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Phase 2a Annabel > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Define pharmacology

A

The study of the effects of drugs

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2
Q

Define pharmokinetics

A

How the body affects the drug

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3
Q

What does MADE stand for (pharmokinetics)

A

M= metabolism
A= absorption
D= distribution
E= excretion

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4
Q

Define pharmacodynamics

A

How the drug affects the body

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5
Q

What is a receptor?

A

A component of a cell that interacts with a specific ligand and initiates a change of biochemical events leading to the ligands observed effects

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6
Q

What are the 2 types of ligands?

A

Exogenous: eg drugs
Endogenous: eg hormones and neurotransmitters

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7
Q

What are 3 chemical types that interact with receptors?

A

Neurotransmitters
Autoacids
Hormones

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8
Q

What are 2 examples of a neurotransmitter?

A

Acetylcholine
Serotonin

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9
Q

What are 2 examples of an autoacid?

A

Local hormones:
Cytokines
Histamine

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10
Q

What are 2 examples of a hormone?

A

Testosterone
Hydrocortisone

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11
Q

What are 4 types of receptors?

A

Ligand gated ion channels
G coupled protein receptors (GPCRs)
Kinase linked receptors
Cytosolic/ nuclear receptors

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12
Q

What is an example of a ligand gated ion channel?

A

Nicotinic ACh receptor

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13
Q

What are ligand gated ion channels used for?

A

ACh binding opens pore and allows ions to move into cell and change the cells electric charge distribution

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14
Q

Give an example of a GPCR

A

Beta adrenoreceptors

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15
Q

What are the largest and most diverse group of membrane receptors in eukaryotes?

A

GPCRs

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16
Q

What is the function of GPCRs?

A

On ligand binding, GPCRs catalyse the exchange of GDP to GTP

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17
Q

What are kinases?

A

Enzymes that catalyze the transfer of phosphate groups between proteins - process is known as phosphorylation

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18
Q

Describe the mechanism of kinase linked receptor activation

A

Ligand binding causes conformational change
Phosphorylation
Signal transduction

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19
Q

What type of hormones use cytosolic/nuclear receptors?

A

Steroid hormones

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20
Q

How do nuclear receptors work?

A

Modify gene transcription

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21
Q

How do zinc fingers aid nuclear receptors?

A

Recognise discrete regions of DNA

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22
Q

Give 2 examples of a chemical imbalance leading to pathology

A

Allergy- inc. histamine
Parkinson’s- dec. dopamine

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23
Q

Give 2 examples of receptor imbalance leading to pathology

A

Myasthenia gravis- loss of nicotinic ACh receptors
Mastocytosis- increased C-kit receptors

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24
Q

What is EC50?

A

Concentration that gives half the maximal response

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25
Q

Define agonist

A

Compound that binds to a receptor and activates it

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26
Q

Define antagonist

A

A compound that binds to a receptor but does not activate it

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27
Q

How is intrinsic activity calculated?

A

Emax of partial agonist
———————————
Emax of full agonist

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28
Q

Can antagonists activate a receptor?

A

No

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29
Q

Define ligand

A

A molecule that binds to another (usually larger) molecule

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30
Q

What does the 2 state model of receptor activation describe?

A

describes how drugs activate receptors by inducing or supporting a conformational change in the receptor from “off” to “on”.

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31
Q

How does competitive antagonists work?

A

Reverse effects of agonists by competing with the agonist to bind to a receptor- prevents activation by blocking agonist binding

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32
Q

What effect does adding a competitive antagonist have on a dose response curve?

A

Curve shifts to the right
-more agonist needed to illicit the same response

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33
Q

How does a non-competitive antagonist work?

A

Binds near the receptor and prevents activation but doesn’t bind directly so agonist can still bind but not activate it

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34
Q

What effect does adding a non-competitive antagonist have on a dose response curve?

A

Shifts right and down- agonist can bind but not activate it

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35
Q

What is a partial agonist?

A

An agonist which is unable to induce maximal activation of a receptor population, regardless of the amount of drug applied

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36
Q

What are the 2 categories of cholinergic receptors?

A

Nicotinic and muscarine

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37
Q

What the ACh receptor for muscarinics?

A

mAChR

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38
Q

What is the receptor for nicotinics?

A

nAChR

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39
Q

What is the antagonist of muscarinic receptors?

A

Atropine

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40
Q

What is the antagonist of nicotinic receptors?

A

Curare

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41
Q

What are the agonist and antagonists of histamine receptors?

