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BDS2 BAMS > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

hazards/risks associated with giving medicine

A 
death 
- allergy to drug
- toxicity of the drug
drug interactions 
- effect on absorption or metabolism of other essential medicines, such as: warfarin (anticogulant), carbamazepeine (anticonvulsant)
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2
Q

5 drug classes

A
  • local anesthetics
  • antimicrobials e.g. antibiotics
  • drugs in pain and inflammation (analgesics)
  • drugs in sedation
  • emergency medical drugs
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3
Q

local anaesthetics use

A

to reduce awareness of Pain

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4
Q

local anaesthetics action

A

LA act on nerve ion channels to block propagation

- stop signals passing to a nerve

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5
Q

4 types of local anaesthtics

A
  • lignocaine (lidocaine)
  • prilocaine
  • bupivicaine
  • mepivicaine

all pH sensitive in tissues

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6
Q

what is often added to local anesthetics?

A

vasoconstrictor to prolong duration of action by keeping blood flow to a minimum so LA stays longer - reduced clearance

patient can have extra distressing reaction to LA - e.g. pulse racing

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7
Q

what do vasodilators do?

A

open blood flow - lowering time of effect

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8
Q

3 types of antimicrobials

A
  • antibiotics
  • antivirals
  • antifungals
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9
Q

commonly prescribed antibiotics

A
  • Amoxycillin
  • Metronidazole
  • Doxicycline
  • Clindamycin
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10
Q

antibiotics method of action

A

varies

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11
Q

what is the most commonly prescribed antiviral drug in dentistry?

A

aciclovir

- can be systemic (tablet to all tissues) or topical (apply to area where problem is e.g. cold sore cream)

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12
Q

2 antifungal drugs

A

nystatin (topical)

fluconazole (systemic - oral)

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13
Q

what increases incidence of oral fungal infections?

A

use of inhalers, dentures or orthodontics

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14
Q

analgesics are

A

drugs in pain and inflammtion

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15
Q

what are non-steroidal anti-inflammatory drugs? (NSAID)

A

drugs used to reduce the inflammatory mediators

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16
Q

what are corticosteroids?

A

drugs used to reduce the inflammation process

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17
Q

what is paracetamol’s mechanism of action?

A

its uncertain
- unknown is peripherally or central (in brain or where pain is)
reduces temperature via thermoregulation in the brain

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18
Q

what type of drug is paracetamol?

A

anti-pyretic and analgesic
- little to no anti-inflammatory action
few side effects

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19
Q

co-codamol

A

paracetamol and codeine

paracetamol is often combine with other drugs to make more potetn

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20
Q

3 types of anti-inflammatory analgesics (NSAID)

A

salicylates
- aspirin

propionic acid derivatives
- ibuprofen

phenylacetic acid derivatives
- diclofenac (prescription only)

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21
Q

what is a dental prescription for diclofnec?

A

very effective analgesic for inflammtion based pain e.g. wisdom teeth

(phenylacetic acid derivative)

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22
Q

what do non-steroidal anti-inflammatory drugs do?

A

inhibit prostaglandin synthesis
(true action unknown)

  • change the balance of PGE1 and PGE2
  • cyclo-ocygenase (COX 1 & 2) enzyme inhibitor

both large mediators of pain in body - so prohibit feeling

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23
Q

how do non-steroidal inflammatory drugs work?

A

Work by inhibiting Arachidonic Acid

All come from same precursor
- Prostaglandins lead to thromboxane – cause platelets stick together

Side effect of non-steroidal anti-inflammatory can cause more bleeding as less platelet adhesion e.g. if tooth removed

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24
Q

reason why you can’t have aspirin

A

if have kidney issue

either lower dose or none (300-600mg up to 4 times a day)

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25
Q

pharmacokinetics of aspirin q

A

Rapid absorption from GIT
- Elimination by 1st order kinetics – easy to eliminate

Unless overdose (enzyme saturation)
- Toxic effects - acidosis
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26
Q

action of aspirin

A

Inhibits COX 1

  • Reduced synthesis of prostaglandins
  • Reduced production of inflammatory mediators

