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Phase 2a Stuff > ICS Pharmacology > Flashcards

ICS Pharmacology Flashcards

1
Q

What are the 4 types of drug interactions?

A
  • Synergy
  • Antagonism
  • Summation
  • Potentiation
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2
Q

Describe Synergy

A

Interaction of drugs such that the total effect is greater than the sum of the individual effects

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3
Q

Describe Antagonism

A

An antagonist is a substance that acts against and block an action (2 drugs opposed to each other)

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4
Q

Describe Summation

A

Drugs used together have the same effect that a single drug would

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5
Q

Describe Potentiation

A

Enhancement of one drug by another so that the combine effect is greater than the sum of each one alone.

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6
Q

Define Pharmacodynamics

A

The effect that the drug has on the body

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7
Q

Define Pharmacokinetics

A

What the body does with the drug

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8
Q

Patient risk factors for drug interaction

A

Polypharmacy, old age, genetic factors, hepatic disease, renal disease

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9
Q

Drug risk factors for interaction

A

Narrow therapeutic curve, steep dose/response curve, saturable metabolism

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10
Q

What is the order of the pharmacokinetic mechanism?

A

Absorption
Distribution
Metabolism
Excretion

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11
Q

How do you avoid drug interactions?

A

Prescribe rationally using the BNF, medicines information service or ward pharmacist.

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12
Q

What is an enzyme inhibitor?

A

A molecule that binds to an enzyme and decreases its activity. Prevents the catalysing of reactions.

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13
Q

Difference between reversible and irreversible inhibitors.

A

Irreversible inhibitors form covalent bonds with the enzyme and change it chemically. Reversible inhibitors bind non-covalently to the enzyme, substrate or both.

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14
Q

3 main types of protein ports

A

Uniporters
Symporters
Antiporters

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15
Q

What are the targets of drugs?

A

PROTEINS!

  • receptors
  • enzymes
  • transporters
  • ion channels
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16
Q

Define a ligand

A

A molecule that binds to another molecule

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17
Q

Give an example of an exogenous ligand

A

Drugs

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18
Q

Give some examples of endogenous ligands

A

Hormones, neurotransmitters

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19
Q

Types of receptor

A
  1. Ligand-gated ion channels
  2. G-protein coupled receptors
  3. Kinase-linked receptors
  4. Cytosolic or nuclear receptors
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20
Q

Agonist and antagonist of muscarinic receptors

A

Agonist is muscarine. Antagonist is atropine.

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21
Q

Agonist and antagonist of nicotinic receptors

A

Agonist is nicotine. Antagonist is curare.

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22
Q

Define affinity

A

How well a ligand binds to the receptor

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23
Q

Define efficacy

A

How well the ligand activates the receptor

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24
Q

Describe an antagonist’s affinity and efficacy

A

Antagonists have some affinity but NO EFFICACY.

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25
Q

Describe signal transduction

A

A basic process involving the conversion of a signal from outside the cell to a functional change within the cell

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26
Q

Purpose of signal amplification

A

To increase the strength of a signal (duh)

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27
Q

Describe allosteric modification

A

When an allosteric ligand binds to a different site on the molecule and prevents the signal from being transmitted (non-competitive inhibition)

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28
Q

Describe tolerance

A

Reduction in drug effect over time at same dose. Caused by repeated high concentrations of that drug

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29
Q

Molecular reasons for someone becoming desensitised to a drug

A

Uncoupling of receptor-ligand relationship
Internalised receptor due to conformational change
Receptor degradation

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30
Q

Define adherence

A

The extent to which a patient follows agreed recommendations

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31
Q

Define necessity beliefs

A

A patient’s perceptions of personal need for treatment (including concerns about side-effects)

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32
Q

What does patient centeredness encourage

A

Holistic view of patient care

Shared control of consultation with patient

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33
Q

Impacts of good Dr-patient communication

A

Better health outcomes
Higher adherence!
Higher patient and clinician satisfaction
Decrease in risk of malpractice

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34
Q

Key principles of patient centred care

A 
Improve communication
Increase patient involvement
Understand the patient's perspective
Provide information
Assess adherence routinely
Review medicines (including the patient's knowledge and concerns of them)
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35
Q

What is concordance?

A

Extension of patient centred medicine (patients are equals and involved in care)

36
Q

Barriers to concordance (not exhaustive)

A

Increased worry
Patients want the doctor to just tell them what to do
Communication skills
Patient choice vs evidence

37
Q

Ethical considerations of concordance

A

Mental capacity
Decision that may be harmful to patient or others
When patient is a child (Gillick)

38
Q

Describe drug ionisation

A

Basic property of most drugs that are weak acids or weak bases
Ionisable groups essential for mechanism of action of most drugs as ionic forces are part of ligand-receptor interaction

39
Q

Obstacles for oral absorption into circulation

A

Drug structure - need to be lipid soluble and stable at low pH

Drug formulation - capsule must disintegrate and dissolve at the right point

Gastric emptying - rate determines how soon a drug is delivered to small intestine

First pass metabolism - have to pass through intestinal lumen, intestinal wall, liver and lungs to circulate

40
Q

Describe intradermal and subcutaneous absorption

A

Limited by blood flow so only a small volume can be given. Used for local effect or to limit rate of absorption

41
Q

Describe intramuscular absorption

A

Depends on blood flow and water solubility of drug. Can make a depot which release drug over days/weeks.

42
Q

Describe inhalational absorption

A

Limited by risks of toxicity, largely restricted to volatiles e.g. general anaesthetics (asthma drugs non-volatile so need to be given as aerosol or dry powder)

43
Q

Most common reversible protein binding of drugs in blood

A

Good ole Albumin

binding creates a depot

44
Q

Where do lipid soluble drugs readily pass?

