. Histo of Negri bodies
  3. CSF may be normal or pleocytosis
27
Q

What is the first thing you do for suspected rabies case

A

Contact state vet

28
Q

After contacting state vet what are the next steps in rabies treatment/biosecurity

A
  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
Q

What is prognosis for rabies

A

100% fatal

30
Q

What is metabolic encephalopathy characterized by

A

Abnormal mental status and elevation of ammonia in blood

31
Q

What is the pathogenesis of metabolic encephalopathy

A
  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
Q

What cell is indicative of metabolic encephalopathy

A

Type III astrocytes

33
Q

What are some clinical signs of metabolic encephalopathy

A

Behavior changes, depression, head pressing, circling, mild ataxia

34
Q

What can cause hyperammonemia

A
  1. Hepatic dysfunction: liver failure or PSS
  2. Excessive ammonia produced in intestinal tract
35
Q

What can cause renal (uremic) encephalopathy

A

Accumulation of metabolic wastes in the brain

36
Q

How do you dx metabolic encephalopathy

A
  1. Blood-ammonia levels
  2. Liver enzymes may or may not be elevated
37
Q

What is tx for metabolic encephalopathy

A

Lactulose

38
Q

What does a true seizure look like

A

Repetitive and rhythmic muscle movements, premonitory signs and aura, postictal signs, not aware or responsive, rapid eye movement

39
Q

What is affected in partial seizure

A

Discrete area of cerebrum affected

40
Q

What is affected in generalized seizure

A

Arises from both cerebral hemispheres simultaneously

41
Q

What is a status epilepticus

A

Succession of seizures without regaining consciousness or continual seizures for 5 minutes

42
Q

What cardiovascular events mimic seizures

A

Syncopal episode from arrhythmia, ruptured chordae tendinae, myocardial infarction

43
Q

What circulatory shock events mimic seizures

A

Hemorrhage, volume depletion

44
Q

What electrolyte disorders mimic seizures

A

Hypocalcemia, hypo magnesium

45
Q

What muscle diseases mimic seizures

A

HYPP, recumbency myopathy, exertional rhabdomylosis

46
Q

What development abnormality can be a differential for seizures

A

Hydrocephalus

47
Q

What metabolic abnormalities are differentials for seizures

A

Hyperammonemia, hypo/hyperosmolality, electrolyte disorders

48
Q

What neoplasms can be differentials for seizures

A

Cholesterol granuloma, PPID

49
Q

What are some iatrogenic differentials for seizures

A

Air embolism, intracarotid injection, fluphenazine

50
Q

What is a differential dx for idiopathic seizures

A

Epilepsy

51
Q

What are some differential dx for infectious seizures

A

Encephalitis, meningitis

52
Q

What are some toxic differential dx for toxic

A

Locoism, moldy corn

53
Q

What is used for immediate control of seizures

A

Diazepam- increase GABA

54
Q

What drugs can be used for prevention of seizures

A

Phenobarbital, potassium bromide, phenytoin

Equine Med and Surgery II (4 decks)

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