Tox exam 2 Flashcards
o Preferred specimens for chemical detection of strychnine?
Antemortem: stomach contents, bait, serum, urine
Postmortem: stomach contents, liver (where metabolism happening in liver)
IDEXX TC 1030: 138$ tat 5-7 working days
what increases absorption of strychnine in lavage fluids?
antacids or bicarb
what drugs do you avoid with strychnine?
o Avoid opioids, phenothiazines, neuromuscular blockers and dissociative anesthetics
These exert extra-parametal signs and increased muscle tone
what lesions are associated with strychnine?
o Generally few to no lesions
Hemorrhage, congestion, cyanosis
o Rapid rigor mortis very quick!
o Stomach contents may still contain bait
what c/s are a characteristic change with strychnine?
Seizures are elicitable by external stimuli (light, sound, touch)
• Important when it comes to Tx quiet calm darker room
May exhibit “sardonic grin”
Death is from resp failure
what is the characteristic smell of zinc phosphide?
o Acetylene, garlic or “dead-fish” odor if you smell it, you are IN TROUBLE TOO!!!
acute zinc phosphide toxicity is due to what?
phosphine gas –> causes most toxicity
what enhances toxicity (release of phosphine gas)?
acid
what are the C/S of zinc phosphide?
o Dogs may show CNS excitation: compulsive hypermotility (“mad dog running”), yelping, convulsions (may resemble strychnine)
CNS more quickly affected
o Death within 3-48 hrs (due to tissue anoxia)
No ATP, respiration altered
for zinc phosphide, what is a Good thing that Reduces conversion into gas
antacids
MOA of fluoroacetate
Slowing of TCA cycle and decreaseing celluler resp and energy
• High energy demand organs hit hardest (heart, brain)
Buildup of citrate that cant be used
• Citrate toxicity (binding of calcium) will anticoagulate your body!!
• Inhibition of various enzymes (glutamate, PFK, etc)
Inhibition of aconitase has variable effects in different species
fluoroacetate C/S of dogs, horses, cats, pigs
dog = CNS stim and GI
LA = cardiac predominate in horses
cats, pigs = CAN and cardiac in cat
lesions of fluoroacetate
rapid rigor mortis
fluoroacetate antidote
Acetate donors which compete with the toxin (aconotase) to reduce conversion to fluoroacetate
• Glyceryl monoacetate
o Monacetin 0.55g/kg IV or IM hourly as needed
• Acetic acid / ethanol
o Given orally, less effective
• Acetamide / dextrose
o Infused over 1 hr, used in NZ lower dose for cats
source of phenoxy derivatives
o All sources are the same for herbicides!!!
o Generally sprayed forages in recommended conc don’t cause poisoning
If owner follows the directions on the bottle, usually animals will NOT get poisoned = important to do this!!!
• Levels not high enough to cause toxicosis
phenoxy derivatives increase toxicity by?
o Alter metabolism of plants (b/c they are plant hormones) which increases their toxicity by increasing accumulation of nitrate or cyanide
Important b/c can increase toxicity of poisonous plants!!
Nitrate and cyanide poisoning!!
o Also improving palatability of some poisonous plants increasing poisoning
Normally poisonous plants are unpalatable, hence why animals don’t like to eat them
Spraying poisonous plants with 2,4-D can increase their palatability = increases toxicity!!!
most susceptible species for phenoxy derivatives
o Cattle and dogs are most susceptible
They eat anything!
o Dogs MOST sensitive
_______________ of urine enhances renal excretion of phenoxy derivatives. what is commonly used to do this?
alkalinization, Na bicarb
phenoxy derivatives are excreted primarily by?
urine, unchanged
C/S of phenoxy der?
o Mainly GI and NM, sometimes look like seizures in DOGS
Can cause ulcers in oral cavity!! can become infected
Also see this with the other herbicides
At high doses, onset is rapid (
phenoxy der characteristic finding in ruminants?
rumen stasis with ingested food
what is contraindicated for Tx of phenoxy der?
