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Pharmacology > Toxicology > Flashcards

Toxicology Flashcards

1
Q

Toxicological terms

A

poison: any substance which when introduced into a living organism destroys life or injures health
toxicity: may be due to high dose or high sensitivity

Lethal dose and effective dose

Therapeutic index (TI) is the ratio between Ld50 and Ed50

v. high value=relatively safe

low value=narrow therapeutic range

LD50: dose at which 50% of animals are killed

ED50: dose at which 50% of animals get alleviation from whatever you’re trying to fix.

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2
Q

Five basic routes of intoxication

A

ingestion: food, water source; vomitus, urine, feces
cutaneous: insecticides, topical applications like ectoparasiticides; blood
inhalation: aerosols
injection: blood

ocular

often seen non-specific signs with intoxication

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3
Q

How is a poisoned animal treated?

A

1st: breathing, HR, temp stabilized

information is gathered from owner

continued absorption of poison is prevented

elimination of absorbed poison is attempted

an antidote may be given

symptomatic and supportive care

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4
Q

Prevention of continued absorption of poison

A

wash- cutaneous i.e. bird covered in oil

gastric evacuation

gastric lavage

adsorbent and chelating agents

elimination

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5
Q

Stimulation of gastric evacuation

A

fourth ventricle: chemotrigger zone

vestibular apparatus

medulla: vomiting centre
stomach: vagal and sympathetic afferents from GI tract stimulate trigger zone

small intestine: serotonin is released from enterochromaffin cells in GI tract

3% hydrogen peroxide

syrup of ipecac- toxic alkaloid that causes GI irriation- only give once

Xylazine: alpha 2 agonist- works on MCTZ

Apomorphine (Dopamine agonist: MCTZ)- opioid, but actions via dopamine receptor (agonist). very useful in dogs, can give in eye, gingival mucosa.

Vomiting gets rid of 40-60% of gastric content- not much use after 6 hours. can put salt or mustard at back of tongue.

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6
Q

Contraindications of gastric evacuation

A

seizures

depression/coma

loss of gag reflex

hypoxia

species unable to vomit

ingestion of corrosives/volatile petroleum products

recent abdominal surgery/hernia

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7
Q

Gastric lavage

A

light anaesthesia/cuffed ET tube

tepid tap water/normal saline (5-10ml/kg)

Gravity flow to aspirate

repeat until clear. Useful to keep 1st lavage for analysis

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8
Q

Adsorbents

A

all adsorbents taken orally (cf. chelating agents)

activated charcoal most commonly used- exposed to O2, makes lots of pores and fissures

fuller’s earth

Fecal elimination

no chemical reaction between toxin and adsorbent

good for large non-polar molecules, bad for hydrocarbons, heavy metals or ethanol

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9
Q

Cathartics

A

ways of getting things out of system fast

sodium (glauber’s salts) or magnesium sulphate (epsom salts)- speed transit through gut

sorbitol (often used in activated charcoal which tends to constipate)- or lactulose–helps move things through gut.

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10
Q

Enhancing elimination via urinary tract

A

Acidify: ammonium chloride

Alkalinization: sodium bicarbonate

Close patient monitoring- acid/base balance

Symptomatic, supportive care and monitoring is often sufficient

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11
Q

Chelating agents

A

useful for diagnosis of heavy metal poisoning- usualy eliminated through urine–> can take urine sample to check for heavy metal

Chemical reaction: agent binds metal ions

bound ions are chemically inert and thus prevent poisoning

examples: EDTA, desferrioxamine (particularly good for iron).

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12
Q

Chocolate

A

theobromine (a methylxanthine) in chocolate products

toxicity: white choc 2.2kg/kg
milk: 9g/kg

dark 1.25g/kg

Clinical signs: vomiting, excitability, ataxia, tachycardia

Treatment: decontamination (adsorbent) and symptomatic

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13
Q

Ethylene glycol

A

source: main component of antifreeze

attractive taste; commonly seen in cats and dogs; high mortality

has specific antidote

Toxicity: cats 1.5ml/kg, dogs 6.6ml/kg

Mechanism: metabolites are toxic (glycoaldehyde, glycolic acid and oxalic acid). Calcium+oxalic acid–>crystals in kidney–>renale failure.

