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Block 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Define ‘pharmacology’

A

The branch of medicine concerned with the uses, effects and modes of actions of drugs. The study of drugs in all their aspects.

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2
Q

Define ‘toxicology’

A

Branch of science concerned with nature, effects, and detection of poisons

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3
Q

Define ‘pharmacodynamics’

A

Pharmacodynamics the branch of pharmacology involved with studying the mechanisms of action of drugs. WHAT THE DRUG DOES TO THE BODY, relative efficacy at receptors, the time course of effect, dose/concentration-dependence effect. Concentration vs. effect.

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4
Q

Define ‘pharmacokinetics’

A

Pharmacokinetics is WHAT DOES THE BODY DO WITH THE DRUG. Includes processes of absorption, distribution, metabolism, and elimination (ADME processes) Concentration vs time.

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5
Q

Define ‘clinical pharmacology’

A

Science of drugs and their clinical use

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6
Q

Define ‘therapeutics’

A

The branch of medicine concerned with the treatment of disease and the action of remedial agents. The treatment of clinical illness/disorders.

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7
Q

Define ‘therapeutic effect’

A

Consequence (expected or unexpected) of medical treatment of any kind, the results of which are judged to be desirable and beneficial

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8
Q

Define ‘adverse effect’

A

Consequence (expected or unexpected) of medical treatment of any kind, the results of which are judged to be dentrimental and undesirable.

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9
Q

Define ‘therapeutic index’

A

The therapeutic index is a metric to predict drug toxicity and the relative safety of the drug. It is a ratio taken of the toxic dose to the therapeutic dose. The larger the ratio the greater the relative safety of the drug. (meaning, if you have a toxic dose that requires a high concentration and a therapeutic dose requiring a very low concentration)

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10
Q

Explain Therapeutic index = TD50/ED50

A
  • High therapeutic index = LD50»ED50; this means that the drug should be fairly safe since the lethal dose is at a higher concentration than the effective dose
  • Low therapeutic index = LD50 = ED50; this means that the drug is more dangerous since the lethal dose nears the effective dose
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11
Q

Define ED50

A

Effect dose in 50% of patients

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12
Q

Define TD50

A

Toxic dose in 50% of patients

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13
Q

Outline the process of drug discovery and development

A
  • Broad screen around 5000 to 10,000 drugs for a specified use. Then screened for toxic effects or agents that are known to cause detriment to human health.
  • ~250 enter preclinical trials.
    1) animal models of disease for effects and toxicity
    2) animal studies for chronic toxicity
  • 5/250 will likely enter clinical trials and will result in about one FDA approved drug.
  • About 1 of every 5000-10000 make it to market and costs $800 million.
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14
Q

Define the term ‘clinical trials’

A

A study involving humans to find out whether an intervention including treatments or diagnostic procedures (which it is believed) may improve a person’s health, does so.

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15
Q

Summarize purpose of Phase 1, Phase 2, Phase 3 and Phase 4 clinical trials, and pre-phase 1

A
  • Phase 1 Human Pharmacology: First time in healthy human (explore PK and PD, metabolism, and tolerance)
  • Phase 2 Therapeutic Exploratory: First time in patient (Explore dosage and use)
  • Phase 3 Therapeutic Confirmatory: EFficacy and safety in large clinical trials (Efficacy and safety profile; assess benefit/risk and dose-response relationship)
  • Phase 4 Therapeutic Use: Efficacy and safety in everyday practice (Refine dosage and study rare ADRs)

pre-phase 1: animal studies to determine safety in humans

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16
Q

Outline the purpose of genotyping for drug response and drug toxicity

A

By sequencing genomes of patients, we can determine genetic compatibility with certain drugs and which drugs will be therapeutically more effective. We can also determine adequate doses for individuals and predict potential side-effects that are genetically linked.

e.g. Abacavir - reverse transcriptase inhibitor, is a treatment of HIV. Its side effects include hypersensitivity. In 5.6% of the population patients are more hypersensitive to treatment.

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17
Q

Define ‘pharmacokinetics’

A

Pharmacokinetics is any process that involves the interaction of the body with the drug that is administered.