o Apomorphine and gastric lavage should be CONTRAINDICATED
When you see the ulcers, should not induce vomiting or do gastric lavage BUT if you don’t see ulcers yet you can still do it
what acts as an absorbent like activated charcoal for Dipyridyl herbicides (paraquat and diquat)
soil, paraquat binds strongly to soil
Toxicity of paraquat is enhanced by?
selenium-vit E deficiency, depletion of tissue glutathione and O2 therapy
Giving O2 can increase damage especially before clinical signs are severe, shouldn’t use O2
Selenium and vit E are antioxidants this is a problem with free O2 radicals
These are CONTRAINDICATED
paraquat distribution and excretion?
distributed all over the body and achieves high conc in lung (10x)
Sequestered in lungs!!!
Causes significant damage in lungs!!!
Classified as a Dz that caused severe respiratory deficiency due to sequestration!
o Paraquat excreted within 24hrs mainly unchanged in urine (min metabolism)
is chronic or acute toxicosis more common with paraquat toxicity?
acute
early and delayed signs of acute paraquat toxicity
Early signs = severe GI signs!
• Maybe vomiting, anorexia, depression
• High doses may cause ataxia, dyspnea and seizures
• Signs may not be observed until 3 days after exposure to paraquat
Delayed signs (2-7 days)
• Owner thinks that since the vomiting has stopped, the animal is getting better but it is actually getting WORSE!!!!
o 2 days for lung damage signs to develop
• This is very serious phase
• Resp signs include tachypnea, dyspnea, harsh resp sounds, cyanosis, and reduced pulmonary compliance
that is the preferred absorbent for paraquat toxicity?
activated charcoal
what is contraindicated in early Tx of paraquat tox?
O2 –> increase lung damage, however give if going to die
what does PCP stand for?
pentachlorophenol
use of PCP
o Only used by certified applicators as a wood preservative (to protect lumber from fungal rot and wood-boring insects)
o No longer found in wood preserving solutions or insecticides and herbicides for home and garden use
Used in open, also diluted = not common for toxicity
what is the ost toxic route of exposure with PCP?
Dermal exposure is the most toxic route of exposure especially for newborn animals
what does PCP cause?
systemic overheating (hyperthermia), convulsive seizures and acidosis, along with GIT signs and resp insufficiency and irritation
what increases PCP toxicity?
High ambient temp
Oily or organic solvent vehicles –> highly lipid soluble
Previous exposure
Poor condition
Newborn
Hyperthyroidism issue usually in cats –> high temp!!!
what decreases PCP tox?
Cold temp
Antithyroid drugs
Presence of body fat distributed and stored in fat not toxic when bound to fat, it must be released in blood to be toxic
MOA of PCP?
uncouples oxidative phosphorylation, blocks/decreases ATP = increases O2 demand
what is the pathopneumonic lesion of PCP?
o Hyperkeratosis of the skin and villous like hyperplasia or urinary bladder mucosa in chronic cases =
what are 4 toxicants that caue resp insufficiency?
Nitrate (brown blood, no fever)
CO (bright red blood, no fever)
Pesticides (marked NM signs, autonomic signs)
Peracute infectious Dz’s
Contrary to paraquat, PCP can use ____________ therapy
O2
source of NPN
excess urea in feed, not enough carbohydrates = NH3 NOT UTILIZED!!!
Urea _____ toxic, but ammonia _____. what does this produce?
is not, is
lethal synthesis
1 part urea produces ___ parts protein
3 = 300% increase
what pH enhances hydrolysis of urea by urease?
alkaline
urea and ammonia are basic
is urea reaction fast or slow? what 2 things are important for the rxn?
fast
pH, temp
most susceptible species to urea
ruminants
what is most toxic of all NPN compounds? why?
urea
rxn is rapid
what increases tolerance to NPN in animals?
• Animals preconditioned or adapted to NPN are more tolerant
o Animals fed urea for first time = will take a very low dose to be toxic!!