Alcohol dehydrogenase=enzyme that metabolises. Can lead to metabolic acidosis– need to counteract metabolic acidosis.

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14
Q

Clinical signs and treatment for ethylene glycol

A

Signs: early (1-2 hours): weakness, vomiting, incoordination

Delayed signs (24-96 hours): thirst, anuria, hematuria, convulsions, death d/t renal failure

Treatment: ethanol is an alternative substrate for enzyme alcohol dehydrogenase. Ethanol has 100x more affinity for enzyme than ethylene glycol

20% ethanol with 5% sodium bicarb (to counteract metabolic acidosis)

can also use 4-methylpyrazole but it’s not super available and it’s expensive.

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15
Q

Organophosphates

A

source: ectoparasitic dips, collars, powders; insecticides

Toxicity: inhibit acetylcholinesterase–> stop ACh from being broken down. acts at muscarinic and nicotinic

Clinical signs: parasympathetic and neuromuscular activity

Treatment: atropine- blocks muscarinic receptors

oximes: regenerates acetylcholinesterase.

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16
Q

Arsenic/mercury

A

sources: inorganic arsenic: weed killers, insecticide, seed dressing, wood preservatives, mineral ores
organic: growth promoter

both arsenic and mercury are heavy metals

Occurence: ant baits attractive to cats; over usage of feed additives (arsenic growth promoters banned in EU)

Toxicity: 1-25mg/kg

Mechanism: general tissue poison

  • inactivation of sulphydryl groups on enzymes
  • uncouple oxidative phosphorylation

cause problems in intestinal epithelium and in kidneys, liver and skin

antidote= chelating agents

17
Q

Arsenic/mecury poisoning signs

A

Acute toxicity: GIT most susceptible- severe gastroenteritis, vomiting, diarrhea, shock; massive ulceration and shedding of mucosa

Chronic toxicity: nervous signs; degeneration of peripheral nerves; ataxia, incoordination, blindness

18
Q

Treatment of arsenic/mercury poisoning

A

GI decontamination

Chelating agents: sodium thiosulphate 15-30g in 100-200ml water IV or 30-60g orally every 6 hours

Dimercaprol: 3mg/kg IM every 3-4 hours.

19
Q

Illicit drugs

A

sources: cocaine, amphetamines, narcotics

Toxicity: generally rapid CNS effects

clincial signs depend on agent

tx: decontamination, largely symptomatic, specific antagonists (i.e. naloxone for opiates).

20
Q

Paracetamol

A

cats especially susceptible, deficient in glucuronyl transferase which is required for glucuronide conjugation

Toxicity: 50-100mg/kg in cats

N-acetyl p-benzoquinone (intermediary) oxidises Hb to metHB (affects O2 carriage).

cP450- metabolises paracetamol to NAPB–> lethal to animal

Can be metabolized to mercapteric acid–> glutathione helps excrete this but there’s only a certain amount in the body.

21
Q

Clinical signs and treatment for paracetamol toxicity

A

Clinical signs: facial/pulmonary oedemia, cyanosis; liver damage (hemolysis, jaundice)

Treatment:

decontamination; supportive

N-acetylcysteine (glutathione precursor)

Sodium sulphate: helps alleviate symptoms

Vitamin C and methylene blue: help hemoglobin issues

22
Q

Anticoagulant rodenticides

A

1st gen: warfarin; 2nd gen: difenacoum, bromadiolone (highly toxic, single feeding causes problems)

toxicity depends on agent

mechanism: vitamin K antagonist (reversible)

intereferes with production of clotting factors I, II, VII, IX, and X

23
Q

Clinical signs and treatment for anticoagulant rodenticides

A

Clinical signs: depression and anorexia even before bleeding

Acute ingestion of very high doses: vascular collapse

Repeated intake: hemorrhage- internal/external (and symptoms of this e.g. weakness)

Diagnosis: prolonged clotting time, urine analysis; hemorrhage at PM

Treatment: vitamin K1 0.25-2.5 mg/kg subcut for warfarin, or 2.5-5mg/kg in case of long acting formulations

Menadione (vitamin K2) not effective.

24
Q

Poisonous plants

A

occur in fields, hedgerows, hillsides, woods, gardens and in house

herbivores graze, browse, touch or are fed with them in hay or straw or other fodder

Carnivores will eat plants in house or in garden or on walks or get fed poisonous plants.

