Pharmacology Flashcards

1
Q

What are the dangers of drug use?

A

Allergies = death

Toxicity = death

Interactions with other drugs which can have an effect on absorption and metabolism of other drugs.

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2
Q

What do LA work on?

A

Block propagation of impulses on ion channels

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3
Q

What is a positive action of adrenaline (vasoconstrictor)?

A

Constricts the blood vessels and allows the drug to remain in the desired area for longer.

Allows lower volume of the drug to be used.

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4
Q

What are the negative actions of adrenaline (vasoconstrictor)?

A

Constricts vessels allows drug to remain in the area for longer which can be toxic to the nerve tissue.

People can also have a reaction.

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5
Q

Name examples of local anaesthetics.

A
Lignocaine.
Prilocaine.
Articaine.
Bupivivaine.
Mepivicaine.
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6
Q

Name commonly prescribed antibiotics.

A

Amoxycillin
Metronidazole.

Doxycycline.
Clindamycin.

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7
Q

Name antiviral drugs and how they can be used.

A

Aciclovir: topical/systemic

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8
Q

What are the drugs used in treating pain and inflammation called?

A

Analgesics.

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9
Q

What type of analgesic reduces inflammatory mediators?

A

NSAIDs

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10
Q

What type of analgesics reduce he inflammation process?

A

Corticosteroids.

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11
Q

How do NSAID work?

A

inhibit prostaglandin synthesis.

Change balance of PGE1 and PGE2.

Inhibit COX 1 and 2 enzymes.

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12
Q

What effect can NSAIDs have on blood?

A

NSAID has an effect on thromboxanes which makes the platelets less adhesive = more bleeding.

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13
Q

Where is aspirin rapidly absorbed from?

A

The GIT

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14
Q

What kind of clearance does aspirin have?

A

Fast

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15
Q

What are the actions of aspirin (NSAID)?

A

Reduces synthesis of prostaglandins.

Reduces production of inflammatory mediators.

Anti-pyrexic. (Reduces fever)

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16
Q

What is an advantage of using aspirin (NSAID)?

A

It is a pre-emptive analgesic. Can be taken before the inflammatory process begins.

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17
Q

List the side effects of Aspirin (NSAID). (5)

A

Gastric irritation= ulcerations.

Inhibition of platelet function = enhanced bleeding.

Bronchospasm = Effect on asthma.

Drug interactions (protein binding)

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18
Q

How do corticosteroids reduce inflammation?

A

Inhibits capillary permeability.

Inhibits the formation of bradykinin.

Inhibits the migration of white blood cells.

Reduces eicosanoid synthesis.

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19
Q

What is the disadvantage of using corticosteroids?

A

They suppress the inflammation but do not address the cause.

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20
Q

What are the ways that corticosteroids can be administered?

A

Topically

Systemically

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21
Q

Give 2 examples of topical corticosteroids.

A
Steroid inhalers.
Hydrocortisone cream (eczema)
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22
Q

List the 3 steroid treatments for mouth ulcers.

A

Beclomethasone inhalers.

Hydrocortisone adhesive tablets.

Betamethasone solutions.

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23
Q

Prednisolone tablets are systemic corticosteroids, what are the uses of these tablets?

A

Prevent transplant rejection.

Treat immunological diseases.

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24
Q

Dexamethasone injections are systemic corticosteroids, what are the uses of these injections?

A

Reduce swelling after surgery.

i.e wisdom tooth removal.

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25
Q

What is the danger with taking systemic steroids for a prolonged period of time?

A

If you take the steroids for a prolonged period of time side effects WILL occur.

The longer u take the steroid the more serious the side effects will become.
High BP
Weight gain
Change is fat distribution (centripetal obesity)
Gastric ulcers
Adrenal suppression
Osteoporosis
Diabetes
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26
Q

What are the side effects of systemic steroids?

A
High BP
Weight gain
Change is fat distribution (centripetal obesity)
Gastric ulcers
Adrenal suppression
Osteoporosis
Diabetes
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27
Q

Name anxiolytic drugs.

A

Benzodiazepines:

Diazepam, midazolam.

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28
Q

What is the action of benzodiazepines?

A

Have an effect on the gamma receptor in membranes.

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29
Q

What are the dangers of using benzodiazepines?

A

The drug is helpful whilst in use but problems occur once the medication is removed.

