• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/73

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

73 Cards in this Set

  • Front
  • Back

Any substance that when introduced into a living organism destroys life or injures health.

POISON

Injury do to high dose or high sensitivity

TOXICITY

LD50

LETHAL DOSE (50)


- Dose which, when given, kills half of the animals it's given to.

ED50

EFFECTIVE DOSE (50)


- Dose which, when given, effects half of the animals it's given to.

LD50/ED50 =

THERAPEUTIC INDEX (TI)


- High therapeutic index = safer


e.g. TI = 200 = 200(LD)/1(ED)



- Lower TIs are more dangerous/risky to give and must be very careful when dosing!

What are the five basic routes of intoxication? Give examples of common toxins that enter via that route.

1. Ingestion


--> food, water source


2. Cutaneous


--> insecticides, topicals like ectoparasiticides & other lipophilic substances (corticosteroids)


3. Inhalation


4. Injection


5. Ocular

Describe the typical protocol for treating an animal suspected to be poisoned.

1. Stabilize vital signs!


- HR, RR, temps


2. Gather info from owner (but take with grain of salt)


3. Continued absorption of poison is prevented


- e.g. washing out mouth, gastric evacuation/lavage, & adsorbents


4. Elimination of the absorbed poison is attempted


5. Antidote given if available


6. Symptomatic & supportive care is given

VPIS

Veterinary Poisons Information Service


- Provided by Medical Toxicology and Info Services


- Subscription service provided privately to clinics

Aims of VPIS (Veterinary Poisons Information Service)?

1. Give info/advice by telephone on management of acute poisoning


2. Provide risk assessment for such cases


- Toxic doses, effects, breed specifics


3. Lab services


4. Referral to 'expert' contacts


5. Identifying tablets/capsules/foreign drugs


6. Antidote/antivenom supply


7. Access to ToxBox

What is ToxBox?

VPIS in collaboration with VetsNow and consists of:


- Activated Charcoal (slurry)


- Apomorphine (emetic)


- European viper venom antiserum


- Fresh frozen plasma


- Acetylcystine


- Vitamin K1 (treatment of rodent/warfarin poisoning)

What are the top 10 most common enquiries to VPIS? (list in order of most common to less common)

1. Anticoagulant rodenticides


2. NSAIDs


3. Chocolate


4. Paracetamol


5. Permethrin


6. Metaldehyde


7. Lilie (cats particularly susceptible to)


8. Grapes


9. Benzalkonium chloride (floor cleaners)


10. Adder (snake) bites

What are the main areas of the body that can be targeted for triggering emesis in an animal?

1. MEDULLA


- Vomiting center


2. MEDULLARY CHEMORECEPTOR TRIGGER ZONE


- Located in the fourth ventricle


3. Vestibular apparatus


4. Stomach


- Vagal & sympathetic afferents from GI tract stimulate trigger zone


5. Small Intestine


- Serotonin is released in GIT


6. Cerebral cortex

In order for gastric evacuation to be semi-successive, it must be done within _____ hours of ingestion of toxin.

< 2 hours or less depending on the toxin


- Rate of absorption varies depending on what was ingested

Gastric evacuation drugs? At home quick tricks?

1. 3% Hydrogen peroxide


- Evacuates 30-40% of gut contents, so still a good portion remains.


2. Syrup of ipecac


- Gut irritant and triggers the MCTZ


- Overdose is a risk, so don't dose again if it doesn't work the first time.


3. XYLAZINE (dogs & cats)


- MCTZ effects


4. APOMORPHINE (dogs only)


- Dopamine agonist and effects MCTZ



At home quick tricks:


- Mustard or salt placed on back of tongue triggers the gag reflex!

CONTRAINDICATIONS FOR GASTRIC EVACUATION?

1. Seizures - risk of aspiration


2. Depression/coma


3. Loss of gag reflex


4. Hypoxia


5. Species that can't vomit naturally (rodents, rabbits, birds and HORSES)


6. Ingestion of corrosives which would irritate the alimentary tract on the way back up


7. Recent abdominal surgery/hernia

Describe the protocol of gastric lavaging.

