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BDS stage 2 > Basic Pharmacology > Flashcards

Basic Pharmacology Flashcards

1
Q

Why do dentists need to know about the principles of drug action ?

A

To be able to use and prescribe drugs rationally
Dental patients might already be taking drugs
To be able to keep up with the latest developments in therapeutics

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2
Q

What is pharmacology ?

A

What the drug does to the body

What the body does to the drug

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3
Q

What is pharmacodynamics ?

A

the effect of the drug on the body

includes the molecular interactions and the effect of the concentration on the magnitude of the response

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4
Q

What does the study of pharmacodynamics allow us to do ?

A

allows us to determine the correct dosage

allows us to compare drugs effectiveness

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5
Q

What is pharmacokinetics ?

A

the effect of the body on the drug

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6
Q

What are the 4 disciplines of pharmacokinetics ?

A

absorption
distribution
metabolism
excretion

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7
Q

What is absorption ?

A

how the drug travels from the site of administration to the blood via the stomach, small intestine, liver and then the systemic circulation.

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8
Q

What is distribution ?

A

drugs can leave the bloodstream and travel in the interstitial fluid or in the intracellular fluid

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9
Q

What is metabolism ?

A

the body can inactivate the drug via enzymatic action

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10
Q

What is excretion ?

A

Drug can be eliminated from the body in the urine, faeces or bile. Kidney removes the drug from the blood.

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11
Q

What does the study of pharmacokinetics allow us to do ?

A

determine the route of administration
the frequency of the drug administration
the duration of the treatment

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12
Q

What are the 2 sources of drugs ?

A

Naturally occuring

Synthetic drugs

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13
Q

What are biologics ?

A

chemically produced biological entities

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14
Q

What 2 properties determine the ability of a dug to bind to its target ?q

A

the shape of the drug and whether it is complementary to the target receptor
charge distribution- determines the forces that will hold the drug to the target

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15
Q

What are the 4 types of interactions that can happen between the drug and the receptor ?

A

van der waals forces
hydrogen bonds
ionic interactions
covalent bonds

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16
Q

What are further considerations that should be made regarding the properties of the drug ?

A

hydrophobicity
ionisation- change charge in solutions
conformation
stereochemistry- isomers

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17
Q

What are the 4 types of proteins that are targets ?

A

receptors
ion channels
enzymes
carriers

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18
Q

What is an example of a receptor ?

A

B2 adrenoreceptor
drug salbutamol works on it
asthma

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19
Q

What is an example of an ion channel ?

A

voltage gated sodium channel
lidocaine acts on this to block a sodium influx
acts as a local anaesthetic

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20
Q

What is an example of an enzyme ?

A

cyloxygenase
aspirin works on it
analgesic

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21
Q

What is an example of a carrier ?

A

proton pump
omeprazole works on it- pumps out protons
anti-ulcer

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22
Q

How can drugs work without a target interaction ?

A

by virtue of their physico-chemical properties

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23
Q

What are some examples of drugs that work via their physico-chemical properties ?

A

Osmotic laxatives- lactulose
Antidotes-acetylcysteine for paracetamol poisoning
antacids- aluminium hydroxides in indigestion

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24
Q

What are targets fro drug action ?

A

receptors
enzymes
ion channels
carrier molecules

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25
Q

What does agonist do ?

A

activate the receptor

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26
Q

What does an antagonist do ?

A

block the action of the antagonist- inhibit

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27
Q

How can drugs act to change ion channles ?

A

block the ion channel from opening
modulate the frequency of opening and closing
(change frequency or capacity)

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28
Q

How can drugs act on enzymes ?

A

inhibiting the enzyme

act as a false substrate for the enzyme

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29
Q

How can drugs act on carrier molecules ?

A

they can be transported instead of the endogenous substrate or inhibit carrier transport

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30
Q

What is GABA and what does it do ?

A

GABA is a neurotransmitter which causes hyperpolarisation by increasing chloride permeability
this leads to a decrease in excitability

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31
Q

How do benzodiazepines work ?

A

they work in the presence of GABA - enhancing the effects of GABA
benzodiazepine binds to an allosteric site which changes the conformation of the GABA receptor and increases the chances of GABA binding as well

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32
Q

What is benzodiazepine used for ?

A

anti-anxiety

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33
Q

What is an orthosteric site ?

A

natural normal binding sure for the endogenous product like a hormone or neurotransmitter- the active site

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34
Q

What is the allosteric site ?

A

a different binding site other than the active site

drugs bind to the allosteric site and not the orthosteric site.

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35
Q

What is an example of an NSAID ?

A

Ibuprofen

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36
Q

What is the normal pathway for cell injury leading to symptoms ?

A

Immune activation and cell injury
phospholipids in the plasma membrane convered to arachidonic acid by Phospholipase A2
Arachadonic acid converted to prostaglandinsm cause inflammation via cyclooxygenase

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37
Q

How do NSAIDs work ?

A

they interact with the enzyme cascade (Cyclooxygenase and Phospholipse A2)
prevent cyclooxygenase converting arachadonic acid into prostaglandinds
stops pro-inflammatory meditors

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38
Q

What are the 4 types of receptor ?

A

ligand gated ion channels (ionotropic)
G protein coupled receptor (metabotropic)
Enzyme linked receptor (kinase)
intracellular receptors

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39
Q

What are the 2 types of ionotropic receptors ?

A

voltage gated and ligand gated

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40
Q

What are ligand gated receptor channels ?