  • Includes processes of absorption, distribution, metabolism and elimination of the drug within the body.
  • What the body does with the drug
  • Absorption, distribution, metabolism, elimination (ADME processes)
  • Measurable data: Tmax, Peak/trough concentration
  • Individual parameters: Bioavailability, clearance, half life, volume of distribution.
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18
Q

Outline the process of drug absorption

A

Drugs entering the blood stream

  • For compounds to reach thte tissues intended they need to enter the bloodstream first.
  • The amount of compound absorbed into the blood will determine the bioavailability of the drug.
  • Different methods will yield different bio-availabilities:
    1) Gastrointestinal endothelial cells can influence uptake: stomach doesn’t absorb much drugs, intestines can have negative feedback on stomach to prevent emptying and lower absorbance
    2) Direct entry into the blood stream via intravenous injection is faster
  • If a % of drug ends up in urine, you can sure at least that % of drug was absorbed
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19
Q

Outline the process of drug distribution

A

Transferring of drugs from blood plasma to the tissues/interstitial fluids of organs

  • Affected by:
    1) polarity/solubility of molecules
    2) Binding to serum proteins
    3) Molecular size
    4) Blood flow rates
    5) Barriers e.g. blood-brain barrier
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20
Q

Outline the process of drug metabolism

A

Drugs are converted to water soluble substances and excreted by kidneys:

  • Phase 1: DRug’s functional groups are modified
  • Phase 2: Metabolites added to drug (conjugation)
  • Occasionally, drug metabolite can be more active than initial drug
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21
Q

Outline the process of drug elimination

A

Drug removed from the body via urine mainly (also respiration and faeces)

  • Unless elimination occurs, accumulation of drug or metabolites can adversely affect the patient.
  • Factors that influence urinary elimination:
    1) Glomerular filtration rate
    2) Secretion into nephron tubules
    3) Movement through GI tract
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22
Q

Define ‘bioavailability (f)’

A

The proportion of drug that reaches the SYSTEMIC circulation (must make it past gut and liver).
- Drug into the body = f*dose

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23
Q

Define ‘volume of distribution (L)’

A

The theoretical volume that would be necessary to contain the total amount of administered drug at the same concentration that is observed in the blood plasma.

  • Vd=A/C where A = amount of drug administered (dose) and C = plasma concentration of the drug administered
  • Determine Vd from In(C plasma) vs Time plot: Extrapolate linear part of plot to y-axis for IV dose -> this point is C(plasma 0), A is drug administered (only known as time 0)
  • High Vd = drug is mostly in the tissues (high distribution)
  • Represent degree which drug is distributed in the body tissue rather than the plasma
  • Reduced by plasma protein binding and increased by tissue protein binding
  • Used to determine loading dose (i.e. initial dose to achieve C-plasma ASAP)
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24
Q

Define ‘clearance’ (vol/time)

A

Volume of plasma from which drug is completely removed per unit of time:

  • Clearance (vol/time) = rate of drug elimination (mole/time) / the plasma concentration (mole/vol)
  • Clearance = elimination rate constant (1/time) x Volume of distribution (L)
  • For each organ of elimination, they have their respective clearance (renal is most important)
  • Single most important pharmacokinetic parameter: determines maintenance dose-rate
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25
Q

Define ‘half-life’

A

Half-life is the time that it takes for the plasma concentration or the amount of the drug in the body to be reduced by 50%. The half-life of a drug depends on its clearance and volume of distribution.

  • Index for time-course of drug elimination and drug accumulation
  • Used to guide dose intervals (frequency of dose)
  • Steady state is usually reached after 5 half-lives
  • T(1/2) is proportional to the ratio of Vd/Cl: T(1/2) = 0.7Vd/Cl
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26
Q

Define ‘first-pass metabolism’

A

The amount of metabolism that occurs after the drug is absorbed but before the drug reaches the systemic circulation (by gut wall and liver)
- Cirrhosis = liver due to long term damage (scar tissue replaces liver cells): decreases first-pass metabolism

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27
Q

Define ‘extraction ratio’

A

Extraction ratio is the proportion of drug removed by a particular organ from the blood plasma

  • Excretion is a function of the amount of blood flow that passes through that organ, extraction ratio, and drug concentration
  • Elimination(renal) = Renal blood flow * drug plasma concentration * renal extraction ratio
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28
Q

Define ‘steady state’

A

Amount of drug into the body equals the amount of drug out of the body:

  • Drug in = Drug out
  • Bioavailability * dose = Clearance *C-plasma (steady state)
  • Practical definition is when drug plasma concentration in each dosing interval are within 5-10% of those in the previous interval: approximately after 5 half-lives the variation in concentration is so slight it’s considered steady state
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29
Q

Describe concepts of drug distribution: blood flow

A

The cardiovascular system varies between individuals in terms of its efficiency, heart rate and contraction volume

  • Increased blood flow can influence how easily compounds can be absorbed
  • Higher blood pressures and blood flow increase elimination
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30
Q

Describe body composition

A

Body composition varies between individuals and distribution of drugs and compounds within tissues varies between fat, muscle, etc.