Anti-pyrexic

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27
Q

important characteristic of aspirin

A

can be taken BEFORE inflammatory process starts
- Pre-emptive analgesia
any non-steroidal taken in anticipation of inflammation (e.g. extraction) is more effective

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28
Q

what are potential side effects of any non-steroidal anti-inflammatory drug? (5)

A

Gastric irritation

  • Erosions, ulceration
  • Worse with alcohol

Inhibition of platelet function
- Enhanced bleeding

Bronchospasm
- Exacerbate asthma

Allergic reactions (rash)

Drug interactions
- Significant protein binding – WARFARIN (anti-coagulant) potentiation

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29
Q

what is ibuprofen?

A

NSAID

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30
Q

benefit of ibuprofen over aspirin

A

fewer side effects - less common

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31
Q

how can you get diclofenac?

A

prescription only

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32
Q

results of diclofenac being more potent than ibuprofen

A

more potent = more side effects = more effective

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33
Q

how to corticosteroids reduce inflammation?

A

by inhibiting

  • Capillary permeability
  • Formation of bradykinin
  • Migration of white blood cells
  • Reduce eicosanoid synthesis

Suppress features of inflammation – do not address the cause!

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34
Q

how do topical drugs work?

A

on the surface of the desired tissue

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35
Q

examples of topical drugs

A
  • Steroid inhalers in asthma
  • Hydrocortisone cream – eczema
  • Steroid treatments for mouth ulcers e.g. Beclomethasone inhalers; Hydrocortisone adhesive tablets; Betamethasone solutions (mouthwashes)
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36
Q

how to systemic drugs work/

A

given to the whole organism?

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37
Q

do dentists get encouraged to use systemic drugs?

A

generally, no
mainly used for chronic immunological diseases
(in hospitals)

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38
Q

examples of systemic drugs

A

Prednisolone (tablets)

  • Prevent transplant rejection
  • Treat immunological diseases

Dexamethasone (injection)

  • To reduce swelling after surgery
  • e.g. Wisdom tooth removal
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39
Q

systemic steroid side effects

A
  • High blood pressure
  • Weight gain (fluid)
  • Fat distribution change (Centripital obesity + ‘buffalo hump’)
  • Gastric ulceration
  • Adrenal suppression
  • Osteoporosis
  • Diabetes
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40
Q

what drugs are used to reduce anxiety?

A

anxiolytics

Benzodiazepines – diazepam, midazolam
- Forget what happened – no short to long term memory

Gas – Nitrous Oxide

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41
Q

after effect of benzodiazepines is

A

Forget what happened – no short to long term memory

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42
Q

benzodiazepines action

A 
Stick to GABA receptors
- Change ion flow into cells 
- Can affect GABA receptors
Pain modifier
Analgesics 
Anxiolytic

Habituate
- Longer taking become less effective

Stop taking cause rebound - increased anxiety

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43
Q

benzodiazepines metabolism

A

Metabolise to metabolites that do the same job
- Still sticks to receptor
Different lasts for different lengths of time

Diazepam has 24hrs approx. length of action
- reflexes impaired
long half life

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44
Q

describe the drug nitrous oxide

A

inhalation sedation

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45
Q

positives of nitrous oxide

A
  • amount of effect can be adjusted during procedure

- no organ metabolism issues - excreted unchanged as a gas

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46
Q

downside of nitrous oxide

A

intereferes with folic acid metabolism

- avoid in pregnancy for both patients and staff

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47
Q

instances where medical emergency drugs used

A
  • asthsma
  • heart attacks
  • diabetic emergencies
  • seizures
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48
Q

definition of a drug

A

“external substance that acts on living tissue to produce a measurable change in the function of that tissue”

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49
Q

what does the term side effect of drug mean?

A

unwanted effect

- same action in every person sometimes unwanted results

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50
Q

what do you need to balance when prescribing a drug?

A

benefits against unwanted effects

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51
Q

what are the 3 general mechanisms of drug actions?

A
  • stimulate normal body communications
  • interrupt normal body communications
  • act on non-host organisms to aid body defences
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52
Q

what are the 2 main types of host communications?

