2 biotoxins Flashcards

1
Q

what is the difference between a toxin and a toxicant?

A

-toxin=biologically produced
-toxicant=anthropogenically produced

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2
Q

what is the most potent toxin on the planet?

A

-botulinum toxin
-produced by clostridium botulinum
-LD50 of 0.5 ng/kg

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3
Q

what is are the classes of degrees of toxicity?

A
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4
Q

what are the differences between venom and poison?

A

poison
-ingestion
-dermal exposure
-inhalation

venom
-must be “injected”
-requires a venom apparatus and gland

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5
Q

what is the graph of toxic organisms?

A
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6
Q

what is the venn diagram of routes of exposure?

A
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7
Q

what happens when you get dermal exposure from poisonous plants?

A

poison ivy, oak, and sumac, gympie
-actually an allergic reaction
-caused by a compound called urushiol
-urushiol=hapten=hapten+protein=allergic response=dermatitis

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8
Q

is the stinging nettle a venomous plant?

A

yes, tiny hair-like protrusions “inject” poison within the skin
-formic acid (also found in bee/wasp venom)
-histamine
-acetylcholine
-serotonin

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9
Q

what are cyanogenic glycosides?

A

poisonous plants through oral exposure

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10
Q

how does cyanogenic glycoside turn into cyanide?

A
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11
Q

what is the graph of potency of oral consumption plants?

A
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12
Q

what is cyanide MOA?

A

-attacks cytochrome C halting oxidative phosphorylation (ATP synthesis)
-symptoms include weakness, nausea, seizure and even cardiac arrest and death

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13
Q

what is cyanide toxicity?

A

acute
-cardiac arrest and possible death
-bright cherry red blood (increased oxygen)

chronic (cassava)
-called konzo (tropical ataxic neuropathy)
-damage to spinal nerves leads to paralysis
-can also present as thyroid goiter caused by a build-up of the detoxification metabolite thiocyanate

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14
Q

what are the treatments of cyanide toxicity?

A

hydroxocobalamin (B12)
-capable of binding one CN molecule each (ex: cyanokit)

sodium nitrite
-converts hemoglobin to methemoglobin
-cyanide binds methemoglobin (called cyanomethemoglobin)

thiosulfate
-often administered with sodium nitrite to increase CN removal via urine
-sodium nitrite+thiosulfate = nithiodote

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15
Q

what are some toxins found in your garden?

A
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16
Q

what is foxglove (digiitalis purpurea)?

A

-common garden plant
-native to temperate europe
-biennial herb, up to 4 feet tall
-trumpet shaped flowers in many colours
-toxic compound=cardiac glycosides (CG)
-main CGs: digitoxin, gitotoxin, gitaloxin
-highly toxic
-all parts of the plant contain toxin

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17
Q

what are cardiac glycosides?

A

-organic compounds
-steroid attached to a sugar moiety and a lactone moiety

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18
Q

what is cardiac glycoside MOA?

A

-interfere with Na/K ATPase
-this decreases intracellular potassium and increases intracellular sodium leading to an increased in intracellular calcium
-this disrupts normal electrical conductivity in the myocardium leading to cardiac arrest

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19
Q

what is the clinical presentation of cardiac glycosides?

A

-symptoms within 5-24 hours of ingestion
-begins with GI symptoms: vomiting, diarrhea, etc
-followed by cardiac symptom: bradycardia, arrhythmia
-weakness, depression, tremors, convulsions, coma
-death from cardiac insufficiency

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20
Q

what is wolfsbane?

A

aconitum
-native to mountainous regions in europe and asia
-prefers damp, cool environments, often found in meadows and woodland areas
-flowers vary in color (blue, purple and white)
-palmate leaves, resembling a wolf’s foot
-contains alkaloid compounds = aconitine
-all parts of the plant are toxic, including roots, leaves and flowers
-ingestion or even skin contact can lead to severe symptoms and in come cases, prove fatal

21
Q

what is aconitine MOA?

A

binds and persistently activates voltage-gated sodium channels

symptoms
-begins in the GI tract, burning and numbness in the mouth and stomach
-followed by severe vomiting
-death by asphyxia caused by the poison’s effects on the heart
-could also be due to respiratory paralysis

22
Q

what are castor beans?

A

-seeds of the ricinus communis plant
-beans contain a toxin called ricin
-native to the southeastern mediterranean, eastern africa and india
-often growth ornamentally in NA in warmer months
-one of only two naturally occurring c=schedule 1 chemical warfare agents

23
Q

what does ricin do?

A

-estimated human LD50 (oral) is 1mg/kg
-acts by irreversibly inhibiting protein production

24
Q

what are the symptoms of ricin poisoning through inhalation?

A

-onset: within a few hours or up to a day
-respiratory distress, fever, cough, nausea, tight chest
-heavy sweating, pulmonary edema
-low blood pressure, respiratory failure, death

25
Q

what are the symptoms of ricin poisoning due to ingestion?

A

-onset: 10 hours
-vomiting and diarrhea (could be bloody)
-resulting in dehydration, low blood pressure
-seizures, and blood in urine
-death by organ failure (next few days)- liver, spleen and kidneys

26
Q

what is the most toxic plant in western canada?

A

western water hemlock (cicuta douglasii)
-perennial herb
-tall, purple streaked stems
-chambered root/tuber with resinous yellow liquid
-large terminal inflorescence with white fowers
-obligate aquatic plant
-common in marshy areas or along permanent streams
-toxic compound = cicutoxin
-found mostly in leaves and roots

27
Q

what is the cicutoxin MOA?