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31
Q

Describe ‘transporter expression’

A

Genetic expression of transporter proteins can alter the rate of absorption and hence the bioavailability of any drug administered:

  • Increased gene expression of protein transporters will lead to more efficient translocation of the drug between compartments:
    1) increased absorption
    2) increased elimination
32
Q

Describe ‘protein binding’

A

Albumin is an example of a protein that binds substances to be carried within the blood. If drug is bound to proteins with higher affinity than the transporters that distribute them within the tissues, then there will result in an accumulation within the blood of drug-protein complex.

33
Q

Describe ‘organ failure’

A

Organ failure, especially those which deal with metabolism and elimination will alter the effects of drug by slowing down clearance. Decreased clearance of a drug leads to increased/prolonged effects

34
Q

Describe ‘barriers and integrity of barriers’

A

Barriers between compartments and tissues can decrease distribution with decreased permeability or increase distribution with increased permeability
- E.g. blood brain barrier decreases drugs that go to the brain.

35
Q

Give examples of how various clinical states (e.g. age, drug dose) can affect the absorption, distribution, metabolism and elimination of a drug

A

Age:

  • Important age change: decreased renal elimination of drugs
    1) e.g. creatine clearance decreases by 8mL/min/1.73 m^2 per decade
  • Age change: increase body fat and decrease body water
    2) Increase distribution of lipophilic drugs and their half-lives
36
Q

Describe paracetamol overdose case study

A
  • Delayed absorption - stomach has limited absorption whereas intestines absorb most of drug
  • Paracetamol overdose occurs hours after initial peak
  • Paracetamol is metabolized as: Paracetamol > NAPQI > NAPQI-glutathione
  • The toxic element is the NAPQI intermediate (converted from Paracetamol via CYP450 enzyme)
  • Factors affecting toxicity:
    1) increase toxicity: CYP450 Induction, Glutathione depletion
    2) Decrease toxicity: CYP450 inhibition, Enhanced sulphation (of Paracetamol)
37
Q

Outline the range of mechanisms by which available drugs produce their effects

A

Drugs are compounds which can produce effects via interactions with the cells of the body particularly on protein receptors, enzymes, channels, transporters and other functional proteins. It is the binding of drugs to proteins that alters the functions of proteins and leads to drug effects.
Examples:
- Drugs can mimic endogenous substances to activate receptors within the body to yield a certain effect
- Replacement - replacement of deficient substances to replace deficient precursor molecules required for synthesis
- Activating/deactivating receptors
- Enzyme inhibition
- Binding to and inactivating cytokines and other signalling molecules
- Inactivation of immune cells

38
Q

Explain how the mechanism of action of a drug underlies dose response relationship and possible side effects

A

Understanding the mechanism of action of a drug allows for prediction of effects and side effects of the drug:

  • Whether drugs are an agonist or antagonist of an enzyme result in opposite outcomes
  • Binding efficiency and mode of competition give indicator on overall effect on body
  • Dose-response relationships are metrics used to monitor changes in an organism caused by different levels of exposure to a substance
  • e.g. Pharmacokinetics = Concentration vs Time, Pharmacodynamics = Concentration vs. Effect
39
Q

Summarize mimicking/replacing an endogenous substance of drug action

A

Mimicking: Administering a structural analogue of a deficient or absent substance

  • E.g. Addison’s disease
  • Adrenal glands do not form cortisol or aldosterone
  • Replacement with analogues like fludrocortisone

Replacement: giving the absent/deficient substance

  • e.g. Diabetes type 1
  • Autoimmune disease prevents synthesis of insulin
  • Receptors will still respond to insulin, but it is just not synthesized
  • Receptors will bind replacement insulin
40
Q

Summarize activating or blocking a receptor of drug action (including receptors with second messengers, ion channels and transporters)

A
  • Activation of receptors: agonist binds and increase activity of the mechanism it is a part of.
  • Inhibition of receptors: Antagonist binds and decrease activity of the mechanism it is a part of.
  • Examples:
    1) G-Protein coupled receptors (GPCR):
  • Adrenergic receptors (Beta-receptor)
  • Adrenaline is agonist
  • Salbutomol - low concentrations will bind to beta-2 adrenergic receptors (dilates airways) and at high concentrations will bind to Beta-1 adrenergic receptors (increase heart rate).

