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401 - Toxicology, Drug Abuse, Pharmacology > 37/38: Intentional Poisonings > Flashcards

37/38: Intentional Poisonings Flashcards

1
Q

nerve agents are designed to be

A

undetectable

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2
Q

nerve agents are very potent _____ that inhibit _______

A

organophosphates
cholinesterase

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3
Q

nerve agent properties

A

colorless, odorless, tasteless, clear

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4
Q

which nerve agents are volatile

A

GA, GB, GD

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5
Q

which nerve agents are oily liquids

A

VX

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6
Q

what is the LD50 for aerosol doses of GA and GB

A

10-400mg-min/m3

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7
Q

what is the dermal dose LD50 for VX and sarin (GB)

A

10-1700mg

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8
Q

GA is

A

tabun

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9
Q

GB is

A

sarin

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10
Q

GD is

A

soman

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11
Q

nerve agents are part of the _____ toxidrome

A

cholinergic

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12
Q

onset of nerve agents (vapors and liquids)

A

Vapors = seconds to minutes
Liquids = slightly delayed due to absorption

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13
Q

AEs of nerve agent vapors

A

most common eye issues (miosis, pain, dim vision, loss of acuity), HA, nausea, cough

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14
Q

AEs of dermal exposure from nerve agent

A

sweating, fasciculations, vomiting, diarrhea, weakness, seizures, loss of consciousness

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15
Q

LT effects of nerve agents are mostly

A

psychological sequelae

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16
Q

the lethality of nerve agents comes from

A

asphyxiation or cardiac arrest

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17
Q

T or F: secondary exposure is a major issue for nerve agents

A

T- can evaporate from pt’s clothing and permeate HCP’s clothing

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18
Q

5 tx for nerve agent toxicity

A

atropine
2-PAM
decontamination
antiepileptics
pyridostigmine

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19
Q

what is always the first step to treating a patient exposed to a nerve agent`

A

decontamination to limit secondary exposure

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20
Q

atropine is a _______ antidote for nerve agents due to it’s _______ effects

A

anticholinergic
muscarinic

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21
Q

2-PAM are _____ which are nucleophilic. Their MOA is _____________

A

oximes
reactivate cholinesterase by removing dialkyl phosphoryl moiety

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22
Q

2-PAM has ________ dependent use

A

time

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23
Q

2-PAM must be used within ____ (time) for
- soman
- sarin
- tabun
- VX

A

Soman = 2-6 min
Sarin = 3-5hrs
Tabun = 14h
VX = 48h

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24
Q

pyridostigmine MOA in soman exposure

A

pretreatment often- is a carbamate acetylcholinesterase inhibitor which outcompetes nerve agents

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25
Q

describe the structure of dioxin

A

is part of a family of isomers- dibenzo-p-dioxin

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26
Q

dioxin is
1 highly lipophilic
2. very specific in dose response
3. a minor environmental pollutant
4. has a half life of 7-11rhs

A

1
- is very wide variation in dose response, major pollutant, half life 7-11yrs

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27
Q

what is the most potent dioxin

A

TCDD

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28
Q

dioxin MOA

A

binds to AHR = inappropriate activation of CYP and phase 2 enzymes

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29
Q

dioxins are considered class ________ and _______ disruptors

A

class 1 carcinogens
endocrine disruptors

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30
Q

what is the impact of dioxin

A

impact on repro function, immunologically suppressive, carcinogenic
causes chloracne

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31
Q

what happens when someone gets chloracne

A

is a systemic toxicity which starts with excessively oily skin = whiteheads, balckheads, cysts, thickened skin, flakiness, scaring, and change in coloration

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32
Q

what is the MOA of chloracne

A

MOA unknown- probably involves alterations of cellularty

33
Q

ricin can be exposed via

A

injection, inhalation, ingestion

34
Q

select all of the above that is true about ricin
1. is water soluble
2. is composed of 2 proteins linked by disulfide bond
3. is 1C + 3N
4. there are no tx for ricin toxicity
5. inhibits many enzymes

A

1, 2, 4

35
Q

what does ricin’s chain B do?

A

facilitates binding and entry into the cell + localizing into ER

36
Q

what does chain A of ricin do?