Could be 2-3x difference in dose
what animals are more sensitive to NPN and why?
• Animals less than one year more sensitive
o Because of rumen microflora and fxn
explain the non/ionized forms of NH3 and how it relates to pH
o NH3 prod in rumen at normal pH (5-6.5) is in ionized form (NH4) which is not absorbed
o Too much urea and NH3 result in elevation of rumen pH (8-9) and NH3 in nonionized form
what is increased (blood levels of these values) due to NH3?
blood NH3, anaerobic glycolysis, blood lactate and systemic acidosis, blood glucose, BUN, serum K and Phos
what are the main C/S of NPN toxicosis?
o Severe colic, bloat, NO DIARRHEA (but if is present = mild), abnormal posture (front limbs down, hind up)
DDx for NPN toxicosis?
inorganic arsenic
Generally cause diarrhea (often bloody) and no nervous signs
o Lead, metaldehyde and chlorinated hydrocarbon pesticides
No abnormal posturing, jumping over objects and maniacal behavior in urea as in chlorinated hydrocarbon poisoning
o Organophosphate
Cause parasympathomimetic signs and respond to atropine therapy
Tx of NPN tox?
o Bloat should be relieved first
o Acetic acid 5% or vinegar to cattle (2-6L) or sheep and goats (0.5-1L) followed by large vol of cold water
what are ionophores used for?
o Anticoccidial in cattle, poultry, and goats
Only used to PREVENT coccidiosis
Sulfonamides can be used to Tx and prevent coccidiosis
o Growth promoter feed additive in cattle = main use
what is the most common source of ionophores?
monensin
also can be malicious poisoning in horses
Drug of first choice to Tx intracellular infections
tetracyclines, then fluoroquinolones
does Monensin accumulate in tissues of animals when given in high doses
NO
how is monensin metabolized?
o Rapidly metabolized by P-450 oxidative demethylation enzymes in liver (slow metabolism in equines b/c they have lowest oxidative demethylases than other domestic species) and excreted mainly in bile
Microsomal enzymes = p450
• Liver enzymes that can be induced or inhibited
Methylases hydroxylases are oxidative enzymes
• Horses deficient in oxidative demethylase enzymes = slow metabolism leads to high conc
why are horses more sensitive to monensin?
100% absorption in horses vs 50% in ruminants
Deficient in oxidative demethylases conc may go up
Mainly excreted in bile horses don’t have gall bladder
what is the main MOA of monensin? what other MOAs does it have?
Sequestering of Ca by mitochondria and inhibition of mitochondria and decreased ATP and energy
o Also catecholamine release results in oxidation products and free radicals causing sarcolemmal memb damage
o Disruption of ions conc in excitable cells alters their fxn
what are the lesions associated with monensin tox?
o Mainly cardiac muscle lesions in horses (pale cardiac muscles, white streaks of necrosis in myocardium), skeletal muscle lesions
o Mainly skeletal muscle lesions in sheep, swine and dogs (pale skeletal muscles)
o Both skeletal and cardiac muscle lesions in poultry and cattle
what enzymes are elevated in monensin tox? decreased?
Elevated enzymes of muscle origin (CPK, AST)
Other enzymes elevated (LDH, AP)
Decreased serum Ca and K (during first 12 hrs)
DDx for monensin tox?
Horses
Colic, BLISTER BEETLE INGESTION (cantharidin toxicosis), azoturia(renal failure)
• Blister beetle damage stomach wall and cause severe clinical signs of colic
Cattle
Vitamin E/selenium deficiency
• Both are antioxidants = deficiency in EITHER or BOTH could cause muscle damage
for monensin, what do you use for supportive Tx? what is important for horses?
IV fluid and electrolyte therapy (to correct hypovolemia and support CV and renal fxns)
K to correct hypokalemia (
what are the factors that cause excess Na an H2O deprivation?
Overcrowding
Frozen water
Unpalatable (medicated) water
Lack of water
what species are most susceptible to Water deprivation-sodium ion toxicosis?
