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AMP > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what is meant by an agonist drug?

A

binds to and activates receptors to produce a biological response.

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2
Q

what is meant by an antagonist drug?/

A

blocks the action of agonists from stimulating receptors.

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3
Q

what is meant by pharmacokinetics?

A

how the drug is absorbed, distributed, metabolized or excreted.
What the body does with the drug.

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4
Q

how do drugs work in the body?

A

they act by binding to receptors causing either activation or inhabition of a regualr body process to give a biological response.

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5
Q

what is meant by pharmacodynamics?

A

what the drug does to the body. - physiological effects on the bosy and the mechanisms of the drug action/ the relationship between drug concentration and effect.

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6
Q

why do drugs target receptors?

A

becuase receptors coordinate the function of all cells in the body. They are chemical messengers.

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7
Q

what would an agonist drug do to a receptrs?

A

activate the receptor.

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8
Q

what would an antagonist drug do to a receptor

A

block the receptor.

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9
Q

why do drugs target ion channels?

A

becuase they are gateways into the cell.

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10
Q

what do blocker drugs do to ion channels?

A

block the channel.

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11
Q

what do modulator drugs doe to ion channels?

A

increase or decrease opening probability.

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12
Q

why do drugs target enzymes?

A

because often the drug molecule is a substrate analogue that acts as a competitive inhibitor of the enzyme.

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13
Q

what effect does an inhibitor drug have on enzymes?

A

normal reaction inhibited.

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14
Q

what effect does a false substrate drug have on enzymes?

A

abnormal metabolite produced.

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15
Q

what effect does a prodrug have on enzymes?

A

active drug roduced.

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16
Q

why do drugs target transporters?

A

because they transport the movement of ions ad small organic molecules across cell memebranes.

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17
Q

what effect do inhibitor drugs have on transporters?

A

block transport.

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18
Q

what effect do false substrate drugs have on transporters?

A

abnormal compound accumulated.

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19
Q

with Pharmacokinetics what 2 assumptions need to be made?

A
  • plasma concentration bears a precise relation to the concentration of drug in the immediate environment of its target.
  • drug response depends only on the concentration of the drug on the immediate environment of its target.
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20
Q

what type of pain is most likely to bring a pt to the dentist?

A

acute pain.

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21
Q

what are corticosteriod medications used for?

A

used for inflammation to relieve discomfort and redness of the mouth.

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22
Q

what are narcotic analgesic medicationd given for?

A

may be given for severe pain conditions.

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23
Q

what is codeine metabolised by?

A

CYP2D6

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24
Q

what are the effects of Nitrous oxide?

A
  • tingling sensation
  • warm sensation
  • feeling of euphoria
  • sleepiness
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25
Q

what are the 2 sedation drugs commonly used in dentistry?

A
  • Nitrous oxide

- midazolam

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26
Q

what is a problem with midazolam if it is used with other CNS depressants?

A

can increase possibility of hypotention, respiratory depression/arrest and death.

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27
Q

what is metronidazole used for? (types of bacteria)

A

anaerobic bacteria and protozoa

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28
Q

what are the effects of prolonged use of antibiotics?

A
  • normal oral/gut flora is destroyed.
  • selection of resistant strains.
  • colonisation by harmful microbes that are not normal residents.
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29
Q

what side effects to the oral cavity can antidepressants have?

A

dry mouth.

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30
Q

How effects do anti-depressants have on the body?

A

block the action of neurotransmitter acetylcholine.

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31
Q

what side effects do nitrates have on the body?

A

can cause headaches.

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32
Q

what are nitrates given to patients?

A

used to prevent and reliece chest pains (angina) as they are vasodilators.

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33
Q

what effects do antihypertensives have on the body?

A

prevent postural hypotension (excessive fall in BP when moving in to an upright position)

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34
Q

what kind of behaviour would you often seen in patients taking opiods?

A

addictive-related behaviour.

often have poor dental health due to neglect.

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35
Q

patients taking insulin are at higher risk of what?

A

dry mouth, gum inflamation, poor healing of oral tissues and thrush.

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36
Q

what medical emergency is most likely to happen with a patient taking insulin?

A

hypoglycaemic episode - severe decline in blood glucose levels.

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37
Q

what are patients taking steriods at a higher risk of complications?