A

Histamine = agonist
-contracts ileum and acid secretion
Mepyramine = antagonist
-reversed contraction of ileum, no effect on acid secretion

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42
Q

Define affinity

A

How well a ligand BINDS to the receptor

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43
Q

Is affinity shown by antagonists or agonists?

A

Both

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44
Q

Define efficacy

A

How well a ligand ACTIVATES the receptor

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45
Q

Do agonist or antagonists show efficacy?

A

Only agonists

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46
Q

Name a drug that will permanently inactivate a receptor

A

BAAM irreversibly antagonises B-adrenoreceptors

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47
Q

Describe receptor reserve

A

Some agonists need only a small amount of receptors to be activated to produce the maximum response

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48
Q

Do partial agonists have a receptor reserve?

A

No- maximal response never seen

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49
Q

What does signal amplification determine?

A

How powerful the response will be

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50
Q

What determines how powerful a signal amplification is?

A

The type of tissue the receptor is based on

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51
Q

Describe allosteric modulation

A

Binding of an allosteric ligand at another site can effect an agonists effect on the receptor

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52
Q

Define Emax

A

Maximum effect a drug can produce

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53
Q

Define intrinsic activity (IA)

A

Refers to the ability of a drug-receptor complex to produce a maximum functional response

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54
Q

Describe inverse antagonism

A

A drug binds to the same receptor as an agonist but induces a response opposite to that of the agonist

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55
Q

Define tolerance

A

The reduction in a drug (agonist) effect over time

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56
Q

What are 3 causes of receptor desensitisation?

A

Uncoupled (receptor can interact with G-protein)
Receptor internalised in cell vesicle
Receptor is degraded

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57
Q

How do NSAIDs work?

A

Inhibit COX which breaks arachidoic acid to PGH2 via competitive inhibition

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58
Q

How do ACE inhibitors work?

A

Inhibit ACE by preventing angiotensin 1 converting to angiotensin 2 So less bind to receptors

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59
Q

What is the effect of ACE inhibitors?

A

-Lack of binding to AT1 receptors results in reduced vasoconstriction-> reduced hypertension
-Also reduced aldosterone -> reduced hypertension

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60
Q

What type of drugs are captopril and enalapril?

A

ACE inhibitors

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61
Q

How do B-lactam antibiotics work?

A

Inhibit biosynthesis of peptidoglycan bacteria cell walls by inhibiting enzyme activity

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62
Q

What are the 3 types of protein ports?

A

Uniporters
Symporters
Antiporters

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63
Q

Describe the function of a uniporter

A

Use energy from ATP to pull molecules in

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64
Q

Describe the function of a symporter

A

Use the movement in of one molecule to pull in another molecule against a concentration gradient

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65
Q

Describe the function of an antiporter

A

One substance moves against its gradient, using energy from the second substance (mostly Na+, K+ or H+) moving down its gradient.

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66
Q

What is the suffix for a proton pump inhibitor?

A

Prazolone

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67
Q

What is the function of a proton pump inhibitor (PPI)?

A

Inhibit acid secretion and reduce acidity to help with reflux ect

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68
Q

Describe the mechanism of PPIs

A

Irreversibly inactivate proton pumps of parietal cell causing a reduction in stomach acidity

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69
Q

Describe the function of diuretics

A

Removes water from the blood to reduce blood volume and therefore blood pressure

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70
Q

How do thiazides work as diuretics?

A

Inhibit Na+/Cl- co transporter on distal tubule of nephron to increase water loss

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71
Q

How does furosemide act as a diuretic?

A

Inhibits NKCC2 pump on thick ascending limb of LOH reducing ions in three interstitium
-reduces hyperosmolarity so less water diffuses into the blood causing water loss

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72
Q

What are calcium channel blockers used to treat?

A

Hypertension

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73
Q

How are calcium channel blockers used to treat hypertension?

A

Block Ca2+ channels in the cardiac muscle, preventing influx of Ca2+ and therefore preventing vasoconstriction

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74
Q

What is the suffix for general anaesthetics?

A

Ocaine/caine

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75
Q

How do local anaesthetics work?

A

Block voltage dependent Na channels preventing depolarisation so the action potential can not be generated- so pain is not transmitted

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76
Q

Which enzyme is responsible for 75% of drug metabolism?

A

CYPs

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77
Q

What are the 3 phases of pharmacokinetics at the plasma level?

A

UPTAKE into plasma
DISTRIBUTION from the plasma
ELIMINATION from the plasma

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78
Q

What occurs in a first order reaction?

A

Rate is directly proportional to the concentration of the drug

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79
Q

What occurs in a second order reaction?

A

Rate directly proportional to the concentration squared

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80
Q

What occurs in a third order reaction?

