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3rd BDS IHD > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what affects does cyclosporine have on the body and what is it used for

A

used as an immunosuppressant to reduce rejection of organ transplants
Causes Gingival Hyperplasia
Particularly affects T cells by affecting IL-2 production

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2
Q

what is pharmacology

A

study of drugs on living organisms

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3
Q

what is pharmacodynamics

A

deals with the study of the biochemical and physiological effects of drugs and their mechanism of action. Effect of the drug on the body.

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4
Q

what is pharmacokinetics

A

absorption, distribution, biotransformation and excretion of drugs. Effect of the body on the drug.

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5
Q

Drugs do not create new pathways but they alter existing ones. which 2 ways can they act?

A

Returns a function to normal operation

Changes a function away from the normal condition

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6
Q

what is a drug

A

a chemical substance of known structure which, when given to a living organism, produces a biological effect.

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7
Q

what is specificity

A

The capacity of a drug to manifest only one kind of action

Goal of theraputics is to reach specificity

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8
Q

what is selectivity

A

Drug ability to predominantly produce one effect. One effect predominates over a particular dose range – this is called the “therapeutic window” – within this range, the drug may be termed “selective”.

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9
Q

compare specificity and selectivity

A

Selectivity is concerned with site of action; specificity, with the kinds of action at a site

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10
Q

at what point does a drug become toxic and what happens before this

A

when above the therapeutic window

in the high end of the therapeutic window we can get adverse effects

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11
Q

what are the 4 types of effect a drug can have

A

Therapeutic effect: The desired or anticipated effect - specificity
Side effect: Other than therapeutic effects occurring at therapeutic doses
Toxic or adverse effect: Deleterious effects usually occurring at higher doses
Lethal effect: Death caused by very high drug dose

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12
Q

what is the therapeutic effect

A

Therapeutic effect: The desired or anticipated effect - specificity

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13
Q

what is a side effect (2)

A

Side effect: Other than therapeutic effects occurring at therapeutic doses

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14
Q

what is a toxic/adverse effect

A

Toxic or adverse effect: Deleterious effects usually occurring at higher doses within the therapeutic window

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15
Q

what is lethal effect

A

Lethal effect: Death caused by very high drug dose

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16
Q

what is an acceptor

A

Acceptor: Substances drugs bind to without causing any effect (e.g. plasma proteins)

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17
Q

what is a receptor

A

Component of a cell or organism that interacts with a drug and initiates the chain events leading to the drug’s observed effect.

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18
Q

what type of receptor is a target for all therapeutic drug

A

heptahelical G-coupled receptors

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19
Q

what is efficacy

A

Efficacy: relationship between receptor occupancy and ability to initiate a response at molecular, tissue or cellular level.

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20
Q

what is affinity

A

Affinity: ability to bind a receptor. Drug/Receptor interaction

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21
Q

what is EC50

A

EC50: [drug] that produces 50% of the maximal effect on semilog scale - above this, we get the toxic effect

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22
Q

what is potency

A

how much drug is required to produce a particular effect. Depend on both affinity and efficacy
Adrenalin similar affinity than propranolol but very different efficacy

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23
Q

how can we differentiate a full agonist from a partial agonist

A

Full agonist or Partial agonist: based on the maximal pharmacological response that occurs when all the receptors are occupied.
on a graph, partial agonist will plateau at lower concentration

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24
Q

what affect does an effective antagonist have on the action of an agonist

A

shifts its affect to the right
agonist requires higher concentrations to have the same affect
antagonist reduces effects of agonist

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25
Q

give examples of where receptors are found in the cell

A

cell membrane receptors: G-coupled receptors, ion channels, enzyme linked

cytoplasm: lipophilic receptors e.g. steroid receptors
nucelus: tyrosine receptors, insulin sensitivity

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26
Q

explain how an adrenal receptor works

A

can be beta (stimulating) or alpha (inhibiting)
binding of ligand leads to G protein activation
by swapping inactive GDP for GTP on G protein
leads to conversion of cAMP for ATP of adenylyl Cyclase
If beta - stimulates cascade of phsophrylation, if alpha - inhibits

