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My Phase 2a > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Four main drug targets

A
  1. Receptors
  2. Enzymes
  3. Transporters
  4. Ion channels
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2
Q

T/F most drug targets are carbohydrates

A

FALSE
Most are proteins

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3
Q

What is a receptor

A

A cell component that interacts with a specific ligand and initiates a change of biochemical events ➡️ the ligands observed effect

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4
Q

Types of ligand

A
  • exogenous - drugs
  • endogenous - hormones N-transmitters etc.
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5
Q

Types of receptors

A
  • Ligand gated ion channels
  • G-protein coupled receptor
  • kinase-linked receptors
  • Nuclear receptors [AKA cytosolic receptors]
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6
Q

Example of a ligand gated ion channels

A

Nicotine ACh receptors

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7
Q

Example of a kinase-linked receptor

A

Receptors for growth factor

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8
Q

Example of nuclear receptors

A

Steroid hormone receptors e.g. oestrogen

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9
Q

Example of G-protein coupled receptors

A

Beta adrenoceptors

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10
Q

What is an ion channel

A

Pore forming membrane proteins that allow ions to pass into the cell and cause a shift in electric charge distribution by diffusion of +ve of -ve ions in or out

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11
Q

What is the largest group of membrane receptors

A

G-coupled proteins

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12
Q

Describe the structure of a GCPR

A

7 transmembrane helices

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13
Q

Examples of GPCR ligands

A

Light energy
Peptides
Lipids
Sugars
Proteins

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14
Q

What are G proteins

A

A family of proteins that transmit signals from GPCRs

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15
Q

What factors regulate GPCR activity

A
  • factors that control the ability to bind and hydrolyse GTP ➡️ GDP
    = guanosine triphosphate = guanosine diphosphate
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16
Q

Describe the mechanism of action of kinase liked receptors

A
  • Kinase enzymes are linked to the receptor and catalyse the transfer of phosphate groups to tyrosine proteins via phosphorylation.
  • Transmembrane receptors are activated when an extracellular ligand binds ➡️ enzymatic activity on the intracellular side.
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17
Q

Mechanism of action of nuclear receptors

A

Modifies gene transcription by binding to ligand binding site on DNA.

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18
Q

Example of a nuclear receptor drug target

A

Tamoxifen acts as aselective estrogen receptor modulator(SERM), or as apartial agonistof theestrogen receptors.

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19
Q

Define an agonist

A

a compound that binds to a receptor and activates it

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20
Q

Define an antagonist

A

a compound that reduces the effect of at a receptor

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21
Q

What is the 2 state model of receptor activation

A

Where a drug activates receptors by inducing or supporting a conformational change in the receptor to switch it on.

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22
Q

Define potency

A
  • Concentration or amount of a drug that is needed to produce a defined effect
  • measured using EC50
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23
Q

What is EC50

A

The concentration that gives half the maximal response.

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24
Q

What is a full agonist

A

An agonist that ➡️ full activation of the receptor and full response even with few receptors occupied

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25
Q

What is a partial agonist

A

A ligand that ➡️ a sub-maximal response no matter the number of receptors occupied or the concentration of ligand

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26
Q

Which compound is more potent and by how much?

A

Compound B is 30 fold more potent

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27
Q

Which compound is more efficacious

A

Compound A

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28
Q

What is intrinsic activity

A

The efficacy of a drug

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29
Q

Define efficacy

A

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

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30
Q

T/F Agonist and antagonists have efficacy

A

False only agonists have efficacy
Antagonists have ZERO efficacy

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31
Q

Describe the activity of these agonists

A

Compound D is more potent than compound A
compound A is more efficacious than compound D

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32
Q

T/F antagonists can activate receptors

A

False

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33
Q

What type of antagonism does this graph show

A

Competitive antagonism as it binds to the same site as the ligand which reduced the “potency”

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34
Q

What type of antagonism does this show

A

Non-competitive antagonism as the antagonist prevents the ligand binding to the receptor ➡️ reduced response [efficacy]