A

Rate directly proportional to the concentration cubed

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81
Q

What occurs in a zero order reaction?

A

Rate unrelated to the concentration of the drug

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82
Q

What are the 5 ways a drug can move from the site of administration to its target?

A
  1. Simple diffusion
  2. Facilitated diffusion
  3. Active transport
  4. Through extracellular spaces
  5. Non-ionic diffusion
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83
Q

Define bioavailability

A

Amount of drug taken up as a proportion of the amount administered

84
Q

What is the ideal bioavailability?

A

1 or 100%

85
Q

What 2 routes of administration have the highest bioavailability?

A

Intravenous and intramuscular

86
Q

What are some routes of drug administration?

A

Oral
Intramuscular
Intravenous
Transcutaneous (skin patch)
Intrathecal (into CSF)
Sublingual
Inhalation
Topical
Rectal

87
Q

What are the 4 barriers a drug passes through?

A

Intestinal wall
Intestinal lumen
Lungs
Liver

88
Q

What effect does gastric pH have on aspirin uptake?

A

Aspirin is ACIDIC
-Raised pH = reduced uptake of aspirin from the stomach and therefore a reduction in bioavailability

89
Q

Where are proteins and large molecules active?

A

Plasma compartment

90
Q

Where are water soluble molecules active?

A

Plasma and interstitial compartment

91
Q

Where are lipid soluble molecules active?

A

Intracellular fluid

92
Q

How is volume of distribution calculated?

A

Total amount of drug in body
——————————————
Concentration of drug in plasma

93
Q

What is volume of distribution?

A

The volume the drug would occupy if it was distributed through all the compartments as if they were plasma

94
Q

What drugs and molecules are found in the plasma compartment?

A

Warfarin
Immunoglobulin

95
Q

What drugs are found in the interstitial compartment?

A

Aspirin/NSAIDs
Antibiotics
Muscle relaxants

96
Q

What drugs are found in the intracellular compartment?

A

Steroids
Paracetamol
Amiodarone (easily taken up by tissue)
Opioids
Local anaesthetics

97
Q

What compartment are drugs eliminated from?

A

Plasma compartment

98
Q

What are the most common routes of drug elimination?

A

Renal or hepatic

99
Q

Define clearance (2 definitions)

A
  1. The volume of plasma that can be completely cleared of drug per unit of time
  2. The rate at which plasma drug is eliminated per unit plasma concentration
100
Q

What are the units of clearance?

A

Mils minute-1 (ml/min)

101
Q

How is renal clearance calculated?

A

Rate of appearance in urine
—————————————
Plasma concentration

102
Q

What is the adult renal blood flow?

A

18% of cardiac output = 1L/min

103
Q

What is the adult plasma flow?

A

60% of blood flow = 600 mls/min

104
Q

What is the adult glomelular filtration rate?

A

12% of renal blood flow = around 130 mils/min

105
Q

How are drugs administered enterally?

A

Oral
Rectal suppository

106
Q

How are drugs administered parentrerally?

A

Subcutaneous
IM
IV
Sublingual
Inhaler

107
Q

Define potency

A

The relative strength of the drug
- lower dose needed to initiate a response

108
Q

Define therapeutic range

A

Upper and lower bounds of safe doses of a drug

109
Q

What occurs in phase 1 of drug metabolism?

A

Non-conjugation
- increases hydrophilicity via enzymes like CYP450

110
Q

What occurs in phase 2 of drug metabolism?

A

Conjugation
- Adds functional group to MASSIVELY increase hydrophilicity

111
Q

Define specificity in terms of pharmacology

A

Acts on a certain target

112
Q

Define selectivity in terms of pharmacology

A

Acts on subtype of target

113
Q

What organ contributes to most of the drug excretion in the body?

A

Kidneys

114
Q

What hormones act at a parasympathetic neurotransmitter?

A

Presynaptic = ACh (n)
Postsynaptic = ACh (m)

115
Q

What hormones act at a sympathetic neurotransmitter?

A

Presynaptic= ACh (n)
Postsynaptic = NAd

116
Q

What hormones act on a skeletal muscle motor neuron?

A

ACh at NMJ (n)

Motor neuron -> NMJ

117
Q

Where are M1 receptors found?

A

Brain

118
Q

Where are M2 receptors found?

A

Heart

119
Q

Where are m3 receptors found?

A

Lungs

120
Q

Which cholinergic receptors are usually Presynaptic?

A

Nicotinic

121
Q

Which cholinergic receptors are usually Postsynaptic?

A

Muscarinic

122
Q

What are the consequences of overstimulation of ACh?

