Discoveries in Pharmacology and the Risk : Benefit Ratio of Drugs Flashcards

1
Q

Other than to treat or prevent diseases, what can drugs be used to prevent?

A

Pregnancy (contraception).
(Lecture 1, Slide 6)

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2
Q

What are 3 adverse reactions patients can have to drugs?

A

Overdoses, idiosyncratic reactions (cannot be explained by known mechanisms) and hypersensitivity.
(Lecture 1, Slide 7)

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3
Q

What types of drugs can be abused?

A

Illegal - Illegal drugs such as heroin, cocaine, cannabis, ecstasy
Legal - such as nicotine, alcohol
(Lecture 1, Slide 7)

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4
Q

What are the three ways in which drugs can be used to combat a condition?

A

Curative (Eliminate underlying condition)
Suppressive (Doesn’t eliminate underlying condition)
Preventative (Stops condition occurring)
(Lecture 1, Slide 9)

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5
Q

What are the 3 positive impacts of drugs?

A

Can save lives, improve quality of life (such as diabetes or epilepsy), or even seeming trivial things (such as avoiding sleepless nights or embarrassment / discomfort)
(Lecture 1, Slide 10)

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6
Q

What are the 3 negative impacts of drugs?

A

Seemingly trivial (e.g drowsiness), Reduced quality of life (erectile disfunction) and can be life-threatening (Overdose, addiction / abuse)
(Lecture 1, Slide 11)

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7
Q

What is the Risk : Benefit ratio?

A

The toxicity of the drug must be weighed against the severity of the condition, e.g you wouldn’t use a very toxic drug on a mild condition but you would use a mildly unpleasant drug on a life-threatening condition
(Lecture 1, Slide 15)

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8
Q

What 3 things would a theoretically risk free drug be?

A

Physician must know exactly what action is required and use the drug correctly.
Drug had only the desired reaction and did nothing else.
Exactly the right amount of action was easily achieved.
(Lecture 1, Slide 16)

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9
Q

Do risk free drugs exist?

A

No.
(Lecture 1, Slide 16)

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10
Q

Why are many drugs insufficiently selective?

A

As dose increases, other organs and tissues are affected.
(Lecture 1, Slide 17)

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11
Q

How may a drug produce permanent changes?

A

Prolonged modification of a tissue.
(Lecture 1, Slide 17)

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12
Q

Why do drugs affect patients differently?

A

Many patients are heterogenous.
(Lecture 1, Slide 18)

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13
Q

Why are dosage adjustments imprecise and crude?

A

Table dose increases often involve doubling of dosages e.g 10 > 25 > 50 > 100 mg.
(Lecture 1, Slide 18)

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14
Q

State 3 ways we can reduce drug risk.

A

By gaining more knowledge of the disease we are trying to treat.
Site-specific delivery.
Site-specific effects.
Informed, careful prescribing.
Pharmacogenomics and Personalised Medicine.
(Lecture 1, Slide 19)

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15
Q

What are some problems in drug development? (Name 3)

A

The need to use animals
Alternatives to animals aren’t representative
Ethical concerns
Legislation
Costs ~ $2.7 billion ( ~ £2.2 billion) to bring a new drug to market.
(Lecture 1, Slide 22)

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16
Q

What are Naturopathic medicines?

A

Include things such as Chinese herbal medicine and can contain pharmacologically active ingredients but the dose and composition is unknown.
(Lecture 1, Slide 27)

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17
Q

What are Homeopathic medicines?

A

Made by dilutions in water down to a10^-60 volume of the original compound that contain no active molecules unless taken in extremely massive volumes.
(Lecture 1, Slide 27)

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18
Q

What is a placebo?

A

An inert (chemically inactive) substance or sham (bogus/fake) therapy
(Lecture 1, Slide 28)

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19
Q

Why does the placebo effect work?

A

All diseases have a psychosomatic component, i.e. belief in therapy results in improved health.
(Lecture 1, Slide 28)

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20
Q

What are the 3 aims of Clinical Pharmacology?

A

To explain drug action at a molecular level, enable development of new drugs and to show that candidate drugs ( a compound with strong therapeutic potential) are safe.
(Lecture 1, Slide 29)

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21
Q

State 3 ways clinical pharmacology achieves its aims.

A

Animal and human studies
Research into drugs and drug action at a molecular cellular, tissue and organ levels
By using placebo controlled, double blind (where the patient doesn’t know what drug they are given and the administrator doesn’t know what drug they are giving) trials.
(Lecture 1, Slide 29)

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22
Q

What was pharmacology initially based on?

A

Acquired learning; a trial and error approach done without knowledge of either disease or treatment.
(Lecture 2, Slide 4)

23
Q

What is drug discovery?

A

A rational approach to identifying biologically active agents that often originate from natural sources, finding out how they work and then using knowledge to find new and better agents.
(Lecture 2, Slide 5)

24
Q

What did Hippocrates (born 460 BC) believe about disease treatment?

A

Believed diseases could be treated.
(Lecture 2, Slide 7)

25
Q

What did Galen (130 - 201 AD) believe about disease treatment?

A

Believed disease was caused by disturbance of liquid components (humours) of the body and that these had properties similar to seasons and ageing.
(Lecture 2, Slide 7)

26
Q

How did people “balance the humours” in ancient times?