Pigs, cows, and poultry are most susceptible
Na enters and exits brain by?
enters by passive diffusion, exits by active transport
Excess Na (and water deprivation) results in ______________ of blood and toxicosis
hypertonicity
high Na in brain inhibits what MOA? what does it cause?
brain inhibits anaerobic glycolysis resulting in lack of energy necessary for active transport of Na
o Na trapped in brain attracts H2O b/c of osmotic gradient, resulting in CEREBRAL EDEMA!!!!
Even if you start to give water, Na in plasma can be dissolved and excreted in urine and start to go down, NA IS STILL ____________
TRAPPED IN BRAIN
what is the c/s difference between Na toxicosis and strychnine tox?
Na = Intermittent convulsive seizures
• Last from 0.5 to 2-3 mins
• Interrupted by other signs
• NOT elicitable by external stimuli (strychnine is)
what is the pathognomonic lesion in pigs for Na toxicosis only if animal dies early (first 24 hrs)?
eosinophilic meningioencephalitis (filling of cerebral and menengeal perivascular spaces with eosinophils)
DDx in pigs for Na tox?
Chlorinated hydrocarbon insecticides
Pigs arsenic poisoning only causes peripheral neurotoxicity not CNS
• Roxarsone
Tx of Na tox
o Give small amounts of fresh water (0.5% of BW) gradually over 2-3 days, if animal is able to drink (recovery = 50%)
Giving water in large amounts may kill animal by aggravating cerebral edema
o IV fluids (5% dextrose) and furosemide in small animals
do metals and minerals cross the BBB?
ONLY lead and organic mercury!!!
what are the sources of inorganic arsenic tox?
ant and roach bait, wood preservative, milk from poisoned cows (lead does this too), paint
what inorganic arsenic oxidative state is the most toxic?
trivalent (arsenite) > pentavalent (arsenate) > elemental (arsenide)
how toxic is inorganic arsenic?
1-25mg/kg = HIGHLY TOXIC
explain the peracute, acute and subacute stages of inorganic arsenic
• If amount is very high can cause hypovolemia, shock and death
o Amount is less and happens over an hour or so = acute
o Amount is less and happens over hours to days = subacute
IN ADDITION TO GI SIGNS, WILL GET POSTERIOR PARALYSIS
what species are most susceptible to inorganic arsenic?
herbivores
where does inorganic arsenic achieve higher concentration at in the body?
liver and kidney and also hair, hoof, nail and skin
MOA of inorganic arsenic
o Trivalent binds to 2-SH goups of lipoic (thioctic acid)
Inhibits thioctic acid (aka lipoic acid) important for energy
what cells are most sensitive to Inorg arsenic?
o Capillary endothelial cells are most sensitive
Very important!!!!!
Wall of capillaries requires very high levels of oxidative enzymes
Will lead to hemorrhage
inorganic arsenic causes wat signs in all types (acute, etc) of poisoning?
GI SIGNS
best specimens for inorganic arsenic
Urine is best antimortem specimen
Liver and kidney re best postmortem specimens
• Because of high blood flow
what toxicity is associated with mucosal shreds in the feces?
inorganic arsenic
what is the emergency life saving Tx for inorg arsenic?
Fluids and elecrolytes and maybe blood transfusion
o If there Is evidence of blood or ulcers in GIT, ________________________are contraindicated
gastric lavage and emetics
chelator of choice for inorganic arcenic
o Dimercaprol (BAL, british antilewisite) --> know both!!! MUST CONFIRM IT IS INORG ARSENIC
what are the target species for arsanilic acid and roxarsone?
Arsanilic acid is mainly used in swine
Roxarsone is mainly used in poultry
what do organic arsinicals cause in target species?
o Cause peripheral neurotoxicity in target species!!!!
Peripheral seen as locomotor signs!!
In swine, what it the biggest difference between arsanilic acid and roxarsone?