A

SLUDGE

-salivation
-lacrimation
-urination
-defacation
-GI distress
-emesis

123
Q

Where are alpha adrenoreceptors found?

A

Vessels and sphincters

124
Q

What is an example of an alpha adrenoreceptor blocker/antagonist?

A

Tamulosin
Doxazosin

125
Q

What are alpha adrenoreceptor blockers/anatagonists used to treat?

A

Hypertension
Benign prostatic Hypertrophy

126
Q

What is the effect of beta1 adrenoreceptor agonists?

A

Act on HEART
-increase inotropy (force) and chronotropy (rate) of cardiac contraction

127
Q

Give an example of a beta1 adrenoreceptor agonist

A

Dobutamine

128
Q

What is an example of a beta1 receptor antagonist?

A

Beta blocker
-propanalol
-bisoprolol
-metoprolol

129
Q

What are beta1 receptor antagonists used to treat?

A

AF
Angina
Heart attack
Angina

130
Q

What are beta1 receptor agonists used to treat?

A

Cardiogenic shock
Severe heart failure

131
Q

Where are beta2 adrenoreceptors found?

A

Lungs (remember 2 = 2 lungs)

132
Q

What is an example of a beta2 receptor agonist?

A

SABAs (salbutamol)

133
Q

What are beta2 agonists used to treat?

A

Asthma
COPD

134
Q

Define hepatic extraction ratio

A

The proportion of drug removed by one passage through the liver

135
Q

How does cytochrome P450 oxidise substances?

A

Adds haem group Fe2+

136
Q

Name 2 cytochrome P450 inhibitors

A

Amiodarone
Cimetidine

137
Q

What are cytochrome P450 inhibitors used for?

A

Makes drugs last longer- they are not eliminated as fast

138
Q

What percentage of liver function must be lost before drug metabolism is affected?

A

70%

139
Q

What are the effects of alpha1 adrenoreceptors?

A

Vasoconstriction
Pupil dilation
Bladder contraction

140
Q

What are the effects of alpha2 adrenoreceptors?

A

Reduce insulin secretion
-found in the pancreas
-stimulated to reduce noradrenaline release

141
Q

What are the effects of beta3 adrenoreceptors?

A

Increased lipolysis
Releases bladder

142
Q

What is an example of a beta 3 agonist?

A

Mirabergon

143
Q

When are beta blockers contraindicated and why?

A

Asthmatics
- They will likely be on beta-2 antagonists anyway

144
Q

Define pain

A

Unpleasant sensory and emotional experience associated with actual or potential tissue damage

145
Q

What are the 3 components of pain?

A

Sensory
Emotional
Actual/potential tissue damage

146
Q

What are 3 positive aspects of pain?

A

Warning of tissue damage
Immobilisation for healing
Protects species- memories of pain

147
Q

What are 3 physiological effects of pain?

A

Increased heart rate
Inc blood pressure
Inc respiratory rate

148
Q

What is nociceptive pain?

A

Inflammatory chemicals reach nerves to stimulate pain

149
Q

Define neuropathic pain

A

Nerve is directly injured- pain originates in nervous system

150
Q

Define chronic pain

A

Ongoing persistent pain greater than 3-6 months

151
Q

Define adverse drug reaction

A

A response to a drug which is noxious and unintended

152
Q

What is the oral bioavailability of opiates?

A

50%

153
Q

What are the 6 types of ADR?

A

A- augmented
B- bizarre
C- chronic
D- delayed
E- end of use
F- failure

154
Q

What is the most common type of ADR?

A

Type A- augmented
80%

155
Q

What are the qualities of a type A ADR?

A

Predictable
Dose related
Self-limited

156
Q

What is the morbidity and mortality like for type A ADRs?

A

Low mortality high morbidity

157
Q

What is an example of a type A ADR?

A

Diuretic causes dehydration
Anticoagulant causes bleeding
Hypertension drug causing hypotension

158
Q

What are the qualities of a type B ADR?

A

Unexpected
Unrelated to dose
Unpredictable
Mostly immunological eg hypersensitivity

159
Q

What is the morbidity and mortality like for type B ADRs?

A

Low morbidity high mortality

160
Q

What is an example of a type B ADR?

A

Penicillin causes anaphylaxis
Heparin causes hair loss

161
Q

What are the qualities of a type C ADR?

A

Occurs after long term therapy
May not be immediately obvious after starting new medication

162
Q

Define idiosyncrasy?

A

Inherent abnormal response to a drug

163
Q

What is an example of a type C ADR?

