Toxicology Exam 1

Front 1

Study of chemicals, drugs, or other substances that produce harmful effects in or on biological tissues.

Back 1

Toxicology

Front 2

What is the central concept of toxiclogy?

Back 2

DOSE RESPONSE

Front 3

What information is provided by a dose-response curve?

Back 3

LD50
ED50
TI= LD50/ED50
SSM = LD1/ED99

Front 4

What is the difference between a poison and a toxin?

Back 4

poison: ANY solid, liquid, gas that interferes with the normal life proesses of that organism

toxin: toxicants/poisons originating from a BIOLOGICAL source

Front 5

What is the difference between Acute and Chronic Toxicity?

Back 5

Acute = <24hr

Chronic = 6mo-2yr

Front 6

T/F: there is no such thing as a NONtoxic substance.

Back 6

true

*dose makes the poison

Front 7

1ppm = ____

Back 7

1 mg/kg --> 1 mg/L

or

1ug/g

Front 8

What are the 3 rules of thumb?

Back 8

1- % --> ppm (4 places right)

2- 100 g/ton --> 110 ppm
1 g/ton --> 1.1ppm

3- 1 lb/acre --> 7 mg/kg BW exposure
1 lb/acre --> 230 ppm forage

Front 9

How should tissue samples be stored?

Back 9

unwashed
double bagged
labeled
plastic/glass container

frozen
refrigerated (whole blood)

Front 10

How is the brain sampled?

Back 10

Whole:

1/2 in formalin
1/2 frozen

Front 11

What are the contraindications for emesis?

Back 11

unconscious, depressed
convulsing, convulsant poison
corrosive/caustic agents
petroleum distillates
volatile hydrocarbons

Front 12

How much fluid do you need for an appropriate gastric lavage?

Back 12

5-10 ml water/kg bw

careful not to overextend stomach

Front 13

How much Activated Charcoal is necessary to act as a GI adsorbent?

Back 13

10-20% slurry
1-2 g/kg (ALL SPECIES)

Front 14

T/F: Toxicants stored in Fat or Bone have little or no biological activity.

Back 14

True

p.10

Front 15

This poison frequents the top 5 list of toxicoses in cats and dogs.

Back 15

Ethylene glycol

Front 16

Common toxicoses affecting the CNS in Dogs.

Back 16

OP
Carbamate
Ethylene Glycol
Theobromine
Tremorgens

Front 17

Common toxicoses affecting the Pulmonary system of dogs and cats.

Back 17

OP
Carbamates

Front 18

What systems are affected by theobromine?

Back 18

CNS, GI, Cardiac, Renal

Front 19

What drug toxicosis in cats has hepatic and hemostatic effects?

Back 19

Acetaminophen

Front 20

What size particles make it to the alveolae for absorption? What size particles are removed by cilia?

Back 20

< or = 1um absorbed

1 - 5 um removed

Front 21

Which is more toxic, bolus or powder form? Why?

Back 21

powder: exposed to a larger absorptive surface

Front 22

What 3 factors affect transfer of toxic agents across biological membranes?

Back 22

lipid solubility
ionization
protein binding

Front 23

Give an example of an excipient.

Back 23

adjuvants
binding agents
enteric coatings
surfactants
solvents
unintentional additives

Front 24

T/F: Fractionation usually increases toxicity.

Back 24

False

Fractionation usually decreases toxicity.

Front 25

What does the season have to do with the toxicity of a synthetic drug?

Back 25

seasons may affect hormone levels/ metabolic activity

*testosterone is highly correlated with cytP450 activity

Front 26

Ruminant urine is ____ (ph range), while canine urine is ___ (ph range).

Back 26

ruminant- alkaline

canine- acid

Front 27

Ruminants are deficient in ______ which makes them particularly susceptible to lidocaine.

Back 27

pseudocholinesterase

Front 28

____ are deficient in sulfate conjugation.

Back 28

Pigs (and pigeons)

Front 29

____ are deficient in glucuronyl transferase.

Back 29

Cats

*also lower mehemoglobin reductase

Front 30

Name 3 factors that decrease cytP450.

Back 30

Vitamin/mineral deficiencies
Proein deficiency
Fatty acid deficiency
High Carbohydrates
Starvation >48hours
High Fat diet (may increase or decrease)

Front 31

Why are newborns so susceptible to toxicoses?

