Household Products Part 2

Question 1

Different bleaches used?

Answer 1

household bleaches (clorox) contain 3-6% sodium hypochlorite; swimming pool products may contain up to 50% hypochlorite; non-chlorine bleaches (colorfast bleach) contain sodium peroxide, sodium perborate and enzymatic detergents

Question 2

Toxicity of bleach is dependent upon what?

Answer 2

the products hypochlorite ion concentration and resulting pH–rather than the ingested dose/quantity

Question 3

In stomach acid bleach forms _________ which penetrates MMs and causes local coagulation.

Answer 3

hypochlorous acid

Question 4

T/F Toxicity more likely from bleaching powders and concentrated solutions than household chlorine bleach.

Answer 4

TRUE

Question 5

MOA of bleach toxicosis?

Answer 5

when combined w/ acid or ammonia solutions, chlorine bleaches cause release of chlorine or chloramine gas and hypochlorous acid–chlorine or chloramine gases cause severe respiratory and eye irritation–concentrated solutions are highly corrosive to MMs (hypochlorite ion is oxidizing)

Question 6

Clinical signs of bleach toxicosis?

Answer 6

signs of oropharyngeal, GI and respiratory irritation–may small of chlorine

Question 7

Treatment of bleach toxicosis?

Answer 7

milk or water (avoid acids), possibly Mg Oxide to neutralize stomach acids; wash dermal exposure w/ water and soap; symptomatic and supportive tx

Question 8

Dr Shokry’s former student’s case!!

Answer 8

The horse was found drooling, refusing to swallow, grinding his teeth and refusing food. Knowing bruxism is often a sign of gastric ulcers, a thorough history revealed the smell of bleach in the drinking water and further questioning of the barn owner revealed a the use of a quarter cup bleach to 20 gallons of water daily and the horse had been off feed for about a week.

Question 9

Properties of xylitol?

Answer 9

sugar alcohol that looks and tastes like sugar

Question 10

Uses of xylitol?

Answer 10

sugar substitute in sugar free gum, candy, diabetic and low carb products; used in dental care products; flavoring in some medications; some parenteral nutrition solutions

Question 11

Source of xylitol toxicosis?

Answer 11

accidental ingestion of xylitol sweetened products

Question 12

T/F FDA requires xylitol to be listed as an active ingredient in products.

Answer 12

FALSE!!! inactive ingredients are NOT listed in order of quantity
also companies may or may not divulge the presence of xylitol

Question 13

T/F Caution must be taken when using human oral hygiene products extra-label in canines.

Answer 13

TRUE–ex infant toothpaste w/ 35% xylitol

Question 14

What species are the most susceptible to xylitol toxicosis?

Answer 14

dogs–so far the only confirmed species

Question 15

What dose of xylitol can cause acute hepatic failure in dogs?

Answer 15

1.6-2.0 g/kg

Question 16

Xylitol-sweetened chewing gum can contain ____g per piece.

Answer 16

1-2 grams

Question 17

ADME of xylitol?

Answer 17

A=readily but incompletely from GIT
D=peak plasma levels 30 minutes post ingestion
M=converted to glucose then glycogen in the liver (liver does about 80% of metabolism)

Question 18

MOA of xylitol toxicosis?

Answer 18

potent promoter of insulin release in dogs–resulting in hypoglycemia. large doses can cause liver failure, GI hemorrhage and DIC

Question 19

Clinical signs of xylitol toxicosis?

Answer 19

hypoglycemia within 30-60 minutes or may take several hours depending on amount ingested; signs related to hypoglycemia–weakness, ataxia, collapse, seizures (may last 12-24 hrs); later onset lethargy, V+, liver failure, coagulopathy (within 48 hrs PI); dogs suffer from liver failure may not show hypoglycemia

Question 20

Lesions seen in xylitol toxicosis?

Answer 20

if only hypoglycemic–no lesions but if liver failure–petechial ecchymotic or GI hemorrhages, severe hepatocyte loss or atrophy and hepatic necrosis

Question 21

Laboratory diagnosis of xylitol toxicosis?

Answer 21

hypoglycemia, +/- hypokalemia, hypophosphatemia. liver failure–>ALT elevation, ALP, Tbili, moderate hypoglycemia, prolonged PT/PTT, thrombocytopenia, hyperphosphatemia

Question 22

Differential diagnosis for xylitol toxicosis?

Answer 22

other causes of hypoglycemia–insulin overload, insulinoma.

other causes of acute hepatic necrosis–hepatotoxins (acetaminophen, aflatoxin, sago palm)

Question 23

Treatment of xylitol toxicosis?

Answer 23

decontamination by inducing V+, 50% dextrose IV followed by IV infusion (5% dextrose) until blood glucose returns to normal–response w/in 12-24 hrs, oral feeding of high carb diet, antiemetics, fluid therapy to treat dehydration

Question 24

T/F Activated charcoal is not effective in decontaminating xylitol.

Answer 24

TRUE

Question 25

Treatment for liver failure caused by xylitol toxicosis?

Answer 25

antacids and GI protectants; liver protectants (SAMe, silymarin, vit E, N-acetylcysteine), antibiotics, transfusions if needed, Vit K1

Question 26

Prognosis of xylitol toxicosis?

