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Tox > Tox Definations > Flashcards

Tox Definations Flashcards

1
Q

Toxicology

A

Toxicology is the science of poisons (toxicants)- their physical and chemical properties, sources, toxicity, toxicokinetics, mechanisms of action, clinical signs, lesions, laboratory diagnosis, diagnosis, differential diagnosis and treatment (or prevention) of diseases caused by toxicants

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2
Q

Poison/Toxicant

A

Poison/Toxicant; can be natural or synthetic

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3
Q

Toxin (biotoxin):

A

Toxin (biotoxin): poison from a biologic process (e.g., zootoxins or animal toxins, phytotoxins or plant toxins, bacterial toxins and mycotoxins)

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4
Q

Toxic:

A

Toxic: deleterious or undesirable effects of poisons

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5
Q

Toxic: deleterious or undesirable effects of poisons

A

Toxic: deleterious or undesirable effects of poisons

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6
Q

Toxicity:

A

Toxicity: amount of a poison that under certain circumstances will cause toxic effects –“heart and sole”

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7
Q

LD50

A

• In mammals is usually expressed as LD50 (lethal dose fifty) in mg/kg body weight

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8
Q

LC50

A

• In birds is expressed as LC50 (lethal concentration fifty) in mg/kg feed and in fish as LC50 in mg/liter water

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9
Q

Acute toxicity -

A

Acute toxicity - effect of a single dose or multiple dose during a 24‐hour period

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10
Q

Subacute toxicity -

A

Subacute toxicity - effect produced by daily exposure from one day to 30 days

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11
Q

Subchronic toxicity

A

Subchronic toxicity- effect of exposure from 30 days to 90 days

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12
Q

Chronic toxicity

A

Chronic toxicity - effect produced by daily exposure for a period of 3 months or more

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13
Q

Chronocity factor

A

Chronocity factor- ratio between acute LD50 and chronic LD50
• the higher it is (>2), the toxicant is more toxic/cummulative with repeated exposure and a single exposure may not toxic
• if low (

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14
Q

toxic dose low (TDL):

A

• toxic dose low (TDL): lowest dose which produces toxic alterations and administering twice this dose will not cause death

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15
Q

toxic dose high (TDH):

A

• toxic dose high (TDH): toxic alterations and administering twice this dose will result in death

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16
Q

No‐effect level (maximum non toxic level):

A

• No‐effect level (maximum non toxic level): amount of a chemical that can be ingested without causing any deaths, illness or toxic alterations in any of the animals for the stated period (usually 90 days to two years or more depending on the species), used for feed additi

17
Q

highest non toxic dose (HNTD)

A

Maximum tolerated dose or minimal toxic dose (MTD)

18
Q

LD0

A

highest dose that does not cause any death

19
Q

LD50

A

dose that kills 50% of animals in a group

20
Q

LD100

A

lowest dose that kills all the animals in a group

21
Q

TOXICOKINETICS-

A

TOXICOKINETICS- the study of absorption, distribution, biotransformation and excretion of toxic agents

22
Q

Importance of studying toxicokinetics

A

• Importance of studying toxicokinetics
o Knowing the routes of exposure
o Knowing distribution of the poison to target organs (sites of action) which will be manifested as clinical signs and lesion
♣ Ex. Lead is the only toxic metal that causes major issues..
o Knowing absorption (if local or systemic effects)
o Selection of proper specimens for chemical analysis
o Knowing the sites of storage
♣ Ex paraquat (sp?) gets stored in lungs, thus is in higher concentrations
o Elimination and the half‐life can be of some use in knowing withdrawal or quarantine periods due to excessive chemical residues in food‐producing animals

23
Q

xenobiotics

A

• Drugs and toxicants are xenobiotics (foreign chemicals)

24
Q

Drug Disposition

A

Drug Disposition – study of movement of drugs in the body across bio-membranes from the site of absorption until elimination

25
Q

Stages of Drug Disposition:

A

Stages of Drug Disposition: (1) Absorption (2) Distribution (3) Biotransformation (4) Excretion

26
Q

Absorption-

A
  1. Absorption- transfer of the drug from the site of administration (ingestion > inhalation > mucous membranes>injection) to circulation
    a. Factors related to the drug
    i. Molecular size
    ii. Lipid solubility
    iii. Ionization- higher the ration b/w N/I, the greater the absorption
    iv. Dissolution in water
    v. Concentration
    vi. Route of Administration/Exposure
  2. Sublinqual & inhalation= vary rapid > IM > SQ> Oral
    b. Factors related to the animal
    i. Blood Flow**
  3. Heat or massage of the IM injection site increases blood flow and absorption
  4. Sympathetic stim increases blood flow to skeletal muscles(β2) and decreases blood flow to GI tract and skin (α1)
  5. Shock and edema decrease blood flow
    ii. Absorption Surface Area
    iii. Connective tissue
    iv. Species
    v. Individual
    c. Absorption from the GI tract
    i. The upper small intestines in the main site of absorption due to extensive surface area and blood flow
    ii. Rate of absorption depends on the rate of gastric emptying – can be changed by disease and drugs (atropine, morphine etc)
    iii. Oral absorption of solid drugs depends on the rate of dissolution (“slow release”, ”fast release” )
    iv. Can be altered by activity, other substances (food decreases absorption, except if it is related to acidity- food increases acidity - ex. Ketoconazole) , blood flow, and species/individual differences
27
Q