Back 31

deficienty enzyme activity
increased permeability of BBB
lower renal fx
eat more

Front 32

Malathion and chlorpyrifos are what class of pesticide?

Back 32

organophosphates

Front 33

OPs bind to the esteratic site of AChE irreversibly. This is called ____.

Back 33

aging

*depends on compound and kinetic but usually expected in < 60 min

Front 34

Where is "true" ChE found?

Back 34

RBCs

Front 35

OPs act on muscarinic, nicotinic, and CNS receptors. What are the clinical signs?

Back 35

PNS: muscarinic--> SLUD

nicotinic: NMJ stimulate/block

CNS: stimulate/block

Front 36

How much inhibition of AChE must occur before clinical signs appear?

Back 36

70% in brain

50% in RBCs

Front 37

what does pralidoxime (2-PAM) do?

Back 37

regeneration of acetylcholinesterase (muscarinic and nicotinic sites)

*otherwise: takes ~20+days to generate new enzye (1-5%/day)

Front 38

Does atropine alleviate all the signs of OP toxicosis?

Back 38

only muscarinic signs

-- nicotinic signs will decrease w. time

Front 39

____ inhibition and "_____" can predict if Organophosphate-induced delayed neuropathy (OPIDN) will occur.

Back 39

Neurotoxic esterase

"aging"

Front 40

Delayed effects of OP toxicosis show up _____ later with progressive irreversible ataxia.

Back 40

1 week-- 2mo

Front 41

OPs are metabolized by type A and type B enzymes. Which type is inhibited by OPs?

Back 41

type B

Front 42

the physiologic function of B esterases like pChE and CbxE is to protect ___.

Back 42

AChE

Front 43

Carbamates differ from OPs

Back 43

active toxicant (op- protoxicant)
reversible (op- irreversible)
carbamic acid derivative (op- phosphoric acid derivative)

Front 44

T/F: Nicotinic Agonists have no antidote. Treatment is symptomatic.

Back 44

True

Front 45

Excitement due to a GABA antagonist like Fipronil may be treated with GABA agonists such as...

Back 45

barbiturates
benzopdiazepines

Front 46

OPs and pyrethrins are both ___ (chemistry).

Back 46

esters

Front 47

Why are there 2 separate syndromes for pyrethroid toxicosis?

Back 47

T syndrome--> Type 1 pyrethroids: tremors

CNS syndrome --> type 2 pyrethroids: seizures

Front 48

Organochlorines have a (high/low) LD50; acute toxicities are (common/rare).

Back 48

HIGH LD50

Rare

*biomagnification possible with chronic toxicities p 43

Front 49

What might you use yohimbine or tolazoline to treat?

Back 49

these are alpha 2 antagonists so they would be used to treat alpha 2 agonist overdose--> Amitraz

Front 50

Most of the side effects of natural insecticides are:

Back 50

dermal
GI

Front 51

What is the relative toxicity of ethylene glycol in dogs, poultry, kids, cats?

Back 51

kids=cats> dog> poultry

Front 52

T/F: Ethylene Glycol metabolites are more toxic than unchanged EG.

Back 52

true

* so try to block metabolism

Front 53

___ is the rate-limiting step of EG metabolism.

Back 53

Alcohol dehydrogenase

Front 54

___ and ___ are the metabolites responsible for the CNS toxicity associated with EG.

Back 54

Ethylene glycol
Glycoaldehyde

Front 55

What is the relative toxicity of EG metabolites?

Back 55

Glyoxilic > Glycoaldehyde > Glycolic > EG

Front 56

____ is the metabolite of EG responsible for acidosis.

Back 56

Glycolic acid

Front 57

What are the stages of clinical signs that are associated with EG toxicosis?

Back 57

(1) <12hours: CNS
(2) 12-24 hours: Cardiopulmonary
(3) 24+ : Renal

Front 58

Why doesn't the EG kit test work for cats?

Back 58

not sensitive enough to detect the low levels that are toxic in the cat

Front 59

How does 4-methylpyrazole work?

Back 59

inhibits Alcohol Dehydrogenase: prevents formation of toxic EG metabolites

Front 60

What can you use to treat EG toxicosis if you don't have 4-MP?