1. Provide light anesthesia & cuffed endotracheal tube


2. Tepid water or normal saline is used to flush out the stomach


3. Gravity used for flow to aspirate


4. Repeat until clear


* Keep first lavage in cases where you're not sure of the toxin.

Adsorbents? Examples?

A material, such as activated charcoal, on which absorption can occur.


- Always given orally!


- No chemical reactions occurring; just absorbing toxic contents which are then excreted in feces with adsorbent.


- E.g. Activated charcoal, Fullers earth (banned in UK)

Describe how activated charcoal is made and it's function.

ADSORBENT


Activated Charcoal is treated with oxygen to make it very porous, with many holes and cracks, which allow for better absorption of toxins.


- No chemical reactions occurring, just absorbing the toxins and then being excreted in the feces.


* Not good for heavy metal or hydrocarbon poisonings!

Catharctics?

Substance that accelerates defecation


Examples:


- Sodium (Glaubers salts)


- Magnesium sulphate (Epsom salts)


- Sorbitol = often combined with activated charcoal because charcoal tends to cause slight constipation and this helps keep things moving

What methods are possible for enhancing elimination of toxins via urinary tract?

1. Acidifying compartments with ammonium chloride


2. Alkalinization with sodium bicarbonate


* Must monitor patient closely for acid/base balance!

Function of chelating agents?

STRONGLY bind toxic METAL IONS such as lead & mercury.


- Bound ions are chemically inert, preventing poisoning


(unlike with adsorbents which only physically absorb toxins)

Most common chelating agent used in vet med?

EDTA - Ethylenediaminetetraacetic acid

What is the toxic component of chocolate?

THEOBROMINE (a methylxanthine)

Clinical signs of chocolate (theobromine) toxicity? Treatment?

CLINICAL SIGNS:


- Vomiting, excitability, ataxia, and tachycardia


* All common symptoms in most toxicity cases, so getting a good history from owner is crucial!



TREATMENT:


- Decontamination


- Symptomatic treatment

List six poisons that have specific antidotes:

1. Ethylene glycol


2. Organophosphates


3. Arsenic (mercury)


4. Opiates


5. Paracetamol


6. Warfarin (anticoagulant rodenticides)

Main component of antifreeze mixtures.


- Attractive taste & common in cats/dogs with high mortality rate


- Cats much more susceptible than dogs


What type of poisoning is this?

ETHYLENE GLYCOL

Mechanism of poisoning via ethylene glycol?

METABOLITES ARE TOXIC (not ethylene glycol itself)


Ethylene glycol -> converted by Alcohol Dehydrogenase to -> Metabolites


Metabolites include:


- Glycoaldehyde


- Glycolic acid


- Oxalic acid, which form crystals that eventually block up the kidneys = death

Ethylene Glycol poisoning early clinical signs? Delayed signs? Treatment?

EARLY CLINICAL SIGNS (1-2 hours):


- Weakness, vomiting, incoordination



DELAYED SIGNS (24-96 hours):


- Thirst, anuria (non-passage of urine), hematuria (blood in urine), convulsions, . . . death



TREATMENTS:


1. Ethanol is an alternative substrate to alcohol DH and has a higher affinity for it that ethylene glycol = metabolites of ethylene glycol not produced!


2. 4-methylpyrazole (4MP; Fomepizole) - also binds to alcohol DH; very safe & can be given before confirmation of ethylene glycol poisoning, but problem is it's expensive..

Sources of organophosphate poisoning?

- Ectoparasitic dips, collars, & powders


- Insecticides

Toxicity of organophosphates results in ______________________________________.

INHIBITION OF ACETYLCHOLINESTERASE


- Results in build up of Ach in synaptic cleft = overstimulation and saturation of parasympathetic and neuromuscular activity, mainly affecting the muscarinic receptors


- Symptoms: "DUMBLES"


Diarrhea, Urination, Mitosis, Bronchi constriction, Lacrimation, Emesis, Salivation

Clinical signs of organophosphate poisoning?

"DUMBLES"


Diarrhea, Urination, Mitosis, Bronchi constriction, Lacrimation, Emesis, Salivation

Treatment of organophosphate poisoning?