A
  • adrenal suppression caused by steroid therapy.
  • disease/condition which requires them to take steroids.
  • oral yeast infections and blood blister (if chronic user)
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38
Q

why can lidocain not be given to patients taking Beta blockers?

A

as beta blockers can decrease hepatic blood flow and/or inhibit hapatic enzymes, this reduces metabolism of lidocain. Leading to increased serum levels and possible toxicity of lidocain.
so taking both lidocain and beat blockers can result in myocardial depression.

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39
Q

what is the effect of beat blockers on the body?

A

block sympathetic influences on cardiac B1 adrenoreceptors.

40
Q

why can patient taking beta blockers not be given vasosupressors in LA?

A

due to non-selective beta-blockers patient has hightened sensitivity to the systemic effects of vasosupressors. so they are at a high risk of an acute hypertensive episode.

41
Q

if a patient is taking monoamine oxidase ihhibitors why can they not have La with a wasoconstrictor?

A

could cause acute hypertensive crisis.

42
Q

why are the effects of warfrin and antiplatelet drugs on patient?

A

they are anticoagulants. So they inhibit the synthesis of vit K-dependent coagulation factors.

43
Q

what should be the normal INR for a patient?

A

1

44
Q

what are the risks to warfarin patients if their INR rises above 1?

A

increased risk of bleeding.

45
Q

how soon before treatment should an IRN be taken?

A

at least 72 hours before.

46
Q

why would a patient be taking bisphosponates?

A

prevent bone resorption in osteoporosis and bone cancer.

47
Q

what can be a problem with patients taking bisphosponates with surgery?

A

impaired wound healing.

48
Q

why can suppressing bone resorption due to taking bisphosponates become a problem to bone?

A

any damaged bone will be left in situ instead of being resorbed.

49
Q

what are the effects of Stevens-Johnson Syndrome?

A

Hypersensitivity complex - effects the skin and mucous membrane.

  • ulcers and other lesions appear in the mucous membrane.
  • extremely painful and reduces the patient ability to eat and drink.
50
Q

How does LA work in the body?

A
  • reversible blocking of nerve conduction.
  • blocks entry of sodium ions into cell.
  • memebrane expansion theory.
  • specific binding hypothersis.
51
Q

what are the 3 different types of LA?

A
  • Ester based
  • Amino-amides
  • Articaine.
52
Q

what is an example of an ester based La?

A

Procaine and benzocaine.

53
Q

what are some examples of an amino-amide LA?

A
  • Lidocaine
  • Mepivocaine
  • Prilocain
  • Bupivocaine.
54
Q

why do you have to be careful when using amino-amids LA with a patient with liver disease?

A

because amino-amids are metabolised by the liver and excreted via the kidneys.

55
Q

what are the benefits of using a vasoconstrictor in LA?

A
  • increases duration of action via reducing LA systemic absorption and increasing anaesthetic concentration near nerve fibres.
  • reduce plasma levels - reducing the dose of LA required.
56
Q

what are some examples of vasoconstrictos used in LA?

A

adrenalin/epinephrine and felypressin.

57
Q

patients with what conditions should you be careful when using adrenalin/epinephrine?

A

patients with heart disease, hypertension and unstable angina.

58
Q

For what patients should you not use felypressin and why?

A

pregnant patients because it can induce labour.

59
Q

what LA causes vasoconstriction?

A

bupivacain.

60
Q

How can you maximise LA effectiveness?

A
  • use of topical
  • good technique
  • careful puncture
  • explain sensation.
  • good communication
  • solution at room temp.
  • stretch tissues
  • slow injection.
61
Q

What types of topical are used in dentistry?

A
  • Xylonor gell (5% lidocain)
  • 20% Benzocaine
  • Lidocain 4% ointment or gel
  • 10% lidocaine intraoral sray.
62
Q

How many cartridges can an Adult be given of 2% lidocain LA?

A

7x 2.2ml.

63
Q

How many cartridges can an child be given of 2% lidocain LA?

A

2x 2.2 ml

64
Q

How many cartridges can an Adult be given of 4% articaine LA?

A

5x 2.2ml

65
Q

How many cartridges can an child be given of 4% articaine LA?

A

2x 2.2ml.

66
Q

How much do you reduce LA dosage by for elderly (65+) patients?

A

reduce by 50%

67
Q

why do you reduce LA does for elderly patients?