Back 60

ethanol (max 20%)-- will competitively use ADH and slow EG metabolism

Front 61

How soon do you have to catch EG poisoning in order to have a good prognosis?

Back 61

Dogs: 5-8 hours

Cats: 3 hours

Front 62

___ can cause Blindness in Primates, because they have less folates (important for 1Carbon metabolism).

Back 62

Short chain alcohols

*takes up to 24hours to show up

Front 63

What toxicant causes the "Energizer Bunny" syndrome?

Back 63

Methylxanthines (Caffeine, Theobromine)

Front 64

What toxicant causes the dog to "bounce like a ball"?

Back 64

Methylxanthines (caffeine, Theobromine)

*CNS, Cardiac, Urinary, GI

Front 65

What is unique about Ibuprofen toxicosis clinical signs?

Back 65

biphasic
GI <6hours

Renal 12hr-5days

Front 66

Who is likely to suffer from ivermectin toxicosis?

Back 66

puppies
foals
collies (different BBB)

Front 67

Foal: Onset of clinical signs 10hours. Mydriasis, blindness, bradycardia, convulsions.

Name the toxicosis.

Back 67

Ivermectin

*blindness is reversible

Front 68

Physostigmine is a treatment for Ivermectin toxicosis. What does it do?

Back 68

inhibits AChE

wakes up from coma (30-90min)

Front 69

Piperazine Toxicosis has CNS signs.
V/D
circulatory collapse
head pressing
hyperesthesia
convulsions
ataxia
muscle tremors
myoclonus

What is the main diagnostic sign?

Back 69

myoclonus

- head neck forward, legs back

Front 70

pseudoephedrine toxicosis is basically a worse form of methylxanthine toxicosis. The treatments are similar:

Back 70

diazepam/pentobarb

propranolol/lidocaine

cool baths

Front 71

Why are dogs particularly susceptible to 24D toxicosis?

Back 71

renal anion transport becomes saturated (dogs are deficient in anion transport secretion in renal proximal tubules)

Front 72

This toxicosis generally affects GI and MUSCLE and causes nonspecific signs in cattle, and Myotonia and hindlimb paresis.

Back 72

phenoxyacetic acid
(2,4-D)

Front 73

Give an example of a Dipyridil Herbicide.

Back 73

Diquat
Paraquat

Front 74

What is the difference in the clinical signs that occur with moderate dose vs high dose PARAQUAT?

Back 74

High dose (<2hr): CNS

Moderate dose (1-3d): GI, RESP, Renal

*diquat is similar but NO respiratory signs

Front 75

Atrazine is the most common agriculatural herbicide in the US (it is a triazine). Who is most commonly affected and what system?

Back 75

Cattle: CNS

Front 76

T/F: Thiocarbamate is a cholinesterase inhibitor.

Back 76

FALSE

mechanism of action is unknown, but it is NOT a cholinesterase inhibitor: do NOT treate with atropine

Front 77

What should you suspect if your dog comes back from running covered in orange-yellow dye?

Back 77

dinitroanaline herbicide (pendimethalin)

Front 78

Round up is a ____ herbicide that mainly affects the GI system.

Back 78

Glyphosphate

Front 79

What should you expect if you feed your cattle pink corn?

Back 79

Captan (carboximide) fungicide toxicosis

Respiratory signs

Front 80

T/F: the antidote for carbamate toxicosis is atropine.

Back 80

False

Carbamate is NOT a cholinergic-- do NOT treat with atropine (PsL)

Front 81

What toxicosis should you suspect in your chickens that have soft shelled, abnormal eggs and weak, deformed legs?

Back 81

Thiram (Carbamate)

*sheep are also susceptible (anorexia, dyspnea, abortion, depres;leth)

Front 82

T/F: Relay toxicosis is common with Cholecalciferol.

Back 82

False

Front 83

Describe the mechanism of action of Cholecalciferol.

Back 83

D3 + active metabolites (25-OH cholecalciferol (liver), 1,25-OH cholecalciferol (kidney)) increase absorption of calcium from small intestine, stimulate bone reabsorption, and promote reabsorption of calcium by renal tubular epithelia

Front 84

A dog comes in for indiscriminate eating. The owner doesn't know what it ate, because there were only a few pieces of soggy cardboard left hanging out of his mouth. This just happened within the last 6 hours. You're a dumb vet and you run a CBC and Chem because you think the toxin will show up on the chem panel. Stupid... of course you see no toxins, but you do notice that the phosphorus is markedly elevated. Now what do you think? What else should spike in the next 24 hours?