A

require an agonist to bind and open a channel
binding leads to change in conformation
channel opens

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41
Q

Where can you find ligand gated channels ?

A

nervosu system - eg. acetylcholine receptor

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42
Q

What are voltage gated channels ?

A

they require a change in membrane potential to open and close

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43
Q

What is an example of a voltage gated channel ?

A

voltage gated Na channels

lidocaine works by binding to these channels and blocking their action to work as an anaesthetic

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44
Q

What is the structure of ionotropic receptors ?

A

pentimetric- 5 parts
have an inward kin which keeps them closed usually
agonist binding leads to conformational change

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45
Q

What are nictonic Ach receptor agonsits used for ?

A

muscle relaxants

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46
Q

What are examples of GPCRs ?

A

Alpha and beta adrenorecepetors

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47
Q

What does GPCR activation lead to ?

A

second messenger activation

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48
Q

What is the structure of a GPCR ?

A

7 pass transmembrane structure
consists of alpha, beta and gamma sub units
have a ligand binding domain and a G-protein binding domain

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49
Q

How can the alpha subunits be specified ?

A

they can be classified as Gs (stimulatory)
Gi (inhibitory) and Gq and G0
these determine the second messenger system

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50
Q

What is the action of Gs sub units ?

A

they activate adenylyl cyclase and calcium channels

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51
Q

What is the action of Gi sub units ?

A

inhibit adenylyl cyclase and activate potassium channels

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52
Q

What is the action of Gq sub sub units ?

A

activate phospholipase C

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53
Q

In the inactive state which G-protein is bound ?

A

GDP

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54
Q

In the active state which G-protein is bound ?

A

GTP

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55
Q

What happens when a drug binds to a GPCR ?

A

leads to conformational change
alpha subunit changes conformation
exchange of GDP for GTP
trigger second mesenger system

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56
Q

What are the classes of adrenoreceptors ?

A 
alpha 1
alpha 2
beta 1
beta 2
these will have the various G subunits
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57
Q

What does the alpha 1 adrenrecetor do ?

A

it has the Gq subunit
this will activate adenylyl cyclase
lead to vasoconstriction

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58
Q

What does the alpha 2 adrenreceptor do ?

A

it has the Gi subunit
this inhibits adenylyl cyclase
leads to auto-inhibition of neurotransmitter release

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59
Q

What does the beta 2 adrenoreceptor do ?

A

it has the Gq subunit
this will activate adenylyl cylase
lead to accelerated HR

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60
Q

What does the beta 2 adrenoreceptor do ?

A

has the Gs subunit
stimulates adenylyl cyclase
leads to bronchodilation

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61
Q

What is atenolol ?

A

beta 1 adrenoreceptor antagonist

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62
Q

What is salbutamol ?

A

beta 2 adrenoreceptor agonist- will lead to bronchodilation in asthma patients

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63
Q

What is the purpose of kinase linked receptors ?

A

they enhance phosphorylation of proteins to activate processes like protein synthesis

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64
Q

What is the structure of kinase linked receptors ?

A

they have a large extracellular ligand binding domain - made of alpha units and an intracellular binding domain made of beta units
single membrane spanning helix

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65
Q

What is an example of a kinase linked receptor ?

A

receptor tyrosine kinase

the receptor for insulin

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66
Q

What happens when a ligand binds to a kinase linked receptor

A

a ligand binding event leads to the dimerisation and the combining of 2 transmembrane helices - this leads to autophosphorylation.

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67
Q

What happens when insulin binds to a receptor tyrosine kinase ?

A

insulin binding to receptor tyrosine kinase activates the intracellular beta unit
tyrosine is phosphorylated by the beta unit
other molecules are phosphorylated - IRS
phosphorylated IRS lead to the effects of insulin

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68
Q

What are agonists ?

A

They mimic the actions of endogenous chemical messengers - the bind to receptors and elicit a cellular response

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69
Q

What is an antagonist ?

A

a drug which blocks the response to the agonist

they block the action of the endogenous product

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70
Q

Give an example of an agonist ?

A

histamine acts at the H1 receptor in smooth muscle to increase local blood flow

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71
Q

Give an example of an antagonist to histamine ?

A

terefenadine

acts as an antagonist at the H1 receptor, - blocks histamine and decreases local blood flow

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72
Q

How can we identify receptor sub types ?

A

ligand binding essays

cloning techniques

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73
Q

What are the 4 histamine receptor sub types ?

A

H1
H2
H3
H4

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74
Q

What is the antagonist to H1 receptor ?

A

terfenidine

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75
Q

What is the antagonist to the H2 receptor ?

A

cimetidine

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76
Q

What is the antagonist to the H3 receptor ?

A

thioperamide

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77
Q

What is the antagonist to the H4 receptor ?

A

Thioperamide

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78
Q

Give an example of intracellular receptors ?

A

oestrogen receptors

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79
Q

What is the purpose of intracellular receptors ?

A

leads to changes in gene transcription and protein synthesis

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80
Q

How many different intracellular receptors are there ?

A

48 - divided into class I and class II

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81
Q

What are class I intracellular receptors ?

A

located in the cytoplasm
form homodimers- made of 2 identical proteins
ligands are endocrine

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82
Q

What are class II intracellular receptors ?

A

located in the nucleus
form heterodimers
ligands are lipids

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83
Q

What properties must a drug have to bind to intracellular receptors ?

A

lipid soluble to bind to nuclear receptors and cause conformational change

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84
Q

What is the mechanism of action of an intracellular receptor ?