• Blindness may develop (NOT with roxarsone)
swine become hyperexciteable with what organic arsenical?
roxarsone
lesions of organic arsenic in swine?
Microscopically, peripheral nerve and optic nerve degen, demyelination, and gliosis
• Demyelination = damage is irreversible
in sheep, what is Cu toxicosis due to?
high copper or low molybdenum, or both
what is the most common Cu toxicosis?
chronic
what is really important about chronic Cu tox?
hemolytic crisis!!!!
what may cause copper accumulation by hepatocytes (secondary copper toxicosis)
liver damage
• Liver actually stores copper = liver will be damaged
• Any other liver damage can make copper accumulate in the liver = 2ndary copper toxicosis
o Primary is low molybdenum or high Cu
• Even though the liver has high amounts of Cu, you may not see C/S
what does stress do to Cu and the liver?
sudden loss of copper from liver into blood
• Stress is predisposing factor liver releases copper that has been stored over time = hemolytic crisis
o Onset of C/S is sudden!!!
what is Cu mainly excreted in
bile
what is characteristic of Cu tox?
Cu also oxidizes hemoglobin to methemoglobin (can’t carry O2)
• Brown chocolate color = characteristic!!!!
what are the lesions associated with Cu tox?
Icterus, hemolysis, methemoglobinemia
Liver is enlarged, yellow and friable
Kidneys are enlarged, hemorrhagic, bluish-dark and friable (gunmetal kidneys)
Spleen is enlarged and dark brown/black (blackberry jam spleen)
Red wine urine!
what is very good indicator of Dz (if you suspect Cu toxicity)
Elevated liver enzymes before acute onset
name the hemolytic agents (10)
• Zinc, naphthalene, phenolics, DMSO, guaifenesin(centrally acting muscle relaxant)
• Poisonous plants
o Onion, glossypol (cottonseed), red maple (Acer rubrum), mustard
• Certain snake venoms
• Infectious Dz’s
o Lepto, babesiosis, anaplasmosis, bacilliary hemoglobinuria
Most of the time the Tx copper poisoning with?
molybdenum because of the imbalance
• Same for molybdenum poisoning, Tx with Cu
• MOST EFFECTIVE CHELATING AGENT FOR COPPER = SPECIFIC ANTIDOTE
D-penicillamine
reduces hepatic Cu accumulation
Supplemental zinc (250ppm) , molybdenum
Bedlington terrier has genetic disposition to this Dz
Cu tox
states that have increased molybdenum, deficiency in Cu
Florida, California, Oregon, Nevada
wat is molybdenum tox usually due to?
Cu deficiency
what species are most susceptible to molybdenum tox? which species are resistant?
CATTLE
horses and pigs = resistant
what 3 things are excreted in toxic levels into milk?
MOLYBDENUM, INORGANIC ARSENIC AND LEAD
does molybdenum tox have bloody diarrhea?
Diarrhea IS NOT HEMORRHAGIC green/yellow with many gas bubbles
what can you use as a test for molybdenum tox?
Can use cytochrome oxidase as a test blood ample will indicate LOW CYTOCHROME OXIDASE LEVELS
what are the main c/s for molybdenum?
o Severe diarrhea (greenish with fluid and gas bubbles) after 8-10 days following exposure
o Rough hair coat and depigmentation (achromotrichia) of hair especially around the eyes (“spectacled” appearance)
o Infertility
what is increased and decreased in the blood for molybdenum tox? what is almost characteristic?
o Elevated molybdenum in the blood (>0.1 ppm) and in liver (>5 ppm)
o Decreased Cu in blood ( almost characteristic!!
what are the Se deficiency Dz’s?
o White muscle Dz (WMD) or nutritional muscle dystrophy (NMD) in lambs, but also seen in calves and foals
o Hepatosis dietetica in young pigs
o Exudative diathesis in chicks
o Nutritional pancreatic atrophy in chickens
o Porcine stress syndrome in pigs
number one source for selenium toxicosis in large animals and poultry
Soil that is high in selenium plants will have high levels of it
what states have high Se soil?