2) Ligand-gated ion channels -NAChR
3) Voltage-gated ion channels and transporters

41
Q

Summarize inhibiting an enzyme of drug action

A

Inhibition of an enzyme will cause accumulation of substrate and decrease product.
Example:
- Cyclo-oxygenase (COX): catalyzes production of pro-inflammatory proteins (prostaglandins)
- NSAIDs inhibit COX -> NSAIDs are inflammatory

42
Q

Summarize binding to and inactivating cytokines or causing cell death

A
  • When drugs/compounds bind to cytokines and signalling molecules they can either turn off the signal or turn on signals.
  • Activation of cell death can result from activation of caspase-3 pathway
  • Example: TNF-alpha
    1) TNF-alpha can cause inflammation
    2) Drugs/compounds can competitively bind TNF-alpha and cause less activation of endogenous receptors
    3) Binding decreases inflammation
43
Q

Outline an example of a drug (and the condition for which it is used) to demonstrate each of the mechanisms described above

A

Mimicking or replacing endogenous substances

  • Cortisone (Addison’s disease)
  • Insulin (Type 1 Diabetes)

Activating or antagonizing receptors
- Salbutamol (beta-2 selective adrenoreceptor agonist for asthma)

Enzyme inhibition
- NSAIDs (COX inhibitor) for anti-inflammatory

Cytotoxic mechanisms

  • Mostly not targeted
  • Many now use biological techniques to target
44
Q

Define Selectivity vs Specificity

A

Selectivity - the ability of a drug to bind to a particular receptor and not others. Measure of affinity of drug for its receptor.

Specificity - the ability of a drug to elicit only a narrow range of effect. Measure of how narrow the effects of the drug are on the body. More related to where the receptors are found in the body. A low specificity drug binds to receptors found on many organs and locations.

45
Q

Define ‘agonist’

A

Chemical that binds to a receptor and activates the receptor to produce a biological response

46
Q

Define ‘antagonist’

A

Chemical that binds to a receptor and results in no activation of the receptor and blocks or dampens the agonist-mediated response instead of producing the biological response

47
Q

Define ‘potency’

A

Concentration to get half the maximum effect of the drug (EC50). Lower EC50 means higher potency. Measure of effect of drug per quantity.

48
Q

Define ‘pharmacodynamics’

A

Pharmacodynamics is the branch of pharmacology involved in the study of drugs and their mechanisms of action. WHAT THE DRUG DOES TO THE BODY.

49
Q

Define ‘EC50’

A

EC50 is the effective concentration of drug administered where 50% of the receptors are activated (Concentration at half Vmax).

50
Q

Define ‘Efficacy’

A

Overall maximum effect of the drug, regardless of quantity. Measured by Vmax. You can have drugs that are equally efficacious but not equally potent. Efficacy is measured by the maximal response whereas potency is determined by EC50.

51
Q

Define ‘inverse agonsit’

A

Inverse agonists binds to the same receptor as the agonist but causes an opposite biological effect of the agonist.

52
Q

Describe the concentration response curves and be able to identify the EC50 and compare potency of agonists

A

EC50 - effective concentrations are determined by finding the concentration at which 50% of the enzyme -substrate complexes are formed.

Potency - potency can be compared by comparing EC50. The lower the EC50 the more potent a drug/compound is.

53
Q

Using adrenergic receptor agonists as an example, explain the concept of drug selectivity

A

Drug selectivity - ability (ratio) of a drug to bind with a certain receptor and not receptor

  • Selectivity = EC50 selected receptor/EC50 other receptor
  • Example:
    1) Beta-2 binds to beta-2 receptors with a 1000:1 ratio over Beta-1 receptors.
    2) Beta-2 receptors hit EC50 much earlier (i.e. much higher potency)
    3) Selectivity = EC50 for Heart rate (beta-2) / EC50 for Airway SM (beta-1)
    4) Selective drugs will only bind to one type of receptor and this will be determined by the effects that are manifested in the patient.
54
Q

Using atropine as an example, explain the mechanism of action of drugs which are defined as ‘antagonists’

A

Atropine is a competitive antagonist.

