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2 - Diseases Of The Human System > Clinical Pharmacology > Flashcards

Clinical Pharmacology Flashcards

1
Q

What are drug categories in dentistry an what is their role?

A

Local anaesthetic - Prevent pain!

Antimicrobials -Treat and prevent infections

Anxiolytics - Reduce anxiety

Analgesics - Reduce postoperative pain

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2
Q

What are the types of host communication?

A

Hormone messages
- General information to ALL tissues

Neural messages
- Targeted information for SPECIFIC tissues

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3
Q

What are examples of hormone systems in the body?

A

Thyroid Hormones – T3 & T4

Insulin/glucagon

Cortisol/Aldosterone

Sex Hormones

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4
Q

What do thyroid hormones do?

A

balance body’s metabolism

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5
Q

How can hypothryroidism be treated?

A

Drugs can replace the missing active hormone - T3 & T4

Thyroxine dose adjusted to correct level gradually

Replacement medicine acts directly in the TISSUES, no direct effect on thyroid gland

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6
Q

How does the automomic nervous system communicate? (what types)

A

Sympathetic - Adrenaline

Parasympathetic - Acetylcholine

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7
Q

How does the sympathetic system speed up heart rate?

A

Sympathetic - adrenergic stimulation

Speeds up the heart via Beta-receptors (B1)

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8
Q

How does the parasympathetic system slow down heart rate?

A

Parasympathetic – cholinergic stimulation

Slows the heart via cholinergic receptors (M2)

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9
Q

What are examples of autonomic drugs?

A

Adrenaline (beta agonist)
Atenolol (beta blocker)

Pilocarpine (cholinergic agonist)
Atropine (cholinergic blocker)

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10
Q

What are the routes of administration?

A

Transdermal - drug applied to the skin for adsorption

Subcutaneous - drug injected into the tissues of the skin

Intramuscular - drug injected into muscle

Intravenous - drug injected into a vein

Transmucosal - drug applied to the mucosa for adsorption

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11
Q

What is a drug applied to the tissue where it acts called?

A

topical

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12
Q

What is a drug applied to the whole organism called?

A

systemic

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13
Q

What is the main purpose of aspirin and what side effect is also useful?

A

aspirin reduces pain (NSAIDS)

side effect - platelet inhibitor for heart attacks

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14
Q

What reaction is commonly seen in penicillan allergy?

A

mild maculopapular rash

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15
Q

What happens in anaphylaxis?

A

Swelling of tissues
narrowing of airways
leadings to circulatory failure

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16
Q

What are drug interactions?

A

One Drug interferes with the absorption, action or metabolism of another

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17
Q

What drugs have interactions commonly in dentistry?

A

warfarins and NSAIDs (aspirin)

protein bind

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18
Q

What is another example where warfarin interacts with another medication?

A

warfarin and erythromycin/ fluconazole/ carbamazepine

decreases drug metabolism of warfarin

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19
Q

What can acute toxic reactions lead to?

A

Bone marrow suppression

Hepatotoxicity & biliary stasis

Acute nephrotoxicity

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20
Q

What should be considering before prescirbing?

A

would a different treatment be a better option? (surgery, filling)

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21
Q

What can prescribing the wrong drug cause?

A

ADR - adverse drug reaction

ineffective

less effective

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22
Q

When is the prescription valid for?

A

six months from date issued

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23
Q

What is different for private prescriptions?

A

GDC number added instead of NHS list number

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24
Q

What are advantages of written instructions?

A

Stressed patient may not remember instructions

Language issues may prevent proper understanding
Multilingual options, large print options

Contact number for Patient if Issues arise with the medicine

Legal protection if post-treatment course questioned

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25
Q

What should advice to patients be?

A

Take drugs at correct time and finish the course

Unexpected reactions: STOP! and contact prescriber

Known side-effects should be discussed e.g. Metronidazole and alcohol

Keep medicines safe: especially from children

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26
Q

Where can dentists refer to regarding drugs?

A

BNF
SDCEP

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27
Q

What are the 4 modes of action?

A

Activation or blocking of Receptors

Activating or blocking Enzyme function

Opening or blocking Ion Channels

Facilitation or blocking Transport systems

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28
Q

What is the difference between antagonist and agonist and inverse agonist?

A
  • Agonist: Increases activity above baseline.
  • Inverse Agonist: Decreases (already present) activity below baseline.
  • Antagonist: Blocks the effects of both agonists and inverse agonists, but has no effect on its own.
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29
Q

Why is the drug/receptor interaction not enough?

A

a cascade is required which happens due to the conformational changes in transmembrane proteins

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30
Q

What is the effect of the drug determined by?