Answer 26

if only hypoglycemia–good and if liver failure–more guarded

Question 27

Properties of methylxanthines?

Answer 27

methylxanthine alkaloids include caffeine, theophylline and theobromine

Question 28

Where else can caffeine be found?

Answer 28

found in beans of the coffee plant (Coffee arabica), leaves of the tea plant (Thea sinensis), is added to cola and energy drinks, chocolate products

Question 29

Where else can theophylline be found?

Answer 29

tea and used in asthma medication

Question 30

Where else can you find theobromine?

Answer 30

occurs in cacao beans of the chocolate plant (Theobroma cacao)

Question 31

Sources of methylxanthine toxicosis?

Answer 31

ingestions of large amounts of chocolate (esp dark), cocoa byproducts, cacao bean mulch, OTC caffeine tablets, diet pills, excedrin (contains caffeine)

Question 32

What species are the most susceptible to methylxanthine toxicosis?

Answer 32

dogs–but cats can be poisoned too

Question 33

What is the LD50 in dogs and cats for caffeine?

Answer 33

dogs–140mg/kg

cats–100-150mg/kg

Question 34

What is the LD50 in dogs and cats for theobromine?

Answer 34

dogs–250-500mg/kg

cats–200mg/kg

Question 35

ADME of methylxanthine?

Answer 35

A=readily absorbed from GIT
D=widely throughout body including CNS
M=by liver and undergo enterohepatic recycling
E=in urine unchanged and as metabolites

Question 36

MOA of methylxanthine toxicosis?

Answer 36

inhibit phosphodiesterases (raise cAMP) and antagonize adenosine receptors–cerebral cortical stimulation, seizures, myocardial contraction, smooth muscle relaxation and diuresis

Question 37

MOA of caffeine toxicosis?

Answer 37

stimulation of the release of catecholamines from the adrenal medulla, respiratory, vasomotor and vagal centers with greater skeletal muscle stimulation

Question 38

MOA of theobromine toxicosis?

Answer 38

greater cardiac stimulation than caffeine

Question 39

Clinical signs of theophylline toxicosis?

Answer 39

nausea, V+, abdominal pain, mild acidosis, tachycardia

Question 40

Clinical signs of caffeine/theobromine toxicosis?

Answer 40

signs may start w/in 2 hrs; restlessness, hyperactivity, panting, V+; tachycardia weakness, ataxia, diuresis, D+, hyper excitability, muscle tremors, hyperthermia; clonic convulsions, progression to arrhythmias, muscle rigidity, hyperreflexia, terminal seizures, coma; HR may exceed 200 bpm w/ VPCs

Question 41

How long do the clinical signs of methylxanthine toxicosis last?

Answer 41

12-72 hours depending on the dose ingested

Question 42

Death of methylxanthine toxicosis is due to?

Answer 42

cardiac arrhythmias, respiratory failure or terminal seizures

Question 43

Lesions caused by methylxanthine toxicosis?

Answer 43

chocolate or caffeine-containing products may be found in the GIT; no gross or histopathologic findings except gastroenteritis and congestion of internal organs may not be present

Question 44

Laboratory diagnosis for methylxanthine toxicosis?

Answer 44

low potassium, phosphorus, magnesium and elevated glucose–can be detected in stomach contents, plasma, serum, urine and liver

Question 45

Differential diagnosis of methylxanthine toxicosis?

Answer 45

strychnine, amphetamine or nicotine, and other CNS stimulating toxins (metaldehyde, etc)–cardiac and CNS disease

Question 46

Prognosis of methylxanthine toxicosis?

Answer 46

if effective decontamination and supportive care for duration (12-26 hrs) favorable prognosis–seizures or arrhythmias on presentation worsen prognosis

Question 47

Decontamination of methylxanthine toxicosis?

Answer 47

early decont by inducing V+ if ingestion w/in 2-6 hrs; activated charcoal to prevent further absorption–continue activated charcoal tx for up to 36-72 hours

Question 48

Treatment of methylxanthines?

Answer 48

IV fluid therapy prevent dehydration and enhance urinary excretion–empty bladder frequently to prevent reabsorption of metabolites from urine. methocarbomal for tremors. diazepam/midazolam for seizures. beta blockers such as propanolol or metoprolol to tx tachyarrhythmias. lidocaine is frequent VPCs. Uncommonly brachycardia occurs and use atropine to tx as long as it is not a reflex brachycardia. ECG should be monitored continuously.

Question 49

Difference between using propranolol and metoprolol in treating tachyarrhythmias?

Answer 49

metoprolol may exhibit less competition for urinary excretion–faster elimination than w/ propanolol

Question 50

List some generally non-toxic household items.

Answer 50

ballpoint pen inks, chalk, crayons, indelible markers, modeling clay, brand name Play-doh, silly putty, newspaper, indoor acrylic paint, pencil lead (graphite), silica gel packs, ant traps, toilet water, cosmetics/related products–>bath oils, body conditioners, calamine lotion, lipstick, deodorants, ingestion of packaging material or large quantities may cause obstruction of the GIT