A

Blood to brain

Across placenta

45
Q

What is bioavailability?

A

The fraction of the administered drug that reaches the systemic circulation unaltered.

46
Q

What is clearance?

A

The volume of bloods cleared of a drug per unit time

47
Q

What is the apparent volume of distribution?

A

The total amount of drug in the body / plasma concentration (that is a division btw)

48
Q

What is the relationship of clearance and apparent volume of distribution?

A

They are inversely proportional (K=CL/Vd)

49
Q

What is steady state?

A

A balance between drug input and elimination (rate of infusion/CL)

50
Q

What is the antagonist to opioids?

A

NALOXONE

51
Q

Some examples opioids

A

Morphine, Codeine, Oxycodone, Fentanyl, Alfentanil etc.

52
Q

What are the four opioid receptors and which one is acted on by all the drugs used?

A

MOP (mu), KOP (kappa), DOP (delta) and NOP (nociception).

All the drugs used are mu agonists (MOP)

53
Q

Define potency of a drug

A

How well the drug binds to a receptor (affinity)

54
Q

Define tolerance

A

Down regulation of receptors with prolonged use. Need higher doses for same effect

55
Q

When does opioid withdrawal start and how long does it last?

A

Starts around 24 hours after last dose, lasts around 72 hours

56
Q

Side effects of opioids

A 
Respiratory depression
Sedation
Nausea
Constipation
Itching
Immune suppression
Endocrine effects
57
Q

Metabolism of morphine

A

Metabolised to morphine-6-glucuronide. Excreted renally and can build up in renal failure.

58
Q

What do sympathetic and parasympathetic fibres from the CNS release to what receptors on the ganglia they synapse with?

A

Acetylcholine to nicotinic receptors

59
Q

What neurotransmitter do sympathetic fibres release at the effector and to what receptors?

A

Noradrenaline to adrenergic receptors

60
Q

What neurotransmitter do parasympathetic fibres release at the effector and to what receptors?

A

Acetylcholine to muscarinic receptors

61
Q

Difference between ganglia in sympathetic and those in parasympathetic systems

A

Sympathetic = ganglia near spinal cord

Parasympathetic = ganglia near targets

62
Q

What type of receptors are muscarinic receptors?

A

G-protein-coupled receptors (GPCRs)

63
Q

How many types of muscarinic receptors are there and where are they?

A

5

M1 = brain
M2 = heart
M3 = glands and smooth muscle
M4/5 = CNS
64
Q

Side effects of anti-cholinergics

A 
Worsen memory
Confusion
Constipation
Dry mouth
Blurred vision
Worsening of glaucoma
65
Q

What do alpha agonists cause?

A

Alpha 1 = raise BP (vasoconstriction)

Alpha 2 = lower BP

(alpha blockers do the opposite)

66
Q

What do beta agonists cause?

A

Beta 1 = increased heart rate and chronotropic effects

Beta 2 = smooth muscle cells in asthma (bronchodilation)

Beta 3 = reduce over-active bladder symptoms

67
Q

What to beta blockers do?

A

LOWER BP

Reduce cardiac work and can treat arrhythmias

68
Q

Uses for beta blockers

A

Angina
MI prevention
High BP
Heart Failure

69
Q

Side effects of beta blockers

A

Fatigue
Bronchoconstriction
Bradycardia
Cardiac depression

70
Q

Define druggability

A

The ability of a protein target to bind small molecules with high affinity

71
Q

Recombinant proteins in clinical use

A 
Insulin
Erythropoietin
GH
IL-2
Gamma interferon
IL-1 receptor
72
Q

What is an adverse drug reaction?

A

Unwanted or harmful reactions following administration of drugs under normal conditions of use

73
Q

Difference between adverse drug reaction and side effect

A

Something CAN be both.

Adverse drug reactions are always bad but side effects can be beneficial.

74
Q

What are hyper-susceptibility effects?

A

When a dose of a drug that is too low to provide a physiological effect results in an ADR.

e.g. Tiny amount of penicillin causing anaphylaxis

75
Q

What are toxic effects?

A

When a very high dose of a drug (beyond therapeutic range) causes damage.

76
Q

Example of a collateral effect ADR

A

Beta blockers can cause bronchospasm as a secondary adverse effect

77
Q

Describe Type A Rawlins Thompson Classification

A

Augmented

predictable, dose dependent and common

78
Q

Describe Type B Rawlins Thompson Classification

A

Bizarre

unpredictable, not dose dependent (e.g. anaphylaxis and penicillin)

79
Q

Describe Type C Rawlins Thompson Classification

A

Chronic

Osteoporosis and steroids

80
Q

Describe Type D Rawlins Thompson Classification

A

Delayed

Malignancies after immunosuppression

81
Q

Describe Type E Rawlins Thompson Classification

A

End of treatment

After abrupt drug withdrawal

82
Q

Describe Type F Rawlins Thompson Classification

A

Failure of therapy

e.g. failure of contraceptive pill in presence of enzyme inducer

83
Q

Causes of ADRs

A

Pharmaceutical variation, receptor abnormality, abnormal biological system unmasked by drug, drug-drug interaction etc.

84
Q

When to suspect an ADR

A

Symptoms soon after starting a new drug, after an increase in dose, disappear when drug is stopped and reappear when restarted.

85
Q

What to include on a yellow card

A

Suspected drug and reaction. Patient and reporter details.

86
Q

When should the yellow card scheme be used?

A

All reactions with herbal medicine or black triangle drugs. Reported on any serious reaction with any drugs.

Phase 2a Stuff (7 decks)

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