Toxicants

Question 1

Xylitol: Systems affected

Answer 1

Hypoglycemia&raquo_space; hepatic failure
MOA: tricks pancreas into releasing insulin leading to hypoglycemia.
Vomiting, diarrhea, melena
Monitor for liver damage: Acute hepatic necrosis, elev. liver enzymes, icterus, coagulopathy, seizures
Behavioral changes, weakness, ataxia, tremors

Question 2

Xylitol: Treatment

Answer 2

Early decontamination/emesis
BG monitoring +/- dextrose treatment
Liver protectants: SAme/silymarin/NAC

Question 3

Methylxanthines

Answer 3

Theophylline: Tea/Drugs
Caffeine: coffee, tea, chocolate
Theobromine: chocolate, cocoa, teas
readily absorbed orally
Elimination thru hepatic metabolism

Question 4

Methylxanthines: MOA

Answer 4

Binding adenosine receptors and blocking receptor activation. Increase intracellular Ca2+ levels
CV: Tachycardia, hypertension, arrhythmias
Nervous: Hyperexcitability, ataxia, seizures
Also: nausea, diarrhea, muscle tremors, PU/PD, resp failure, hypokalemia

Question 5

Methylxanthines: Treatment

Answer 5

Decontamination: emesis (1-2hr w/ caffeine; 6 hrs w/ chocolate)
Activated charcoal w/ cathartic
U-Cath to prevent reabsorption
Supportive care: IV fluids, sedation (ace), seizures (midazolam), hypertension (beta blockers)

Question 6

Acids: MOA and Toxicosis

Answer 6

Rapid surface protein coagulation > coagulation necrosis > formation of thick eschar
Stricture formation
Mild tissue irritation > sign. ulceration

Question 7

Alkalines: MOA and Toxicosis

Answer 7

large ingestion may occur b/c lack of taste
Liquefactive necrosis with edema and inflammation (transmural necrosis across tissue layers)
Membrane lysis, denatured proteins, thrombosis, stricture formation

Question 8

Acid + Alkalis Diagnostics

Answer 8

Endoscopy
CBC/PCV (blood loss anemia, WBC change w/ sepsis + GI perforation

Question 9

Acids and Alkalis Treatment

Answer 9

Decontamination w/ lots of water or saline
GI decontam contraindicated
IV vs PO drugs
Gastroprotectants
Fluid therapy
Analgesia
No neutralization

Question 10

Essential Oils

Answer 10

Absorbed thru mucous membranes
Cats are more sensitive
Depending on oil: hepatobiliary, GI, nervous, resp etc

Question 11

Essential Oil Treatment

Answer 11

Decontamination w/ washing/irrigation
Non-caustic: emesis + activated charcoal
Caustic: dilution w/ milk or water
Hepatoprotectants (silymarin. NAC, SAMe)
Dose/oil dependent

Question 12

Lithium Disc Batteries

Answer 12

Li Disk: no corrosive compounds but can cause tissue damage/perforation from current
Often passes unchanged in feces

Question 13

Dry cell (alkaline) Batteries

Answer 13

Tissue damage from rupture of casing
Heavy metals in casing if battery lodged in GI

Question 14

Batteries: Treatment/Outcomes

Answer 14

Endoscopic or surgical removal
GI protectants and antacids to allow for ulcerations to heal
Analgesics

Question 15

Fertilizers

Answer 15

Usually poor GI or dermal absorption. V/D, anorexia, abd. discomfort
Milorganite: GI signs, muscle pain, stiffness
Cacao bean mulch: methylxanthine tox
Anhydrous ammonia = corrosive
Added herbicides, fungicides insecticides
Treatmet: emesis, supportive care

Question 16

Ethylene Glycol MOA

Answer 16

Rapidly absorbed in GI
> metabolized by alcohol dehydrogenase > oxalic acid
Symptoms: vomiting, mental dullness, ataxia, metabolic acidosis, renal failure (oxalate crystalluria).

