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Toxicology > Tox exam 2 > Flashcards

Tox exam 2 Flashcards

1
Q

o Preferred specimens for chemical detection of strychnine?

A

 Antemortem: stomach contents, bait, serum, urine
 Postmortem: stomach contents, liver (where metabolism happening in liver)
 IDEXX TC 1030: 138$ tat 5-7 working days

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2
Q

what increases absorption of strychnine in lavage fluids?

A

antacids or bicarb

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3
Q

what drugs do you avoid with strychnine?

A

o Avoid opioids, phenothiazines, neuromuscular blockers and dissociative anesthetics
 These exert extra-parametal signs and increased muscle tone

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4
Q

what lesions are associated with strychnine?

A

o Generally few to no lesions
 Hemorrhage, congestion, cyanosis
o Rapid rigor mortis  very quick!
o Stomach contents may still contain bait

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5
Q

what c/s are a characteristic change with strychnine?

A

 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

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6
Q

what is the characteristic smell of zinc phosphide?

A

o Acetylene, garlic or “dead-fish” odor  if you smell it, you are IN TROUBLE TOO!!!

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7
Q

acute zinc phosphide toxicity is due to what?

A

phosphine gas –> causes most toxicity

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8
Q

what enhances toxicity (release of phosphine gas)?

A

acid

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9
Q

what are the C/S of zinc phosphide?

A

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

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10
Q

for zinc phosphide, what is a Good thing that Reduces conversion into gas

A

antacids

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11
Q

MOA of fluoroacetate

A

 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

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12
Q

fluoroacetate C/S of dogs, horses, cats, pigs

A

dog = CNS stim and GI
LA = cardiac predominate in horses
cats, pigs = CAN and cardiac in cat

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13
Q

lesions of fluoroacetate

A

rapid rigor mortis

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14
Q

fluoroacetate antidote

A

 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

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15
Q

source of phenoxy derivatives

A

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

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16
Q

phenoxy derivatives increase toxicity by?

A

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!!!

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17
Q

most susceptible species for phenoxy derivatives

A

o Cattle and dogs are most susceptible
 They eat anything!
o Dogs MOST sensitive

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18
Q

_______________ of urine enhances renal excretion of phenoxy derivatives. what is commonly used to do this?

A

alkalinization, Na bicarb

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19
Q

phenoxy derivatives are excreted primarily by?

A

urine, unchanged

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20
Q

C/S of phenoxy der?

A

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 (

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21
Q

phenoxy der characteristic finding in ruminants?

A

rumen stasis with ingested food

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22
Q

what is contraindicated for Tx of phenoxy der?

A

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

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23
Q

what acts as an absorbent like activated charcoal for Dipyridyl herbicides (paraquat and diquat)

A

soil, paraquat binds strongly to soil

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24
Q

Toxicity of paraquat is enhanced by?

A

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

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25
Q

paraquat distribution and excretion?

A

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)

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26
Q

is chronic or acute toxicosis more common with paraquat toxicity?

A

acute

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27
Q

early and delayed signs of acute paraquat toxicity

A

 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

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28
Q

that is the preferred absorbent for paraquat toxicity?

A

activated charcoal

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29
Q

what is contraindicated in early Tx of paraquat tox?

A

O2 –> increase lung damage, however give if going to die

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30
Q

what does PCP stand for?

A

pentachlorophenol

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31
Q

use of PCP

A

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

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32
Q

what is the ost toxic route of exposure with PCP?

A

 Dermal exposure is the most toxic route of exposure especially for newborn animals

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33
Q

what does PCP cause?

A

systemic overheating (hyperthermia), convulsive seizures and acidosis, along with GIT signs and resp insufficiency and irritation

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34
Q

what increases PCP toxicity?

A

 High ambient temp
 Oily or organic solvent vehicles –> highly lipid soluble
 Previous exposure
 Poor condition
 Newborn
 Hyperthyroidism  issue usually in cats –> high temp!!!

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35
Q

what decreases PCP tox?

A

 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

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36
Q

MOA of PCP?

A

uncouples oxidative phosphorylation, blocks/decreases ATP = increases O2 demand

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37
Q

what is the pathopneumonic lesion of PCP?

