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Environmental Health > 7/11/16 > Flashcards

7/11/16 Flashcards

1
Q

Toxic action of a substance

A

a consequence of the physical/chemical interaction of the active form of that substance with a molecular target within the living organism

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2
Q

Magnitude of toxic effect

A

a function of the concentration of altered molecular targets, which in turn is related to the concentration of the active form of the toxicant at the site where the molecular targets are located

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3
Q

Toxicokinetics

A 
what the body does to the agent 
Absorption 
Distribution
Metabolism
Excretion
Storage
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4
Q

Toxicodynamics

A

what the agent does to the body - the active form of the agent at the sensitive target

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5
Q

TK/TD are affected by

A
  • other drugs/xenobiotics
  • genetic polymorphisms
  • infection/GI flora
  • age, weight, diet
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6
Q

Absorption and distribution

A

enteral (oral, sublingual, rectal)
parenteral (IV, IM, SC)
other routes (inhalation, topical, transderaml)

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7
Q

What is the common feature of all routes of administration (except IV)?

A

Absorption - epithelial cells line our body cavities and surfaces (epithelial cells lines our body cavities and surfaces)

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8
Q

Physicochemical factors that affect kinetics of absorption

A

pH, blood flow, gastric emptying, bowel transit, surface area (lung 140m2, GI 300m2, skin 1.5-2m2)

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9
Q

Diffusion

A

low MW, lipophilic compounds, requires concentration gradient

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10
Q

Carrier-mediated transport

A

ligand binds receptor on cell surface

ex: cholesterol/lipoprotein bind to LDL

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11
Q

Facilitated transport

A

mediated by membrane transport proteins
energy provided by concentration gradient
- glucose transporter

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12
Q

Active transport

A

major form of drug transport

  • mediated by membrane transport proteins
  • transports AGAINST a concentration gradient
  • temeperature-dependent and saturable
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13
Q

Why is the blood-brain barrier less permeable to toxicants?

A

Capillary endothelial cells (tightly joined, contains ATP transporter - efflux pump)
Capillaries in CNS are surrounded by glial cells
Low protein content of interstitial fluid in brain limits movement of water-insoluble molecules by paracellular transport

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14
Q

Purpose of biotransformation (metabolism)

A

convert xenobiotics to water soluble forms so that they can be excreted in feces and urine

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15
Q

Why does biotransformation make resulting compound more toxic?

A

Most xenobiotics are liophilic and body readily excretes water soluble compounds so the body transform via Phase 1 or 2 reaction to make them more soluble.

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16
Q

Primary enzyme in phase 1 reactions

A

cytochrome p-450 (mixed function oxidase)

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17
Q

Phase 2 reaction enzymes

A

glucuronyltransferase
sulfotransferase
glutathione-S-transferase
acetyltransferase

18
Q

Excretion pathways

A 
respiratory (mucociliary exchange, gas exchange)
GI (biliary excretion, entero-hepatic circulation)
urinary excretion (glomerular filtration, trans-tubular secretion)
19
Q

Other routes of excretion

A

milk, sweat, hair, nails, saliva

20
Q

biological half-life

A

time required for chemical in the body to decrease to 1/2 its current value

21
Q

toxicological endpoints

A

cell death, cellular/organ dysfunction, teratology, genetic changes, cancer

22
Q

LD50

A

lethal dose to 50% of test population, lower ld50 - more toxic

23
Q

Exposure

A

any condition which provides an opportunity for an external environmental agent to enter the body

24
Q

Agent

A

any chemical, biological, or physical material capable of eliciting a biological response (diff than vector or carrier - air, water, soil, food)

25
Q

Dose

A

amount of agent actually deposited within the body, distinction between exposure and dose is blurred

26
Q

exposure assessment

A

exposure = intensity x frequency x duration

27
Q

Vectors for exposure in context of environmental health

A

water, air, food, soil

28
Q

toxicokinetics in the toxicological paradigm

A

exposure, internal dose, biologic effective dose

29
Q

toxicodynamics in the toxicological paradigm

A

early biologic effects, altered structure & function, clinical disease

30
Q

Patterns of exposure

A 
continuous (cigarette)
intermittent (uranium mining)
cyclic 
random
concentrated
31
Q

Hierarchy of “exposure” data

A

Quantitative personal dosimeter measurements
quantitative ambient measurements in the vicinity
quantitative surrogates of exposure (estimates of drinking water or food consumption x conc.)
residence or employment in proximity to the source of exposure
residence or employment in the general geographic area of the source of exposure

32
Q

Uncertainties in toxicology

A

high to low dose extrapolation

interspecies comparisons

33
Q

Define dose-responser relationship

A

the relationship between the quantity of response and the dose of the drug or toxicant

  • response is due to agent
  • degree of response is due to compound concentration
  • have a quantifiable response parament
34
Q

Potency

A

Range of doses over which a drug produces increasing responses

35
Q

Efficacy

A

maximal response; plateau of the dose-response curve

36
Q

“Random” model

A

Risk of response is a function of dose, assumes no threshold, no dose is safe, any dose increases the risk (ex cancer)

37
Q

“Deterministic” Model

A

Severity of response is a function of dose, assumes a threshold, a “safe” dose exist(ex radiation, chloracne)

38
Q

Interactive responses

A

Additive (2+4=6)
Synergistic (2+5=20)
Potentiation (0+4=10)
Antagonism (2+6=3; 4+1=0)

39
Q

Interactions of chemicals - additive

A

operating through same molecular mechanism - specific receptor or very specific interaction (ex 2 diff organophosphates interacting with cholinesterase receptor)

40
Q

Interactions of chemicals -synergistic

A

Carbon tetrachloride w/ ethyl alcohol - people living above dry cleaning exposed and drink alcohol - synergy response -> liver toxicity
lung cancer & asbestos

41
Q

Interactions of chemicals - potentiation

A

only one chemical has toxic effect at site of action

ex: isopropyl alcohol (rubbing alcohol, antifreeze, solvent not toxic to liver CNS depression w/ gastritis, pain, N+V) -> potentiates CCl4
* In the absence of pretreatment, little response

42
Q

Interactions of chemicals - antagonism

A

1) functional mechanism, 2 chemicals counterbalance each other
- chemical producing convulsions plus anticonvulsant drug (diazepam)
2) dispositional mechanism, alters concentrations or residence time of toxin (ipecac, charcoal)
3) metabolic mechanism - modulation of CP450
4) receptor block mechanism (competitive inhibitors - naloxone, tamoxifen, atropine)

Environmental Health (2 decks)

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