25
Q

Common ragwort (senecio jacobea)

A

very common, widely distributed in permanent pasture

basal rossette of leaves (year 1 most toxic)

yellow daisy like flowers (may-october)

all parts of plant, including root, are poisonous.

seeds are prachute types and spread easily

herbicides cause wilting–>concentrates toxin.

remains poisonous even when dried and stored.

26
Q

Common ragwort- mechanism of action and symptoms

A

Toxic components are pyrrolizidine aklaloids

Cattle and horses are particularly susceptible, especially young animals. Outdoor pigs and chickens are also very sensitive. Sheep, goats and deer are more tolerant.

Hepatotoxic

Symptoms:

cattle: poor appetite, either constipation or diarrhea, juandice, head pressing
horses: lethargy and yawning (sleepy staggers), blindness, animals may walk in circles or in straight lines for long distances

Death after acute ingestion may be in a few days. Effects are cumulative and chronic exposure is more likely.

NB: no antidotes for ragwort posisoning. No specific treatments.

27
Q

Bracken (pteridium aquilinum)

A

wide upland distribution

leaves and rhizomes are toxic, even when dried

young plant is most toxic

mostly affects cattle but sheep, pigs and horses can also be affected.

Main toxic components: thiaminase, carcinogens, cyanogenic glycosides

Causes: bone marrow depletion in ruminants, thiamine deficiency in monogastrates; tumours in bladder and GI tract.

28
Q

Symptoms of bracken poisoning

A

Acute: hemorrhagic syndrom esp cattle- carcinogens affect platelets; depression weakness, anorexia, death (4-10 days)

Chronic: enzootic hematuria (cattle)- bladder hemorrhage

Bright blindness- retina degeneration, hyper reflectivity of tapetum (cattle and sheep)

GIT tumors in conjunction with BPV-4

Thiamine deficiency (horses and pigs)- counteract by giving vitamin B

Clinical features: horses- bracken staggers; pig-appears like heart failure; cattle: weakness, weight loss, bleeding, blood in feces, breathing difficulties

Treatment: supportive and possible blood transfusion (cattle and sheep); thiamine supplement for pigs and horses.

29
Q

Yew (taxus baccata)

A

evergreen tree with red fruits in autumn

all parts of tree are poisonous except fleshy aril; also when dried

taxines=toxins; inhibit Na and Ca currents

also contain irritant oils which are rapidly absorbed

60% of reported poisonings are in dogs

symptoms in dogs start 2 hours after ingestion: vomiting, diarrhea, and salivation, hypothermia, bradycardia, resp. depression, convulsions, heart and resp. failure

30
Q

Yew susceptibilities and treatment

A

horses, sheep, cattle and goats are also susceptible in addition to dogs

poisoning can result in sudden death, reasons may be uncertain

on PM: findings may include empty right heart, and left heart, spleen, liver and luns filled with dark tarry blood

no antidotes

31
Q

Oak (Quercus robur)

A

poisoning in cattle, sheep, horses and goats

leaves and acorns are toxic

usually seasonal

tannins=poisonous compounds

cause kidney damage and gastroenteritis

symptoms: lack of appetite, depression, constipation, follower by diarrhea with blood in feces, blood in urine, colic

not seen in pigs

no antidote

32
Q

Onion and garlic poisoning in dogs and cats

A

oxidant toxins. contain thiosulphates. cats and dogs don’t have enzymes to digest these.

symptoms: weakness, vomiting, diarrhea, breathlessness, blood in urine

eventually hemolytic anemia

lag time to symptoms ~2 days

33
Q

Grapes, raisins, sultanas, currants

A

Mostly in dogs, but some in cats and ferrets

Mode of action is unclear: tannins? mycotoxins? pesticides?

Large invidual variation

causes vomiting and diarrhea

acute renal failure, casts in urine

34
Q

Lillies

A

different species, toxic to cats

contain calcium oxalate and oxalic acid crystals

irritate mucous membranes, may cause histamine release

hypersalivation, vomiting, diarrhea, anorexia, irritation of buccal membranes–> non specific signs lead to renal failure

seen within 3-6 hours of ingestion.

try to rinse calcium crystals out of mouth with water or milk.

Pharmacology (12 decks)

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