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Toxicology > Lecture 3 > Flashcards

Lecture 3 Flashcards

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0
Q

DDT is a ____?

A

organochlorine

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1
Q

strychnine is a _____?

A

rodenticide that was isolated from a plant

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2
Q

what are general characteristics of organophosphates?

A

organophosphate = pesticide
degrades fast
used in flea collars, dips, fly, ant and roach bates

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3
Q

mechanism of action of organophosphates?

A

inhibits AchE causing cholinergic overstimulation

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4
Q

symptoms of anticholinesterase toxicity (organophosphates)

A
  1. muscarinic (SLUDGE-M) - from excessive stimulation of GABA receptors
  2. nicotinic receptors (responsible for shuttling ions back and forth across neurons and muscular junctions)
  3. CNS - seizures
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5
Q

species specific symptoms of organophosphates (AChE inhibition)

A

horses = colic and dehdyration
ruminants = rumen stasis
dogs & cats = convulsions
cats = chlorpyrifos more nicotinic signs

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6
Q

how do you diagnose organophosphate (AchE inhibition) toxicity?

A
  1. history and clinical signs
  2. atropine challenge (if there is response to atropine its not OP toxicity)
  3. decreased RBC AChE
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7
Q

treating organophosphate (AChE inhibition) toxicity

A
  1. GI decontamination
  2. atropine sulfate for muscarinic signs
  3. oximes (protopam, 2-PAM) to reactivate AChE - bumps OP off AChE
  4. diazepam
  5. time
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8
Q

organophosphate-induced delayed neurotoxicity (OPIDN)

A

OP compounds that produce significant inhibition of neuropathy target esterase (NTE) which cause delayed neuropathy

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9
Q

what are symptoms of organophosphate-induced delayed neurotoxicity?

A

axonal degradation of long motor neurons - signs are hindlimb weakness and paralysis

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10
Q

what is the tx for organophosphate-induced delayed neurotoxicity?

A

none

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11
Q

general characteristics of ivermectin

A
  • produced by soil fungus: streptomyces avermitils
  • crosses the BBB!!
  • collies, aussie shephards, shelties are super sensitive to ivermectin
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12
Q

what is fibrinil?

A

a GABA-A antagonist that works against roaches and is widely used

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13
Q

ivermectin: mechanism of action

A

GABA agonist

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14
Q

symptoms of ivermectin toxicity

A 
mydriasis
respiratory depression
ataxia
coma
blindness
bradycardia
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15
Q

how to dx ivermectin toxicity

A

history
brain ivermectin concentration (>1000ppb)
can measure GI content, liver, fat and feces

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16
Q

treatment of ivermectin toxicity

A

GI decontamination (activated charcoal and saline cathartics)
short acting barbituates for convulsions
supportive care
epinephrine, fluids for anaphylaxis

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17
Q

what are mycotoxins

A

fungal metabolites that cause pathological, physiological and/or biochemical alterations usually on several organ systems simultaneously

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18
Q

slaframine - how is it produced?

A

by “black patch” fungus on red clover

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19
Q

where does slaframine toxicity generally occur?

A

central, south-east and south-west US where its humid, rainy and cool weather triggers growth

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20
Q

what is the MoA of slaframine?

A

it is an ACh mimic - acts primarily as a muscarinic cholinergic agonist especially in exocrine glands

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21
Q

symptoms of slaframine?

A

seen mostly in horses and cattle
“slobbers” - excessive salivation (sometimes only sign)
bloat, diarrhea, frequent urination
feed refusal

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22
Q

dx and tx of slaframine

A

dx by consumption, differentiate from OPs or botulism

tx by removing source, maintaining hydration and electrolytes, atropine

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23
Q

fumonisin is a metabolite of what?