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35
Q

What are the categories of cholinergic receptors

A
  1. Nicotinic
  2. Muscarinic
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36
Q

What is a muscarinic receptor agonist

A

Muscarine

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37
Q

What is a muscarinic receptor antagonist

A

Atropine

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38
Q

What is a nicotinic receptor agonist

A

Nicotine

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39
Q

What is a nicotinic receptor antagonist

A

Curare

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40
Q

What happens when H1 receptors are activated

A

Allergic reactions

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41
Q

what happens when H2 receptors are activated

A

Gastric acid secretion

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42
Q

What happens when H4 receptors are activated

A
  • immune system activation
  • inflammatory conditions - such as rhinitis, asthma and pruritus
  • inflammatory pain
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43
Q

What type of receptors are histamine receptors

A

GPCR

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44
Q

2 receptor related factors governing drug action

A
  • affinity
  • efficacy
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45
Q

2 tissue related factors governing drug action

A
  • receptor number
  • signal amplification
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46
Q

Define affinity

A

How well a ligand binds to a receptor

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47
Q

T/F affinity is a property shown only by agonists

A

FALSE
Both agonists and antagonists display affinity

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48
Q

T/F partial agonists have a receptor reserve

A

False
Even at 100% occupancy a maximal response is not seen

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49
Q

Define a receptor reserve

A

The condition where the agonist produces a maximal response by occupying a small fraction of the available receptors, leaving spare receptors as the receptor reserve.

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50
Q

Define signal transduction

A

Receptor activation ➡️ a series of molecular events inside the cell ➡️ cellular response

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51
Q

Define signal amplification

A

an increase in the intensity of a signal through networks of intracellular reactions

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52
Q

Define inverse agonism

A

When a drug that binds to the same receptor as anagonistbut induces a pharmacological response opposite to that of theagonist.

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53
Q

What is allosteric modulation

A

A ligand binding to a separate site to the receptor active site ➡️ a conformational change in the active site ➡️ increased or decreased affinity of the ligand to the receptor

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54
Q

What is tolerance

A
  • A reduction in the agonist effect over time
  • caused by continuous or repeated high concentrations
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55
Q

What is desensitisation

A
  • The rapid duction in response to an agonist.
  • a defence mechanism to prevent overstimulation
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56
Q

T/F.
Desensitisation is a slow process and tolerance is a rapid one

A

FALSE

Desensitisation is a rapid process and tolerance is a slow one

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57
Q

Define selectivity

A

The ability to affect 1 subtype of a receptor and not another
- e.g. salbutamol selectively agonises on B2 adrenoceptors

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58
Q

What is the bioavailability of morphine

A

50%

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59
Q

Convert a 20mg oral dose of morphine to a parenteral dose

A

10mg
Half the dose because 50% bioavailability

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60
Q

How long does a single dose of immediate release morphine last

A

3-4 hours

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61
Q

How long does it take for IV preparations to take effect

A

~ 1min because the blood travels around the whole body in about 1 min

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62
Q

How long does it take for SC preparations to take effect

A

~30mins

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63
Q

How long does it take for oral preparations to take effect

A

~ 1 hour

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64
Q

Difference between morphine and diamorphine

A

Diamorphine is a modified version of morphine that is more potent and faster acting as it crosses the BBB faster

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65
Q

How do opioids work

A

By descending inhibition of pain via blocking opioid receptors

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66
Q

Types of opioid receptors

A
  • miu - MOP
  • kappa - KOP
  • delta - DOP
  • nociceptin opioid-like receptor - NOP
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67
Q

TOLERANCE =

A

Down regulation of the receptors with prolonged use
Need higher doses to achieve the same effect

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68
Q

Dependence =

A

Psychological - craving and euphoria
Physical dependence

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69
Q

Common side effects of opioids

A
  • respiratory depression
  • constipation
  • sedation
  • N+V
  • itching
  • Immune suppression
  • Endocrine effects
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70
Q

What is used to treat opioid induced respiratory depression

A

Naloxone
- IV is fastest
- has a host half life therefore, give depot first in case pt runs off when they come around