A
  • hormone messages

- neural messages

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53
Q

describe hormone messages

A

general information to all tissues

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54
Q

describe neural messages

A

targeted information for Specific tissues

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55
Q

similarities between hormones and nerve messengers

A

both chemical messengers

both can be stimulated or interrupted

56
Q

role of thyroid hormones

A

balance’s body’s metabolism

  • control metabolism and function of tissue - whole range of responses altered
  • Large physiological change
57
Q

what condition is too much thyroid hormone?

A

hyperthyroidism

Sweaty, hot, anxious 
Eyeball pushed forward in socket
•	Proliferation of fat in socket 
•	Problem with antibody in thyroid gland 
Proptosis - u Sweaty, hot, anxious 
Staring 
Eyeball pushed forward in socket
58
Q

what condition is too little thyroid hormone?

A 
hypothyroidism
o	Cold intolerant
o	Slow mental activity
o	Hair loss
o	Slow pulse & low Blood pressure
59
Q

what does thyroxine tablet replace?

A

missing T3 and T4

- dose adjusted to correct level gradually to normal metabolism

60
Q

where does thyroxone tablet work?

A

directly in the tissues - no direct effect on thyroid gland

61
Q

sympathetic nerve communication

A

adrenaline

part of autonomic nervous system

62
Q

parasympathetic nerve communication

A

acetylcholine
(muscarininc cholinergic)

(part of autonomic nervous system)

63
Q

sympathetic control of heart rate

A

adrenergic stimulation

- speeds up heart rate via beta-receptors

64
Q

parasympathetic control of heart rate

A

cholinergic stimulation

- slows the heart rate via cholinergic receptors

65
Q

what does anticholinergic drugs do?

A

stops saliva production in the mouth

66
Q

4 ‘autonomic’ drugs

A

adrenaline
atenolol
pilocarpine
atropine

67
Q

what is adrenaline?

A

beta agonist
- speed up heart rate

‘autonomic’ drug

68
Q

what is atenolol?

A

beta blocker

  • slow down heart rate
  • blocks adrenaline receptor so stopping action

reduce arrythmias, lower BP

‘autonomic’ drug

69
Q

what is pilocarpine?

A

cholinergic agonist

‘autonomic’ drug

70
Q

what is atropine?

A

cholinergic blocker

take away effect on heart
HR is kept artificially low at rest by cholinergic system

‘autonomic’ drug

71
Q

3 ways drugs can interact with tissues

A
  • receptors
  • enzymes
  • ion channels
72
Q

how do receptors for drugs work?

A

Pick up drug like an aerial on outside of cell

By themselves not enough!

  • coupled to ion channels – cause to channel to open, allow to flow in
  • coupled to G-proteins – change conformation to trigger cascade
  • coupled to gene transcription
73
Q

occupancy

A

the fraction of bound receptors

74
Q

affinity

A

how avidly the drug binds to its receptor

75
Q

efficacy

A

maximum response achievable and capacity for sufficient effect or beneficial change

76
Q

higher affinity and occupancy

A

greater response of drug

77
Q

2 ways drug can bind

A

Form bonds which cannot be broken
- drug cannot come away and receptor cannot be reused e.g. aspirin

Receptor binds to the drug but is dependent on the concentration of the drugs and affinity of drug.

  • Eqm balance
  • Normal state some activated receptors some not and some free drug in blood.
  • The higher the affinity the longer the drug will be on the receptor activating it and more time change in cell
78
Q

what is the ‘law of mass action’?

A

drug in vicinity of receptor

- increase concentration of drug around receptor more drug will bind

79
Q

agonist

A

bind to receptor and cause an effect

  • directly causes an effect inside the cell
80
Q

partial agonist

A

more difficult to produce the drug/receptor effect than with an agonist
- causes part change and part response but not full response, dynamic process

increase partial agonist concentration will improve efficacy for some but not all

81
Q

antagonist

A

no effect but block receptor action

competitive and non-competitive

82
Q

competitive antagonist

A

Reversible

  • Antagonist effect reduced by increasing the concentration of the agonist
  • Competitive reversible antagonist removed from receptor means agonist can still bind

Example: atenolol (β1 blocker)

83
Q

non-competitive antagonist

A

irreversible

  • Binds and reduces available receptors for the agonist
  • Non-competitive irreversible antagonist causes conformational change so substrate can no longer bind

Example: phenoxybenzamine (α1 blocker)

84
Q

way enzymes work can be described as

A

substrate antagonism

85
Q

types of enzyme modification

A

reversible modification or irreversible modification

86
Q

how can drugs effect enzymes?

