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PA 2306- MOD 7 > Toxicity > Flashcards

Toxicity Flashcards

1
Q

What is cytotoxicity vs genotoxicity

A

cytotoxicity- cellular destruction

Genotoxicity- Changes in genetic material that is passed along

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2
Q

What is an example of cytotoxicity and genotoxicity

A

Cytotoxicity- lipid peroxidation

Genotoxicity- Covalent binding

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3
Q

What is receptor mediated toxicicity and how long does it last

A

toxicity is caused by binding of the parent compound to receptor/enzyme/ion channel (very targeted)
-adverse rxn is usually disapates when drug administeration is discontinued or further expose terminated

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4
Q

What is naloxone and what receptor does it work on

A

Naloxone for emergency tx for opiod addiction tx

-antagonist at mu receptor site for opiote (has short half life so needs to be repeatdly admined)

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5
Q

How does acetaminophen work and what does it target

A

Works on cyclooxgenase enyme to inhibit protaglandin systhesis

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6
Q

Where does acetaminophen work better

A

Works better on cyclooxgenase in CNS compared to the peripherry

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7
Q

What will happen when too much acetaminophen is injested

A

Will go thru phase II using p450 and create reactive intermediate which can leads to covalent binding to sulfhydryl groups of hepatic pros

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8
Q

How can the reactive intermediate in acetaminophen phase II be delt with

A

Glutathione (GSH) will protect + convert it to a non reactive product

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9
Q

What is used to produce more GSH for aceaminophen overdoses

A

N-acytl-cystein

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10
Q

What is the mathew rumack nomogram used for

A

To determine if one has acetaminophen poisining or if there is a potential for it

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11
Q

What does a depletion of GSH in phase II cause

A

Cause an increase of intracellular calcium (damaging)

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12
Q

How can acetaminophen be used as a marker for liver damage

A

If half life of acetaminophen increases from 4 to 8 hours

-it indicates that biotransformation of acetaminophen is taking a hit aka liver damage

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13
Q

What is the typical route of biotransformation of isoniazid

A

will be transformed to acetylisoniazid then to either isonicotinic acid or diacetylyhrazine which are both non tox

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14
Q

Why does isoniazid go thru phase I rxn

A

Slow acetylators are more suseptible as there is a greater degree of intermediate Acetylhdrazine that will instead go thru phase I then to the non toxic substance

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15
Q

What is the phase I rxn of isoniazid

A

Intermediate (acetylhydrazine) will go through phase I rxn and generate free radicals that can lead to covelent binding (causing liver necrosis)

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16
Q

What happens in iproniazid biotransformation in slow acetalators

A

intermediate (isopropyl hydrazine) will go thru phase I pathway in slow acetylators and be biotransformed in to free rads that cause damage

17
Q

What happens in normal ox dissociation curve

A

as PO2 goes down more o2 will be released

18
Q

what occurs in the presence of CO for the oxygen dissociation curve

A

In presense of CO; it will bind to hemoglobin and shift curve to right and reduce carrying capacity

-Need more of a reduction of PO2 to release O2

19
Q

At 50% COHb what percentage decrease do you need in PO2 to release 1 o2 at tissues

A

90% reduction in PO2

20
Q

What is the mechanism of action for cyanide posioning

A

reversible binding to cytochrome oxidase in the mitochondria blocking electron transport

21
Q

How is cynanide delt with in the body

A

Enzymes rhodanese and thiosulfate ion (50% of cyanide in 1 hour)

22
Q

What can be formed to clean up cyanide and how is it made

A

Methemoglobin

-can be produced with sodium nitrite

23
Q

What is the mechanism of toxicity for organophosphate pesticides

A
  • toxicity is caused by inhibition of cholinesterase (responsible for hydrolysis of acetylcholine)
  • blocks active site (pseudosubstrate)
24
Q

What is the tx for organophosphate pesticides

A

Tx involves pralidozime and atrophine- bind out inhibitor

25
Q

How do free rads cause cell injury

A

Free radicals can initiate chain rxns by taking an electron from a stable molecule which then becomes an unstable free radical itself

26
Q

What is the defense mechanism against free radicals and what does it form

A

GSH

-will donate proton (H) to deal with substrate (free rad) then form GSGS

27
Q

What are the 3 ways nucleophilic thiol group (GSH) helps deal with free rads

A
  1. Conjugation catalyzed by glutathione transferase
  2. Donation of a proton to reactive metabolites or free radicals
  3. Chemical rxn with rective metabolite to form a conjugate
28
Q

How is GSH remade after it is made to GSGS

A

Must be transfered back through the use of NADPH and GSSG reductase

29
Q

Where does the NADPH come from that is needed for the formation of GSH

A

NADPH comes from NADP using G6P dehydrogenase

30
Q

What does a deficiency in the conc of GSH in the rbcs cause

A

Leads to hemolysis

31
Q

What are the most significant reactive oxygen species (3)

A

Superoxide anion
Hydroxyl radical
hydrogen peroxide

32
Q

What is redox cycling and example of it

A

Production of reactive oxygen species

ex- quinone is reduced to produce unstable semiquinone which is oxidized again (process keeps repeating)

33
Q

What doe reactive oxygen species do in the body

A

Damage DNA
Oxidise fatty acids in lipids
Oxidation of amino acids in pro
Oxidation of enzyme cofactors

34
Q

What systems deal with reactive oxygen species (3)

A

Superoxide dismutase
Glutathion peroxidase
catalase

35
Q

What vits are natural scavengers of ROS

A

Vit C + E

36
Q

What are the steps to deal with superoxide (2)

A
  1. Superoxide–> Hydrogen peroxide by Superoxide dimutase

2. Hydrogen peroxide–>water by Catalase/ Glutathione peroxidase

37
Q

How are hydroxyl radicals delt with and what enzyme is utalized

A

Glutathione peroxidase is used with GSH

38
Q

Which are the major pathways that a cell can go thru that has no point of return (cytotoxic events) (5)

A
  1. Lipid peroxidation (#1 for cell damage)
  2. Covalent binding to macromolecules
  3. Changes in Thiol status
  4. Enzyme inhibition
  5. Ischemia
39
Q

How does lipid peroxidation develop and what is responsible for it

A

A hydroxyl radical removes a hydrogen atom from the unstaurated fatty acid of the membrane phospholipid and produces a free radical

-Lipid radical reacts w molecular oxygen and produces a lipid peroxide radical (and continues again and again)

PA 2306- MOD 7 (8 decks)

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