A

drug binds to nuclear receptors
causes conformational change
drug goes to the nucleus and allows gene transcription to occur by unwinding chromatin
mRNA is translated

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85
Q

Most receptor operated channels have how many binding sites ?

A

multiple

binding at one site will allow binding at another

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86
Q

How many binding sites do Ach homomers have ?

A

5

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87
Q

How many binding sites do Ach heteromers have ?

A

2

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88
Q

What is the mechanism of action of salbutamol ?

A

salbutamol binds to beta 2 adrenoreceptor
leads to complex
activates adenylyl cyclase (Gq of alpha unit)
increased cyclic cAMP
leads to bronchodilation

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89
Q

What is the concentration of a drug ?

A

the concentration in the plasma

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90
Q

Why is dose important ?

A

wrong drugs give toxic effects

different dosages are sub therapeutic for different conditions

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91
Q

What is the shape of a dose response curve that has agonist concnetration on the x axis and percentage response on the y axis ?

A

hyperbolic curve

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92
Q

What is the shape of a dose response curve that has agonist concentration on the x axis and percentage response on the y axis ?

A

sigmoid curve

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93
Q

What is the advantage of using logarithims ?

A

shows threshold - when activity starts
shows linear response
shows max response

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94
Q

What are the 2 types of dose-response curves ?

A

quantal and graded

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95
Q

What do graded response curves show ?

A

show response of a particular isolated system or tissue

its measured against agonist concentration

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96
Q

What do quantal response curves show ?

A

population based effectd
specific response determined in each member of the population
cumulative on the y axis

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97
Q

Why plot a dose response curve ?

A

estimation of the emax
estimation of the Ec50
allow efficacy and potency to be measured

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98
Q

What is the EC50 ?

A

estimation of the concentration of drug required to produce a 50% maximal response

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99
Q

the further to the left the curve is …

A

the more potent the drug is

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100
Q

What is affinity ?

A

the strength at which an agonist and drug will bind to the receptor

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101
Q

What does the 2 state hypothesis predict ?

A

at any given point the receptor can be rested or active and there is a balance between the 2

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102
Q

What happens to balance between rested or active when a drug binds ?

A

if a drug binds depending on its affinity will bind to a receptor and change conformation, destroy the equilibrium and lead to an activated receptor.

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103
Q

What is the B max ?

A

maximum saturation of binding sites

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104
Q

What are the values of k1 and k-1 ?

A

k1- rate of association of agonist with the receptor

k-1- rate of AR complex dissociation

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105
Q

How do we quantify affinity ?

A

k1/k-1= Kd

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106
Q

Will a high affinity drug have a larger K1 or K-1 ?

A

larger K1

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107
Q

What is Kd ?

A

The concentration of ligand needed to occupy 50% or receptors
it is a constant and is the same for that specific drug receptor combination in any tissue

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108
Q

What can Kd values be used to compare ?

A

the affinity of different drugs for the same receptor

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109
Q

What is the relationship between ligand-receptor interaction and Kd ?

A

the lower the Kd the tighter the ligand/receptor interaction

inverse relationship

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110
Q

How can we measure Kd on a dose-response curve ?

A

find the Ec50

the further to the left the lower the Kd value and therefore the greater the affinity

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111
Q

What does potency depend on ?

A

affinity of the drug
efficacy of the drug
receptor density
efficiency of the stimulus

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112
Q

What is potency ?

A

the amount of drug needed to produce a given effect (50% of emax)
the lower the ec50 the greater the potency

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113
Q

How is potency represented graphically ?

A

percentage response on the y axis agaisnt log conc

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114
Q

How is efficacy represented graphically ?

A

binding on the y axis agaisnt log conc

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115
Q

Why is binding not a good measure of effectiveness of a drug ?

A

only a small number receptors might be needed to elicit a response- leads to spare receptors
many receptors amplify signals

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116
Q

What does efficacy describe ?

A

ability of an agonist to activate a receptor

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117
Q

What is a full agonist ?

A

they have a high efficacy and an activated receptor is likely. They produce a max response whilst only occupying a small number of receptors.

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118
Q

What is a partial agonist ?

A

have a low efficacy and AR is less likely
unable to produce a maximal response even when occupying all receptors
they have a different receptor-signal mechanism
the max response is short of the max response the system is capable of producing

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119
Q

What is the use of partial agonists ?

A

they are used to alleviate side effects
they bind to the orthosteric site and prevent the full agonist binding
reduces the number of side effects

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120
Q

Give an example of a partial agonist ?

A

vereniciline- partial agonist for the nicotine receptor

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121
Q

What are the limitations of the 2 state hypothesis ?

A

some receptors can be activated in the absence of ligands - constitutive activity
some receptors bind to other receptors leading to G-protein activation which actually activates the receptor

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122
Q

What are inverse agonists ?

A

they have a higher affinity for the inactive state than for the active state.

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123
Q

How do inverse agonists work ?

A

they work by stimulating and turning off rather than acting like an antagonist and blocking.

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124
Q

What are allosteric modulators ?

A

the bind to the allosteric site and alter the efficacy and the affinity of the agonist for the orthosteric site

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125
Q

How do positive allosteric modulators work ?

A

they dont act alone
increase the affinity and the efficacy of the agonist
eg. Benzo will bind to the allosteric site increasing the affinity and efficacy of GABA to the orhtosteric site

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126
Q

How do negative allosteric modualators work ?

A

not active alone

decrease affinity and efficacy of endogenous agents

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127
Q

What happens with continual repeated administrations of the drug ?