A

due to liver function decreasing with age.

68
Q

what actions should you take before giving any patient with liver damage La?

A

contact their GP regarding liver function tests.

69
Q

what are other ways in which you can locally anestise an area without LA drugs?

A
  • cooling with ethyl chloride
  • pressure
  • hypoxia
70
Q

what are the different methods of LA using drugs?

A
  • topical applcation
  • subcutaheous injection (inflitration)
  • nerve block
  • epidural
  • intrathecal (in spine)
71
Q

what are the idea properties of LA?

A
  • stabel in solution
  • non-irritating to tissues
  • no permanent damage
  • no allergic response
  • rapid onset of action
  • predictable duration of action
  • more of sensory block.
  • no systemic toxicity
  • potent
  • no active metabolites.
72
Q

why in LA is the aromatic terminal essential?

A

allows the LA to penetrate fatty tissues.

73
Q

why does LA need to penetrate through fatty tissues?

A

to gain access to the nerve cell membrane through the lipid sheath to allow it to reach its site of action,

74
Q

why in LA is the hydrophilic amino terminal needed?

A

at certain pH it can gain a charge enhancing solubility in water and prohibit its solubility into lipids.

75
Q

what is LA solubility in water important?

A
  • to allow for the dissolution in a solvent to permit injection.
  • allow penetration through body fluid following administration.
76
Q

what is different about the structre of articaine when compared to both amide and ester LAs?

A

articaine contains both an amide with an ester side chain.

77
Q

what is an example of a ketone-type agent?

A

Dyclonine (a liquid topical applied with a swab or as a mouth rinse- has bactericidal and fungicidal properties)

78
Q

what is the pKa value of LA between?

A

8.0-9.0

79
Q

at pH 7.4 what percentage of LA will be in the non-ironized form?

A

5-20%

80
Q

how is the non-ironizing form of LA important?

A

allows for rapid penetration of cell membrane.

81
Q

how is the ironizing form of LA important?

A

once LA has diffused into the nerve trunk - the ionized form binds to the sodium channels/

82
Q

what does pKa indicate?

A

the pH at which the ionized and non-ironized forms of LA are equal.

83
Q

what are the major determinants of an LA drug allowing for diffusion into nerve fibres?

A
  • pKa
  • lipid solubility
  • pathophysiological factor (eg inflammation etc)
84
Q

what types of nerves are most sensitive to LA?

A

ones with a smaller diameter and that are also myelinated.

85
Q

what type of channels do sodium channel blockers bind to? and why?

A

activated ones -so that LA only works where it needs to.

86
Q

what is the only type of LA that binds to any sodium channel?

A

Benzocain

87
Q

what are the effects of injecting LA into an area with acidosis? and why?

A

will partly reduce the action of LA - this is due to most La’s being ironized therefor unable to cross the cell membrane.

88
Q

what is acidosis? and when is it likely to occur?

A

it is an icrease acidity of blood plasma, and happens with inflamation.

89
Q

at what pH does blood plasma need to be at for acidosis?

A

less than 7.35

90
Q

at what pH does blood plasma need to be at for alkalosis?

A

more than 7.45

91
Q

what is nerve blockage dependent upon? (in regards to the nerves themselves)

A
  • length of axon (short)
  • frequency dependence (resting nerves are less sensitive)
  • nerve fibre size (small and myelinated)
  • arrangement of fibre bundles in nerve sheath.
92
Q

what are some of the side effects of LA toxicity?

A
  • hypersensitivity (allergic response)
  • unconsciousness/respiratory arrest (due to CNS depressant)
  • circulatory collapse (due to possible decrease in cardiac output)
  • methaemoglobinaemia (toxic efffect of prilocaine/articaine in high does)
93
Q

How much epinephrine (adrenaline) is normally found in LA?

A

1:200,000

94
Q

how much norepinephrine (norarrenaline) is normally found in LA?

A

1:100,000

95
Q

why are vasoconstrictors not used in LA when injected into extremities (ie fingers and toes)?

A

because it limits circulation, and there is a higher risk of hypoxia of tissues.

96
Q

why would adrenaline be used over felypressin as a vasoconstrictor?

A

because it is more effective at constricting blood vessels.

97
Q

why would felypressin be used over adrenaline as a vasoconstrictor?

A

because it has no effect on the heart conduction / contraction.

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