o South Dakota, north Dakota, Wyoming, montana, Nebraska, Kansas, Utah, Colorado, new Mexico
= mid-west and western states
Seleniferous plants that are oblgate accumulators = _____ Se
o Require Se for growth o Astragalus (locoweed, milk vetch), Stanleya (prince’s plume), Oonopsis (golden wood), and Xylorrhiza (woody aster) Unpalatable = usually don’t eat unless they have to
Seleniferous plants that are facultative accumulators = _____ Se
o Do not require Se but that can accumulate it
o Examples are Aster (aster), Atriplex (saltbush), and Castilleja (paint brush)
Seleniferous plants that are passive accumulators = _____ Se
o Accumulate Se passively in Se-rich soil
o Many plants including crop plants such as corn, wheat, oats, barley, grass, and hay, and other plants
o Most common source b/c they are edible!!!
what type of soil does Se stay in?
arid, alkaline soil
Se is a component of this enzyme
glutathione peroxidase
most toxic form of Se
organic Se in plants
how toxic is Se?
HIGHLY
how is Se toxicity reduced
HIGH PROTEIN DIET AND INGESTION OF OTHER ELEMENTS THAT BIND SE SUCH AS COPPER
chronic exposure of Se leaves high concentrations of Se in what?
high conc in hoof and hair
Subacute or chronic
what explains why Se causes hoof and hair abnormalities?
o Se replaces sulfur in AA causing abnormal proteins
Se has relationship with arsenic and sulfur
C/S of acute Se tox?
• Mainly resp signs labored respiration w/ fluid sounds in lungs, bloody froth from nares, cyanosis
subacute Se toxicosis produces what syndrome unique to swine?
NEUROPARALYTC SYNDROME
• Porcine focal symmetrical poliomyelomalacia
• Unique to swine!!!
• Similar to arsenic poisoning but don’t have hoof or hair abnormalities ad loss of appetite with arsenic
what is subacute Se toxicosis in cattle called?
“Blind staggers” in cattle are not really blind and they don’t really stagger but oh well
what is chronic Se toxicosis in cattle called?
alkali Dz
what samples are best for acute and chronic Se tox?
o Acute blood is best sample in live animal
o Chronic = hoof and hair samples
Remember earlier we said shouldn’t wash specimens EXCEPTION HERE = HOOF SHOULD BE WASHED
o Elevated blood or plasma glutathione peroxidase
DDx for chronic Se tox?
Molybdenum toxicosis anemia, poor hair coat, etc
Fluoride toxicosis causes bone and teeth abnormalities, wasting, poor hair coat, locomotor signs
Freezing, ergotism and laminitis
Chronic Se most common
Tx for subacute and chronic Se tox?
No Tx but you can prevent
Adding Cu, high protein and sulfur-containing proteins may reduce absorption
Adding organic arenicals to diet increases biliary excretion of Se
are younger or more mature animals more sensitive to lead tox?
Young animals are more senstitive than adults (greater absorption and immature BBB)
what decreases absorption of lead?
Ca, zinc or protein –> have deficieny in these (esp. Ca) will increase absorption due to upregulation
what indication makes lead the top DDx?
basophilic stippling of RBCs
target tissues of lead
cNS, GIT, blood
lead tox MOA
competes with Ca ions (ie in bone) and alters Ca movement across membs
Leads to cerebral edema
this rarely causes megaesophagus
lead tox
what type of RBCs do you see with lead tox?
o Increase in nRBCs
See nonregen anemia with inappropriate release of nRBCs
lead tox antemortem specimen of choice
whole blood
>90% of lead is bound to circulating RBCs
Chelation therapy for lead tox is most commonly? Cu?