A 
effect of the drug reduces 
internalisation of the receptor 
stops the potential for binding 
long periods lead to desensitisation 
reapplying the drug can lead to a heightened response
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128
Q

What is an antagonist ?

A

drug which blocks response to the agonist

binds to the receptor and prevents the endogenous product binding

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129
Q

What is the mechanism of action of antagonists ?

A

they dont have a mechanism of action, they just bind to the receptor and prevent the agonist binding

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130
Q

What are the 3 classes of antagonists ?

A

chemical
physiological
pharmacological

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131
Q

What are chemical antagonists ?

A

binding of 2 agents to make an active drug inactive

known as chelating agents

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132
Q

Give an example of chemical antagonism ?

A

heparin (-) binds to potamine (+) this stops the risk of bleeding

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133
Q

What is physiological antagonism ?

A

two agents with opposite effects that can cancel each other out

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134
Q

Give an example of physiological antagonism ?

A

glucorticoids have a risk of inducing hyperglycaemia so they are administered with insulin

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135
Q

What is pharmacological antagonism ?

A

binds to receptor and blocks the normal action of agonist on the receptor

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136
Q

What are the 2 types of receptor antagonists ?

A

allosteric binding

active site binding

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137
Q

At the binding sites anatagonists can bind …. ?

A

reversibly or irreversibly

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138
Q

What is a reversible active site antagonist called ?

A

competitive antagonist - binds at the orthosteric site- comeptes with the agonist

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139
Q

What is an irreversible active site anatagonist called ?

A

non-comeptitive active site antagonist- works at the allosteric site so the orthosteric site is still avaialble so endogenous product can still bind. - there is no competitive element

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140
Q

What are allosteric binding antagonists called ?

A

non-competitive antagonists - they dont compete for the orthosteric site

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141
Q

Does the agonist have any efficacy ?

A

no because it does not result in the AR* state

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142
Q

What is competitive orthosteric antagonism ?

A

antagonist will bind to receptor and prevent agonist binding but this can be overcome with increased agonist concentrations.

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143
Q

How is competitive orthosteric antagonism visible on the dose response curve ? (competitive antagonist)

A

parallel shift to the right of the agonist curve

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144
Q

How is non competitive orthosteric antagonism visible on the dose response curve ? (non-competitive active site antagonist)

A

the antagonist binds irreversibly to the orthosteric site
this is due to irreversible covalent bonds forming
this is visible as a shift to the right and a reduced maximal assymptote

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145
Q

What are non receptor antagonists ?

A

they dont bind to orthosteric sites but they still manage to inhibit the ability of the agonist to produce a response.
it occurs at the molecular level and works by inhibiting downstream molecules in a pathway

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146
Q

How are non receptor antagonists visible on the dose response curve ?

A

reduced slope

reduced maximal assymptote

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147
Q

With competitive antagonists how is the dose response curve produced ?

A

you cant measure antagonist response so you have to measure the agonist and the antagonist response

148
Q

Why is the curve shifted to the right for competitive antagonists ?

A

because more agonist is needed to get the same response

the curve has the same form and max response because the antagonist binds irreversibly.

149
Q

How do we work out the dose ratio ?

A

Antagonist + Agonist EC50 / Agonist EC50

150
Q

What is the schild equation used for ?

A

calculated for different antagonists and then plotted as a straight line- where the line intercepts the x axis- amount of antagonist needed to reduce the agonist by 50%

151
Q

What can we use schild values for ?

A

comapring the effectiveness of antagonists

152
Q

What are pH2 values ?

A

they are the negative logarithim of the molar concentration of antagonsit required to make a dose ratio of 2

153
Q

When can you only use schild plot values?

A

if a linear relationship and schild plot= 1

154
Q

What does the extent of antagonist inhibition depend on ?

A

the amount of competing antagonist

actual amount of antagonist- differences between individuals

155
Q

What does the irrevesible antagonist dose response curve look like ?

A

curve doesnt have the same form
shifted to the right
reduced maximal response
increased EC50

156
Q

Why is the curve different for irreversible antagonism ?

A

antagonist binds with the orthosteric site irreversibly reducing the max reponse - cant be overcome by increasing agonist concentrations

157
Q

How is the duration of the effects of irreversible antagonism determined ?

A

the longer it takes for receptors to turn over the longer the effect of the irreversible antagonist

158
Q

What is the curve for irreversible agonists similar to ?

A

the curve for partial agonsits

159
Q

How can you determine if something is an irreversible antagonist or a partial agonist based on the dose response curves ?

A

if you know the experimental conditions- know if antagonist was purposefully added

160
Q

Which antagonists are more common ?

A

competitive antagonists

161
Q

Give an example of a competitive antagonist ?

A

tamoxifen at the oestrogen receptor

162
Q

Give an example of an irreversible antagonist ?

A

phenoxybenzamine at the alpha 1 adrenoreceptor

163
Q

What does the curve look like for non-competitive antagonists ?

A

reduced slope

rediced maximal effect

164
Q

Give an example of a non-competitive antagonist ?

A

nitedipine

165
Q

How do we measure the therapeutic index ?

A

TD50/LD50 - therapeutic/lethal

166
Q

Why do we have the therapeutic index ?

A

to give the range of concentrations of therapeutic and toxic effects

167
Q

What does a large therapeutic index mean ?

A

there is a large gap between the theraputic doses and the lethal doses - not likely to get toxic

168
Q

What is pharmcokinetics ?