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27
Q

which protein does a G protein effect ad how

A 
Adenolyl Cyclase
either activates (beta) or inhibits (alpha) cAMP --> ATP
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28
Q

what type of adrenal receptors are there

A

Alpha 2 blood vessels
β1 Heart
β2 Lung
β3 Bladder

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29
Q

where are beta 1 receptors found

A

heart

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30
Q

where are beta 2 receptors found

A

lungs

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31
Q

where are beta 3 receptors found

A

bladder

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32
Q

where are alpha 2 receptors found

A

smooth muscle, vessels

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33
Q

how does adrenal beta receptor activation cause smooth muscle contraction

A

heptahelical receptor activated swaps GDP for GTP
causes swapping of ATP for cAMP on adenylyl cyclase
increases intracellular cAMP
which is used for muscle contraction

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34
Q

how do benzodiazepines work

A

ion channel activater by binding to GABA
increases frequency of chloride channel opening
hyperpolarization
CNS depression

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35
Q

what is GABA and what works on this

A

an amino acid that functions as the primary inhibitory neurotransmitter for the central nervous system
Benzodiazepines bind to this to cause Cl- channel opening = hyperpolarization = CNS depression

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36
Q

compare Benzodiazepines and Barbiturates

A

Benzodiazepines increase FREQUENCY of chloride channel opening
Barbiturates increase DURATION of chloride channel opening
both cause hyperpolarization and depress CNS

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37
Q

how do omeprazole and other anti- acids work

A

Act by irreversibly blocking the H+/K+ ATPase (gastric proton pump)
reducing acid release in stomach

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38
Q

how many hospitalization are due to adverse effects of drugs

A

3-4%

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39
Q

how many hospitalized patients experience adverse drug effects

A

20-30%

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40
Q

what is a type A adverse effect

A

pharmacological or toxic effect
Exaggerated therapeutic responses - determined by pharmacokinetics
Secondary unwanted action
More predictable or anticipated effects and preventable

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41
Q

what is a type B adverse effect

A

Pharmacologically unexpected, unpredictable, or idiosyncratic adverse reactions
Immunologic (Allergic or anaphylactic)
Idiosyncratic (Qualitatively abnormal adverse reactions that occur in a given individual and whose mechanism is not yet understood)

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42
Q

what does the theraputic index lie between

A

MTC and MEC
minimum toxic concentration
maximum effective concentration

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43
Q

what medicines have low therapeutic index

A

Anticoagulant i.e. warfarin
Aminoglycoside antibiotics i.e. gentamicin
Anticonvulsants i.e. phenytoin

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44
Q

state some major and minor concerns of type A adverse effects

A 
Major concerns
Respiratory depression (i.e. narcotic agents)
Cardiac toxicity (i.e. overdose of intravascular injection of local anaesthetic)

Minor concerns
Diarrhoea (Broad spectrum antibiotics)
Dry mouth (Anticholinergics i.e. antidepressant)
Drowsiness (CNS drugs i.e. benzodiazepines)

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45
Q

what are some risk situations for type A adverse effects

A 
Childhood - **
Elderly - polypharmacy, disease
Pregnancy - placental diffusion
Lactation - diffusion into milk
Renal failure - metabolised in the kidney/excreted 
Haemodialysis
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46
Q

what are the four stages of pharm kinetics

A 
Absorption
Distribution
Metabolism
Excretion
Each step is a target for adverse effect
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47
Q

what is chelation and how might this affect pharmokinetics

A

bonding to metal ions

some drugs chelate leading to less/more absorption

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48
Q

who should not receive tetracycline antibiotic and why

A

Distribution sequestration of tetracycline in bone (tissue binding) leading to depression of bone growth in children and irreversible staining of tooth enamel
Not to be prescribed in pregnant women and children under 12.

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49
Q

what can affect absorption of drugs

A

if we have eaten
what we have eaten
when e have eaten
chelation to metal ions e.g. tannins prevent absorption of iron

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50
Q

give some possible factors that effect drug metabolism

A

Diseases may alter drug metabolism (i.e. renal and hepatic dysfunction)
Abnormal drug metabolism may be due to inherited factors of either
Phase I oxidation
Phase II conjugation
Polypharmacy risk of drug interactions

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51
Q

what may lead to in-proper excretion of drugs

A

renal failure
Kidney disease
Polypharmacy

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52
Q

compare type A and B adverse effects

A

A:

  • predictable
  • dose dependence
  • high incidence
  • low mortality
  • treatment = lower dose

B:

  • unpredictable
  • not dose dependent
  • low incidence
  • high mortality
  • treatment = stop treatment
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53
Q

what is and what causes VPS

A 
Valproate syndrome
Valproic acid used for anticonvulsant in pregnant women
causes child to have:
Broad forehead
Odd finger numery
Thin upper lip
Long philtrum
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54
Q

what is valproic acid, when should it be avoided and why

A

anticonvulsant
avoid in pregnancy
causes VPS in children

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55
Q

what is Cross sensitisation

A

reactivity either to drugs with a close structural chemical relationship or to immunochemical similar metabolites

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56
Q

what age are we most likely to get allergic reactions

A

20 and 49

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57
Q

what host factors effect susceptibility to allergic reactions

A

Age (between 20 and 49 at higher risk of allergic reactions)
Sex (slightly more common in women) - related to hormones e..g oestrogen
Genetic factors
Diseases
Previous exposure

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58
Q

what is the incidence in drug related anaphylaxis and how many die from it

A

3 per 100,000

1-2 die per 100,000

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59
Q

what are the 3 most likely causes of death within dentistry

A

Penicillin (75% of anaphylactic deaths)
Aspirin
Local anaesthetics: procaine, lidocaine (rare)

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60
Q

what percent of anaphylactic deaths are from penicillin

A

75%

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61
Q

what is treatment for anaphylaxis

A

Adrenaline (im)
Antihistamine (chlorphenamine)
Steroids (hydrocortisone)
Bronchodilator (β agonist/aminophylline)

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62
Q

what is stephan/johnson syndrome and what causes it

A

spots all around the body

type B adverse reaction due to anticonvulsants, anti-gout medications, pain relivers, peniccilin

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63
Q

pt gets spots all around the body after taking anti-gout medication,. What is this likely to be?

A

Stephan/Johnson Syndrome

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64
Q

what food should be avoided when on warfarin and why

A

grapefruit

enhances function of warfarin making blood too thin

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65
Q

what does teratogenic mean

A

‘monster baby’

deformaties in baby due to medicine for mother

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66
Q

what antibiotic should be avoided with warfarin

A

Metronidazole

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67
Q

what antibiotic shouldn’t be given to pregnant women and why

A

metronidazole = teratogenic

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68
Q

are penecillins water or lipid soluble

A

water

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69
Q

what is cytochrome P450 and why is it important

A

superfamily of enzymes containing heme as a cofactor
these proteins oxidize and metabolise steroids, fatty acids, and drugs in the liver
any drugs which act on cytochrome p450 will alter metabolism in the liver

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70
Q

what is a major inhibitor of p450 and what affects does this have on warfarin and other drugs metabolised in liver

A

Erythromyocin

inhibits metabolism = prolongs effect of drug = lower dose of other drug or lower dose of ertyhromyocin

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71
Q

what drugs/foods might affect midazolam plasma concentrations and what might this lead to

A

Cytochrome p450 inhibitors e.g. Erythromycin, omeprozole, grapefruit juice
lead to over sedation and respiratory failure

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72
Q

what are some inducers of cytochrome p450

A

phenytoin
carbamazapeine
Rifampicin
Glucocorticoids

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73
Q

What is Rifamapcin used for

A

TB treatment

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74
Q

what is st johns wort and when should we avoid this and why

A

flower extract
used for depression
avoid when having organ transplant or on OCP
induces cytochrome p450 = more metabolism of drugs = less effective

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75
Q

what must we tell a patient on metronidazole

A

side effects = call 111
no alcohol = increase side effects
Nausea, vomiting, flushing, tachycardia, shortness of breath, headache

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76
Q

what does alcohol chemically do when taken with metronidazole

A

decreases acetaldehyde dehydrogenase

so increases acetaldehyde from alcohol

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77
Q

what are the initial and after effects of local anaesthetic

A

Initially CNS stimulation by depressing inhibitory pathways: tremor/convulsion
Followed by CNS depression: lethargy, respiratory depression, unconsciousness

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78
Q

what is local anaesthetic metabolised by and what alters clearence time

A

CYP3A4

Clearance limited by hepatic blood flow rather than metabolism (45 min half life)

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79
Q

how does adrenaline act on the body

A

alpha 1 receptors = vasoconstriction of smooth muscle and blood vessels
beta 2 receptors = muscle relaxation (lungs)

