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Toxicology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Give 2 examples of 2nd generation anti-coagulants

A

Brodifacoum

Bromadiolone

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2
Q

Describe how 2nd generation anti-coag rodenticides work (MOA)

A

antagonize the action of vitamin K1 epoxide reductase –> can’t make active vitamin K –> depletion of vitamin K1 dependent factors (2,7,9,10)

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3
Q

Which coag factor has the shortest half-life? Bc of this, which coag panel test becomes prolonged first

A

factor 7

prothrombin time (PT) prolongs first

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4
Q

At what time frame after ingestion do we check PT? If it’s prolonged, what therapy do we provide?

A

after 48hr

oral vitamin K1 for 4 weeks

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5
Q

Two important products of COX pathway that can be inhibited by NSAIDs & their general effect on platelets

A

Thromboxane A2– increases platelet aggregation

Prostacyclin (PGI2)– inhibits platelet aggregation

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6
Q

What is the shock fluid dose for:

1) dogs
2) cats

A

1) 90ml/kg

2) 40-50ml/kg

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7
Q

Which type of fluids (generally) should be avoided with pit viper envenomation

A

Colloids (may interfere with coagulation)

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8
Q

When choosing an analgesic for a patient follow pit viper bite, which category of drug should be avoided and why?

A

NSAIDs–inhibitory effects on platelet aggregation

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9
Q

Coral snake venom is primarily _____ and therefore causes minimal _______

A

neurotoxic;

minimal tissue reaction & pain

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10
Q

Describe how coral snake venom works

A

it’s a post-synaptic alpha-neurotoxin–> blocks nicotinic ACh receptors of NMJs

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11
Q

Cats are extremely sensitive to the venom of ____ and it is often fatal

A

Black widows

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12
Q

Black widow venom is primarily a ______ and causes release of?

A

Neurotoxin;

release of Norepi & ACh

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13
Q

Name 2 types of rodenticides that are not anti-coagulant

A

Cholecalciferol

Bromethalin

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14
Q

Net result of cholecalciferol toxicity?

A

Hypercalcemia

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15
Q

Describe the MOA of bromethalin toxicity

A

uncouples oxidative phosphorylation (decreased ATP–> messed up Na/K ATPase–> Na builds in cells)

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16
Q

Why would multiple doses of activated charcoal be indicated for cholecalciferol or bromethalin toxicity?

A

Due to enterohepatic circulation

esp. bromethalin which is excreted in bile

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17
Q

What is the risk assoc. with inducing emesis in a dog that’s ingested zinc phosphide?

A

the gas that comes up (phosphine gas) can be toxic to staff!

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18
Q

Which route of exposure to zinc phosphide is worse and why?

A

Inhalation–readily absorbed into systemic circulation

with ingestion, it’s corrosive to the mucosa and induces vomiting

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19
Q

How does strychnine cause clinical signs (MOA)?

A

blocks the inhibitory actions of glycine (CNS upregulated)

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20
Q

Which toxic gases are

1) heavier than air
2) lighter than air

A

1) CO2, H2S

2) NH3, CO

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21
Q

Acute levels of ____ppm of which gas can lead to olfactory paralysis

A

> 100ppm of H2S

22
Q

Primary source of H2S as it relates to animal exposure?

A

decomposition of fecal material

gets mixed or stirred, releasing the gas

23
Q

Why are pulse oximeters not helpful in diagnosis of CO toxicity?

A

They only measure dissolved gas in the blood–cannot tell if it’s Hgb bound to O2 or CO

24
Q

Levels of CO2 must reach _____ppm for clinical signs to appear

A

50,000ppm

*300ppm is normal ambient level

25
Q

How do amyl nitrite and sodium nitrite treat HCN toxicity

A

they induce the formation of methemoglobin which has a higher affinity for HCN

GOAL= 25% MetHgb

26
Q

Which spp. is highly susceptible to heated teflon (PTFE)

A

birds/poultry

27
Q

Lethal dose of ethylene glycol in

1) dogs
2) cats

A

1) 4 ml/kg

2) 1.5 ml/kg

28
Q

EG toxicity requires early diagnosis and treatment. What is the treatment window (time frame) in dogs? Cats?