A

-GABA receptor antagonist
-8oz of mature plant could kill a horse/cow
-a single root can be fatal
-poisoning common in livestock as toxin is still active when dry
-human intoxication does occur
-mistaken for wild carrot or parsnip

28
Q

what are the clinical signs of wolfbanes?

A

-rapid onset, violent symptoms
-salivation, apprehension, muscle twitching, jaw clamping, teeth grinding
-spasms, jerking movements, running fits, seizures, coma
-death from respiratory paralysis within 45-90 min of ingestion

29
Q

what are the differences between primary and secondary photosensitization?

A
30
Q

what is st. john’s wort?

A

hypericum perforatum
-perennial, 1-3 feet tall
-bright yellow flowers, terminal clusters
-common along roadsides, pastures, rangeland, wasteland
-like dry gravelly, sandy soil
-toxic compound: hypericin
-found in pigment granules in leaves and flowers

31
Q

what is the hypericin mechanism of toxicity?

A

-direct acting photodynamic agent
-causes primary photosensitization
-hypericin+lightly pigmented skin+UVA exposure+molecular oxygen=photosensitivity reaction

32
Q

what are the clinical signs of hypericin?

A

-most common incidences of poisoning=livestock
-many species at risk, especially those with unpigmented skin
-erythema, edema, vesiculation, necrosis, skin shedding
-can present as tachycardia, tachypnea, pyrexia, salivation, diarrhea
-shedding of conjunctival and buccal mucosa, blindness, feed refusal, starvation
-shock, hypotension, convulsions and death in extreme cases

33
Q

what are the treatments of hypericin?

A

-terminate UV exposure
-treat lesions like burns
-antihistamines for swelling

34
Q

what are the plants containing pyrrolizidine alkaloids?

A

-very diverse group of plants, mostly perennial
-common genera: senecio, amsinickia, heliotropium, echium, trichodesma, and crotolaria
-throughout western canada, often contaminate grainfields, pastures, etc
-toxic compound= >100 different pyrrolizidine alkaloids but only a few have been proven to be toxic
-contained in the foliage and seeds

35
Q

what is pyrrolizidine alkaloid MOA?

A

-enters liver where it’s metabolized to toxic pyrrole derivatives
-pyrrole derivatives bind cellular macromolecules
-this can result in DNA adduct formation, impaired cell division, cell death, hepatic necrosis and eventual liver failure

36
Q

what is pyrrolizidine alkaloid toxicity?

A

-chronic toxicity more common than acute
-cattle and horses at higher risk
-contamination of feed (grains, hay), pasture grazing
-some degree of toxicity to humans as alkaloids can transfer to milk

37
Q

what are the clinical signs of pyrrolizidine alkaloid toxicity?

A

-sudden onset lover failure (after chronic exposure)
-horses: progressive weakness, sometimes jaundice, staggering, sleepiness, biting the ground/themselves/others, delirium and eventual coma and death within 1 week of symptoms
-cattle: mania, colic, diarrhea, tenesmus, rectal prolapse, hepatogenous photosensitization, eventual death

38
Q

what is hepatogenous photosensitization?

A

-secondary photosensitization=most frequent type observed in livestock
-phylloerythrin accumulates in plasma due to liver damage causing impaired hepatobiliary excretion
-phylloerythrin is derived from the breakdown of chlorophyll by microorganisms
-increased phylloerythrin in circulation then reaches the skin where it absorbs and releases light energy causing lesions/burns

39
Q

what are some toxic house plants?

A
40
Q

what is the mechanism of action of calcium oxalate crystals?

A

-mechanical irritation

41
Q

what is the toxicity of calcium oxalate crystals?

A

-incurred from ingesting/chewing on leaves
-usually mild

42
Q

what are the clinical signs of calcium oxalate crystals?

A

-salivation, head shaking, oral pain, swelling of oral mucosa
-difficulty breathing
-colic, vomiting, diarrhea +(dehydration)

43
Q

what are the treatments for calcium oxalate crystals?

A

-rinse mouth
-antihistamines
-symptomatic/supportive

44
Q

what are proteolytic enzymes?

A

-suggested that dieffenbachia toxicity could also be attributed to proteolytic enzymes
-discovered when leaf extracts treated with trypsin (protein cleaving enzyme) were not as toxic

45
Q

what is the bulgarian umbrella?

A

intentional poisonings
-victim: bulgarian dissident writer georgi markov
-date: sept 7, 1978
-location: london, waterloo bridge
-method: umbrella rigged to inject ricin-laced pellet
-outcome: markov fell ill and died a few days later
-suspected perpetrators: bulgarian secret police, assisted by the KGB
-context: cold war era espionage and assassination

46
Q

what happened in you season 3?

A

intentional poisonings
-Love Quinn and Joe Goldberg attempt to murder each other using wolfsbane
-Love coats a knife in the poison which Joe grabs to defend himself supposedly poisoning him
-he then uses a needle filled with the same poison to kill Love and saves himself using adrenaline (epinephrine)

47
Q

what are the medical uses of st. johnswort?

A

-historically use for kidney and lung problems, insomnia, depression and to aid wound healing
-still used today for mental disorders
-topical use is promoted for wounds, bruises and muscle pain
-being investigated for cancer diagnosis and treatment (hypericin accumulates in neoplastic tissue, can induce apoptosis)
-however, more research is required to fully validate some of these claims

48
Q

what is lanoxin (digoxin)?

A

-used to treat heart failure
-specifically atrial fibrillation

49
Q

what is digibind/digifab?

A

-digoxin antidote
-contains fab antibody fragments designed to bind digoxin
-has higher affinity for digoxin than the Na/K ATPase
-eliminated in urine