A

change the way it folds so changes enzyme effect - irreversible e.g. cholesterol forming

block receptor site or change way it folds

87
Q

ion channels

A

disrupt cell ion balance

influence electrical activity and ion influx

88
Q

examples of drugs which work on ion channels

A
  • local anesthetics - prevent conduction of AP, communication
  • anti-diabetic drugs
89
Q

how do ion channels work?

A
  • Agonist come along changes cell
  • Changes transmembrane protein
  • Allows pore to open so ion can flow through
  • Specific to type of ion
90
Q

pharmacokinetics

A

what body does to a drug
refers to the movement of drug into, through and out of the body

(the time course of its absorption, bioavailibilty, distribution, metabolism and excretion)

91
Q

pharmacodynamics

A

study of the biochemical and physiological effects of drugs

how the drug effect the organism

92
Q

4 phases of drug from intake

A

absorption
clinical effect
metabolism
excretion

93
Q

advantage of oral drug administration

A

Socially acceptable

94
Q

disadvantages of oral drug administration

A
  • Slow onset – not useful in emergency
  • Variable absorption – some maybe lost in stomach acid, gut
  • Gastric acid may destroy drug
  • ‘first-pass’ metabolism – liver metabolises before enters circulation
95
Q

advantage of ‘first-pass’ liver metabolism

A

makes an active form of an inactive drug

less needed by oral rout
e.g. valavivlovie -> aciclovir

96
Q

disadvantage of ‘first-pass- liver metabolism

A

more needed by oral route to get desired clinical effect

e.g. glceryl trinitrate

97
Q

what is important to factor into dosage when prescribing a drug?

A

if it is ‘first-pass’ metabolised and liver functionability

98
Q

when can you get abnormal liver function?

A
  • extremes of life
  • liver disease
  • drug interactions changing drug metabolism
99
Q

6 factors affecting oral absorption

A
  • ‘first-pass’ liver metabolism
  • lipid solubility and ionisation
  • drug formulation
  • gastrointestinal motility
  • interactions with other substances in the gut
  • GI tract disease`
100
Q

5 forms of drug administration

A
  • oral
  • intravenous
  • intramuscular
  • subcutaneous
  • inhalation
101
Q

advantage of non-oral drug administration

A
  • predictable plasma levels

- no first pass metabolism (good for emergencies)

102
Q

disadvantages of non-oral administration

A
  • allergic reactions more severe adn faster
  • access difficulties/self-medication
  • drug cost higher
103
Q

bioavailbilty

A

proportion of an ingested drug that is available for clinical effect

104
Q

4 things that modify bioavailability

A
  • dosage form
  • destruction in the gut
  • poor absorption
  • first pass metabolism
105
Q

volume of distribution

A

amount of the body the drug diluted in

- compartments

106
Q

3 things that impact drug distribution

A

Lipid binding

  • Bound to lipids in plasma
  • Slow release from accumulation

Drug binding to plasma proteins
- Bound drug is inactive
- Can act as a reservoir
Drug interactions possible by competitive binding
- Warfarin & aspirin
Warfarin binds to plasmin protein – top up what’s used already
However if start taking a drug with a higher affinity then less will bind meaning one drug will have an emphasised response

107
Q

how many stages are in preparing drugs for elimination from body?

A

2

108
Q

phase 1 drug elimination reaction

A

Oxidation, reduction, hydrolysis – little changes to molecule, changes conformation, no longer bind to receptor, inactivate it

109
Q

phase 2 drug elimination reaction

A

Conjugation for excretion
- Glucuronidation, sulphation, methylation, acetylation, glutathione

Tag with enzyme onto molecule which will be excreted so increased the amount excreted from body

110
Q

5 methods of drug excretion

A
  • renal (urine)
  • liver (bile)
  • lungs (exhale gas)
  • sweat
  • saliva
111
Q

method of excretion for most drugs

A

renal excretion

112
Q

how can renal excretion be modified?