A

o Hyperkeratosis of the skin and villous like hyperplasia or urinary bladder mucosa in chronic cases =

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38
Q

what are 4 toxicants that caue resp insufficiency?

A

 Nitrate (brown blood, no fever)
 CO (bright red blood, no fever)
 Pesticides (marked NM signs, autonomic signs)
 Peracute infectious Dz’s

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39
Q

Contrary to paraquat, PCP can use ____________ therapy

A

O2

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40
Q

source of NPN

A

excess urea in feed, not enough carbohydrates = NH3 NOT UTILIZED!!!

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41
Q

Urea _____ toxic, but ammonia _____. what does this produce?

A

is not, is

lethal synthesis

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42
Q

1 part urea produces ___ parts protein

A

3 = 300% increase

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43
Q

what pH enhances hydrolysis of urea by urease?

A

alkaline

urea and ammonia are basic

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44
Q

is urea reaction fast or slow? what 2 things are important for the rxn?

A

fast

pH, temp

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45
Q

most susceptible species to urea

A

ruminants

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46
Q

what is most toxic of all NPN compounds? why?

A

urea

rxn is rapid

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47
Q

what increases tolerance to NPN in animals?

A

• 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

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48
Q

what animals are more sensitive to NPN and why?

A

• Animals less than one year more sensitive

o Because of rumen microflora and fxn

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49
Q

explain the non/ionized forms of NH3 and how it relates to pH

A

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

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50
Q

what is increased (blood levels of these values) due to NH3?

A

blood NH3, anaerobic glycolysis, blood lactate and systemic acidosis, blood glucose, BUN, serum K and Phos

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51
Q

what are the main C/S of NPN toxicosis?

A

o Severe colic, bloat, NO DIARRHEA (but if is present = mild), abnormal posture (front limbs down, hind up)

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52
Q

DDx for NPN toxicosis?

A

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

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53
Q

Tx of NPN tox?

A

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

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54
Q

what are ionophores used for?

A

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

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55
Q

what is the most common source of ionophores?

A

monensin

also can be malicious poisoning in horses

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56
Q

Drug of first choice to Tx intracellular infections

A

tetracyclines, then fluoroquinolones

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57
Q

does Monensin accumulate in tissues of animals when given in high doses

A

NO

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58
Q

how is monensin metabolized?

A

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

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59
Q

why are horses more sensitive to monensin?

A

 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

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60
Q

what is the main MOA of monensin? what other MOAs does it have?

A

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

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61
Q

what are the lesions associated with monensin tox?

A

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

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62
Q

what enzymes are elevated in monensin tox? decreased?

A

 Elevated enzymes of muscle origin (CPK, AST)
 Other enzymes elevated (LDH, AP)
 Decreased serum Ca and K (during first 12 hrs)

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63
Q

DDx for monensin tox?

A

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

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64
Q

for monensin, what do you use for supportive Tx? what is important for horses?

A

 IV fluid and electrolyte therapy (to correct hypovolemia and support CV and renal fxns)
 K to correct hypokalemia (

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65
Q

what are the factors that cause excess Na an H2O deprivation?

A

 Overcrowding
 Frozen water
 Unpalatable (medicated) water
 Lack of water

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66
Q

what species are most susceptible to Water deprivation-sodium ion toxicosis?

A

Pigs, cows, and poultry are most susceptible

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67
Q

Na enters and exits brain by?

A

enters by passive diffusion, exits by active transport

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68
Q

Excess Na (and water deprivation) results in ______________ of blood and toxicosis

A

hypertonicity

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69
Q

high Na in brain inhibits what MOA? what does it cause?

A

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!!!!

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70
Q

 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 ____________

A

TRAPPED IN BRAIN

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71
Q

what is the c/s difference between Na toxicosis and strychnine tox?

A

Na =  Intermittent convulsive seizures
• Last from 0.5 to 2-3 mins
• Interrupted by other signs
• NOT elicitable by external stimuli (strychnine is)

72
Q

what is the pathognomonic lesion in pigs for Na toxicosis only if animal dies early (first 24 hrs)?

A

eosinophilic meningioencephalitis (filling of cerebral and menengeal perivascular spaces with eosinophils)

73
Q

DDx in pigs for Na tox?