A

mathematics of processes ADME which govern the amount of drug in the body and how this changes with time

169
Q

What is absorption ?

A

movement of the drug across membranes

170
Q

What is metabolism ?

A

how the drug is broken down

171
Q

What is distribution ?

A

where the drug goes in the body

172
Q

What is excretion ?

A

how the drug is removed from the body

173
Q

What happens in absorption ?

A

transfer of an exogenous compound from the site of administration to the systemic circulation

174
Q

Which type of compounds are likely to be absorbed ?

A

lipid soluble and unionised

175
Q

Is the stomach important in drug absorption ?

A

no - weak acids and alcohols are absorbed here

176
Q

How can substances pass across membranes ?

A

passive diffusion and active transport

177
Q

Why is the rate of gastric emptying important ?

A

it determines the delivery of drugs to the small intestine and absorption there

178
Q

Why is the small intestine significant ?

A

it is the site of absorption of most drugs

179
Q

Why is the small intestine a good site of absorption ?

A

large
highly vascularised
permeable

180
Q

What type of drugs are absorbed in the small intestine ?

A

weak basic drugs

181
Q

What is the range of pH in the small intestine ?

A

6 in the duodenum and 7.4 in the terminal ileum

182
Q

Why are enterocytes significant ?

A

site of drug metabolising enzymes

transporters

183
Q

What are the factors affecting GI absorption ?

A

Gut motility
gut pH
physico-chemical interactions
particle size and formulation

184
Q

Why is gut motility important ?

A

decreased motility leads to decreased absorption

excessive rapid movement leads to reduced absorption

185
Q

Why is gut pH important ?

A

strong bases and acids are poorly absorbed

186
Q

Why are physico-chemical interactions important ?

A

eg. tetracycline can bind to calcium rich foods

187
Q

Why is particle size and formulation important ?

A

drugs are prepared to have a certain absorption

like resistant coatings

188
Q

What is bioavailability ?

A

the fraction of the adminstred dose that enters the systemic circulation

189
Q

What is first pass metabolism ?

A

metabolism that occurs in the liver and small intestine first before reaching the systemic circulation

190
Q

What is a parameter of absorption ?

A

area under the curve

191
Q

How do we work out area under the curve ?

A

Add concentrations and divide by 2
multiply by time
trapezium rule

192
Q

What is another way of representing bioavailbility ?

A

F

193
Q

What is the F for an intravenous dose ?

A

1 - goes straight into the systemic circulation

194
Q

What is the F for an extracellular dose ?

A

less than 1

195
Q

What are the disadvantages of using F as a parameter?

A

does not consider rate of absorption

196
Q

What is the C max ?

A

the maximum concentration of a compound after it has been administered

197
Q

What is the t max ?

A

the time taken to get to C max

198
Q

What is sublingual administration ?

A

placing under the tongue
goes straight into the superior vena cava
avoids first pass metabolism

199
Q

What is the rectal/vaginal route ?

A

bypasses the GI/hepatic systems
rapid absorption
useful if patient is vomiting

200
Q

What is the venous drainage from the rectum ?

A

two thirds systemic - middle and inferior veins

one third liver- superior rectal vein

201
Q

What are advantages of IV injection ?

A

very rapid

alternative to IM

202
Q

What are the disadvantages of IV injection ?

A

risk of infection

immediate adverse effects

203
Q

What are advantages of IM injections ?

A

faster systemic effect and faster local effect

204
Q

What are the parenteral routes of adminsitration ?

A 
IV 
IM 
Subcutaneous 
transdermal 
inhaled
intrathecal - reaches the CSF
205
Q

What are the ways that drugs can cross cell membranes ?

A

passive diffusion through lipid
diffusion across aquaporins
carrier mediated

206
Q

Which substances are likely to dissolve in lipid ?

A

non-polar

unionised

207
Q

Do ionised species have a high or low lipid solubility ?

A

low

208
Q

Drugs that are weak acids and weak bases are….

A

can be both ionised and unionised

209
Q

What determines the ratio of ionised:unionised ?

A

pH

210
Q

What is enterohepatic recirculation ?

A

drugs pass twice through enteric metabolism before getting to the tissues `

211
Q

What is the route of enterohepatic recirculation ?

A

drugs go to the gut and the liver and are secreted as bile into the duodenum
the bile is abosorbed by enterocytes and the transported back the liver

212
Q

What is an example of a drug that passes through enterohepatic recirculation ?

A

morphine

213
Q

What are the 2 processes behind elimination ?

A

metabolism and excretion

214
Q

What are the systems assocaited with elimination ?

A

kidneys
hepato-billary system
lungs

215
Q

With most drugs being lipophilic what must be done to them prior to elimination ?

A

they must be made water soluble and hydrophilic

this happens in metabolism

216
Q

What is drug metabolism ?

A

enzymatic modification of the drug

phase I and phase II

217
Q

What is phase I reactions ?

A

usually oxidation
adding a fucntional group
increases pharamcological activity

218
Q

What are phase II reactions ?

A

conjugation

adding a conjugate to make more hydrophilic and water soluble

219
Q

What are the reactions of aspirin in metabolism ?

A
  1. Aspirin is oxidised to salicylic acid

2. Salicylic acid is conjugated to gluconoride

220
Q

Why does aspirin need to be metabolised ?

A

it is a prodrug - retaina activity until in right tissue

221
Q

What are typical phase I reactions ?

A

oxidation
reduction
hydrolysis

222
Q

What happens in phase I reactions ?