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71
Q

MHRA advice for prescribing opioids in chronic, non-cancer pain

A
  • Before prescribing opioids, discuss with the patient the risks and features of tolerance, dependence, and addiction - use short term courses
  • Agree a treatment strategy and plan for end of treatment
  • Warnings have been added to the drug labels and packaging of opioids to support patient awareness
  • At the end of treatment, taper dosage slowly to reduce the risk of withdrawal effects - may take weeks
72
Q

What is codeine metabolised into

A

Morphine

73
Q

Which enzyme metabolises morphine and codeine

A

CYP2D6

74
Q

What is morphine metabolised into

A

morphine 6 glucuronide - a more potent drug than morphine

75
Q

How is morphine excreted

A

morphine 6 glucuronide is renally excreted.

76
Q

What patient factors need to be considered when prescribing morphine

A
  • renal function: reduced renal function ➡️ respiratory depression due to build up of morphine 6 glucuronide - a more potent version.
  • pharmacogenetics: CYP2D6 presence and activity in individuals varies ➡️ reduced or absent responses.
77
Q

What do you prescribe for opioid pain relief in pts with renal function <30%

A

Morphine cannot be effectively cleared so oxycodone is given instead as its metabolite is weaker than the parent drug and accumulation is not as dangerous

78
Q

Which enzyme breaks down tramadol

A

CYP2D6

79
Q

Tramadol primary and secondary effects

A
  • primary
    • weak opioid agonist
  • secondary
    • SNRI - serotonin and nor-epinephrine reuptake inhibitor.
80
Q

Define bioavailability

A

The proportion of a drug that reaches systemic circulation after administration, and is able to have an effect.

81
Q

Define pharmacodynamics

A

What the drug does to the body.

82
Q

Define pharmacokinetics.

A

What the body does to the Drug.
- Absorption
- Distribution
- Metabolism
- Elimination / excretion.

83
Q

What is an irreversible inhibitor

A

A molecule that binds to the active site of an enzyme and changes it chemically eg by covalent bonds.

84
Q

What is a reversible inhibitor

A

A molecule that binds non-covalently and produce different types of inhibition based on whether these inhibitors bind to:
-the enzyme
- the enzyme-substrate complex
- both

85
Q

Define active transport.

A
  • Movement of ions from low concentration to higher concentration.
  • needs energy to work.
  • needed for cells to get ions, glucose, amino acids etc.
86
Q

Types of protein ports

A
  • uniporters: use ATP to pull molecules in
  • symporters: the movement in of one molecule to pull in another molecule against a concentration gradient.
  • antiporters: one substance moves against its gradient, using energy from the second substance one substance moves against its gradient, using energy from the second substance
87
Q

Where can you find symporters?
Give an example

A

In organs that secrete fluids
NKCC - Na-K-Cl cotransporter in kidney

88
Q

What are the main drug targets in the body

A
  1. Receptors
  2. Enzymes
  3. Transporters
  4. Ion channels
89
Q

Where can opioid receptors be found

A
  • CNS
  • GIT
  • respiratory system
90
Q

How does naloxone work

A

A competitive opioid receptor inhibitor

91
Q

Why are ADRs concerning

A
  1. Adversely affect patients’ quality of life
  2. Increase costs of patient care
  3. Preclude use of drug in most patients, although they may occur in only a few patients
  4. May mimic disease
  5. Very common cause of death, behind heart disease, cancer and stroke
92
Q

What is an ADR

A
  • An unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use and is suspected to be related to the drug.
  • Has to be noxious and unintended
93
Q

Difference between ADR and side effects

A
  • ADRs are unexpected and harmful
  • Side effects are minor, predictable and can be beneficial
94
Q

How do toxic effects occur

A
  • dose too high
  • drug interactions
  • reduced excretion due to renal or hepatic impairment
95
Q

3 broad ADR risks

A
  1. Patient risk
  2. Drug risk
  3. Prescriber risk
96
Q

Examples of patient risk factors for ADRs

A

Gender (F>M)
Elderly
Neonates
Polypharmacy (21% 5 or more drugs)
Genetic predisposition
Hypersensitivity/allergies
Hepatic/renal impairment
Adherence problems

97
Q

Examples of drug risk factors for ADRs

A
  • low therapeutic index
  • commonly causes ADRs
  • steep dose-response curve
98
Q

T/F
All ADRs occur immediately

A

False
- ADRs can occur rapidly, late, delayed or intermediate.