Question 17

Ethylene Glycol: Treatment

Answer 17

Inhibit metabolism: fomepizole or ethanol
Correct acid-base + electrolyte derangements
Correct fluid imbalances
Remove parent compound and metabolites: hemodialysis
Supportive care for acute kidney injury: antiemetics/GI protectants/ phosphate binders

Question 18

Ibuprofen Toxicity

Answer 18

V/D anorexia, gastric ulceration, abd. pain.
Very high doses: seizure, ataxia, coma
Cats are twice as sensitive
Renal damage: decrease renal blood flow and GFR etc
Platelet aggregation inhibited

Question 19

Ibuprofen Treatment

Answer 19

Prevent gastric ulceration: misoprostol, sucralfate
Renal failure: fluids
+CNS effects
Stabilization: respirations seizures
Decontamination: activated charcoal

Question 20

Why is Carprofen less toxic than Ibuprofen?

Answer 20

Stereochemistry
Equal amounts of R and S, S more specific for COX2 than COX 1, which is related more to GI tox, which is the form that accumulates in the gut.

Question 21

Naproxen (Aleve)

Answer 21

toxicity at dose close to analgesia
Dogs are animals most sens.

Question 22

Glucoronidation

Answer 22

Major pathway of xenobiotic biotransformation in mammalian species except for members of the cat family.

Question 23

UGT Enzyme

Answer 23

Cats are deficient in aspects of a major drug metabolizing pathway that is involved in both drug elimination and drug detoxification
So: more drug exposure (longer t1/2) and toxic, reactive forms can accumulate

Question 24

Acetominophen Damage

Answer 24

Tissue damage and toxicity occur due to the accumulation of the reactive N-acetyl benzylquinoneimine metabolite. Causes cell damage and necrosis.

Question 25

Acetominophen: Toxicity

Answer 25

Hepatocellular injury and necrosis
-vomiting, anorexia, tachycardia, tachypnea
-high doses: methemoglobinemia: cyanosis, hemoglobinuria, hematuria

Question 26

Acetominophen Cats

Answer 26

Predominant toxic effect is methemoglobinemia

Question 27

Acetominophen Treatment

Answer 27

GI decontamination: emesis, activated charcoal
O2 and fluids
Whole blood if bad anemia
N-acetylcysteine IV to counteract toxic mechanism (or SAMe)

Question 28

N-acetylcysteine

Answer 28

Thiol donor and frees up regular cysteine to be used in glutathione (GSH) anabolism
AKA increased GSH levels allowing for detoxification of reactive metabolites.

Question 29

Acetominophen Prognosis

Answer 29

Treatment most effective within 8 hrs
8-24 hrs lowers mortality but incomplete protection from hepatotoxicosis
Guarded in cats w/ CS

Question 30

Pseudoephedrine (cold and allergy products)

Answer 30

Acts as symphathomimetics: alpha + beta adrenergic agonist
-Peripheral vasocontriction
-cardiac stimulation
-enhanced CNS output

Question 31

Pseudoephedrine CS

Answer 31

restlessness, agitation, pacing, hallucinations, tachycardia, hypertension, muscle tremors, seizure, head bobbing, hyperthermia, death

Question 32

Pseudoephedrine Treatment

Answer 32

Emesis (if <30 min), activated charcoal, cathartic
treat seizures, tremors (ace, barbituate)
Cardiac function (beta blocker, propranolol)

Question 33

Thyroid Hormone CS

Answer 33

Affects metabolism, increases O2 consumption, temp, HR, blood volume, enzyme activity.
CS: V/D, hyperactivity to lethargy, hypertension, tachycardia, tachypnea, dyspnea, abnormal PLR

Question 34

Thyroid Hormone Treatment

Answer 34

Emesis, charcoal, carthartics
Supportive care and treat symptoms

Question 35

Venlafaxine (SRI)

Answer 35

Cats most common
Mydriasis, vomiting, techypnea, tachycardia, ataxia, agitation
Tx: emesis, charcoal, monitor HR and BP
Cyproheptadine as serotonin antagonist

Question 36

Amphetamines

Answer 36

CNS stimulant, agitation, hyperthermia, tremors, seizures, tachycardia, hypertension, cardiac arrhythmias, coma
Tx: emesis, charcoal, cathartics
supportive care + symptomatic tx, fluids

Question 37

Urine Acidification

Answer 37

The more basic the pH, the more reabsorption, so as pH drops, the compounds are more charged adn there is less reabsorption.

Question 38

Carbon Dioxide (CO2) Sources

Answer 38

Sources: end product metabolism, fuel burning heaters, decomposing manure.

Question 39

Methane Source

Answer 39

Microbial degradation, rumen microflora in cows, goats, sheep and other ruminants

Question 40

Ammonia Source

Answer 40

animal facilities where excrement can decompose on a solid floor