A

Dogs: < 8-12hr

Cats: < 3 hr

29
Q

Two treatment options for EG toxicity? Their MOAs?

A

4-MP–> inhibits alcohol dehydrogenase

Ethanol–> shifts alcohol dehydrogenase to itself for metabolism so EG doesn’t get broken down

30
Q

Why is methanol associated with formation of blindness in humans and primates?

A

inability to breakdown formic acid (metabolite)

31
Q

Ethanol and 4-MP are not indicated in the tx of?

A

Methanol toxicity

32
Q

Which toxic substance is assoc. with heinz body anemia in cats

A

Propylene glycol

33
Q

Why might we see a strong metabolic acidosis with proplyene glycol ingestion?

A

one of it’s breakdown products is lactic acid (high lactate= metabolic acidosis)

34
Q

Would 4-MP be indicated for tx of propylene glycol?

A

No

35
Q

Pyrethrin & pyrethroid MOA?

Name a few clinical signs you might see

A

Prolonged Na channel conduction

hyperesthesia (tx somewhere quiet), muscle tremors, ear twitching

36
Q

Lipid therapy would be effective for any drug with a Log P _____

A

> 1

*higher number= more it mixes with fat

37
Q

How do Organophosphates and Carbamates differ? (2)

A

OPs–> irreversible inhibition of AChE
Carbamates–> REVERSIBLE inhibition of AChE

OPs undergo “aging” which strengthens their bond to the enzyme & carbamates do not

38
Q

OPs and carbamates primarily cause ______ signs. Name 4

A

Muscarinic signs

SLUD (salivation, lacrimation, urination, defecation)

39
Q

Tx of choice for OPs and carbamate toxicity? What is our main goal?

A

Atropine

Goal= treat bradycardia & bronchial secretions

Atropine doesn’t help nicotinic signs!!

40
Q

Which drug is considered an antidote for OP/Carbamate toxicity

A

2-PAM

*helps nicotinic signs

41
Q

The presence of muscle tremors combined with HYPOthermia might be indicative of which toxicity?

A

Citrus oil

42
Q

Toxin assoc. with snail/slug bait? Assoc. clinical signs?

A

Metaldehyde

“Shake and bake”–> muscle tremors + secondary hyperthermia

43
Q

On which channels does Ivermectin exert its effects?

A

activates glutamate-gated chloride channels

**causes hyperpolarization

44
Q

Dogs with the ____ mutation can only handle ____ mg/kg of ivermectin.

Is HW prevention safe for these affected dogs?

A

MDR1 mutation can only get 0.15mg/kg

HW prevention is safe (0.006mg/kg)

45
Q

How does Amitraz cause clinical signs?

A

increases alpha-2 adrenergic activity (sedation, ataxia, bradycardia)

46
Q

Concerning Amitraz toxicity:

1) why might we see hyperglycemia
2) what drug can be used for tx

A

1) alpha-2 agonists inhibit insulin release

2) Atipamezole (alpha-2 antagonist)

47
Q

If you’re not sure which type of moth ball a dog or cat ate, which test can you use?

A

Mix salt with water

Bad type will float, other will sink

48
Q

2 reasons corrosive alkalies are worse than corrosive acids

A

corrosive acids are painful upon ingestion which limits the amount ingested (unlike alkalines…large amounts can be ingested)

Alkalines cause more severe necrosis (liquefactive compared to coagulative)

49
Q

Treatment for corrosives includes decontamination? (T/F)

A

FALSE–no emesis or activated charcoal

DILUTE with water or milk instead

50
Q

The risk with homemade playdough is assoc. with its ____ content

A

salt (hypernatremia)

*>180 causes seizures

Toxicology (5 decks)

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