Back 84

Not such a dumb vet after all.

It is likely D3 toxicosis-- Phosphorus spikes within the first 12 hours followed by a Calcium elevation at 24 hours post exposure

Front 85

What systems are affected by D3 toxicosis? (think-- what can calcium mess up?)

Back 85

Cardiac
Renal
GI

Front 86

What is the treatment for D3 toxicosis?

Back 86

pred +/- furosemide for several weeks

+/- calcitonin if serum Ca++ is unresponsive

Front 87

What is the relative toxicity of bromethalin in:

mouse
rat
dog
cat

Back 87

Most : Cat (0.54)> Rat (2.3)> Dog (3.7)> Mouse (6.7) : Least

Front 88

This rodenticide works by uncoupling oxidative phosphorylation in the CNS allowing fluid to accumulate in myelin sheaths. This decreases nerve trasmission and will eventually result in respiratory arrest.

Back 88

Bromethalin

Front 89

What is unique about the clinical signs associated with Bromethalin toxicosis?

Back 89

2 syndromes based on dose (like

@> LD50 Convulsant Syndrome

<LD50 Paralytic Syndrome

Front 90

What toxicosis have 2 different syndromes?

Back 90

Based on Dose:
Dipyridil Herbicides (High dose : CNS, Moderate Dose: gi, resp, renal)
Bromethalin (>LD50: Convulsant vs <LD50 Paralytic)
*** these also affect Onset times...


Based on Type (1 or 2)
Pyrethroids
(CNS vs Tremors)

Front 91

What toxicosis causes loss of bark early on?

Back 91

Bromethalin

* this is associated with <LD50
* other signs: miosis, anisocoria, paralysis (forelimb extensor rigidity)

Front 92

Why would you give activated charcoal to a dog that ingested Bromethalin 4 days ago?

Back 92

decrease enterohepatic circulation

Front 93

Describe a typical Zinc Phosphide gopher bait.

Back 93

gray
grain
fishy/garlic

Front 94

How much Zn in ppm is in 1% gopher bait?

Back 94

10,000ppm

10,000 mg/kg

Front 95

What produces the acute effects of Zinc Phosphide Toxicosis?

Back 95

Phosphine gas (PH3)
-produced in the stomach: responsible for free radical production & possibly blockage of mitochondrial cytochrom oxidase

(zinc causes later hepatic and renal damage)

Front 96

Clinical signs of Zinc Phosphide toxicosis include consistent Vomiting, dyspnea, tonic convulsions and arrhythmias. What is the onset and course of this disease?

Back 96

onset 15min-4hr (can be delayed up to 12 hr)

duration 4-48hr

Front 97

You live next to a dairy. Your dog stays outside during the day. You come home from work 4hours after leaving your dog perfectly healthy, and find your dog dead in the yard. He is already very stiff. On necropsy, they find whole corn in his stomach. Guess!

Back 97

Avitrol

*used to control pigeons and starlings at the dairy next door

Front 98

Like Antiesterases Avitrol increases acetylcholine. Why might it act so much more rapidly than Antiesterases?

Back 98

blocks K+ current of repolarization following an action potential

Front 99

What is an Inandione?

Back 99

Anticoagulant-- similar clinical signs as coumarins

Front 100

Which anticoagulant is safer, 1st or 2nd generation?

Back 100

1st generation: requires multiple doses to kill (warfarin)

2nd generation: 1 dose (brodifacoum)
10-100x more potent

Front 101

T/F: Cats are more resistant to anticoagulant rodenticides thatn dogs.

Back 101

True

Front 102

Anticoagulant Rodenticides act as Vit K antagonists blocking synthesis/carboxylation of factors 2, 7, 9, 10. Therefore these factors caannot bind ___.

Back 102

Ca++

Front 103

T/F: Anticoagulant Rodenticides have a direct effect on capillaries.