Distribution-

A
  1. Distribution- transport of drugs from the plasma to the tissues (site of action/storage/biotransformation)
    Factors Affecting Distribution:
    • Drug properties – lipid solubulity
    • Concentration gradient
    • Plasma protein binding- generally reversible, prolongs half-life, inactivates it, rate of binding depends on the amount of drug
    o Acid= albumin
    o Basic= glycoproteins & lipoproteins
    o Steroids= globulin
    • Blood flow – brain, liver, kidney, endocrine &raquo_space; muscle , skin&raquo_space; bone, adipose tissue
    • Tissue barriers
    o Brain (BBB)- tight endothelial junctions (prevent hydrophilic, not lipophilic), glial cells, CSF flushing, active transport of organic acids/bases
    ♣ Influenced by age, inflammation, trauma, allergies, hypotension, hypoxia, organic solvents (alcohol), heavy metals
    o Eye, Testicles, Placenta, Mammary glands
    • Affinity to certain tissues (Sequestation)
    o Tetracycline – to calcium in skeletam tissues
    o Iodine – thyroid
    o Aminoglycosides – kidney
    Redistribution- movement of drug from the tissue to the blood
    Ex. Thiopental vs. phenobarbital
28
Q

Passive Diffusion

A
  1. Passive Diffusion- simple (if lipid soluable/hydrophobic- majority of drugs), transmembrane and paracellular
    a. Factors affecting simple diffusion
    i. Concentration Gradient – “dose”
    ii. Lipid solubility – measured by lipid partition coefficient (the ratio b/w solubility of drug in lipid to solubility in water)
  2. The higher the lipid solubility, the faster the drug crosses cell membranes
    iii. Degree of ionization- drugs cross membranes in the NON-ionized form (=lipid soluble & no electrical charge)
  3. Rate of diffusion depends on the ratio of non-ionized form of the drug to the ionized form (N/I)
  4. Depends on pH & pK of the drug and the pH of the environment
    a. Acidic drugs ionize in alkaline medium & vice-versa
    b. Hendersan Hasselbalch =
    i. pK Acid= pH + log (N/I) (ANI)
    ii. pK Base = pH + log (I/N) (BIN)
  5. Ex. Quaternary ammonia compounds such as d-tubocurarine are mostly ionized
29
Q

Facilitated Diffusion

A
  1. Facilitated Diffusion- carrier mediated, no energy, downhill
    a. Ex. Glucose (insulin lowers K and glucose levels)
30
Q

Active Transport

A
  1. Active Transport- requires energy, uphill, primary & secondary
    a. Characterized by saturability, selectivity and competitive inhibition by cotransporter compounds
    b. Ex. Active tubular secretion
31
Q

Pinocytosis-

A
  1. Pinocytosis- engulf drug molecules dissolved in water

a. Ex. Aminoglycoside sequestration by the renal tubular cells – do not use with amphotericin

32
Q

Drug Metabolism

A 
Drug Metabolism (Biotransformation)
Chemical alteration of the drug molecule by the cells of the animals
33
Q

Results of Biotransformation

A

• Change in physiochemical properties of the drug
o The metabolism is more water soluable, polar and ionized
• Changes in pharmacological activity
o Bioinactivation or detoxification (most drugs)
o Bioactivation of lethal synthesis (few drugs)
o Pro-drug (inactive) active

34
Q

Sites of Biotransformation

A

Sites of Biotransformation
• Liver
o Smooth ER (microsomes)= MAIN SITE
o Hepatocyte cytoplasm, mitochondria, lysosomes, nuclear envelope, plasma membrane
• Other tissues (the nervous tissue, kidney, GI, lungs, skin)
• Plasma

35
Q

Hepatic Metabolism

A

Hepatic Metabolism
• Enzymes lack specificity (ex. Cytochrome-P450, CYP P450, MFO)
• Enzymatic reactions are saturable reactions
• Drugs can compete on the same enzyme
• Enzymes can be induced or inhibited by drugs
• Microsomal enzymes cause oxidation, reduction, hydrolysis and conjugation to glucuronic acid

36
Q

Phase 1

A

• Oxidation
o Microsomal – hydroxylation, deamination, dealkylation, desulfuration, sulfoxide formation
o Non-microsomal – cytosol or mitochondria
♣ Alcohol and aldehyde dehydrogenase (ex. Ethanol to acetaldehyde)
♣ Xanthine oxidase (ex. Xanthine to uric acid)
♣ Tyrosine hydroxylase (ex. Tyrosine to dopa)
♣ Monoamine oxidase (ex. Metabolism of catecholamines and serotonin)
o MOST COMMON biotransformation reaction **important!!
♣ High oxidative =insensitive (ruminants and horses)
♣ Low oxidative enzymes= sensitive (cats, birds)

• Reduction
o Microsomal (ex. Nitro reduction of chloramphenicol)
o Non-microsomal (ex. Aldehyde reduction of chloral hydrate)

•	Hydrolysis
o	Microsomal hydrolases
o	Non-microsomal hydrolases
♣	Esterases (ex. Acetylcholine, succinylcholine, procaine)
♣	Amidases (eg. Procainamide)
♣	Peptidases (eg. Proinsulin)
37
Q

Phase II Reaction (synthetic)

A

Phase II Reaction (synthetic)
• Conjugation- combination of a drug or its metabolite with an endogenous substance
o Occurs with foreign compounds and endogenous chemicals
o Conjugation is to glucuronic acid, sulfuric acid, acetyl group, methyl group, glycine, methionine and glutathione
o Conjugation to glucuronic acid is the most common conjugation reaction
♣ Glucuronidation is microsomal but all other conjugationare non-microsomal
o Deficient in the neonates
o Metabolite conjugates are usually inactive and water-soluble
o Certain conjugation reactions may lead to formation of metabolites (acyl glucuronidation of NSAID) that are hepatotoxic
♣ NSAID approved in cats= Meloxicam

Tox (5 decks)

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