A

adding a functional group like OH
decreases lipid solubility
increases pharamcoligical activity

223
Q

What are the phase I reactions catalysed by ?

A

group of enzymes called cytochromes P450s

224
Q

What are the cytochrome P450 enzymes ?

A

superfamility of haem cofactor containing enzymes

225
Q

Why do the cytochomes P450s have haem factors ?

A

allows enzyme to carry out redox cyclically and add fucntional groups

226
Q

Where are CYPs usually expressed ?

A

in the intestine and the liver- hepatocytes and enterocytes
hepatocytes
always in the ER

227
Q

What is the most expressed CYP enzyme ?

A

CYP 3A

228
Q

What are the routes of ethanol metabolism ?

A
  1. ethanol to acetaldehyde by alcohol dehydrogenase
  2. acetaldehyde to acetae by aldehyde dehydrogenase
  3. small amount of metabolism by CYP2E1
229
Q

Where does ethanol metabolism occur ?

A

liver

230
Q

What is aldehyde dehydrogenase inhibited by ?

A

metronidazole
when taking metronidazole dont drink as it can inhibit aldehyde dehydrogenase - stop metabolism at acetaldheyde which is toxic

231
Q

What are phase II reactions ?

A

conjugation
fucntional group is a point of attachment for conjugates decreases lipid solubility and makes a pharmacoligically inactive metabolite

232
Q

What is the most common form of conjugation ?

A

glucoronidation

233
Q

What is glucoronidation mediated by ?

A

UDP -glucoronyltransferases

have a broad substrate specificity

234
Q

Why are glucoronides excreted rapidly ?

A

polar

pharmacolgically inactive

235
Q

What are the routes in paracetamol metabolism ?

A

paracetamol can be conjugated with gluccoronide or sulfates
however some cna be metabolsied by CYP2E1 to NAPQI and then made into a glucoronide with glucathione S transferase and the mercapturic acid

236
Q

What is NAPQI ?

A

a hepatotoxin

237
Q

What happens in paracetamol overdose ?

A

conjugates depleted and system saturated

paracetamol forced to take CYP450 route and amke NAPQI leading to hepatic necrosis

238
Q

What is the problem with alcohol and paracetamol overdose ?

A

CYP2E1 increases in alcohol metbaolism forcing more paracetamol down thia route and making NAPQI

239
Q

What are the fluids that an excrete ?

A 
urine 
bile 
lung 
milk
sweat
240
Q

How is penicillin cleared from the blood ?

A

rapidly

241
Q

How is diazepam cleared from the blood ?

A

slowly

242
Q

Are metabolites or parent compounds excreted faster ?

A

metbaolites

243
Q

What is the limiting factor in glomerular filtration ?

A

molecular weight
must be less than 20000
plasma conc of the drug

244
Q

What is not filtered in glomerular filtration ?

A

plasma proteins

plasma protein bound drugs

245
Q

How are lipid soluble drugs excreted ?

A 
lipid soluble drugs filtered through the glomerulus 
secreted into distal portion 
metabolism to more polar compounds 
secreted back to tubule 
excretion in urine
246
Q

How are water soluble drugs excreted by the kidneys ?

A

they are secreted unchanged

247
Q

How does the nephron enable the drug to be secreted ?

A

the nephron reabsorbs water concentrating the drug so that it can be passed out the urine

248
Q

80% of renal blood flow goes where ?

A

peritubular capilalreis of the PCT

249
Q

How are drugs transported from the peritubular capillareis to the tubular lumen ?

A

2 systems for acids and alkalis
transport against an electrochemical gradient
many drugs share the same transporter- leading to competition
PPB drugs not limited

250
Q

Which drugs use the acid system ?

A

penicllin and furosemide

251
Q

Which drugs use the base system ?

A

amiloride and cimetidine

252
Q

Why are lipid soluble drugs slowly excreted ?

A

high tubular permeability

253
Q

Why do water soluble drugs get excreted quickly ?

A

low tubular permeability

254
Q

What does the extent of tubular reabsorption depend on ?

A

pH of tubular fluid

Drug lipid solubility

255
Q

What happens to drugs in an alkaline fluid ?

A

weak acids become ionised and reasbsorption is diminished

weak bases become unionised and reabsorption increases

256
Q

For weak bases when is the greatest ionisation ?

A

in an acidic pH

257
Q

For weak acids when is the greatest ionisation ?

A

in alkaline pH

258
Q

What does pH partition impact on ?

A

the rate at which drugs permeate membranes and their distribution in compartments

259
Q

Where do weak acids accumulate ?

A

in compartments of alkaline ph

260
Q

How can we rapidly excrete a weak base ?

A

in an acidic urine

261
Q

How can we rapidly excrete a weak acid ?

A

in an alkaline urine

262
Q

How can we eliminate volataile gases ?

A

exhalaton

263
Q

What is clearance ?

A

measure of the ability of eliminating organs to remove a compound from the body

264
Q

How can we work out the total body clearance ?

A

Addition of the organ clearances

265
Q

How can clearance be defined ?

A

volume of plasma cleared per unit of time

266
Q

How can we work out clearance with Ke ?

A

CL= Ek x Vd

267
Q

What are the units of elimination constant ?

A

1/t

hr^-1

268
Q

How can we work out the Ek graphically ?

A

slope of the log transformed graph

269
Q

If the slop of the log graph is linear what does this mean ?

A

0 order kinetics

constant metabolism regardless of dose

270
Q

What is half life ?

A

time it takes for a concentration of a drug to reach 50% of its current value

271
Q

How can we work out half time ?

