toxicology exam 1 Flashcards

1
Q

factors that increase toxicity

A

co-morbidities
loss of protective mechanisms
co-exposures
genetics

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2
Q

most common route of occupational exposure

A

inhalation

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3
Q

most common route of poison exposure

A

ingestion

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4
Q

routes of exposure to toxins

A
inhalation
ingestion
dermal absorption
wounds
occular
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5
Q

effects of acute toxicity

A
cellular/organ dysfunction
receptor interactions
cell death
interference with vital processes
inflammation
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6
Q

effects of chronic toxicity

A
cumulative dysfuntion
chronic inflammation
cell proliferation
dysfunctional repair mechanisms
fibrosis
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7
Q

polypharmacy

A

multiple drugs prescribed

common problem for elderly

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8
Q

risk factors for drug interactions

A

age
multiple prescribers
inadequate monitoring
impaired drug elimination (liver/renal disease)
drugs with narrow therapeutic index (coumadin)

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9
Q

impaired elimination

A

when taking 2 drugs, one can impair the elimination or metabolism of the other, making it more likely to reach a toxic threshold

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10
Q

slow vs fast metabolizers

A

slow metabolizers more likely to get to a toxic level of a drug, fast metabolizers less likely to get to a therapeutic level

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11
Q

6 mechanisms of toxicity

A
receptor-ligand interactions
perturbation of membrane function
interference with ATP generation
interaction with macromolecules
alteration of calcium homeostasis
generation of free radicals
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12
Q

what interferes with receptor-ligand interactions

A

PCBs, bisphenols, estrogen

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13
Q

example of membrane disruption

A

ETOH, Na channel disruption

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14
Q

what interferes with ATP generation

A

CN, Hydrogen sulfide

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15
Q

what interferes with macromolecules

A

CO binds to Fe, metals and sulfhydryl groups, lipid peroxidation

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16
Q

what alters calcium homeostasis

A

foxglove, digoxin

17
Q

what happens to ROS/Carbon radicals in times of oxidative stress

A
Increases:
P450 metabolism
reperfusion
ischemia
xenobiotics
18
Q

what happens to antioxidants in times of oxidative stress

A

Decreases:
GSH depletion
low SOD fxn
malnutrition

19
Q

what is an antioxidant

A

can donate an electron to a free radical

ex. GSH, readily donates a H

20
Q

what happens with Paraquat exposure

A

pulmonary fibrosis

lung toxicity

21
Q

mechanism of paraquat toxicity

A

yields hydroxyl radical

22
Q

organophosphate/carbamate insecticide

A

parathione
inactivates acetyl cholinesterase
inhibits enzyme fxn

23
Q

organophosphate carbamate antidote

A

atropine sulfate/ anti-muscarinic

24
Q

what causes methemoglobin toxicity

A

exposure to nitrates

makes Hb-Fe+++

25
methemoglobin antidote
methylene blue | makes Hb-Fe++
26
what does cyanide do?
interfere with ATP generation binds/inhibits cytochrome oxidase body can't do aerobic respiration
27
cyanide antidote
amyl/sodium nitrite to make Fe+++ | then, hydroxycobalamin or sodium thiosulfate
28
treatment for Pb, As, Hg poisoning
chelation- DMSA, succimer, oral
29
problems with treating metal poisoning
``` cannot penetrate cell membrane can unintentionally redistribute metals can complex/remove essential metals liver/kidney toxicity limited effectiveness ```
30
basket complex
incomplete shielding that occurs when trying to treat metal toxicity, biological targets still have some access
31
why is mercury poisoning so serious
CNS toxicity with very low exposure
32
mercury poisoning mechanism
reacts with sulfhydryl groups on proteins (inhibits) | interacts with selenium
33
mercury antidote
DMSA
34
mechanism of lead poisoning
reacts with sulfhydryl, phosphate carboxyl groups on proteins mimics calcium, interferes with zinc and iron
35
effect of lead toxicity
``` CNS: impaired concentration headache encephalopathy decreased intelligence altered neuro development cognitive decline interferes with vit. d synthesis and heme synthesis ```
36
lead antidote
DMSA