A

Chlorinated hydrocarbon insecticides
 Pigs  arsenic poisoning  only causes peripheral neurotoxicity not CNS
• Roxarsone

74
Q

Tx of Na tox

A

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

75
Q

do metals and minerals cross the BBB?

A

ONLY lead and organic mercury!!!

76
Q

what are the sources of inorganic arsenic tox?

A

ant and roach bait, wood preservative, milk from poisoned cows (lead does this too), paint

77
Q

what inorganic arsenic oxidative state is the most toxic?

A

trivalent (arsenite) > pentavalent (arsenate) > elemental (arsenide)

78
Q

how toxic is inorganic arsenic?

A

1-25mg/kg = HIGHLY TOXIC

79
Q

explain the peracute, acute and subacute stages of inorganic arsenic

A

• 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

80
Q

what species are most susceptible to inorganic arsenic?

A

herbivores

81
Q

where does inorganic arsenic achieve higher concentration at in the body?

A

liver and kidney and also hair, hoof, nail and skin

82
Q

MOA of inorganic arsenic

A

o Trivalent binds to 2-SH goups of lipoic (thioctic acid)

 Inhibits thioctic acid (aka lipoic acid)  important for energy

83
Q

what cells are most sensitive to Inorg arsenic?

A

o Capillary endothelial cells are most sensitive
 Very important!!!!!
 Wall of capillaries requires very high levels of oxidative enzymes
 Will lead to hemorrhage

84
Q

inorganic arsenic causes wat signs in all types (acute, etc) of poisoning?

A

GI SIGNS

85
Q

best specimens for inorganic arsenic

A

 Urine is best antimortem specimen
 Liver and kidney re best postmortem specimens
• Because of high blood flow

86
Q

what toxicity is associated with mucosal shreds in the feces?

A

inorganic arsenic

87
Q

what is the emergency life saving Tx for inorg arsenic?

A

 Fluids and elecrolytes and maybe blood transfusion

88
Q

o If there Is evidence of blood or ulcers in GIT, ________________________are contraindicated

A

gastric lavage and emetics

89
Q

chelator of choice for inorganic arcenic

A 
o	Dimercaprol (BAL, british antilewisite) --> know both!!!
MUST CONFIRM IT IS INORG ARSENIC
90
Q

what are the target species for arsanilic acid and roxarsone?

A

 Arsanilic acid is mainly used in swine

 Roxarsone is mainly used in poultry

91
Q

what do organic arsinicals cause in target species?

A

o Cause peripheral neurotoxicity in target species!!!!

 Peripheral seen as locomotor signs!!

92
Q

In swine, what it the biggest difference between arsanilic acid and roxarsone?

A

• Blindness may develop (NOT with roxarsone)

93
Q

swine become hyperexciteable with what organic arsenical?

A

roxarsone

94
Q

lesions of organic arsenic in swine?

A

 Microscopically, peripheral nerve and optic nerve degen, demyelination, and gliosis
• Demyelination = damage is irreversible

95
Q

in sheep, what is Cu toxicosis due to?

A

high copper or low molybdenum, or both

96
Q

what is the most common Cu toxicosis?

A

chronic

97
Q

what is really important about chronic Cu tox?

A

hemolytic crisis!!!!

98
Q

what may cause copper accumulation by hepatocytes (secondary copper toxicosis)

A

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

99
Q

what does stress do to Cu and the liver?

A

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!!!

100
Q

what is Cu mainly excreted in

A

bile

101
Q

what is characteristic of Cu tox?

A

 Cu also oxidizes hemoglobin to methemoglobin (can’t carry O2)
• Brown chocolate color = characteristic!!!!

102
Q

what are the lesions associated with Cu tox?

A

 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!

103
Q

what is very good indicator of Dz (if you suspect Cu toxicity)

A

Elevated liver enzymes before acute onset

104
Q

name the hemolytic agents (10)

A

• 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

105
Q

Most of the time the Tx copper poisoning with?

A

molybdenum because of the imbalance

• Same for molybdenum poisoning, Tx with Cu

106
Q

• MOST EFFECTIVE CHELATING AGENT FOR COPPER = SPECIFIC ANTIDOTE

A

 D-penicillamine

107
Q

reduces hepatic Cu accumulation

A

 Supplemental zinc (250ppm) , molybdenum

108
Q

 Bedlington terrier has genetic disposition to this Dz

A

Cu tox

109
Q

states that have increased molybdenum, deficiency in Cu

A

Florida, California, Oregon, Nevada

110
Q

wat is molybdenum tox usually due to?