A

Affinity – the tightness of the drug binding to the receptor

Occupancy – how much time the drug spends on the receptor

Efficacy – how effective the drug is at producing a response from the receptor

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31
Q

What is the drug at an equilibrium with?

A

with surrounding tissue fluid
it spends time in receptor and in fluid

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32
Q

What does a low affinity in turn cause?

A

low occupancy > low effect

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33
Q

What can a low affinity be combated by?

A

increasing the dose of the drug
however in some drugs even increasing the concentration will not acheive max efficacy (partial agonist)

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34
Q

Why is butyrylcholine (BCh) a partial agonist?

A

max effect will never be obtained despite the concentration

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35
Q

What law do drugs in vicinity of a receptor obey?

A

law of mass action

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36
Q

What is a non-linear relationship between occupancy and response?

A

an increase in occupancy may not have an effect on the response to the drugs, ie. at half occupancy reponse could be max

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37
Q

What is the linear relationship between occupancy and response?

A

50% receptor occupancy produces 50% response

38
Q

What are partial agonists?

A

More difficult to produce the drug/receptor effect than with an agonist

Increase partial agonist concentration will improve efficacy for some receptors but not for others

39
Q

How are competitive antagonists improved?

A

by increasing the concentrations (bind to more sites, inhibiting more responses)

40
Q

What is the basis of non-competitive antagonists?

A

attaches to seperate site, cannot be improved with concentration
affinity/efficacy rules do not apply

41
Q

What is the difference between competitive and non-competitve antagonists?

A

Reversible (competitive)
Agonist effect reduced by increasing the concentration of the antagonist

Irreversible (non- competitive)
Binds to allosteric site and reduces available receptors for the agonist

42
Q

What temperature do enzymes work optimally at?

A

at body temperature (37-40)

43
Q

Do enzymes change at the end of a reaction?

A

no

44
Q

How can drugs change enzyme action?

A

Substrate antagonism – competitive

Non-competitive substrate inhibition

45
Q

What is an example of a non-competitive antagonist?

A

aspirin - platelet plug inhibitor

46
Q

What can ion channel effects change?

A

cell electrical activity
ion influx

47
Q

What are examples of ion channel drugs?

A

LA
Anti-diabetic drugs

48
Q

Can agonists be competitive?

A

yes competing against the antagonist

49
Q

What is pharmacokinetics?

A

what the body does to drugs

50
Q

What is pharmacodynamics?

A

what drugs do to the body

51
Q

What is the stages of a drug in the body?

A

Administration

Absorption

Transport

Clinical Effect

Metabolism

Excretion

52
Q

What are the enteral (via the gut) ways of administration?

A

oral

53
Q

What are the parenteral (not the gut) ways of administration?

A

Transdermal
Transmucosal
Intravenous (iv)
Intramuscular (im)
Subcutaneous (sc)

54
Q

What is another way of administration?

A

inhalation

55
Q

What are the advantages and disadvantages of oral drug administration?

A

Advantages:

  • Convenient and easy to take yourself (no needles!)
  • Often inexpensive

Disadvantages:

  • May not be absorbed well or broken down by stomach acid
  • Slower onset of action than some methods
  • First pass metabolism
56
Q

What is the ‘first pass’ metabolism?

A

GI blood goes through the liver first ( hepatic portal vein) for metabolism (can inactivate or activate a drug)
Then reaches systemic circulation after passing the liver

57
Q

What veins do not drain to the hepatic portal vein and straight into the systemic circulation?

A

sublingual and rectal

58
Q

What are the two ways the liver metabolises the drug and what are examples of both?

A

Inactivation: This is the more common scenario. The liver’s enzymes often work to break down drugs into inactive metabolites, essentially rendering them ineffective. - More is needed via oral route to make them effective (GTN administered sublingually for angina)

Activation: In some cases, the liver can actually convert an inactive prodrug into its active form. Prodrugs are essentially medications designed to be delivered safely but need liver metabolism to become effective. (Lisinopril, a blood pressure medication, is a prodrug. The liver converts it to lisinoprilat, the active form that lowers blood pressure.)

59
Q

What are the advantages and disadvantages of intravenous/intramuscular administration?

A

Advantages
Very rapid onset
Predictable plasma levels
No first pass metabolism

Disadvantages
Allergic reactions more severe
Short duration of action
Access difficulties/self-medication (patients may feel uncomfortable)
Drug cost higher (purity is important)

60
Q

What are the advantages and disadvantages of transdermal and subcutaneous administration?

A

Advantages
No first pass metabolism
Allergic reactions often very localised
Prolonged action – can be days with transdermal patches (insulin)

Disadvantages
Very slow onset (low blood flow)
Self-medication possible
Drug cost higher
Effect will vary from person to person and site to site

61
Q

What method of administration gives the highest bioavailability?