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30
Q

Name an anxiolytic gas.

A

Nitrous oxide

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31
Q

What are the advantages of nitrous oxide?

A

The amount of effect can be adjusted during the procedure.

No issues with organ metabolism, is excreted unchanged.

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32
Q

When can nitrous oxide not be used and why?

A

In pregnancy.

Interferes with folic acid metabolism which is required for the formation of the brain and spinal cord in an embryo.

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33
Q

What are the functions of the thyroid hormone?

A

Balance bodys metabolism

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34
Q

What messengers (2) does thyroxine replace?

A

T3 and T4

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35
Q

How must the dosage of the thyroxine tablets be altered?

A

Gradually

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36
Q

How do thyroxine tablets act?

A

Directly upon the tissues - no effect on the gland.

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37
Q

Name the 2 types of nerve communication.

A

Sympathetic

Parasympathetic

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38
Q

What drug acts on the sympathetic NS? What is this stimulation called?

A

Adrenaline

Adrenergic stimulation

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39
Q

What drug acts on the parasympathetic NS?What is this stimulation called?

A

Acetylecholine

Cholinergic stimulation

40
Q

What is the effect of the sympathetic NS? How does this occur?

A

Speeds up heart rate via beta-receptors.

41
Q

What is the effect of the parasympathetic NS? How does this occur?

A

Slows the heart via cholinergic receptors.

42
Q

What autonomic drug is a beta agonist?

A

Adrenaline

43
Q

What autonomic drug is a beta blocker?

A

Atenolol

44
Q

What autonomic drug is a cholinergic agonist?

A

Pilocarpine

45
Q

What autonomic drug is a cholinergic blocker?

A

Atropine

46
Q

In terms of drug/receptor interaction, what happens if the drug does not find the receptor?

A

No effect

47
Q

In terms of drug/receptor interaction, what happens if the drug binds to the receptor yet the fit isn’t ideal?

A

Shape of protein remains unaltered so no effect occurs. However, the binding site is blocked.

48
Q

In terms of drug/receptor interaction, what happens if the drug (agonist) binds and the fits the shape of the binding site?

A

Causes a shape change which has an effect with the cell.

49
Q

What are the 2 components in drug-receptor activity?

A

Drug-receptor interaction.

Drug induced response.

50
Q

What are the 2 main points components of drug receptor interaction?

A

AFFINITY

OCCUPANCY

51
Q

In drug-receptor interaction what is the definition of affinity?

A

How well the drug and receptor bind.

52
Q

n drug-receptor interaction what is the definition of occupancy?

A

How long the drug and receptor are bound together.

53
Q

What is the main component in the drug induced response?

A

How effective the drug is in producing a change within the cell.

54
Q

Define AGonist.

A

Binds to a receptor and causes and effect.

55
Q

Define partial AGonists.

A

A drug that is more difficult to produce an effect. Some of the effect is produced but not all.

56
Q

How can the effect of partial AGonists be increased?

A

Increasing the concentration of the partial agonist.

DOESN’T WORK FOR ALL PARTIAL AGONISTS.

57
Q

Name the 2 types of ANTagonists.

A

Competitive

Non-competitive.

58
Q

How can the effect of a reversible antagonist be reduced?

A

By increasing the concentration of the AGonist

59
Q

What is the effect of irreversible ANTagonists?

A

Binds and reduces the availability of receptors for the AGonist.

60
Q

Name an example of a reversible ANTagonist.

A

Atenolol

61
Q

Name an example of an irreversible ANTagonist.

A

Phenoxybenzamine

62
Q

Define ANTagonist.

A

Drug that binds to the binding site and blocks it. No effect produced.

63
Q

Name 5 routes of administration.

A
Oral
Intravenous
Intramuscular
Subcutaneous
Inhalation
64
Q

What type of administration does and inhaler fall into?

A

Topical.

Once inhaled the drug doesn’t reach the alveoli and is absorbed via the surface of airways. = topical

65
Q

What are the advantages of oral administration?

A

Socially acceptable, more people likely to take drugs via oral method.

66
Q

What are the disadvantages of oral administration?

A

Slow onset

Variable absorption: some of the drug is lost on route, never know exactly how much is being directly absorbed.

Drug can be destroyed by gastric acid.

First pass metabolism: drug passes through the portal vein into the liver where is it partially metabolised. Only a portion of the drug actually reaches circulation.