A

Cu deficiency

111
Q

what species are most susceptible to molybdenum tox? which species are resistant?

A

CATTLE

horses and pigs = resistant

112
Q

what 3 things are excreted in toxic levels into milk?

A

MOLYBDENUM, INORGANIC ARSENIC AND LEAD

113
Q

does molybdenum tox have bloody diarrhea?

A

 Diarrhea IS NOT HEMORRHAGIC  green/yellow with many gas bubbles

114
Q

what can you use as a test for molybdenum tox?

A

 Can use cytochrome oxidase as a test  blood ample will indicate LOW CYTOCHROME OXIDASE LEVELS

115
Q

what are the main c/s for molybdenum?

A

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

116
Q

what is increased and decreased in the blood for molybdenum tox? what is almost characteristic?

A

o Elevated molybdenum in the blood (>0.1 ppm) and in liver (>5 ppm)
o Decreased Cu in blood ( almost characteristic!!

117
Q

what are the Se deficiency Dz’s?

A

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

118
Q

number one source for selenium toxicosis in large animals and poultry

A

Soil that is high in selenium  plants will have high levels of it

119
Q

what states have high Se soil?

A

o South Dakota, north Dakota, Wyoming, montana, Nebraska, Kansas, Utah, Colorado, new Mexico
 = mid-west and western states

120
Q

Seleniferous plants that are oblgate accumulators = _____ Se

A 
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
121
Q

Seleniferous plants that are facultative accumulators = _____ Se

A

o Do not require Se but that can accumulate it

o Examples are Aster (aster), Atriplex (saltbush), and Castilleja (paint brush)

122
Q

Seleniferous plants that are passive accumulators = _____ Se

A

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!!!

123
Q

what type of soil does Se stay in?

A

arid, alkaline soil

124
Q

Se is a component of this enzyme

A

glutathione peroxidase

125
Q

most toxic form of Se

A

organic Se in plants

126
Q

how toxic is Se?

A

HIGHLY

127
Q

how is Se toxicity reduced

A

HIGH PROTEIN DIET AND INGESTION OF OTHER ELEMENTS THAT BIND SE SUCH AS COPPER

128
Q

chronic exposure of Se leaves high concentrations of Se in what?

A

high conc in hoof and hair

 Subacute or chronic

129
Q

what explains why Se causes hoof and hair abnormalities?

A

o Se replaces sulfur in AA causing abnormal proteins

 Se has relationship with arsenic and sulfur

130
Q

C/S of acute Se tox?

A

• Mainly resp signs  labored respiration w/ fluid sounds in lungs, bloody froth from nares, cyanosis

131
Q

subacute Se toxicosis produces what syndrome unique to swine?

A

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

132
Q

what is subacute Se toxicosis in cattle called?

A

 “Blind staggers” in cattle  are not really blind and they don’t really stagger but oh well

133
Q

what is chronic Se toxicosis in cattle called?

A

alkali Dz

134
Q

what samples are best for acute and chronic Se tox?

A

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

135
Q

DDx for chronic Se tox?

A

 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

136
Q

Tx for subacute and chronic Se tox?

A

 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

137
Q

are younger or more mature animals more sensitive to lead tox?

A

Young animals are more senstitive than adults (greater absorption and immature BBB)

138
Q

what decreases absorption of lead?

A

Ca, zinc or protein –> have deficieny in these (esp. Ca) will increase absorption due to upregulation

139
Q

what indication makes lead the top DDx?

A

basophilic stippling of RBCs

140
Q

target tissues of lead

A

cNS, GIT, blood

141
Q

lead tox MOA

A

competes with Ca ions (ie in bone) and alters Ca movement across membs
 Leads to cerebral edema

142
Q

this rarely causes megaesophagus

A

lead tox

143
Q

what type of RBCs do you see with lead tox?

A

o Increase in nRBCs

 See nonregen anemia with inappropriate release of nRBCs

144
Q

lead tox antemortem specimen of choice

A

whole blood

 >90% of lead is bound to circulating RBCs

145
Q

Chelation therapy for lead tox is most commonly? Cu?