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80
Q

what drugs affect adrenaline action

A

Non selective β blockers
Tetracycline antidepressants – inhibit uptake
Cocaine – inhibit uptake
Ritalin – ADHD (release endogenous norepinephrine)
Parkinson’s disease (COMT inhibitors reduce breakdown)

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81
Q

what are benzodiazepines a major substrate of

A

cytochrome p450

82
Q

what might affect benzodiazepine plasma levels

A

inducers/inhibitors of cytochrome p450enzyme
Inhibition (increased plasma levels)
Calcium channel blockers /macrolide / azole antifungal/protease inhibitors
Induction (decreased plasma levels)
Anti-TB, anti epileptic

83
Q

where are most drugs absorbed and why

A

small intestine

highest surface area

84
Q

what is bioavailability of a drug

A

Fraction of unchanged drug reaching the system circulation following any route of administration - IV has 100% bioavailability

85
Q

what drug administration method has 100% bioavailability

A

IV

86
Q

what is first pass metabolism

A

drug gets metabolized at a specific location in the body that results in a reduced concentration of the active drug upon reaching its site of action or the systemic circulation

87
Q

what 3 factor affect bioavailability of a drug

A

Absorption
First pass metabolism
Food: can decrease the oral availability of sparingly lipid soluble drugs (i.e. atenolol oral availability decreased by 50% by food) - fed or fasting

88
Q

give 3 physiochemical factors affecting distribution of drugs

A

Molecular size
Oil/water partition coefficient
Degree of ionisation that depends on pKa
Protein binding

89
Q

give 3 physiological factors affecting distribution of a drug

A

Organ or tissue size
Blood flow rate
Physiological barriers blood capillary membrane cell membrane specialised barriers

90
Q

what plasma protein do most acidic drugs bind to

A

albumin

91
Q

what plasma protein do most basic drugs bind to

A

α1-acid glycoprotein

92
Q

what is perfusion

A

bathing an organ or tissue in a fluid

93
Q

what is perfusion limited distribution

A

perfusion is the bathing of an organ in a fluid e.g. blood

the perfusion of an organ alters the distribution of a drug to a organ

94
Q

what are some high and low perfusion organs

A 
high = kidney, liver, heart
low = fat, bone, muscle
95
Q

what 3 barriers affect Permeability rate limitations

A

Blood brain barrier
Blood testis barrier
placenta

96
Q

describe brain blood vessels

A

The blood brain vessels are very tight with little porosities with no pores for water
only small lipid soluble substances can cross this barrier
supported by glial cells
Acidic brain cell ‘traps’ ionised weak bases e..g morphine

97
Q

describe the movements that occur at the placental barrier

A

Sugars, fats and oxygen diffuse from mother’s blood to foetus
Urea and CO2 diffuse from foetus to mother
Maternal antibodies actively transported across placenta Some resistance to disease (passive immunity)
Most bacteria are blocked
Many viruses can pass including rubella, chickenpox, mono, sometimes HIV
Many drugs are toxins and can pass including alcohol, heroin, mercury

98
Q

why can most drugs cross the placental blood barrier

A

Drugs that are lipid soluble and mostly un-ionised can easily pass the barrier to the foetus compared to the more polar and ionised ones.

99
Q

compare active and deactive metabolism

A

active:
pre-drugs are given and metabolised to their active state
they increase in therapeutic effect and toxic effect

deactive:
Structure changed
Decrease of pharmacological effect
Decrease of toxicity

100
Q

breifly explain the metabolism pathways of drugs

A

either phase 1 or 2 initial reaction

if phase 1:

  • phase 2 = conjugate
  • OR straight to excretion

If phase 2:

  • conjugate
  • to excretion
101
Q

explain phase I excretion reaction

A

Introduction, or exposure, of a polar group by oxidation, reduction or hydrolysis (catalysed by cytocrhomeP450 CYP450 - family of enzymes to produce metabolites in phase 1)
At this point if the metabolites are sufficiently polar can be excreted
A C-H group can be turned into a C-OH converting non pharmacological active compound into active.
Production of primary metabolite and can be excreted or go through phase II into conjugate
DANGER: Toxic compound can be created as well if activated

102
Q

do excreting products have to be more polar or more non-polar

A

more polar to be excreted

103
Q

what is a conjugate when referring to phase 2 reactions

A

a near 100% inactivated metabolite ready for excretion

104
Q

what is phase II reaction

A

Attachment of an endogenous molecule (Transferases: Glucoronyl- Sulpho- AcetylMethyl- ) to a drug or Phase I metabolite, glucuronide, sulphate, acetyl forms a conjugate = ~100% inactive