A

Steroids predispose to hypoglycaemia -> diabetes

164
Q

What are the qualities of a type D ADR?

A

Effects not visible until a long time after taking the medication due to prolonged exposure

165
Q

What is an example of a type D ADR?

A

Tardive dyskinesia due to antipsychotics

166
Q

What are the qualities of a type E ADR?

A

Long term use
Withdrawal reaction
Serious complications associated with stopping

167
Q

What would a predictable dose related ADR likely to be?

A

Type A

168
Q

What would a ADR with history of allergy be likely to be?

A

Type B

169
Q

What would an ADR when the patient has been taking the drug for a long time be likely to be?

A

Type C

170
Q

What would an ADR when a patient had been using the drug and is having problems later on be likely to be?

A

Type D

171
Q

What would an ADR associated with withdrawal be likely to be?

A

Type E

172
Q

What is an example of a type E ADR?

A

Opiate withdrawal

173
Q

What factors increase susceptibility to an ADR?

A

Old age
Female sex
Drug interactions
Drug or diet changes
Genes

174
Q

Describe a type 1 hypersensitivity reaction

A

IgE mediated

175
Q

Describe a type 2 hypersensitivity reaction

A

IgG mediated cytotoxicity

176
Q

Describe a type 3 hypersensitivity reaction

A

Immune-complex deposition
- reaction with antibiotics

177
Q

Describe a type 4 hypersensitivity reaction

A

T cell mediated

178
Q

Describe the qualities of a type F ADR

A

Common
Dose related
Often caused by drug interactions

179
Q

What is an example of a type F ADR?

A

Failure of oral contraceptives with enzyme inducers

180
Q

How are ADRs managed?

A
  1. Continue drug and manage ADR
  2. Reduce drug dose
  3. Stop the drug (type B)
181
Q

What are the markers of a type A ADR?

A

Serum concentration

182
Q

What are the markers of a type B ADR?

A

Tryptase (released by mast cells)
Urine methylhistamine (breakdown product of histamine)

183
Q

How are ADRs reported?

A

Yellow card scheme

184
Q

When should ADRs be reported?

A

All suspected ADRs for new medications
All ADRs in children
Fatal, life threatening, disabling, incapacitating or prolonged hospitalisation

185
Q

Define synergy

A

The actions of 2 drugs combine

186
Q

Define drug antagonism

A

One drug blocks the action of another

187
Q

What are the patient risk factors for drug interactions?

A

Poly pharmacy
Old age
Genetics
Hepatic disease
Renal disease

188
Q

What are the drug risk factors for drug interactions?

A

Narrow therapeutic index
Steep dose/response curve
Saturable metabolism

189
Q

What are the factors that affect absorption?

A

Motility
Acidity
Solubility
Non-absorbed complex formation
Direct action on erythrocytes

190
Q

What are factors that affect distribution?

A

Protein binding

191
Q

What is renal excretion dependent on?

A

Urine pH

192
Q

What are 4 drugs that are weak acids?

A

Aspirin
Ibuprofen
Paracetamol
Warfarin

193
Q

What are 4 drugs that are weak bases?

A

Amphetamine
Atropine
Propranolol
Salbutamol

194
Q

What is required for a prescription?

A

Diagnosis
Drug treatment
Indications and contraindications

195
Q

What information is required on a prescription sheet?

A

Patient name
Dose
Route
Frequency
Duration
Total number of tablets
Drug name
Date and signature

196
Q

When and why are oral fluids discontinued before surgery?

A

For 2 hours before
-risk of aspiration under anaesthesia

197
Q

Which drugs should be discontinued prior to surgery?

A

ACE inhibitors
Warfarin (bridge to heparin)
Diabetes drugs

197
Q

What type of drug is morphine?

A

Receptor agonist

198
Q

What are some naturally occurring opioids?

A

Morphine
Codeine

199
Q

What are some simple chemical modified opioids?

A

Diamorphine (heroin)
Oxycodone

200
Q

What are some synthetic opioids?

A

Pethidine
Fentanyl

201
Q

How should oral opioid dose be adapted if given parentally?

A

Halved

202
Q

What is an opioid antagonist?

A

Naloxone

203
Q

What are the side effects of opioids?

A

Respiratory depression
Sedation
Nausea and vomiting
Itching
Immune suppression

204
Q

What is the first line response to opioid induced respiratory depression?

A

Administer naloxone IV
-400 micro grams/ ml

205
Q

What percentage of paracetamol is metabolised in phase 1 and phase 2 reactions?

A

Phase 1= 5%
Phase 2 = 95%

Phase 2a Annabel (12 decks)

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