99
Q

What is the Rawlings Thompson ADR classification system

A
  • Type A: Augmented pharmacological
  • Type B: Bizzare or idiosyncratic
  • Type C: Chronic
  • Type D: Delayed
  • Type E: End of treatment
  • Type F: Failure of therapy
100
Q

What is a type A ADR

A

Augmented pharmacological
- A predictable, dose dependent common ADR
- Accounts for ~80% of all ADRs

101
Q

What is a type B ADR

A

Bizzare
- not predictable and not dose dependent
- e.g. anaphylaxis with penicillin

102
Q

What is a Type C ADR

A

Chronic
- e.g. osteoporosis caused by steroid use

103
Q

What is a type D ADR

A

Delayed
- e.g. malignancies after immunosuppression

104
Q

Type E ADRs

A

End of treatment
- occur after abrupt withdrawal of meds
- e.g. opiate withdrawal syndrome

105
Q

What is a type F ADR

A

Failure of therapy
- Failure of oral contraceptive pill in presence of enzyme inducer

106
Q

What does DoTS stand for

A
  • Dose relatedness (toxic, collateral or hypersusceptibility)
  • Timing eg fast infusion of frusemide hearing loss and tinnitus
  • Patient susceptibility eg patient factors
107
Q

How do Type A ADRs present

A
  • an extension of primary effects - e.g. hypoglycaemia and insulin
  • a secondary effect of the drug - e.g. bronchospasm with beta blockers
108
Q

Features of type B ADRs

A
  • unpredictable and not related to pharmacology
  • not dose dependent
  • cannot readily be reversed
  • less common but more serious and can be life threatening
    • low morbidity and high mortality
  • can be caused by allergy/ hypersensitivity
109
Q

What is idiosyncrasy

A
  • An inherent abnormal response to a drug. Caused by:
    • genetic abnormality ➡️ enzyme deficiency
    • abnormal receptor activity, e.g. Malignant hyperpyrexia with general anaesthetics
  • rare but serious
110
Q

How does one develop an allergy / hypersensitivity reaction

A
  1. Antigen/antibody reaction
  2. First dose acts as antigen
  3. Antibody produced
  4. Second dose causes antibody-antigen reaction
111
Q

What are the types of hypersensitivity reactions

A
  • Type 1:immediate anaphylactic IgE eg penicillin allergy
  • Type 2: cytotoxic antibody IgG, IgM eg methyl dopa and haemolytic anaemia
  • Type 3: immune complexes eg procainamide induced lupus
  • Type 4: delayed hypersensitivity T cell eg contact dermatitis
112
Q

Features of a type C ADR

A
  • chronic [continuous]
  • uncommon
  • related to cumulative dose
  • time related
  • e.g. steroid use ➡️ osteoporosis. Colonic dysfunction due to laxatives
113
Q

Features of a type D ADR

A
  • delayed
  • usually dose related
  • uncommon
  • shows itself some time after the use of the drug
  • e.g. teratogens is and carcinogenesis
114
Q

Features of a type E ADR

A
  • **End of drug use **
  • uncommon
  • occurs soon after drug is withdrawn
  • E.g
    • Opiate withdrawal
    • Glucocorticoid abruptly withdrawn leads to adrenocortical insufficiency
    • Withdrawal seizures when anticonvulsants are stopped
115
Q

Features of Type F ADRs

A
  • Failure
  • common
  • dose related
  • often caused by interactions
  • e.g: failure of oral contraceptive pill with an enzyme inducer
116
Q

When should you suspect an ADR

A
  • Symptoms soon after a new drug is started
  • Symptoms after a dosage increase
  • Symptoms disappear when the drug is stopped
  • Symptoms reappear when the drug is restarted
117
Q