Back 103

True

*damage them = rupture easily

Front 104

Vitamin K gets reused for the activation of clotting factors. When it is used Vit K goes from active--> inactive and coagulation precursor become activated coagulation factors. What enzyme is required to "reactivate" vit K?

Back 104

epoxide reductase

Front 105

What does the PCV, FDP, and Platelets look like on a Rodenticide poisoning patient?

Back 105

PCV low, red cells normal
Fibrinogen/ DFP normal
Platelets normal/ slight decrease

Front 106

Which Vit K should you give in what route?

Back 106

K1
SubQ (other routes increase risk of anaphylaxis)

Front 107

Oral K1 supplementation should be __ weeks for 1st gen anticoagulants and ___ weeks for 2nd gen anticoagulants.

Back 107

2 weeks--> 1st gen

3-5 weeks --> 2nd gen

Front 108

Strychnine's major influence is on the spinal cord and medulla in the CNS. It binds ____ and removes ____ influence.

Back 108

gycine (GABA) receptor

removes neuroinhibitory influence

*results in overstimulation

Front 109

Bilateral, symmetrical tetanic seizures stimulated by bright lights, sounds, or touch are very strong indicators of ____ toxicosis

Back 109

strychnine toxicosis

Front 110

Name 3 ddx that cause clonic/tonic seizures.

Back 110

Carbamates
OP
Chlorinated HC
Metaldehyde

Front 111

Why woud you give Na pentobarb for seizures associated with strychnine poisoning?

Back 111

acts as a GABA mimetic

(strychnine inhibits glycine receptors)

Front 112

T/F: activated charcoal does NOT bind strychnine very well.

Back 112

False

Activated charcoal binds charcoal very well.

Front 113

would you use a urine alkalinizer or acidifier to ion trap strychnine?

Back 113

acidifier

*strychnine is an alkaloid.

Front 114

What causes "Shake and Bake" syndrome?

Back 114

Metaldehyde

(molluscicide)

Front 115

What causes the CNS excitation associated with metaldehyde toxicosis?

Back 115

decrase in serotonin (5HT), GABA and NE concentration

Front 116

You successfully treat a patient with severe metaldehyde poisoning. 3 days later you discharge the patient and he's back within 12 hours relapsing. The owner (who you trust) swears that they did not get back into the molluscicide. What's going on?

Back 116

Dogs can appear to recover if you get the acidosis/ seizure masked with drugs... and will relapse days later with severe liver problems (so make sure you are supporting the liver after the neurologic phase has passed)

Front 117

A cleaning product that has an LD50 of 65mg/kg should have what label? How toxic is it?

Back 117

WARNING (50-500mg/kg)

Moderately toxic

Front 118

Caution labels indicate a slightly toxic substance with an LD50 of ____.

Back 118

0.5-5g/kg

Front 119

The general Clinical signs associated with ingestion of most household cleaners are ____.

Back 119

GI: V/D

*granular detergents, hydrocarbons and disinfectants also have CNS signs

Front 120

order the relative toxicity of soaps:
anionic, amphoteric, nonionic, cationic

Back 120

cationic> amphoteric> anionic > nonionic

Front 121

What is the difference between phenolic soaps and cationic surfactants+nonionic detergents?

Back 121

phenolic soaps/pine oils = hepatic damage (green or Black urine)

Cationic+nonionic = GI, CNS

Front 122

When are you likely to see liquefactive necrosis vs coagulative necrosis?

Back 122

akaline solution: liquefactive

acid solution: coagulative

Front 123

Why wouldn't you use activated charcoal in MOST household chemical exposures?

Back 123

signs are not systemic (mostly GI)

activated charcoal is only indicated when there is potential for systemic effects or if the cleaning product is potentially corrosive.

Front 124

T/F: Hydrocarbon solvent exposures cause Convulsions.

Back 124

False.

*they cause CNS: depres-leth, ataxia, coma, but not convulsions

Front 125

Anionic surfactants cause ____ in high doses.

Back 125

Hemolysis

Front 126

Pine oils and phenols are particularly bad for ____ because they are deficient in glucuronide conjufation.

Back 126

cats

Front 127

This class of toxicants can cause iron toxicosis associated with cardiovascuar collapse and liver necrosis in addition to GI problems.

Back 127

Rose fertilizer

*onset <2hours

general signs: V/D