  • Competitive antagonists bind to the same active site as agonists do but do not elicit a response
  • Occupation of the active site and decrease in the agonist response.
  • Increased concentrations of the agonist will displace the antagonist.
  • Atropine is a muscarinic cholinergic receptor agonist but no blockage of NAChR
55
Q

Describe the different types of antagonists/inverse agonists

A
  • Competitive: can be overcome by more agonist; shifts curve right
  • Irreversible/non-competitive: cannot be overcome by more agonist; lowers Vmax.
  • Inverse Agonist: bind to receptor and causes opposite as agonist
56
Q

Describe the purpose of the ‘adverse drug reactions’ classification

A

Adverse drug reactions account for the fourth most common cause of death in patients and third most cause of hospitalization. With most of the population (requiring medical attention) already undergoing poly-pharmacy drug interactions are hard to predict.

57
Q

Describe dose-related (Type A) adverse reactions and outline the strategies to identify and minimize the occurrence of each sort of adverse drug reaction

A

Dose related (Type A) ADR

  • Extensions of known predictable pharmacological effects.
  • High incidence rate, low morbidity
  • Increased doses of therapeutic agents can cause adverse effects.
  • Treat by adjusting dose to get into therapeutic range
  • International normalized ratios are performed for drugs to determine the lowest risk possible for the highest therapeutic effect.
58
Q

Describe Bizzare/idiosyncratic (Type b) adverse reactions

A
  • Bizarre effects due to individual variation, or mechanisms of drug action/interaction with other agents that we do not yet understand
  • Low incidence rate, high morbidity
  • Treat by stopping (no dose adjustment)
59
Q

Describe other types of adverse reactions

A 
Type C: chronic/statistical
Type D: Delayed
Type E: End of use
Type F: Failure of therapy 
Type G: Genetic
60
Q

Define ‘class effects’ in relation to adverse drug reactions

A

Class effects - The definition of drug class effect is based on three concepts: similarly in chemical structure, similarity in mechanism of action or similar pharmacological effects. Drugs of the same class are expected to have similar ADRs

61
Q

Define ‘dose-related effects’ (ADR)

A

Adverse drug reactions that are a result of too high a dose

62
Q

Define ‘susceptibility’

A

Lack of ability to resist a drug usually because of genetics which are not compatible with the drug administered

63
Q

Define ‘idiosyncratic’

A

Type B reactions are drug reactions which occur rarely and unpredictably among the population. Usually allergic reactions, with enzyme polymorphism, renal or hepatic failure to metabolize the drug, individual variation in pharmacodynamics.

64
Q

Describe the process of predicting drug toxicity via ‘therapeutic index’

A

Therapeutic index - the therapeutic index is a metric to predict drug toxicity and the relative safety of the drug.

  • It is a ratio taken of the toxic dose to the therapeutic dose.
  • The larger the ratio the greater the relative safety of the drug.
  • Therapeutic index = LD50/ED50.
  • High therapeutic index = LD50&raquo_space; ED50. Drug should be fairly safe since the lethal dose is at a higher concentration than the effective dose.
  • Low therapeutic index = LD50 approximately equal to ED50. This means that the drug is more dangerous since the lethal dose nears the effective dose.
65
Q

Outline the logic behind the different way in which causal relationships between a drug and an adverse effect are determined for an individual vs a population.

A

Population - rule of 3’s - If an adverse event occurs on average every 1 in X subjects exposed you need to observe 3X subjects in order to have a >95% chance of observing the adverse event. (e.g. To observe an ADR with 1 in 1000 chance of occurring, need to have a trial of 3000 patients).

Individual - if there are adverse drug reactions in an individual you do a case review and determine what the cause of the adverse drug reaction was. Whether it was a dosage issue or if it was due to idiosyncratic ADR. Stop drug usage or find out other interactions. Discuss deprescribing and determine all the drugs that they were taking. Prioritizing the medicines they are on currently and eliminate to control interactions the ones that are suspected of causing a negative interactions. Wean important drugs that deal with CNS, beta blockers, etc.