What actions should be taken if an ADR is suspected

A
  1. Assess if urgent action is required
  2. Take a history
  3. Review medication history
  4. Review the adverse effect profile of suspected drug
  5. Modify dose, stop or swap
  6. Report
118
Q

What are the most common systems to be affected by ADRs

A
  • GI
  • Renal
  • Haemorrhagic
  • Metabolic
  • Endocrine
  • Dermatological
119
Q

6 common ADRs

A
  1. Confusion
  2. Nausea
  3. Balance problems
  4. Diarrhea
  5. Constipation
  6. Hypotension
120
Q

T/F
Reporting ADRs is a legal requirement

A

FALSE
It is good practice

121
Q

What do you report on a yellow card

A
  • All suspected reactions for
    • herbal medicines
    • black triangle ▼ drugs
  • All serious suspected reactions for
    • established drugs, vaccines and contrast media
    • drug interactions
122
Q

What does the ▼ Black Triangle mean?

A

The black triangle ▼ indicates a medicine is undergoing ‘additional monitoring’

123
Q

Which preparations are given a black triangle

A
  1. New active substances
  2. Biological meds or anything derived from plasma
  3. Anything given conditional approval
  4. Anything that requires additional studies e.g. for side effect monitoring
124
Q

Who can report on a yellow card

A
  • Doctors, dentists, coroners, pharmacists, nurses, including midwives and health visitors, radiographers, optometrists.
  • pts, parents or carers since 2005
125
Q

4 key bits of info to put on a yellow card

A

Suspected drug(s)
Suspect reaction(s)
Patient details
Reporter details
ALSO: Additional useful information

126
Q

Draw out the structure of the nervous system

A
127
Q

What does the somatic nervous system innervate and what is the result of its activation

A

The skeletal muscle
Activation ➡️ muscle excitation

128
Q

How many neutrons lie between the CNS and the skeletal muscle in the somatic nervous system

A

1

129
Q

How many neutrons lie between the CNS and the target organs in the autonomic nervous system

A

2 neutron chain with a ganglion in between

130
Q

What does the autonomic nervous system innervate?

A
  • Smooth muscle
  • cardiac muscle
  • glands
  • GI neutrons
131
Q

What is the result of autonomic system activation

A

Leads to excitation or inhibition

132
Q

Fight or fight is associated with the

A

Sympathetic nervous system

133
Q

Rest and digest is associated with which nervous system

A

Parasympathetic

134
Q

Which nervous system has an autonomic ganglion adjacent to the spinal cord

A

Sympathetic

135
Q

Which nervous system has an autonomic ganglion near the effector organ

A

Parasympathetic

136
Q

What neurotransmitters does the somatic nervous system use

A

Acetylcholine

137
Q

What neurotransmitters does the parasympathetic nervous system use

A

Acetylcholine

138
Q

What neurotransmitters does the sympathetic nervous system use

A

Acetylcholine and noradrenaline

139
Q

Types of acetyl choline receptors and which systems they are found in

A
  • nicotinic - found in somatic nervous systems
  • muscarinic - found in parasympathetic nervous systems
140
Q

Which nervous system and neurotransmitter are responsible for sweat glands

A

ACh released at sympathetic post ganglion if termini

141
Q

Which nervous system and neurotransmitter are responsible for blood vessels

A

Nitric oxide released from the Parasympathetic postganglionic termini

142
Q

Nicotine stimulates which nervous systems

A

Parasympathetic and sympathetic

143
Q

Muscarine stimulates which nervous systems

A

Parasympathetic

144
Q

How many muscarinic receptor types are there and where are they found

A

M1: Brain
M2: Heart
M3: All organs with parasympathetic innervation
M4: Mainly CNS
M5: Mainly CNS

145
Q

What type of receptor are muscarinic receptors

A

GPCR

146
Q

Effect of activation of M2 on heart SA node

A

Decreases the heart rate

147
Q

Effect of activation of M2 on heart AV node

A
  • Decrease in conduction velocity
  • induces AV node block
148
Q

Type of muscarinic receptor found in the respiratory system AND effect of stimulation