105
Q

what is the major comparison between phase I and phase II reactions

A

Phase I predominantly produces more active compounds while Phase II produces less active

106
Q

how does genetic polymorphisms affect drug metabolism

A

CYP2D6 Polymorphism
8% of Caucasian lack CYP2D6
Are POOR METABOLIZERS for cardiovascular, psychiatric and opiate drugs

107
Q

what enzyme do some caucasians lack, what percent lack it and what does this affect

A

CYP2D6
8% lack this enzyme
POOR METABOLIZERS for cardiovascular, psychiatric and opiate drugs

108
Q

what is the major comparison of biliary excretion and renal excretion

A

biliary (stool) = non-polar (conjugates, stable)

renal = polar (metabolites etc)

109
Q

what is the likely excretion pathway of a phase II reaction product

A

Biliary as non-polar

110
Q

what cells produce bile

A

hepatic cells of the liver

111
Q

what percent of bile is re-absorbed in small intestine

A

90%

112
Q

how does polarity effect excretion of drugs

A

Metabolites are more excreted in bile than parent drugs due to increased polarity

113
Q

how might liver secretion of drugs with bile prolong effect of drug?

A

Some drugs and metabolites excreted by the liver cells into bile, pass into the intestine. Reabsorption from the gut during the process of enterohepatic recycling may prolong the pharmacological effect of a drug

114
Q

describe the 3 processes that occur in nephron function

A

Glomerular filtration
Active secretion
Passive reabsorption

115
Q

what is the average glomerular filtration rate

A

120ml.min

116
Q

what is filtered at glomerular filtration

A

unbound proteins - usually not drugs

117
Q

what occur as passive reabsorption

A

non-ionised drugs are re-absorbed into the blood

ionised water soluble drugs are taken to the bladder for urination

118
Q

in terms of secretion, filtration and re-absorbtion. What does excretion =
and what is the term for this

A

excretion = filtration+ secretion - reabsorbtion

CLR rate of renal excretion

119
Q

what is CLR

A

rate of renal clearance

120
Q

what if CLR < GFR

A

net secretion

121
Q

what if CLR > GFR

A

net re-absorption

122
Q

why might there be a high level of rug in a body

A

reduced metabolsim/excretion

excessive dosing

123
Q

give some reaosn why we might have decreased drug clearence

A 
Saturable metabolism 
Genetic enzyme deficiency 
Renal failure 
Liver failure 
Age (neonate or elderly) 
Enzyme inhibition
124
Q

give some reasons why drug clearance might be too high

A 
Normal variation 
Poor absorption 
High first pass metabolism 
Non compliance 
Enzyme induction
125
Q

what is pain

A

An unpleasant sensory and emotional experience which we primarily associate with tissue damage or describe in terms of tissue damage or both (IASP definition).

126
Q

how many people in the UK suffer from persistent pain

A

About 40%, or as many as 28 million people, in the UK suffer from persistent pain.

127
Q

what can SCN9A gene mutations or Nav1.7 voltage-gated sodium channel mutations in the subunit cause

A

loss of pain sensation

128
Q

describe the pain nervous pathay

A

Pain is transduced and travels through sensory fibres to meet the CNS
where it is then taken to the limbic system (perception/learning)
thalamus (transmission)
and somatosensory cortex for pain perception

129
Q

give 4 dental explanations for pain

A

Infection causes Acute and chronic inflammation = prostaglandins, bradykinin
Exposed nerve endings = neurogenic pain
Swelling in confined space = pressure effects
Fear and anxiety

130
Q

give ways in which we can treat dental pain

A 
Reduce tissue damage:
  -Non steroidal anti inflammatory drugs (NSAIDS)
  -Steroids
  -Cooling
Nerve block: Local anaesthetics
Spinal Cord: opioids
Central Nervous system:
  -Opioids
  -Psychological factors
131
Q

what are the WHO’s guidelines on pain management

A 
Believe the patient
History of symptoms
Assessment of severity
Physical examination
Appropriate pain management
132
Q

what is Synergism in pharmacology

A

where multiple drugs have the same effect

133
Q

how has the WHO ladder been since updated from the 1980’s (2)