A

fungas fusarium found on corn

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24
what 3 isoforms does fumonisin form?
B1, B2, and B3 - B3 being most toxic
25
MoA of fumonisin
1. inhibits sphingosine-N-acteyltransferase causing increased levels of sphinganine which is cytotoxic. - sphingosines are lipids that are important in cell signaling and integrity 2. affects vascular endothelial cells leading to stroke, hepatic injury and pulmonary edema.
26
what animals are susceptible to fumonisin?
horses, ponies, donkeys, swine and rabbits
27
what two diseases are linked to fumonisin?
equine leucoencephalomalacia (ELEM) and porcie pulmonar edema
28
porcine pulmonary edema: clinical signs
inactivity, increased respiratory rate, decreased HR, pulmonary edema within 4-7 days, respiratory distress hepatic lesions consisting of apoptosis, necrosis and hepatocyte proliferation
29
porcine pulmonary edema: dx
1. analysis of feed 2. increase in serum and tissue sphingoid bases 3. increased ALT, ALP, GGT, total bilirubin, bile acids and cholesterol (indicating liver damage)
30
Equine Leukoencephalomalacia (ELEM): general characteristics
late fall/early winter main target is brain and liver
31
equine leukoencephalomalacia (ELEM): clinical signs
anorexia, ataxia, circling, drowsiness, blindness and hysteria hyperexcitability, mania, profuse sweating hepatoxicity - icterus, hepatic encephalopathy, coma and convulsions from hepatic encepahlopathy nearly 100% mortality rate
32
equine leukoencephalomalacia (ELEM): dx
1. analysis of feed 2. liver injury: increased liver enzymes such as ALP, ALT, sorbitol dehydroenase, GGT and total bilirubin and bile acids 3. post-mortem CNS necrosis and liquefaction
33
equine leukoencephalomalacia (ELEM) fumonisin toxicity: tx
no treatment available isolate from others change feed
34
tremorgenic mycotoxins where does it come from?
produced by fungi that belong to genera penicillum, aspergillus, claviceps and acremonoium
35
how ar eyou exposed to tremorgenic mycotoxins?
thru grass and spoiled food
36
what is the MoA of tremorgenic mycotoxins?
release of neurotransmitters from synaptosomes in the CNS
37
what are symptoms of tremorgenic mycotoxins?
jerky movements, stiff gait, ataxia can also see photosensitization, icterus (jaundice) and pulmonary edema
38
ammoniated feed toxicosis: general characteristics
non-protein nitrogen (NPN) sources - urea, ammonium salts - added to feed species affected are bovine, caprine, ovine leads to excitability called "bovine bonkers" - they get hyperexcited, run, stop and act normal, then start all over again
39
symptoms of ammoniated feed toxicosis
hyperexcitability - nervousness, rapdi blinking, dilated pupils, trembling, SLUD, etc. - animals will alternate btwn hyperexcited and normal if caused by imidazole - onset of clinical signs is rapid with death in 24 hours - death occurs from ammonia toxicity when blood ammonia reaches > 2mg/dl
40
dx of ammoniated feed toxicosis
- history - clinical signs - increased ammonia, glucose, BUN, decreased blood pH
41
**what is normal blood ammonia concentration**
< 0.5mg/dl
42
tx for imidazole toxicosis and non-protein nitrogen toxicosis (ammoniated feed toxicosis)
just feed removal can try pumping 5 - 10 gallons of cold water and vinegar into stomach to acidify rumen and the tempertaure will reduce urease activity
43
strychnine: general characteristics
very toxic restricted compound large numbers of intentional poisonings use strchnine alkaloid used to controlpocket gophers birds are more tolerant with a higher LD50
44
where does strychnine come from?
seeds of strychnos-nux vomica (indian tree)
45
strychnine: MoA
- competitive antagonist at postsynaptic spinal cord and medulla glycine receptors causing disinhibition of all muscles (= stimulation of muscles) your muscles go into tetanus
46
strychnine symptoms
rapid onset - begins with anxiety, stiff neck and gait, "grinning" - violent tetanic seizurs - sawhorse stance, rigid extension of all 4 limbs - death from respiratory failure, exhaustion
47
dx of strychnine
clinical signs - lack of tonic convulsions - elevated GOT, CPK, LDH in serum - lactic acidosis, hyperkalemia, leukocytosis
48
tx of strychnine
- primary goal is to control seizures and prevent asphyxiation - administer pentobarbitol or methocarbamol - emesis - ion trapping with ammonium chloride
49
salt: general characteristics
water deprivation (dehydration) most common or consumption of large amounts of salt - most common in pigs and cattle
50
salt: MoA
Na crosses the BBB and prevents brain from utilizing energy which prevents Na from being pumped out of hte brain. so Na gets trapped creating an ion disequilibrium. water flows into the brain causing massive swelling leading to neuro impairments.
51
salt: symptoms
CNS - salivation, increased thirst, abdominal pain and diarrhea progresses to circling, wobbling, head pressing, blindness, seizures
52
salt: dx
Na levels > 160mEq/L brain Na concentrations above 2000ppm is diagnositc have to differentiate from polio, lead, pesticides, encephalitis
53
salt: tx
SLOWLY rehydrate IV hyperosmotic fluids low in Na - loop diuretic - furosemide - can be administered to prevent pulmonary edema during fluid therapy
54
furosemide
loop diuretic that blocks the Na/K channels in the loop of Henle which prevents reabsorption of Na helping to decrease Na levels. treatment for salt toxicity
55
MoA of alprazolam (xanax)
benzodiazepine - GABA-a receptor agonist
56
MoA of alprazolam
acts at the limbic, thalamic, hypothalamic levels of the CNS as a GABA-a agonist
57
symptoms of alprazolam (xanax) toxicity
ataxia, depression, vomiting, tremors, tachycardia, diarrhea and ptyalism CNS excitation
58
dx of alprazolam (xanax) toxicity
suspected ingestion and clinical signs
59
tx of alprazolam (xanax)
- emesis with apomorphine - gastric lavage with activted charcoal - a specific benzodiazepine antagonist - flumazenil - used for severe CNS depression associated with toxicosis
60
flumazenil
benzodiazepine GABA-a receptor ANTAGONIST | - its the only GABA-a receptor antagonist you can get on the market
61
zolpidem (ambien): general characteristics
sleep aids that act similar to diazepines
62
zolpidem (ambien): MoA
inhibits neuronal excitation by binding to the benzodiazepine omega-1 receptor rapid absorption; highly available
63
zolpidem (ambien): symptoms
ataxia, vomiting, lethargy, disorientation, hypersalivation, hyperactivity and panting
64
zolpidem (ambien): dx
based on suspected ingestion and clinical signs
65
zolpidem (ambien): tx
generally symptomatic

Toxicology (3 decks)

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