A

Usually by bleeding emetics (a medicine that causes vomiting) or massaging.
(Lecture 2, Slide 7)

27
Q

What did the Arab culture (600 - 1100 AD approx.) contribute to pharmacy?

A

Pharmacy processes of concentration and purification of medicinal herbs (evaporation of extracts, filtration, distillation).
(Lecture 2, Slide 8)

28
Q

What theory did Paracelsus (1493- 1541) develop about vital functions?

A

Developed theory that vital functions are chemical (rather than humours) and that these can be treated with chemicals.
(Lecture 2, Slide 8)

29
Q

What did Paracelsus extract from plants to form crude drugs?

A

Active principles (induces pharmacological activity).
(Lecture 2, Slide 8)

30
Q

What did Langley (1901) suggest?

A

That there must be a “receptive substance” on the target tissue which binds the chemicals - later proven true
(Lecture 2, Slide 10)

31
Q

What did Otto Von Loewi’s experiments in 1921 first demonstrate?

A

The chemical nature of neural transmission.
(Lecture 2, Slide 11)

32
Q

What was the method of Otto Von Loewi’s experiment in 1921?

A

He took 2 isolated berating frog hearts, perfused with saline, and stimulated the vagus nerve in one heart (so the heart beat slowed) and when the saline from the first heart was introduced to the second heart, it’s heart beat also slowed.
(Lecture 2, Slide 12)

33
Q

What did Otto Von Loewi suggest after his transmission experiment?

A

That a substance had been released from the heart. (which later was proven to be acetylcholine)
(Lecture 2, Slide 12)

34
Q

How do agonists show affinity and efficacy?

A

A substance binds to a receptor (affinity), activates the receptor (efficacy) and produces a response.
(Lecture 2, Slide 14)

35
Q

Name 2 examples of a response to an agonist.

A

Change in heart rate
Change in blood pressure
Change in acid secretion in the stomach
Relaxation / Contraction of intestine.
Relaxation of airways in the lungs.
(Lecture 2, Slide 16)

36
Q

What did Henry Dale first witness in 1904?

A

Receptor antagonism
(Lecture 2, Slide 18)

37
Q

What was the method of Henry Dale’s experiment in 1904?

A

He injected adrenaline into a cat, which resulted in a rise of blood pressure.
He then injected adrenaline into a cat which had received ergot and saw no rise in blood pressure.
He then came to the conclusion that Ergot had blocked the effect of adrenaline.
(Lecture 2, Slide 18)

38
Q

How do antagonists show affinity but not efficacy?

A

A substance binds to a receptor (affinity) but does not activate it (no efficacy), producing no response
(Lecture 2, Slide 19)

39
Q

Can an Antagonist produce a response in the body?

A

It can by blocking an agonist from producing its response
(Lecture 2, Slide 19)

40
Q

What did John Henry Gaddum and Heinz Ott Schild develop in the 1940s?

A

A mathematical theory of antagonism.
(Lecture 2, Slide 21)

41
Q

What is Acetylcholine?

A

It is a widespread chemical neurotransmitter in the body
(Lecture 2, Slide 23)

42
Q

What does Acetylcholine control?

A

Autonomic function and voluntary movement, and is involved in arousal, attention, memory and motivation
(Lecture 2, Slide 23)

43
Q

Where is Acetylcholine found?

A

In the brain and periphery.
(Lecture 2, Slide 23)

44
Q

What is Muscarine derived from?

A

The fly agaric mushroom (Amanita muscaria)
(Lecture 2, Slide 24)

45
Q

What does Muscarine do?

A

It mimics the autonomic effects of Acetylcholine.
(Lecture 2, Slide 24)

46
Q

What is Nicotine derived from?

A

Tobacco plant (Nicotinia tabaxum)
(Lecture 2, Slide 25)

47
Q

What does Nicotine do?

A

It mimics the central effects of Acetylcholine. (Decreases appetite, heightens mood, gives better memory and increases alertness)
(Lecture 2, Slide 25)

48
Q

What is a Muscarinic Acetylcholine receptor?

A

A Ligand-gated ion channel that is important in autonomic function.
(Lecture 2, Slides 26 and 27)

49
Q

What are the two Nicotinic Acetylcholine receptors and what do they do?

A

They are G-protein coupled receptors;

Neuronal type, which is important in central functions
Muscle type, important in skeletal muscle functions.
(Lecture 2, Slides 26 and 27)

50
Q

What is Atropine and what is it used for?

A

It is an antagonist that selectively blocks muscarinic acetylcholine receptor.
(Lecture 2, Slide 29)

51
Q

What effect does muscarinic acetylcholine receptor blocked by Atropine have on the body?

A

Reduces salivations and bronchial secretions before surgery, and treats excessively low heart rate.
(Lecture 2, Slide 29)

52
Q

What is Vecuronium and what is it used for?

A

It is an antagonist that selectively blocks muscle-type nicotinic acetylcholine receptor.
(Lecture 2, Slide 29)

53
Q

What effect does muscle-type nicotinic acetylcholine receptor blocked by Vecuronium have on the body?

A

Produces paralysis during surgical procedures.
(Lecture 2, Slide 29)

54
Q

What types of molecules can be used as drugs?

A

Peptides, proteins, antibodies and nucleotides.
(Lecture 2, Slide 31)