CNS Stimulants Flashcards
Which two toxins cause intermittent seizures?
- Lead
- 1080
1080
a rodenticide not available in the US, and also found in some Australian plants
Are seizing animals an emergency?
yes
Strychnine
below ground use restricted pesticide; also found in herbal medications
Strychnine MOA
competitive and reversible inhibition of NT glycine (which would normally open chloride channels) and hyperpolarizes neurons, so the animal has uncontrolled reflex activity especially concerning extensor muscles –> RIGIDITY
Strychnine Clinical Signs
anxiety, violent tetanic (only rigidity) seizures, death d/t respiratory inhibition (can’t expand chest) so they suffocate
Strychnine Tx
no emesis (rapid onset) but can lavage, IV fluids + electrolytes, control seizures, poor prognosis
may also administer lipid therapy
lipid therapy
can be given to fat soluble toxins to keep them BOUND in circulation (remember only free is a problem)
Pros of Lipid Therapy
faster recovery time, can be administered via peripheral catheters (inc. availability beyond ERs), inexpensive with a good shelf life
Cons of Lipid Therapy
must be refrigerated, can have a number of complications (lipemia, pancreatitis, inc. liver enzymes, organ failure, binds other important drugs like diazepam)
Toxins that can be treated with Lipid Therapy
Most common: Marijuana!!
but also ivermectin, Ca channel blockers, permethrin, antidepressants, muscle relaxers
Water Hemlock
one of the most toxic plants in the US (toxin concentrated in root chambers in stem), grows in waterways
Water Hemlock Clinical Signs
rapid onset violent seizures with a similar MOA to strychnine; salivation, muscle twitching, and death
Water Hemlock Tx
not often done because usually animal is found dead, but can use AC and even rumenotomies
Mycotoxin
toxins produced by a fungus, often found on stressed or poorly stored crops
Tremorgenic Mycotoxin Grasses (3)
- Bermuda
- Dallis
- Perennial Rye Grass
Large Animal Tremorgenic Mycotoxin Clinical Signs
“staggers” appear after ~7 days of grazing, fine muscle tremors of head and neck, stiffness
Large Animal Tremorgenic Mycotoxin MOA
reduces GABA and glycine concentrations, and likely cerebral vasoconstriction
Large Animal Tremorgenic Mycotoxin Tx
remove from source, provide supportive care, good prognosis with recovery in 3-7 days
Small Animal Tremorgenic Mycotoxin Sources
“garbage toxicosis” so garbage, compost, indole alkaloids (penicillium spp)
Small Animal Tremorgenic Mycotoxin MOA
inhibits glycine, GABA, and possible increase in Ach
Small Animal Tremorgenic Mycotoxin Clinical Signs
hyperactivity, tremors, seizures (w/in 30-120minutes) with varying severity
Small Animal Tremorgenic Mycotoxin Tx
emesis, maybe AC, seizure and tremor control (via methocarbamol!), supportive care and fluids
Methocarbamol
centrally acting skeletal muscle relaxant
Should you ever induce emesis in a seizing animal?
NO omg please no
3 Ways to Get Hypernatremia
- Ingestion
- Dehydration
- Substances that Cause Fluid Shifts (Osmotic Shifts)
Substances that may DIRECTLY cause Salt Toxicosis
salt (duh), brine, feed mixing errors, rock salt, ice melt, ocean water, bouillon, homemade playdoh
INDIRECT causes of Salt Toxicosis
lack of water (frozen, overcrowded trough, gross, etc), osmotic agents, paintballs, activated charcoal, high fructose corn syrup
Acute Salt Toxicosis MOA
sudden increase in plasma Na and water is pulled out of the brain causing cerebral vascular damage and hemorrhage
Chronic Salt Toxicosis MOA
Na diffuses into brain to protect from dehydration d/t water loss, so glycolysis is inhibited which dec ATP because the Na pump stops working (leads to vomiting, lethargy, ataxia, tremors, seizures)
Is it important to know whether salt toxicosis is acute or chronic?
yes, we don’t want to correct it too quickly, otherwise can cause cerebral edema
Idiogenic osmoles
produced if elevations of Na in the brain are elevated for more than 24 hours in order to counteract the osmotic pull of water out of the brain
This is a pathognomonic lesion of acute salt toxicosis in what species?
SWINE; these are eosinophilic cuffs around blood vessels and are only seen on histopath within the first 48 hours
Acute Salt Toxicosis Tx
low sodium IV fluids given quickly, also plain water enemas
Chronic Salt Toxicosis Tx
slowly drop sodium levels, so administer hypertonic saline (match serum Na levels) over a long period of time and DO NOT ALLOW FREE CHOICE WATER
Amphetamines
many derivatives, available as Rx/OTC/illegal; low margin of safety and have rapid absorption over the blood-brain-barrier
Amphetamine Clinical Signs
agitation, tachycardia with reflex bradycardia, hypertension, hyperthermia, seizures, death
Amphetamine Tx
DO NOT GIVE BENZODIAZAPINES
GIVE ACEPROMAZINE (a lot)
support cardiovascular system (fluids) and acidify the urine to promote excretion
Serotonergic Drugs
increases levels of serotonin in the CNS; found in SSRIs, SNRIs, MAOIs, TCAs and other antidepressants
Serotonin Syndrome
complex combination of clinical signs resulting from the overstimulation of serotonin receptors
Serotonin Syndrome Prognosis in Humans
poor
Serotonin Syndrome Prognosis in Pets
good
3 Main Signs of Serotonin Syndrome
- CNS Effects (agitation, seizures)
- Autonomic Effects (hypersalivation, vomiting, diarrhea, fever)
- Neuromuscular Effects (rigidity, tremors)
mydriasis
dilated pupils
Serotonin Syndrome Tx
acepromazine and cyproheptadine (plus other supportive care, AC charcoal can be given if found soon enough)
Methylxanthine Sources
caffeine, chocolate, tea, coffee
Why does chocolate have a longer time to peak plasma levels?
chocolate increases pyloric sphincter tone, so it doesn’t get into intestines as quickly!
Methylxanthines Clinical Signs
GI/Cardiac/Neuro stimulatory signs
bloating, vomit/diarrhea, hyperactivity, tachyarrhythmias, tremors and seizures
How to determine dose ingested?
add caffeine and theobromine concentrations (mg/oz) together
Methylxanthine Tx
emesis for chocolate and AC if over lethal dose, otherwise supportive care for symptoms