Atropine = muscarinic receptor AGONIST



Oximes IV = reactivates the enzyme acetylcholinesterase!

Common sources of arsenic (or mercury) poisoning? Common occurrences in animals?

SOURCES:


- Inorganic arsenic from weed-killers, insecticides, seed dressing and wood preservatives


- Organic arsenic from growth promoters


OCCURRENCES:


- Ant baits attractive to cats


- Over usage of feed additives


- Cats particularly vulnerable!

Mechanism of arsenic (or mercury) poisoning?

GENERAL TISSUE POISONING


- Acts on rapidly dividing cells, particularly in the intestines, but also in liver and kidneys


- Results in inactivation of sulphydryl groups on enzymes


- Uncouple oxidative phosphorylation

Clinical effects of acute arsenic (or mercury) toxicity? Chronic toxicity?

ACUTE TOXICITY (most common in animals)


- Severe gastroenteritis, vomiting, diarrhea... shock


- Massive ulceration and shedding of mucosa = bloody feces and vomit



CHRONIC TOXICITY (organic arsenicals) = nervous signs


- Rare in animals as they typically are exposed to a single, large amount.


- Degeneration of peripheral nerves


- Ataxia, in-coordination, blindness

Treatment of arsenic (or mercury) poisoning?

GASTROINTESTINAL DECONTAMINATION


Both heavy metals so chelating agents used:


- Sodium thiosulphate = orally or IV


- Dimercaprol = IM


- Broad spectrum antimicrobials as well for animals who've suffered extreme gastroenteritis.

Why are cats especially susceptible to paracetamol poisoning?

- Deficient in glucuronyl transferase, which is required for glucuronide (metabolic byproduct of paracetamol) conjugation

Mechanism of toxicity of paracetomol in animals?

"Toxic intermediary" Byproduct of paracetamol oxidizes Hb to metHb!

Clinical signs of paracetamol poisoning?

1. Facial/pulmonary edema


2. Cyanosis, due to metHb


3. Liver damage


4. Hemolysis


5. Jaundice

Treatment of paracetamol poisoning?

DECONTAMINATION AND SUPPORTIVE CARE


- N-acetylcysteine makes more glutathione, which binds and gets rid of the toxic intermediary byproduct


- Sodium sulphate


- Vit C converts metHb to oxyHb

PARACETAMOL POISONING:


- If caught within _______ hours, there's a good chance of healthy recovery.


- Between _______ hours, recovery likely, but will probably suffer from hepatic damage.


- _______ hours later, prognosis not good.

< 8 hours = good recovery


8-24 hours = recover with some hepatic damage


> 24 hours = poor prognosis

Sources of anticoagulant rodenticides?

1st generation: Warfarin


2nd generation: Difenacoum, bromadiolone (highly toxic)

Mechanism of toxicity with anticoagulant rodenticides?

- Vitamin K antagonists


- Interferes with production of clotting factors (I, II, VII, IX, X)

Clinical signs of anticoagulant rodenticides?

- Depression and anorexia


- Vascular collapse (in acute, very high doses)


- Hemorrhage, internal/external (repeated intake) = weakness

Diagnosis of anticoagulant rodenticide poisoning?

1. Prolonged clotting time


2. Urine analysis


3. PM :(


* Latent period makes rat poisoning difficult to diagnose, so get good history from owner.

Treatment of rat poisoning?

VITAMIN K1 (not K3)!

Very common poisonous plant that's widely distributed in permanent pasture.


- All parts of the plants are poisonous


- Remains poisonous even when dried & stored


- Seeds are parachute type and spread easily.

COMMON RAGWORT


- Basal rosette of leaves = most toxic


- Yellow daisy like flowers = May-Oct

A farmer may be prosecuted if ragwort is present on his/her pasture.



True or False?

TRUE - It's illegal to have on your land.

Toxic components of Common Ragwort?

PYRROLIZIDINE ALKOLOIDS = HEPATOTOXIC


* Cattle, horses, pigs and chickens are particularly susceptible (especially young)


* Sheep, goats & deer are more tolerant.

Symptoms of Ragwort poisoning in cattle? Horses?