A

co-analgesics added e.g. nerve blocks, psychological issues, radiotherapy
More specific with types of drugs e.g. NSAIDs and paracetamol instead of ‘non-opioids’

134
Q

what is the WHO ladder

A

progression of treatment with increasesing severity of pain = stronger analgesics
NSAIDs –> weak opiods +- NSAIDs –> strong opiods

135
Q

what is paracetamol and when is it used and what effects does it have

A

it is a weak non-NSAID COX inhibitor
other mechanisms unknown
Analgesic, antipyretic, not much anti-inflammatory effect
used with mild, non-inflammatory pain

136
Q

how many tablets = overdose of paracetamol and what is the treatment

A

> 30 tablets in a day or toxic dose >4g

N-acetyl-cysteine NAC

137
Q

what can newer NSAIDs do compared to old ones and why is this good

A

differentiate between COX1 and COX2
anti-platelet and GI tract adverse effects usually come from COXI
selective COX2 inhibitors reduce these effects

138
Q

what side/adverse effects do we get with NSAIDs

A

GI Tract: Occult GI blood loss from minor breaches in mucosa (loss of PGE). Peptic ulceration. General GI upset, indigestion
Renal Function: Reduction in intrarenal blood flow can cause renal failure
Platelets: COX inhibition, bleeding tendency, Thromboxane inhibition
Cardiovascular: As a result of altered renal function, fluid retention can precipitate heart failure
Respiratory: Some ‘aspirin sensitive’ asthmatics

139
Q

do COX I or COX II affect platelet function

A

COX I

140
Q

what are some risks with COXII inhibitors

A

Parecoxib, Celecoxib
Slightly pro thrombotic
Increased risk MI and Stroke
Contraindicated in cardiovascular disease

141
Q

what must we do with NSAIDs before surgery and why

A

stop 5 days before elective surgery
platelets have 4 day lifespan and they are irreversibly reduced
need proper platelet function

142
Q

when are weak opioids prescribed and how do they work

A

moderate pain

codeine is metabolised to morphine

143
Q

how might metabolism effect weak opiods

A

e.g. codeine is metabolised by enzymes = morphine

if pt has educed enzymes or inhibition, effect will be less

144
Q

what are some adverse effects of weak opiods

A

Cardiovascular: Reduced sympathetic outflow, increased vagal tone. Bradycardia, hypotension, excitation.
Respiratory: Inhibit cough reflex, respiratory depression.
GI Tract: Reduced gastric motility. Constipation, nausea and vomiting.

145
Q

what are some actions of weak opiods

A

Sedation, euphoria, (dysphoria), excitation
ANALGESIA
Spinal Cord : Reduced pain fibre transmission kappa opioid receptors
Brainstem: Reduced pain projection to higher centres. Mu opioid receptors
Respiratory depression, reduced brainstem response to hypoxia and hypercarbia.

146
Q

what receptors do opioids act on in the body

A

Spinal Cord : Reduced pain fibre transmission kappa opioid receptors
Brainstem: Reduced pain projection to higher centres. Mu opioid receptors

147
Q

what is the reversal agent for weak opiods

A

Naloxone 400 mcg i.v. dramatic reversal of mu receptor opioid effects.
Far less effective on newer synthetic opioid like substances as their effects in the CNS are less well defined.

148
Q

explain opioids dependancy

A

Chronic opioid use: reduced effect as CNS becomes more tolerant. Dose increases.
Acute withdrawal: Hypertension, tachycardia, tachypnoea, diarrhoea, sweating, anxiety, hallucinations.
Any chronic opioid medication will precipitate some withdrawal reaction if stopped suddenly.

149
Q

name 2 newer opiods and why might they be better than codeine

A

Tramadol and Nefopam
As effective as codeine, less variability, much less constipation hence very frequently prescribed. “Oramorph” lower dose oral morphine.

150
Q

why might tramadol not be a good alternative to codeine

A 
Increasing number of fatalities from overdose causing respiratory depression.
Dependency develops with long term use which is difficult to withdraw.
New legislation: Controlled drugs (class 3). Limit to maximum prescription. Must be signed for.
151
Q

can you give paracetamol, NSIADs or opiods to patietns with damaged liverkidney?

