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pharmacology toxicology > toxicology exam 1 > Flashcards

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
Q

methemoglobin antidote

A

methylene blue

makes Hb-Fe++

26
Q

what does cyanide do?

A

interfere with ATP generation
binds/inhibits cytochrome oxidase
body can’t do aerobic respiration

27
Q

cyanide antidote

A

amyl/sodium nitrite to make Fe+++

then, hydroxycobalamin or sodium thiosulfate

28
Q

treatment for Pb, As, Hg poisoning

A

chelation- DMSA, succimer, oral

29
Q

problems with treating metal poisoning

A 
cannot penetrate cell membrane
can unintentionally redistribute metals
can complex/remove essential metals
liver/kidney toxicity
limited effectiveness
30
Q

basket complex

A

incomplete shielding that occurs when trying to treat metal toxicity, biological targets still have some access

31
Q

why is mercury poisoning so serious

A

CNS toxicity with very low exposure

32
Q

mercury poisoning mechanism

A

reacts with sulfhydryl groups on proteins (inhibits)

interacts with selenium

33
Q

mercury antidote

A

DMSA

34
Q

mechanism of lead poisoning

A

reacts with sulfhydryl, phosphate carboxyl groups on proteins
mimics calcium, interferes with zinc and iron

35
Q

effect of lead toxicity

A 
CNS: impaired concentration
headache
encephalopathy
decreased intelligence
altered neuro development
cognitive decline
interferes with vit. d synthesis and heme synthesis
36
Q

lead antidote

A

DMSA

pharmacology toxicology (1 decks)

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