A

changing urine pH - make more alkaline can get rid of excess acidic drug

113
Q

2 disorders of excretion

A

renal disease

  • chronic renal failure
  • drug doses must be reduced

liver disease
- liver failure (drug doses must be reduced)

114
Q

single compartment model

A

drug behaves as if it is evenly distributed throughout the body
- goes everywhere in same concentration

115
Q

two compartment model

A

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

  • blood flow dependent
  • go to large blood flow compartments first then other areas
116
Q

what mainly causes body compartments?

A

largely due to blood flow

more flow = more drug delivery

117
Q

first order kinetics

A

Drug elimination or absorption is by PASSIVE DIFFUSION only

Drug removal is proportional to the drug concentration

  • removed from the body at a rate that is proportional to the concentration
  • Logarithmic graph of elimination is a straight line

most medicines
- Half-life of drug is constant so can predict how long it will be in body

118
Q

zero order kinetics

A

Drug elimination is an ACTIVE process and can be saturated by high drug concentrations

Linear graph of drug elimination
- Zero order has a constant rate of drug elimination whereas first order is proportional to drug concentration

119
Q

use of zero order kinetics

A

Useful for how long drug in body and how fast will be removed
- Need to know half-life, bioavailability
Can work out dosing schedule based on bioavailability and mechanism of excretion
- so what is the required stable level in patient

120
Q

what is drug accumulation?

A

How the plasma concentration builds if repeated doses of a drug are given.

121
Q

too frequent dosing schedule

A

toxic plasma levels

122
Q

too infrequent dosing schedule

A

result in sub-therapeutic plasma levels and no clinical effect

123
Q

Injections Vs Creams as routes of administration

A

injection

  • can get to site quicker
  • know volume absorbed
  • higher plasma peak level

cream
- can be more slow release (effects felt for longer; lower peak plasma level)

injections are more expensive as more HCP time needed

124
Q

what method of administration is best for an infection?

A

injection

- higher peak plasma level faster

125
Q

what method of administration is best for morphine?

A

what lot of pain relief for prolonged time

- transdermal patch

126
Q

what is the only method of administration that involves first pass metabolism?

A

oral

not injection, absorption under tongue, path or cream

127
Q

subcutaneous Vs transdermal method of administration

A

subcutaneous is already in connective tissue

  • quicker action but shorter duration
    e. g. insulin
128
Q

how does blood flow effect duration of action of a drug?

A

higher blood flow = rapid rise in plasma level but short duration

e.g. muscle

129
Q

what is bioavailability/

A

portion of ingested drug available for clinical effect

can be lost by

  • First pass metabolism – lose proportion
  • GI disease – not absorbed
  • Destroyed by gastric acid
130
Q

phase 1 in drug inactivation and excretion

A

adds or takes away sections so cannot bind to receptor (in liver)

  • can go round multiple times with multiple modifications before make a sufficient change to prevent drug working
    e. g. diazepam
131
Q

phase 2 in drug inactivation and excretion

A

conjugate with other molecules so it can be removed by kidney and gut

132
Q

bound and free drug relationship

A

Some will dissolve in plasma some will be bound to plasma proteins. Until concentration drops so that equilibrium from bound to free acting drug move towards more needing to be free so can be used

  • Binidng to plasma means the duration of drug can be prolonged as circulate until eqm shift
133
Q

albumin role

A

can bind to drugs

Determines oncotic pressure of keeping fluid in blood stream and not released into tissues

Made in liver

134
Q

how can excess free drug occur and consequence of this?

A

not enough plasma proteins for drug binding

some drug may not be used efficiently and list

135
Q

what is preferential binding in plasma and how can it be used?

A

preferential binding of one drug to the other if stronger affinity for that drug to the site

can change the amount of drug available in plasma

e. g. warfarin only works when free in plasma
- can increase by introducing a drug with stronger affinity so more free Warfarin

BDS2 BAMS (54 decks)

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