• Created by: Rscottqub
  • Created on: 05-01-20 14:48
the science of poisons, the study of adverse effects of chemical,physical or bio agents on people, animals and the environment
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all things are poisons
there is nothing without poisonous qualities - it is the dose and frequency which makes something toxic
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all drugs have a
dose response curve
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botox in the smallest conc can be
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different drugs have different
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types of sources of poison
1. physical sources, 2. biological sources 3. chemicals
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physical sources
radiation- will damage cells
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biological agents
ie bacteris, viruses, fungi attack and damage cells
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ie drugs, dyes - the biggest source of toxins
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biological toxins
sub type of the bio agents - organism ( ie bacteria) itself doesn't cause damage but it secretes bio toxins which result in damage
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toxicological profile
physio chem properties , route of exposure,
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all drugs are toxic in ......
an OD
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people vary in their
sensitivity to drugs
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what is tested during animal testing?
multiple tests- different species, long term admin, post mortem examin, physio and bio monitoring
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not all adverse effects that occur in animals
will occur in humans and vice versa
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some side eff. are predictable due to
the drugs MOA
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what is a dose
amount of substance administered at one time
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drug dose depends on
number of doses, frequency of doses, treatment period, exposure site , sub properties
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types of dose
administered dose, absorbed dose, target dose
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administered dose
amount administered orally or by injection
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absorbed dose
the amount of sub entering body via eyes, skin,lungs or GIT and was taken up by organs or particular tissues . AKA internal dose
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target dose
amount at the site of action for the necessary period of time
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side effect
drugs will produce many effects but only 1 is associated with the primary objective of therapy - all others are considered side effects
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all side effects are bad
false - some are beneficial
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toxic effect are always
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what sort of dose are we aiming for ?
most effective dose but minimally toxic - balancing act between effective dose and toxic dose
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No observed adverse effect level- the highest dose with no adverse effects seen
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lowesr observed adverse effects level - the lowest dose where first see toxic effects
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which will always be lower NOAEL or LOAEL
NOAEL - will always be lower ***
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types of toxicity
acute , sub chronic , chronic
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occurs almost immediately. usually a single dose or series of doses received in 24hr period
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sub chronic
from repeated exposure for several weeks/months.
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cumulative damage to particular organ system - takes months/years to be recognized as clinical disease
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Classifying undesired effects
5 ways to classify side effects
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1. local or systemic toxicity
local- site of 1st contact systemic - absorption and distribution of toxicant to distant site
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2. REVERSIBLE or irreversible
Reversible - ie liver, kidney , skin - generally as long as you remove the toxin it can make a recovery. Liver can regen. itself
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ie mutagens - perm damage to DNA , carcingogens - cause proliferation. Treatment here is to kill cells affected rather than treat them
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drug which directly/indirectly causes structural changes in the the baby- ie thalidomide . NB most drugs are not teratogens
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3, IMMEDIATE or Delayed toxicity
Immediate toxic eff. - occur quickly after single dose
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delayed toxic effects
occur after a lapse of time
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carcinogens example of
delayed - often 20-30 years before tumors are observed in humans
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4. Allergic reactions (chemical allergy)
immune adverse reaction to a chemical. 1st time take something your allergic to - no effects - only on re exposure - adverse reaction
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most reactions are
just minor skin eruptions - serious anaphalaxis is rare
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5. Idiosyncratic reactions
not an allergic response - it is increased sensitivity . it is a genetically determined reactivity to a chemical
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Bhopal tragedy
Dec 1984, 40 tons methyl ioscynate gas leaked from pesticide plant .0 .5 million exposed - 3800 killed instantly . 20k premature deaths in following decades, 100k chronically ill
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Mechanisms of toxicity
exposure phase, toxixokinetic phase , toxicodynamic phase
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exposure phase
magnitude of toxic effects depends on: form of exposure route of exposure, nature of contact, intentional or accidental, physical state of compound- ie more serious effects if inhaled - as by pass 1st PM
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Toxicokinetic phase
ADME - A, conc, SA od exposure, D- transport proteins, barriers BBB, M- toxication E- kidney damage if excreted via kidneys?
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Toxicodynamic phase
events following drug receptor interaction that will result in toxic effects-
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what is toxicity
molecular reaction bet. sub and endogenous molecule
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types of molecular reaction (ie from prev slide(
non covalent bonding (usually reversible) Covalent binding (practically irreversible - perm alters endogen. mol.) Hydrogen abstraction - free radical formation. Electron transfer (redox rxtions) Enzymatic reactions
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causes injury to cells - Direct (primary) indirect (secondary)
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occurs if toxic sub interacts with one/more of cells components
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results from disruption of microenvironment within cell- ie metabolism,cell activity
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during cell injury what is altered
homeostatis - adaptive responses aim to balance distrubances to cell metabolism etc - if these fail - cell is irreverisbly damaged - cell death
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Drug misuse poisoning deaths are mainly
accidental - most common - opiates
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poisoning is
the 2nd most common method of suicide in the Uk. F>M
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common suicide drug
paracetamol, propranolol - slow HR
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toxicokinetics of propranolol (ADME)
A-rapid ab orally D- rapidly distributed - v lipophillic - into tissue including CNS. M- extensive hepatice met. E- 95-100% ingested dose excreted in urine . T0.5= 3-6hrs
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toxicodynamics of propranolol
decreased HR and CO . Possible bronchospasm and hypoglycaemia. Blockade of Na channels - seizures, ventricular arrthymia
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management of propranolol OD
keep airways clear for breathing. resuscitation with fluid therapy- iv atropine sulphate for bradycardia. iv glucagon- increase HR
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CO poisoning
incomplete combustion of carbon based fuels . Route exposure - inhaltion.
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toxicokinetics of CO poisoning
binds to Hb - reducing Hb O2 carrying capacity . Also inhibits mito respiration. both result in less o2 in the blood
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initial CO poisoning symptoms
dizzy, nausea vomit, tiredness , confusion, stomach pain, shortness of breath
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symptoms could develop to
impaired mental state , vertigo, tacycardia, seizures , loss of consciouness, chest pain/heartv attack
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100% o2 if available- using tight fit mask. until COHb levels are less than 3% in non smokers 10% in smokers .
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Half life of COHb when breathing air
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when breathing 100% o2
80mins - O2 accelerates elimination of COHb Vs air
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all things are poisons


there is nothing without poisonous qualities - it is the dose and frequency which makes something toxic

Card 3


all drugs have a


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botox in the smallest conc can be


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Card 5


different drugs have different


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