A

intravenous

62
Q

What is the bioavailability modified by?

A

Dosage form
Route of administration
Destruction in the gut
Poor absorption
First pass metabolism

63
Q

How is the drug distributed and how can drug interactions occur?

A

Drug is dissolved in the blood and transported bound to carriers

Usually plasma protein – Albumin

Drug binding to plasma proteins
Bound drug is inactive
Can act as a reservoir
Drug interactions possible by competitive binding i.e. Warfarin & aspirin

64
Q

What plasma protein usually transports drugs?

A

albumin

65
Q

What does the speed of diffusion depend on?

A

the blood flow to the area
the blood wall vessel barrier
active secretion of the drug into the tissue

66
Q

single VS two compartment model

A
  • Single compartment: Assumes the drug distributes evenly throughout the body like one big bucket.
  • Two compartment: More realistic, considers the drug moving between a central compartment (blood, organs- heart/brain/kidney) and a peripheral compartment (muscle, fat).
67
Q

What is the volume of distribution?

A

Different parts of the body may receive different drug levels compared with plasma – ‘Compartment model’
Vascular, tissues, CNS

68
Q

What happens if drugs bind to lipids in the tissues and what are examples?

A

Slow release from accumulation – prolonged effect
Examples include the anaesthetic gasses – halothane, isofluorane

69
Q

Where are drugs metabolised?

A

liver mostly
some in plasma (some LAs)

70
Q

What are the Phase 1 reactions and what are examples of them?

A

Change to drug itself
Examples - Oxidation, reduction, hydrolysis

71
Q

What are the phase 2 reactions and what are examples of them?

A

Conjugation to a compound scheduled for excretion
Examples - Glucuronidation, sulphation, methylation, acetylation,

72
Q

What system is used most commonly to remove substances in the body and what can affect drugs trying to leave?

A

P450 Mono-Oxygenase system
drugs may enter competition with other substances/drugs at any step (why knowledge of drug interactions is important)

73
Q

What can the elimination system produce that is unwarranted?

A

produce metabolites that are active, more potent drugs

74
Q

How are drugs eliminated?

A

any body fluid i.e concentration in saliva will mirror concentration in plasma

(drug and alchohol testing by police)

75
Q

Where does the most extensive excretion occur?

A

Renal excretion of water soluble metabolites – urine

Liver metabolism and excretion – bile

Lungs – inhaled gases and volatile fractions of other drugs

76
Q

Where do small proportions (relative to plasma concentration) get excreted?

A

sweat
saliva
tears

77
Q

What does renal excretion depend on?

A

renal function
renal bloodflow

78
Q

How can renal excretion of overdosed aspirin be modified?

A

making urine more alkaline (bicarbonate intravenously) which encourages acid secretion into urine and removes aspirin from body

79
Q

What can cause excretion problems and what should be done?

A

Renal Disease
Chronic renal failure
Drug doses must be reduced

Liver disease
Liver failure
Drug doses must be reduced

80
Q

What should you always do in situations of disease?

A

Always ask advice from the patient’s doctor about how much to reduce a drug use in an individual case
will depend on liver/renal function
Will depend on the drug being used

81
Q

What is the plasma half-life and what does it vary by?

A

Time taken to eliminate half of the drug
varies by mechanism of excretion

82
Q

What is first order kinetics?

A

Drug metabolism increases as drug concentration increases i.e. large amount of drug will increase rate of excretion
Excretion is by PASSIVE DIFFUSION only

83
Q

What is zero order kinetics?

A

Drug metabolism is at a FIXED rate – ACTIVE process
Irrespective of drug concentration
Can lead to the drug accumulation if saturation exceeded

84
Q

What is zero order kinetics fixed by?

A

by max capacity in enzyme systems of body

85
Q

Why are zero order kinetics useful?

A

if drug level in current blood and time ago it was taken is known, it is possible to predict backwards to the max dose taken to assess whether or not it exceeded the hepatic metabolic levels (where above leads to free-radical formation)

applies to paracetemol

86
Q

What is the problem with frequency of dosing?

A

TOO FREQUENT will result in plasma levels that may be toxic

TOO INFREQUENT will result in sub-therapeutic plasma levels and no clinical effect

87
Q

What does drug toxcitiy depend on?

A

Depends upon the drug’s THERAPEUTIC INDEX

88
Q

What route of absorption is least reliable?

A

oral

89
Q

When should treatment be avoided in pregnency?

A

first trimester as crucial development happens during this period

90
Q

Why are drugs used for sedation rarely used orally?

A

orally takes too long and may be unreliable

91
Q

How do most drugs enter the brain?

A

transmembrane passive diffusion

2 - Diseases Of The Human System (19 decks)

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