Ca disodium EDTA is the most commonly used chelating agent - Rebound can look like re-exposure
Tx copper with D-penicillamine
o See this more quickly than lead, also resolves more quickly
zinc tox
Most rapid accumulation and turnover of zinc occurs in ?
in pancreas, liver, kidney and spleen as well as male repro organs
Important for clinical signs
These pts can sometimes develop pancreatitis!
how is zinc excreted?
o Normally primarily excreted in feces via bile, pancreatic juice and mucosal cells
what are the main C/S of zinc tox?
o GI V/D, anorexia, lethargy, abdominal pain, pica o Hematologic HEMOLYTIC ANEMIA (INTRAVASCULAR) • Icterus and hemoglobinuria
what do you use for zinc tox chem analysis?
o USE TRACE ELEMENT TUBES FOR ANALYSIS
Dark blue top
Avoids contamination with zin stearate
what toxicity will you see a reticulocytosis on CBC?
ZINC TOXICOSIS CBC, NOT LEAD
What is possible several days after acute toxicity from metaldehyde and should be monitored for in canines?
liver failure
What are the 3 body systems show C/S in chronic lead toxicosis?
Neuro, GI and hematopoietic systems
what does oral acute iron toxicosis do to absorption?
o Oral acute overdose overwhelms selective absorption mech saturates ferritin in GI mucosal cells leading to absorption of toxic conc of iron
o Free iron causes saturation of transferrin = free circulating iron
Body not designed to upregulate excretion of free iron in blood stream!!!
iron toxicosis MOA is primarily on what systems?
o Primary effect on GIT, liver and CV system leading to hock and death
lesion for iron toxicosis?
Yellow-brown discoloration at injection site
do you use chelation for iron toxicosis? if so, what chelator?
Indicated only in severe toxicosis w/I 12 hours of ingestion
DeFERoxamine (Desferal) by continuous IV infusion at 15 mg/kg/hr or IM (less effective) at 40 mg/kg q4-8hr
• Pulmonary toxicity is most significant adverse effect following continuous IV infusion
• Urine is reddish-brown during Tx
where is amphetamine distributed and what effects does it have?
o Widely distributed including CNS and have peripheral effects
Cross BBB
what is the MOA of amphetamines/
o Block reuptake of norepi and dopamine
Excitatory transmitters
what are the main clinical sign of amphetamine tox in dogs?
circle for hours!!
what is contraindicated in the Tx of amphetamine tox?
o Benzodiazepines may cause CNS stim
increase chance of seizures
MOA of cocaine tox
o CNS stim, indirect sympathomimetic, prevents reuptake of norepi, dopamine and serotonin
Inhibit norepi reuptake in brain = convulsive seizures
• Nicotine can also cause this
Tx that is contraindicated in cocaine tox?
lidocaine –> can cause CNS stim
what is different about marijuana tox metabolism
ENTEROHEPATIC RECIRCULATION
MOA of marijuana tox
- CB1 (cannabinoid receptor) widely distributed in brain (alters activity of various neurotransmitters)
o Has cannabinoid effects on memory, perception and control of movement
what is metaldehyde used for?
kill snails
what special species does metaldehyde affect?
hedgehogs
C/S associated with metaldehyde
shake and bake
what is a characteristic sign of metaldehyde tox?
formaldehyde smell in stomach contents
metaldehyde tox in dogs - do they develop post-recovery liver failure?
uncommon
whats different in ethylene glycol tox in cats vs dogs?
IMPORTANT FOR CATS!!!! EVERYTHING IS GOING TO GO FASTER IN CATS = must be more agressive
what are the late C/S in dogs for ethylene glycol tox?
24-72 hr PI
animals that survive acute develop oliguric renal failure
what is a good indicator of ethylene glycol tox?
Ca ox (monohydrate) crystals in kidney/urine
what are the differences between the Kacey EG and catachem EG tests?
Kacey EG test kit • False positive can result from propylene glycol, mannitol sorbitol, glycerol and ethanol • Neg result doesn’t rule out exposure! Catachem EG test • NO FALSE POS with ethanol
what is the Tx of choice for EG?
o Fomepizole (4-MP) - DOESN’T cause CNS depression, diuresis, hyperosmolality (as ethanol can)