A

 Ca disodium EDTA is the most commonly used chelating agent - Rebound  can look like re-exposure
Tx copper with D-penicillamine

146
Q

o See this more quickly than lead, also resolves more quickly

A

zinc tox

147
Q

Most rapid accumulation and turnover of zinc occurs in ?

A

in pancreas, liver, kidney and spleen as well as male repro organs
 Important for clinical signs
 These pts can sometimes develop pancreatitis!

148
Q

how is zinc excreted?

A

o Normally primarily excreted in feces via bile, pancreatic juice and mucosal cells

149
Q

what are the main C/S of zinc tox?

A 
o	GI
	V/D, anorexia, lethargy, abdominal pain, pica
o	Hematologic
	HEMOLYTIC ANEMIA (INTRAVASCULAR)
•	Icterus and hemoglobinuria
150
Q

what do you use for zinc tox chem analysis?

A

o USE TRACE ELEMENT TUBES FOR ANALYSIS
 Dark blue top
 Avoids contamination with zin stearate

151
Q

what toxicity will you see a reticulocytosis on CBC?

A

ZINC TOXICOSIS CBC, NOT LEAD

152
Q

What is possible several days after acute toxicity from metaldehyde and should be monitored for in canines?

A

liver failure

153
Q

What are the 3 body systems show C/S in chronic lead toxicosis?

A

Neuro, GI and hematopoietic systems

154
Q

what does oral acute iron toxicosis do to absorption?

A

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!!!

155
Q

iron toxicosis MOA is primarily on what systems?

A

o Primary effect on GIT, liver and CV system  leading to hock and death

156
Q

lesion for iron toxicosis?

A

 Yellow-brown discoloration at injection site

157
Q

do you use chelation for iron toxicosis? if so, what chelator?

A

 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

158
Q

where is amphetamine distributed and what effects does it have?

A

o Widely distributed including CNS and have peripheral effects
 Cross BBB

159
Q

what is the MOA of amphetamines/

A

o Block reuptake of norepi and dopamine

 Excitatory transmitters

160
Q

what are the main clinical sign of amphetamine tox in dogs?

A

circle for hours!!

161
Q

what is contraindicated in the Tx of amphetamine tox?

A

o Benzodiazepines may cause CNS stim

increase chance of seizures

162
Q

MOA of cocaine tox

A

o CNS stim, indirect sympathomimetic, prevents reuptake of norepi, dopamine and serotonin
 Inhibit norepi reuptake in brain = convulsive seizures
• Nicotine can also cause this

163
Q

Tx that is contraindicated in cocaine tox?

A

lidocaine –> can cause CNS stim

164
Q

what is different about marijuana tox metabolism

A

ENTEROHEPATIC RECIRCULATION

165
Q

MOA of marijuana tox

A
  • CB1 (cannabinoid receptor) widely distributed in brain (alters activity of various neurotransmitters)
    o Has cannabinoid effects on memory, perception and control of movement
166
Q

what is metaldehyde used for?

A

kill snails

167
Q

what special species does metaldehyde affect?

A

hedgehogs

168
Q

C/S associated with metaldehyde

A

shake and bake

169
Q

what is a characteristic sign of metaldehyde tox?

A

formaldehyde smell in stomach contents

170
Q

metaldehyde tox in dogs - do they develop post-recovery liver failure?

A

uncommon

171
Q

whats different in ethylene glycol tox in cats vs dogs?

A

 IMPORTANT FOR CATS!!!! EVERYTHING IS GOING TO GO FASTER IN CATS = must be more agressive

172
Q

what are the late C/S in dogs for ethylene glycol tox?

A

24-72 hr PI

animals that survive acute develop oliguric renal failure

173
Q

what is a good indicator of ethylene glycol tox?

A

Ca ox (monohydrate) crystals in kidney/urine

174
Q

what are the differences between the Kacey EG and catachem EG tests?

A 
	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
175
Q

what is the Tx of choice for EG?

A

o Fomepizole (4-MP) -  DOESN’T cause CNS depression, diuresis, hyperosmolality (as ethanol can)

Toxicology (4 decks)

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