A

inhibits protein synthesis by inactivating ribosomes by removing an adenine residue from rRNA = rRNA can’t bind to protein elongation factors

37
Q

clinical sx of ricin toxicity

A

resp distress (inh within few hrs), severe vomiting (ingestion), gastroenteritis, hemorrhage, and inflammation, multiple organ failure, death within 48-72hrs

38
Q

what are the tx for ricin toxicity

A

no tx available

39
Q

describe the tylenol poisoning series and outcome

A

drug was tampered with to lace with potassium cyanide = led to development of tamper resistant packaging such as induction seals and quality control measures

40
Q

anthrax, AKA ___________ is a , gram ____, ____ forming bacillus found in soil worldwide

A

bacillus anthracis
gram +
spore forming

41
Q

inhalation of anthrax can cause

A

mediastinitis

42
Q

spores of anthrax taken into the lymphatic sytem can

A

germinate

43
Q

cyanide is a chemical group that consists of

A

1C and 3N

44
Q

plant sources of cyanide include

A

cassava roots, apricot pits, peach pits, almonds

45
Q

which HPTN drug can cause cyanide poisoning

A

nitroprusside

46
Q

________ can react with water to form hydrogen cyanide gas

A

common salts like NaCN, KCN

47
Q

why is cyanide gas the most dangerous

A

less dense than air = rise/ disperse quickly

48
Q

T or F; cyanide crosses membranes easily

A

T - due to low MW

49
Q

nonionized cyanide is metabolized to

A

thiocyanate

50
Q

cyanide metabolism is limited by

A

endogenous stores of sulfur

51
Q

nonionized cyanide is metabolized to thiocyanate by

A

rhodanese, b-mercaptopyruvate, CN sulfurtransferase

52
Q

what is the MOA of cyanide toxicity

A

induces cellular hypoxia and metabolic acidosis by shutting down oxphos = no ATP = enzymes to metabolize cyanide can’t run

inhibits multiple enzymes, succinic acid dehydrogenase, superoxide dismutase, carbonic anhydrase, cytochrome oxidase

53
Q

which 2 organs are majorly impacted by cyanide

A

heart and CNS

54
Q

cyanide survivors can develop delayed _________

A

neuro sequelae

55
Q

cyanide toxicity onset

A

v rapid (seconds to minutes)

56
Q

tx for cyanide toxicity besides antidotes

A

supportive care- ventilate, give 100% oxygen, vasopressors for hypotension, sodium bicarbonate

57
Q

antidotes for cyanide toxicity

A

Hydroxocobalamin

Cyanide antidote kit: amyl nitrile, sodium nitrile, sodium thiosulfate

58
Q

how does hydroxocobalmin work as a cyanide antidote

A

is a metalloprotein with a central cobalt atom that complexes CN forming cyanocobalamin (pref)

59
Q

what is the preferred tx for cyanide toxicity

A

hydroxocobalamin

60
Q

what is the MOA for the cyanide antidote kit

A

the amyl nitrile generates methemoglobin which CN has a higher affinity to compared to cytochrome a3

61
Q

anthrax produces which 3 toxins

A

protective antigen
edema factor
lethal factor

62
Q

what does PA do

A

pore forming that allows EF and LF into cell

63
Q

what does EF do

A

produces cAMP = imbalance in water homeostasis = cellular edema

64
Q

what does lethal factor do

A

metallic protease that breaks down cell and activates immune response to kill cell off

65
Q

anthrax sx starts with ______________ and progresses to ________________

A

Starts with fever, malaise, cough, chest discomfort (2-3 days)
Progresses to severe respiratory distress, dyspnea, diaphoresis, stridor, cyanosis

66
Q

anthrax tx (3)

A

antibiotics (cipro, doxy)
raxibacumab
vaccine

67
Q

what is raxibacumab

A

a monoclonal antibody that blocks the binding of anthrax PA

68
Q

the anthrax vaccine is a __________ strain that produces the PA antigen

A

avirulent nonencapsulated strain

69
Q

the ______ test is used to detect arsenic poisonigns

A

arsenic

70
Q

arsenic is a metalloid existing in multiple forms, including

A

elemental, gaseous (arsine), organic and inorganic (As3+, As 5+)

71
Q

Arsenic trioxide (As2O3) is a __________= easily incorporated into food and drink

A

flavorless, odorless

72
Q

As3+ inhibits

A

pyruvate dehydrogenase

73
Q

As3+ 4 impacts

A

inhibits PDH
inhibits citric acid cycle
decreases gluconeogenesis
affects cardiac repolarization

74
Q

As5+ is readily reduced to ____ and ________

A

As3+ and pentavalent arsenic resembles phosphate (ex- gets incorporated wherever phosphate would be) = uncouple OSPHOS

75
Q

arsenic has ____ metabolism

A

hepatic

76
Q

acute toxicity to arsenic resembles

A

cholera- diarrhea rice water

77
Q

death from acute arsenic poisoning is mostly due to

A

CV collapse and hypovolemic shock

78
Q

chronic arsenic toxicity causes

A

arseniasis
mees lines
GIT, skin, CNS, primary organ damage
N, epigastric pain, colic, diarrhea, paresthesias
cancer

79
Q

arsenic toxicity tx

A

chelation tx with BAL, 2,3-dimercaptosuccinic acid, and dimercaptopropane sulfonate which are vicinal dithiol moieties that bind arsenic

401 - Toxicology, Drug Abuse, Pharmacology (32 decks)

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