A

0.693/Ke

or graphically

272
Q

How long does it take for a compound to reach its steady state ?

A

5 half lives

273
Q

How many half lives does it take to remove a drug ?

A

6/7 half lives

274
Q

What is the average intake of food additives ?

A

8g

275
Q

What does exposure to chemicals do ?

A

can induce or inhibit drug metabolising enzymes

276
Q

What can induction lead to ?

A

increased synthesis of Phase I and II reactions
increased metabolism and reduced pharmacological effectiveness
may need to increase dose
can be complicated in multi drug therapy if you remove the inducer

277
Q

What can act as inducers ?

A

smoking
ethanol
some drugs

278
Q

What can inhibition lead to ?

A

inhibit CYP system
reduced metabolism and increased pharmacological effect
basis of many drug-drug interactions

279
Q

What can act as inhibitors ?

A

ethanol acutely

grapefruit juice components can inhibit CYP3A4

280
Q

What is an adverse drug reaction ?

A

harmful or seriously unpleasant reactions at the dose intended for therapeutic effect

281
Q

What must drug safety take into account ?

A

severity of the ADR
disease
therapetci alternatives
perception of the risk- is it bad or not ?

282
Q

What is the time sequence of an ADR ?

A

most adverse reactions happen in a short period and some can show up in offspring

283
Q

What is a side effect ?

A

unavoidable consequence of the drug administration due to the pharmacology of the drug
mild and expected and dependent on dose

284
Q

What are secondary adverse effects ?

A

indirect causation - taking a drug can cause an increased risk of something else
Glucocorticoids can reduce immunity and then lead to increased risk of opportunistic infections

285
Q

How can age affect ADRs ?

A

elderly more likely to have ADRs due to increased medications and lower phase I metabolism

286
Q

Why dont newborns excrete drugs well ?

A

low GFR

287
Q

How does sex influence ADRs ?

A

females have different levels of growth hormine nad CYP expression

288
Q

How does medical history influence ADRs ?

A

if youve had an ADR to one drug more likely to have an ADR to another drug

289
Q

How can ethnicity affect ADRs ?

A

intrinsic - pharmacokinetic and pharmacodynamic- japanese acetylate fast
or can express different receptors- pharmacodynamic
extrisnsic- alcohol, diet and smoking

290
Q

What is a type A adverse reaction ?

A

heightened response based on what we expected at a conc

291
Q

What is an example of a type A adverse reactions ?

A

beta blockers reduce HR

however can lead to bradycardia

292
Q

What are parasympathetolytics ?

A

muscarinic antagonists that decrease parasympathetic activation

293
Q

What are type B ADRs ?

A

bizarre effects

unpredictable for pharmacology of the drug

294
Q

What happened in the Northwick park clinical trial ?

A

phase I clinical trial of leukaemia treatment led to cytokine response- indiscriminate immune response

295
Q

What are type C ADRs ?

A

Chronic effects

occur as a result of chronic treatment of the drug

296
Q

What is an example of a type C ADR ?

A

iatrogenic cushings syndrome by a tumour due to chronic glucocorticoid therapy

297
Q

What are type D adverse reactions ?

A

occur remote of treatment- in children of treated patients

298
Q

What are type E adverse reactions ?

A

withdrawal effects

299
Q

What is adrenal atrophy ?

A

exogenous glucocorticoids act in the HPA axis in a negative feedback system for a long period of time
leads to adrenal atrophy
termination of treatment means the adrenal gland produce cortisol- leads to addisons disease.

300
Q

Modification can take the form of ?

A

potentiatiob- increase

attenuation- decrease

301
Q

Give an example of pharmacodynamic interactions ?

A

ethanol inceases the sedative effect of antihistamine drugs

302
Q

Give an example of pharmacokinetic reactions ?

A

one drug interferes with anothers shape, metabolism or excretion
some drugs inhibit CYP450 and interfere with drug metabolism

303
Q

What does it mean if a drug is a weak acid ?

A

proton donor

304
Q

What doe sit man if a drug is a weak base ?

A

proton acceptor

305
Q

What is pKa a measure of ?

A

the strength of an acid/base

306
Q

How does the degree of ionisation change ?

A

the pH of the solution

307
Q

What happens when the pKa of the drug equals the pH of sthe solution ?

A

50% of the drug is ionised

308
Q

What happens to an acid and a base if you increase the acidity ?

A

increasing the acidity means the acid drug wil go from ionised to neutral
the base will get ionised

309
Q

What happens to an acid and a base if you increase the basicity ?

A

the base will go from ionised to neutral

the acid will get ionised

310
Q

What is the significance of ionised species ?

A

low solubility - cant pass through lipid bilayer

311
Q

What is pH partitioning ?

A

acidic drugs accumulate in basic fluid compartments and vice versa

312
Q

What happens to aspirin in the stomach ?

A

aspirin is a weak acid
stomach has pH of 2
aspirin is neutral unionised and can pass through lipid bilayer into plasma

313
Q

What happens to aspirin in the plasma ?

A

pH is 7.4

aspirin becomes ionised

314
Q

What affects the ability of a drug to get from the systemic circulation to other tissues ?

A

ability to cross plasma membranes
blood flow to certain tissues
extent of plasma protein binding

315
Q

What is set up between the systemic circulation and the tissue ?

A

an equilibrium

if elimination processes remove the compund then the concentration in the tissue wil also decrease

316
Q

What is drug distribution ?

A

reversible transfer of drug form one location in the body to another

317
Q

How does drug distribution usually occur ?