67
Q

List other factors that can affect oral absorption.

A

Lipid solubility- can only be absorbed if the drug is soluble in lipids.

Drug formulation- Drugs can be coated which allows absorption at different stages in the route.

Problems with GI motility- drug can’t be passed through the GI tract.

Drug can interact with other substances in the gut.

Disease of the GI tract- some patients may not have enough bowel to allow absorption.

68
Q

(First pass metabolism) All blood from the GI tract drains into the hepatic portal vein. Which 2 veins do not?

A

Sublingual

Rectal

69
Q

In terms of managing FPM what do some drugs have the ability to do?

A

Some drugs can become activated after being metabolised in the liver.

70
Q

What is a disadvantage of FPM?

A

More drug needs to be administered orally so the desired amount can reach the circulation- have desired clinical effect.

e.g. Glyceryl Trinitrate.

71
Q

Before administering an oral drug, what is important to consider?

A

If the patient has normal liver function. Cant give high dosages of drugs since the liver cannot metabolise it efficiently.

72
Q

When does abnormal liver function occur?

A

In extremes of life.

Those with liver disease.

73
Q

What are the advantages of non-oral drug administration?

A

Predictable plasma levels

No first pass metabolism.

74
Q

What are the disadvantages of non-oral drug administration?

A

Reactions are more severe: occur all over body not localised.

Difficult to self-medicate.

Drug cost higher.

75
Q

Define bioavailability.

A

Proportion of an administered drug that is available for clinical effect.

e.g.
IV = 100%
Oral = variable

76
Q

In terms of drug distribution what determines where the drug will travel to?

A

Circulation.

Areas with higher blood flow receive more of the drug.

77
Q

Define the 2 phases in drug elimination.

A

Phase 1:
Inactivating the drug via oxidation, reduction, hydrolysis etc. Reactions make changes to the drugs which inactivate them.

Phase 2:
Conjugation. A molecule is bound to the drug which helps the drug be filtered and excreted by the kidney.
i.e glucuronidation, sulphation, methylation etc

78
Q

How can drugs be excreted?

A

Renal-urine, liver-bile, lungs-gas, sweat, saliva.

79
Q

What is the main way drugs are excreted?

A

Kidney-urine.

80
Q

Define single compartment models.

A

Drug behaves as if it is evenly distributed throughout the body.

81
Q

Define two compartment models.

A

Drug behaves as if it is in equilibrium with different tissues in the body.

82
Q

How do you work out drug clearance?

A

Plasma half life. (t 0.5)

First order kinetics
Zero order kinetics

83
Q

Define 1st order kinetics.

A

Most common.

Drug elimination/absorption by PASSIVE DIFFUSION.

Proportional to the drug concentration. The higher the concentration the faster the removal.

Logarithmic graph is a straight line. Constant half life.

84
Q

Define Zero order kinetics.

A

Elimination is and ACTIVE process can be saturated by high drug concentrations.

Linear graph of drug elimination. Constant amount of drug us eliminated per unit time.

85
Q

What are the consequences of a dosing schedule that is too frequent?

A

Toxic plasma levels depends on drugs therapeutic index.

86
Q

What are the consequences of a dosing schedule that is too infrequent?

A

No clinical effect

87
Q

Define pharmacodynamics.

A

The interactions between the drug and the body.

88
Q

Define Pharmacokinetics.

A

How the body processes the drug.

89
Q

Define bioavailability.

A

The amount of drug present in the circulation that is able to produce an effect.

90
Q

What information do you need to know before creating a dosing schedule?

A

The half life of the drug.
The drug clearance time.
The function of the liver/kidney.

91
Q

What are the 2 classes of local anaesthetic?

A

Amides (most common) and esters.

92
Q

How can you tell what LA are amides? (Hack)

A

Amides have an i in the prefix of the name, not the ‘caine’ bit. i.e. Lidocaine.

93
Q

In 1% LA how many milligrams are in 1 millilitre?

A

10 miligrams to 1 millilitre.

94
Q

What drugs should you avoid interacting with warfrin?

A

Antifungals

95
Q

What drugs should you avoid interacting with statins (for lowering cholesterol)?

A

Antifungals.

96
Q

Name anti fungal drugs and how they are administered.

A

Nystatin: Topical
Fluconazole: oral