A
  • M3
  • produces mucus in the airways and nasopharynx
  • induces bronchoconstriction - smooth muscle contraction
149
Q

Type of muscarinic receptor found in the GIT system AND effect of stimulation

A
  • M3
  • Increase saliva production
  • Increases gut motility
  • Stimulates biliary secretion
150
Q

Type of muscarinic receptor found in the skin, which nervous system is responsible AND effect of stimulation

A
  • M3
  • sympathetic system releases ACh
  • stimulates the sweat glands to release sweat
151
Q

Type of muscarinic receptor found in the urinary system AND effect of stimulation

A
  • M3
  • Contracts detrusor muscle
  • Relaxation of internal urethral sphincter
152
Q

Type of muscarinic receptor found in the eye AND effect of stimulation

A
  • M3
  • Causes myosis
  • Increases drainage of aqueous humour
  • Secretion of tears
153
Q

symptoms of Muscarine poisoning

A
  • blurred vision
  • hypersalivation
  • bronchoconstriction
  • bradycardia
  • diarrhoea
  • polyuria
  • hyperhidrosis
154
Q

T/F ACh is implicated in memory and can contribute to memory problems

A

True

155
Q

Cause of myasthenia gravis

A

Blockage of normal ACh transmission ➡️ skeletal muscle weakness, especially on repeated attempts on movement.

156
Q

Myasthenia gravis treatment

A

Anticholinesterase to increase availability of ACh at the NMJ.
- e.g.

157
Q

Where is noradrenaline released from

A

From the sympathetic nerve fibre

158
Q

Where is adrenaline released from

A

Adrenaline glands

159
Q

Alpha 1 receptor agonist

A

Noradrenaline and adrenaline
NAd>Ad

160
Q

Alpha 1 receptor is found where
AND what are the results of activation

A
  • found in blood vessels
  • results in smooth muscle contraction in pupils and blood vessels and skin
161
Q

Alpha 2 receptor agonists

A

Noradrenaline and adrenaline

162
Q

Result of alpha 2 receptor activation

A

Mixed effects on vascular smooth muscle
Also found in the brain

163
Q

Beta 1 receptor agonists

A

Noradrenaline and adrenaline

164
Q

Effects of activation of receptor activation

A

Chronotropic and ionotropic effects on the heart

165
Q

Beta 2 receptor agonists

A

Adrenaline and noradrenaline
Ad> NAd

166
Q

Effects of beta 2 receptor activation

A

Relaxes smooth muscle in the lungs and uterus

167
Q

Beta 3 receptor agonist

A

Noradrenaline and adrenaline
NAd> Ad

168
Q

Consequences of beta 3 receptor activation

A
  • Enhances lipolysis
  • relaxes bladder debris or
169
Q

Alpha 1 blocker uses

A
  • lower BP
  • phaeochromocytoma
  • BPH
170
Q

Clinical uses of alpha 2 blockers

A

Trick question there aren’t any

171
Q

Beta 1 receptor locations

A
  • heart
  • kidney
  • fat cells
172
Q

Effect of beta 1 receptor agonism

A
  • tachycardia
  • increase in stroke volume
  • renin release to increase vascular tone
  • lipolysis and hyperglycaemia
173
Q

Beta 1 receptor blockers effects

A
  • reduced heart rate
  • reduced stroke volume
  • Reduce stroke volume
  • Reduce myocardial oxygen demand and help remodelling in heart failure or post-myocardial infarction
174
Q

What do you use for beta blocker poisoning and why

A
  • glucagon
  • used because glucagon increases the heart rate and myocardial contractility regardless of the presence of beta blockers as it bypasses the beta-adrenergic receptor site
175
Q

5 locations of beta 2 receptors and the effect of their agonism

A
176
Q

Uses of beta 2 receptor agonists

A
  • asthma
  • COPD
  • Tocolysis - delaying preterm labour
177
Q

Side effects of beta 2 receptor agonists

A
  • tremor
  • tachycardia
  • hyperglycaemia - due to glucagon release

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