A

by passive diffusion of an unionised drug across cell membranes until equilibrium is reached

318
Q

What happens with distribution after an IV injection ?

A

Transfer from plasma to tissue
equilibrium
removal of compound by elimination processes from the blood means trnasfer from the blood to the tissue

319
Q

What do capillaries consist of ?

A

basement membrane attached to endothelium

endothelium has slits

320
Q

What affects the rate of distribution ?

A

permeability of the capillaries

amount of vasculature

321
Q

What affects the extent of distribution ?

A

lipid solubility- ionised drugs cant enter cells easily

plasma protein binding

322
Q

What are some key plasma binding proteins ?

A

albumin

alpha 1 acid glyocprotein

323
Q

What is albumin ?

A

produced in the liver
binds to acidic and neutral drugs
decreased in malnutrtition and cirrhosis

324
Q

What is alpha 1 acid glycoprotein ?

A

produced in the liver
binds to basic and neutral drugs
elevated in cancer

325
Q

How do drugs bind to plasma proteins ?

A

reversibly

326
Q

Which form of drug is pharmacologically active ?

A

unbound drug

327
Q

What does extensive protein binding lead to ?

A

slows down drug action
slows down elimination
slower acting
prolonged therapeutic drugs

328
Q

Why can drugs bind to tissues ?

A

due to tissue composition

due to cellular compartments

329
Q

How can drugs bind to tissues due to composition ?

A

lipid soluble drugs can accumulate in fat tissue

330
Q

How can drugs bind based on cellular components ?

A

tetracycline has high calcium affinity- accumulate in bones and teeth
chloroquine - antimalrial- afinity fro melanin so wil bind in the retina leading to ocular toxicity

331
Q

What is the volume of distribution ?

A

measure of the extent of distribution

dilution factor between the drug in the body and the drug in the plasma

332
Q

How do you work out vD for an IV dose ?

A

V= Dose/plasma conc at 0

333
Q

How do you work out vD ?

A

total amount of drug in the body/ drug plasma concentration

334
Q

If drugs are confined to plasma … ?

A

vD will be small

335
Q

If drugs accumulate outside the plasma ?

A

vD is large

336
Q

Why is Vd important ?

A

used to calcualte dose

337
Q

How can vD be used to calculate dose ?

A

plasma concentration dictates the ability of a drug to reach its target organ in an effective concnetration therefore dicatates dose

338
Q

What does a low Vd mean ?

A

confined to te plasma

339
Q

What does a high vD mean ?

A

accumulated in the peripheral tissues

340
Q

if a drug is lipid soluble and confined to body water intracellular will it be low or high vd ?

A

high vD

341
Q

If a drug is confined to the extracellular compartment and cant enter cells will the Vd be low or high ?

A

low

342
Q

If a drug is confned to the plasma will it have a high or low vD?

A

low Vd

343
Q

How do you work out the concentration at t=0 ?

A

extrapolate backwards

344
Q

How do you work out volume of distribution ?

A

dose/plasma conc at 0

345
Q

What are the 2 ways of working out clearance ?

A

dose/AUC

CL= Ek x Vd

346
Q

How can you work out Ek ?

A

Half life= ln2/Ek

ln2=0.693

347
Q

How can you work out the route of administration ?

A

intravenous- straight line plot

348
Q

Why might there be a difference in half life between 1 person on 2 ocassions ?

A

half life can be prolonged if the drug acts as an inhibitor of metabolism
Disease
Age

349
Q

How does genetic constitution affect drug metabolism ?

A

genetic constitution determines if slow or fast metaboliser

350
Q

Why might metabolism differ between 2 different people ?

A

drugs

alcohol

351
Q

What are the characteristics of fast metabolisers ?

A

normal enzyme activity
low plasma drug concnetration
high drug metabolite concentrations
normal therapeutic effect

352
Q

What are the characteristics of slow metabolisers ?

A

low enzyme activity
high plasma cocn of drug
low metabolite conc
exaggerated therapeutic effect

353
Q

What is the effect of neonates on drug metabolism ?

A

low activity of CYPs
glucoronyltransferase
N-acetyltransferase
lack of conjugation activity

354
Q

Why can exposure to chemicals alter drug metabolism ?

A

chemicals can be inhibitors or inducers of drug metabolising enzymes

355
Q

How can chemicals acts as inducers ?

A

induce synthesis of metabolic enzymes
decreased drug effectiveness
increased dose needed

356
Q

How can chemicals act as inhibitors ?

A

reduced rate of metabolism

increased pharmacological effect

357
Q

What is the elimination constant ?

A

fraction of drug in the body removed per unit of time

358
Q

What does an Ek of 0.2 per hour mean ?

A

20% of drug remaining in the body is eliminated per hour

359
Q

What is the half life ?

A

time taken for the plasma cocnetration to reduced by one half

360
Q

How can you work out half life ?

A

graphically

half life= ln2/Ek

361
Q

What is ln2 ?

A

0.693

362
Q

What is the therapeutic index ?

A

the difference between concentration needed to produce a therapeutic effect and that needed for toxicity

363
Q

How to you convert from mg to micrograms ?

A

/1000

364
Q

What is the nicotinic acetylcholine receptor an example of ?

A

Ligand gated ion channel

365
Q

What happens to glucoronidation in paracetamol overdose ?

A

saturated

366
Q

The IV route of adminstration is used for ?

A

drugs which may be easily altered by acidic pH of the stomach

BDS stage 2 (28 decks)

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