66
Q

Give examples of adverse drug reactions of NSAIDs

A

NSAID - Non-steroidal anti-inflammatory drugs (inhibit COX-1 and COX-2)

  • Platelets contain COX-1 but not COX-2
  • Thromboxane A2 is predominant COX product and promotes platelet aggregation.
  • NSAIDs ADRs:
    1) Type A: GIT ulcers, renal impairment, reduced platelet aggregation, asthma.
    2) Type C: Myocardial infarction
  • COX-2 specific inhibitors drugs have similar benefits with less ADRs
67
Q

Give examples of adverse drug reactions of Warfarin

A

Warfarin - anticoagulant (Blood thinner)

  • Do NOT take with CYP2C0 inhibitor
  • Risk of clotting if too little
  • Risk of bleeding if too much
  • Large range of clearance range in patients (risk of improper dosage)
68
Q

Give examples of beta-2 agonist

A

dilation of bronchial passage (asthma treatment)

1) Type A:
- Tremor
- Tachycardia
- Sore throat

2) Type C:
- sudden death

69
Q

Demonstrate how pharmacokinetics is used to achieve optimal antibiotic effect (i.e. concentrations above MIC (minimum inhibitory concentration, MBC (minimum bactericidal concentration) and minimize toxicity

A

MIC (minimum inhibitory concentration) - lowest concentration of a drug or chemical that prevents visible growth of a bacterium (the growth rate = the death rate)

MBC (minimum bactericidal concentration) - the lowest concentration of a drug or chemical that results in microbial death.

Use pharmacokinetics to achieve a steady state concentration above MIC and MBC, while being below the toxicity threshold. Need to consider ADME processes to direct proper dosage for steady state concentrations.

70
Q

Understand the rationale for therapeutic drug monitoring (target concentration interventions)

A
  • Therapeutic drug monitoring = monitoring drug effects while measure blood concentration of drug.
  • Steady state is when dose rate = elimination rate
  • Altering dose rate changes steady state concentration.
  • Therapeutic drug monitoring involves giving dosage, monitoring therapeutic effects, and adjusting dosage to meet targeted concentration.
71
Q

Define ‘volume of distribution’

A

Volume of distribution [L] - the theoretical volume that would be necessary to contain the total amount of administered drug at the same concentration that is observed in the blood plasma.

  • Vd = A/C:
    1) A = amount of drug administered (dose)
    2) C = plasma concentration of the drug administered.
  • Determine Vd from In(Cplasma) vs Time plot
    1) extrapolate linear part of plot to y-axis for IV dose -> this point is C-plasma,0.
    2) A is drug administered (only known at time 0)
  • High Vd = drug is mostly in the tissues (high distribution)
  • Represent degree which drug is distributed in the body tissue rather than the plasma
  • Reduced by plasma protein binding and increased by tissue protein binding.
  • Used to determine loading dose (i.e. initial dose to achieve Cplasma ASAP)
72
Q

Define ‘area under curve’ (AUC)

A

The average plasma concentration of drug exposure over a period of time (i.e. cumulative exposure to the drug)

  • on a plasma concentration vs time graph
  • AUC = bioavailability x Dose / clearance
73
Q

Explain how AUC, volume of distribution, clearance and half-life are used to help achieve dose adjustments that achieve therapeutic concentrations

A

AUC = cumulative exposure to drug
Volume of distribution = metric of drug distribution in body
Clearance = volume of plasma which is cleared of the drug per unit of time
Half-life = time it takes for 50% of the drug in the body to be eliminated

AUC, Vd, clearance, and half-life all measure how long the drug is affecting the body. These metrics can help determine the timing and quantity of the dosage required to reach the target steady state concentration

74
Q

Explain the difference between medicines and ‘natural products’

A

Major difference is natural produces are unregulated. This leads to large variation of dosage and risks in preparation. Some natural products don’t have evidence supporting their effectiveness and can be actually harmful.

Medicine is heavily regulated, supported with evidence, and accurately prepared by professionals.

75
Q

Consider and contrast therapeutic and non-therapeutic use of following: alcohol

A
  • When naturally distilled, can have methanol mixed with ethanol
  • Methanol is poisonous in low dosage
  • Methanol poisoning isn’t immediately distinct from regular ethanol until too late.
76
Q

Consider and contrast therapeutic and non-therapeutic use of following: nicotine

A
  • Stimulates ACh receptors of the autonomous nervous system
  • Natural nicotine sources have large variation of dosage
  • Natural nicotine medicine can have ADR when combined with modern medicine
77
Q

Consider and contrast therapeutic and non-therapeutic use of following: opiates

A
  • OxyContin = regulated drug
  • Heroin = street-version
  • Heroin is unregulated and can be mixed with other drugs for lethal effects
  • Dosage is unknown in illegal version

Block 1 (9 decks)

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