A 
paracetamol = possibly
NSAIDS = no
Opiods = no
152
Q

what might we take for severe pain

A

Morphine; oral, s.c., i.v.
Diamorphine s.c., i.v.
Fentanyl patch (transdermal)

153
Q

if we were to take an opiod PO, what would we do to the IV dose

A

x3 due to less bioavailability

154
Q

why is patient delivered morphine better than nurse deliver morphine post op

A

studies show that patients deliver 1/3 the amount nurses do

155
Q

if a patient is on morphine IV what is co-prescribed

A

anti-emetic

156
Q

what is the minimum morphine given for a patient post op

A

1mg every 5 minutes

157
Q

how much morphine do we give post op until pt is comfortable

A

2mg in 3 minute increments

158
Q

how much morphine is usually needed for recovery setting

A

10-20mg

159
Q

what are Gabapentin and Pregabalin

A

type of Adjuvant therapy
Effective for chronic neurogenic pain
Reduce central transmission and pain projection
Adverse effect: sedation, dizziness, nausea, occasionally hypotension

160
Q

when might antidepressant be used clinically

A

Adjuvant therapy for chronic or neurological pain

161
Q

how might we psychologically support a patient with unexplained pain

A

Sharing experience with other patients, talking about it, BELIEVE the patient
Highly underestimated with pain as it is not related to death or serious illness but it really reduced quality of life
Adjuvant techniques like anti-depressants or Gabapentin and Pregabalin pain killers

162
Q

what are the three antibiotic typs that attack the cell wall

A

β-lactams – penicillins and cephalosporins - inhibit gp formation
Glycopeptides – vancomycin, teicoplanin
Cycloserine – inhibits alanine racemase & D-alanine ligase. TB treatment.

163
Q

how do beta lactams work

A

contain a beta lactam ring and similar structure to D-Alanyl D-alanine
bind to cell wall of bacteria via PBP or DD-transpeptidase
and prevent proper function and formation of crosslinkages

164
Q

what is the structure of penicillin (2)

A

very similar structure to D-alanyl-D-alanine - structural homologue
and contains beta lactam ring 5 member ring

165
Q

how does penicillin work (4)

A

structure very close to D-alanyl-D-alanine
This binds to DD-Transcriptase (PBP)
enzyme needed to form peptidoglycan cross-linkages
when bound, cannot form new cell walls = cell death

166
Q

what is vancomycin and what is it effective against

A

Glycopeptide antibiotic
Effective against Gram positive organisms
Used in MRSA patients

167
Q

how does Vancomycin work

A

Binds to D-alanyl D-alanine dipeptide on side chain of newly synthesised peptidoglycan subunits, preventing them from being incorporated into cell wall by penicillin binding proteins (PBPs)

168
Q

how does Erythromycin work

A

Erythromycin blocks exit of nascent chain during transcription of bacterial DNA

169
Q

how does Tetracyclines work

A

Tetracyclines inhibit tRNA binding to amino acids preventing any synthesis
Inhibit binding of tRNA to mRNA/Ribosome complex
Bacteriostatic compounds
All broad spectrum
penetrates mammalian cells to reach intracellular organisms
Incorporated into developing bone and teeth - contraindicated for children
Use restricted due to widespread resistance

170
Q

how do aminoglycosides selectively work against bacteria (3)

A

bacterias mRNA sub-units are 30s and 50s
humans mRNA sub-untis are 40s and 60s
Bind to 30S subunit = misreading of genetic cod

171
Q

what do aminoglycosides work against

A

Effective against aerobes and facultative anaerobes- Not active against anaerobes
Not effective against anaerobes as bacterial up-take requires oxygen- or nitrate-dependent electron transport

172
Q

how and why do we administer Aminoglycosides

A

Not absorbed from the gut

must be given intravenously or intramuscularly for systemic treatment

173
Q

why can Tetracyclines not be given to children

A

can get implemented into growing teeth and bone

174
Q

are tetracyclines bacteriostatic or bacteriocidic

A

bacteriostatic

175
Q

are macrolides bacteriostatic or bacteriocidic

A

bacteriostatic

176
Q

how do macrolides work and give an example and when it is used

A

Bind to 50S subunit blocking exit of nascent polypeptide chain
Erythromycin
Penicillin allergy

177
Q

what type of antibiotic are metronidazole

A

Nitromidazoles

178
Q

what are nitromidazoles affective against

A

anaeorbic bacteria and parasites

179
Q

how does metronidazole work

A

activated in cell by redox enzyme pyruvate-ferredoxin oxidoreductase
In anaerobes, ferredoxin is an e- transporter molecule that reduces (gives electrons to) Metronidazole
This single electron transfer reduces the nitro group of met. creating highly reactive anion – disrupts DNA helix
intermediate is short-lived and decomposes
Metronidazole is active only against strictly anaerobic organisms
because only these can produce the low redox potential necessary to reduce the drug