CATTLE: Poor appetite, either constipation or diarrhea, jaundice, & head pressing



HORSES: Lethargy and yawning (Sleepy Staggers), blindness, walking in circles or long, straight lines



* More often effects are cumulative and chronic exposure is more likely (causes major liver problems)


* Death after acute ingestion may be in a few days.

There are NO antidotes to common ragwort poisoning.



True or False?

TRUE - so important to remove ragwort from pastures and prevent reinfestations.

Leaves and the rhizomes are toxic even when dried.


- Young plant is most toxic


- Mostly cattle affected, but sheep, pigs and horses can be as well.


- Present year round

BRACKEN

Main toxic components of bracken?

1. Thiaminase


2. Carcinogens


3. Cyanogenic glycosides

Bracken toxicity causes:

1. Bone marrow depletion in ruminants


2. Thiamine deficiency (monogastrates - cattle make their own)


3. Tumors in bladder and GI tract

Acute signs of bracken poisoning? Chronic signs?

ACUTE:
- Hemorrhagic syndrome (esp cattle)


- Depression weakness


- Anorexia


- Death (4-10d)


CHRONIC:


- Enzootic hematurea = blood in urine (cattle)


- Bright blindness (cattle & sheep)


- GIT Tumors in conjunction with BPV4


- Thiamine deficiency (monogastrates)

Clinical features of bracken poisoning in horse? Pigs? Cattle?

HORSE = Bracken staggers


PIGS = Appears like heart failure


CATTLE = Weakness, weight loss, bleeding ,blood in feces & breathing difficulties

Treatment of bracken poisoning?

- Supportive & possible blood transfusion (expensive cattle & sheep)


- Thiamine supplement for pigs and horses

- Seasonal (Spring or Autumn)


- Clitocybe species identified to cause problems in dogs.


- DUMBLES Symptoms


- Treated with atropine

MYCOTOXINS

Evergreen tree with red fruits in Autumn


- All parts poisonous except fleshy, red aril


- Taxines are the toxins, which inhibit Na+ & Ca2+ currents


- Contain irritant oils which are rapidly absorbed


- 60% of poisonings in dogs!

YEW POISONING

Yew poisoning accounts for ____% of plant poisoning in dogs.

60%

Symptoms of Yew poisoning in dogs?

Vomitting, diarrhea, salivation, hypothermia, bradycardia, respiratory depression, convulsion, heart & respiratory failure

Yew poisoning can result in sudden death.



True or False?

TRUE - after death PM findings include an empty right heart and the left heart, liver, spleen and lungs filled with dark tarry blood

Horses, sheep, cattle and goats are susceptible to yew poisoning along with dogs.



True or False?

TRUE

Which species are commonly poisoned by Oak? Which parts are toxic? Poisonous compounds? Results in? Symptoms?

Cattle, horses, sheep & goats (not pigs)


- Leaves & acorns are toxic


- Tannins = poisonous compounds


- Results in = kidney damage & gastroenteritis


SYMPTOMS:


- Lack of appetite, depression, constipation followed by diarrhea (with blood in feces), blood in urine, colic

Poisonous compounds in oak? Antidote?

TANNINS = No antidote

Onion and garlic poisoning occurs in . . .

DOGS & CATS



* Often due to raw, cooked or powdered products being given in leftovers.

What types of toxins are found in onions and garlics?

Oxidant Toxins - contain thiosulphate

Symptoms of onion and garlic poisoning in dogs and cats?

-Weakness


-Vomiting


-Diarrhea


-Breathlessness


-Blood in urine


* Eventually results in hemolytic anemia


* Lag time in symptoms = ~2 days

Grapes, raisins, sultanas, and currants are all toxic to dogs.



True or False?

TRUE

Symptoms of grape poisining?

Vomiting and diarrhea


* Can result in renal failure and casts in urine

Lilies are toxic to __________.

CATS

Toxic component to Lilies?

Calcium oxalate and oxalic acid crystals

Symptoms of lily poisoning?

- Irritated mucous membranes


- May cause histamine release


- Hypersalivation


- Vomiting


- Diarrhea


- Anorexia


* Seen within 3-6 hours! Quick intervention is key!