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Toxicology-soph-c > Mechanisms only > Flashcards

Mechanisms only Flashcards

1
Q

organophosphate pesticides (OPs)

A

irreversible inhibition of acetylcholinesterase (AChE) activity = anticholinesterase

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2
Q

ivermectin

A

GABA receptor agonist (depressive effects)

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3
Q

pyrethroid pesticides

A

binds voltage gated Na+ channel (excitation)

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4
Q

bromethalin

A

damages mitochondrial function (uncouples oxidative phosphorylation in CNS) -> loss of ion gradient ->fluid accumulation in myelin sheaths -> decreased nerve conduction and respiratory arrest
(CEREBRAL EDEMA)

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5
Q

alprazolam (xanax)

A

GABA receptor modulator that acts at the limbic, thalamic, and hypothalamic level of the CNS (depressive effects)

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6
Q

zolpidem (ambien)

A

inhibits neuronal excitation by binding to the benzodiazepine site of GABA receptors (depressive effects)

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7
Q

slaframine

A

muscarinic cholinergic agonist (ACh mimic) especially in exocrine glands
(SLOBBERS)

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8
Q

fumonism

A

inhibits sphingosine-N-acetyltransferase causing increased levels of sphinganine which is cytotoxic
(CORN)

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9
Q

strychnine

A

competitive antagonist at post synaptic spinal cord and medulla glycine receptors; glycine is an inhibitory neurotransmitter, therefore evokes an overstimulation (excitation)

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10
Q

salt

A

diffusion of sodium into CSF when plasma sodium levels are high leading to inhibition of glycolysis and ATP and attraction of water
(Na+ >160 mEq/L)

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11
Q

phenoxyacetic acid herbicides

A

mechanism unknown

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12
Q

ergot alkaloids

A

dopamine and serotonin receptor agonists

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13
Q

ionophores

A

increase intracellular Na+ and Ca++, leading to mitochondiral swelling and cell death, especially in muscle. remember it’s target is the mitochondiral MEMBRANE)
(heart problems)

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14
Q

tetanus

A

blocks release of GABA and glycine (both are inhibitory neurotransmitters) resulting in overstimulation of muscles resulting in stiffness

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15
Q

anticoagulants

A

inhibits vitamin K1 epoxide reductase, preventing formation of vitamin K dependent clotting factors

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16
Q

nitrates

A

nitrate->nitrite->vasodilation and ferrous iron + Hgb -> methemoglobin ->oxygen starvation of tissues

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17
Q

cardiac glycosides

A

inhibits Na+/K+ ATPase through competition with K+ for binding sites

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18
Q

cyanide

A

inhibition of cytochrome oxidase and oxidative phosphorylation

19
Q

methylxanthines

A

competitive antagonist of adenosine receptors (causes CNS stimulation, vasoconstriction, tachycardia); prevents Ca++ reuptake, leading to increased skeletal and cardiac muscle contractility

20
Q

gossypol

A

chelates iron and causes anemia, inhibits dehydrogenase leading to decreased energy and stress (can be cumulative as it is lipophilic)

21
Q

cantharidin

A

inhibits protein phosphatases (dysregulates protein metabolism); mucosal irritant
(muzzle in the water)

22
Q

ethylene glycol

A

major toxic agents of ethylene glycol are metabolites produced by the action of alcohol dehydrogenase; glycolic acid causes acidosis, glyoxilic acid thought to cause CNS signs, oxalate/oxalic acid causes renal damage and hypocalcemia

23
Q

cholecalciferol/vitamin D3

A

causes massive increases in serum Ca++ by increasing GI absorption, decreasing renal excretion, increasing synthesis of calcium binding protein, mobilizing bone calcium

24
Q

grape/raisin

A

unknown

25
Q

acetaminophen

A

formation of NAPQI causes liver tissue necrosis and increased methemoglobin, oxidative damage of erythrocytes in cats (methemoglobin and heinz body production)

26
Q

NSAIDS

A

uncoupled oxidative phosphorylation at high doses, blocks COX-1 and COX-2 decreasing prostaglandins

27
Q

arsenic

A

depends on the form

  • pentavalent (CNS signs): reduced and metabolized in rumen, reduces to metabolic energy and some is converted to trivalent form
  • trivalent (blood): binds to -SH groups -> disrupts cellular metabolism and inhibits oxidative phosphorylation
28
Q

zinc

A

free zinc is released in the stomach’s acidic environment forming zinc salts leading to corrosive effect to stomach and intestinal mucosa; oxidative damage

29
Q

phenols

A

denatures and precipitates cellular proteins thus destroying all contacted cells

30
Q

zearalenone

A

estrogen receptor agonist

think pig vulva

31
Q

bee venom

A

mellitin (latin for SWEET/HONEY) causes pain and histamine release, phospholipase A2 destroys membranes

32
Q

wasp/hornet venom

A

some contain neurotoxins, kinins induce pain

33
Q

ant venom

A

peperidine causes dermal necrosis and formic acid causes burnign sensation and pain

34
Q

holocyclotoxin (tick saliva)

A

impairs acetylcholine release at neuromuscular junction (results in weakness and paralysis)

35
Q

other mechanism associated with dermacentor toxin

A

acts on Na+ channels

36
Q

toad poisoning

A

secretions from the toad include biogenic amines (histamines) and Bufogenins (bufotalin)

37
Q

bufogenins (bufotalin)

A

inhibit Na+/K+ ATPase, produce cardiac arrhythmias

SIMILAR TO CARDIAC GLYCOSIDES AND TX SIMILARLY!

38
Q

alpha-Iatrotoxin (black widow)

A

creates pores in membranes allowing Ca++ entry and releasing massive amounts of neurotransmitter ->sustained muscle spasms

39
Q

sphingomyelinase D (brown recluse)

A

binds to cell membranes and cleaves heads off lipids

40
Q

eastern coral snake venom

A

bungarotoxin is a neurotoxin that prevents binding of Ach, causing paralysis

41
Q

enterotoxins from garbage/carrion toxicity

A

bind to intestinal epithelium, increasing permeability and causing fluid loss (diarrhea) and decreased absorption of nutrients

42
Q

endotoxins

A

LPS - gram negative cell walls

43
Q

botulinum

A

prevents release of ACh at neuromuscular junction causing paralysis

Toxicology-soph-c (4 decks)

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