180
Q

what is ferredoxin

A

an e- transporter molecule that reduces (gives electrons to) Metronidazole
found in anaerobes

181
Q

which type of antibacterial affect DNA polymerase

A

Rifamycins

182
Q

how many antibiotic prescriptions come from dentists

A

10%

183
Q

how much of dental prescriptions are amoxicillin and metronidazole

A

60%amoxicillin

30£ metronidazole

184
Q

how many dental prescriptions did not fit the NICE guidelines in 2015

A

1 in 5

185
Q

what is the general clasificatio of most anti-virals

A

very narrow and low in number

virostatic not virocidal

186
Q

give a few methods of antiviral machinery

A

Prevent fusion of viral envelope with cell membrane
Zidovudine (AZT - HIV) acts as substrate for & inhibitors of viral reverse transcriptase (viral enzyme to create DNA copy of its RNA, necessary for integration into host genome)
Acyclovir – inhibits HSV DNA polymerase

187
Q

what is Zidovudine used for

A

antiviral for HIV
acts as substrate for & inhibitors of viral reverse transcriptase (viral enzyme to create DNA copy of its RNA, necessary for integration into host genome)

188
Q

what is

Acyclovir used for

A

HSV antiviral

inhibits HSV DNA polymerase

189
Q

for a dental abscess, what anti-biotic can we provide under NICE guidelines

A

Amoxicillin 500mg tds x 5/7

Penicillin V 500mg qds x 5/7

190
Q

what is the treatment for a localised dental abscess

A

pulpectomy/drainage
analgesia
not recommended to use antibiotics

191
Q

when are antibiotics indicated with a dental abscess

A

No possibility of immediate attention by a dental practitioner,
Signs of severe infection e.g. fever, lymphadenopathy, cellulitis, diffuse swelling.
Systemic symptoms e.g. fever or malaise.
A high risk of complications e.g. people who are immunocompromised or diabetic or have valvular heart disease.

192
Q

a pt has a large swollen neck. What are some other diagnosis other than abscess (non-infectious, neoplasm and viral)

A

Non infectious
Localised lymphadenopathy due to other inflammation or a neoplasm.
Salivary gland problem due to stone, infection (parotitis), or dehydration/dry mouth.
Neoplasm: Intraoral, Salivary gland.
Unerupted teeth.
Viral : Mumps

193
Q

what do we prescribe for an odontogenic neck space infection

A

Oral metronidazole 8 hourly

194
Q

what can we treat MRSA bacteraemia with

A

Vancomycin
Intravenous
Twice daily
2 weeks

195
Q

what is the 5 C’s

A

five drugs starting with C that may lead to out competition of good bacteria and lead to a drug induced C. Difficile infection

196
Q

briefly explain antimicrobial stewardship

A

start smart:

  • thorough drug allergy history
  • immediate therapy with narrow spectrum antibiotics if sepsis
  • blood samples before if possible but do not delay
  • document everything

then focus:
-reviewing the clinical diagnosis and the continuing need for antibiotics at 48*-72 hours
and documenting a clear plan of action - the ‘antimicrobial prescribing decision’
-possible switch from IV to PO
-specific antibiotics

197
Q

what are the five ‘antimicrobial prescribing decision’ options

A

Stop antibiotics if there is no evidence of infection
Switch antibiotics from intravenous to oral
Change antibiotics – ideally to a narrower spectrum – or broader if required
Continue and document next review date or stop date
Outpatient Parenteral Antibiotic Therapy (OPAT)

198
Q

compare floxacillin and Vancomycin

A

Flucox is first line, broad as it is small and may not land on target site
Vancomycin is much larger and has more effect, needed IV as not absorbed in gut

199
Q

expalin the indication of no,large and small zone of inhibition

A

no zone = not effective against bacteria
small zone = effective but need very high concentrations = not suitable
largezone = effective and suitable

200
Q

how can we avoid C.Difficle outbreaks

A

good hygiene and hand washing
avoid unnecessary antibiotics
avoid the 5 C’s antibiotics

3rd BDS IHD (14 decks)

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