ICS Pharmacology Flashcards
1
Q
What are the 4 types of drug interactions?
A
- Synergy
- Antagonism
- Summation
- Potentiation
2
Q
Describe Synergy
A
Interaction of drugs such that the total effect is greater than the sum of the individual effects
3
Q
Describe Antagonism
A
An antagonist is a substance that acts against and block an action (2 drugs opposed to each other)
4
Q
Describe Summation
A
Drugs used together have the same effect that a single drug would
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.
6
Q
Define Pharmacodynamics
A
The effect that the drug has on the body
7
Q
Define Pharmacokinetics
A
What the body does with the drug
8
Q
Patient risk factors for drug interaction
A
Polypharmacy, old age, genetic factors, hepatic disease, renal disease
9
Q
Drug risk factors for interaction
A
Narrow therapeutic curve, steep dose/response curve, saturable metabolism
10
Q
What is the order of the pharmacokinetic mechanism?
A
Absorption
Distribution
Metabolism
Excretion
11
Q
How do you avoid drug interactions?
A
Prescribe rationally using the BNF, medicines information service or ward pharmacist.
12
Q
What is an enzyme inhibitor?
A
A molecule that binds to an enzyme and decreases its activity. Prevents the catalysing of reactions.
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.
14
Q
3 main types of protein ports
A
Uniporters
Symporters
Antiporters
15
Q
What are the targets of drugs?
A
PROTEINS!
- receptors
- enzymes
- transporters
- ion channels
16
Q
Define a ligand
A
A molecule that binds to another molecule
17
Q
Give an example of an exogenous ligand
A
Drugs
18
Q
Give some examples of endogenous ligands
A
Hormones, neurotransmitters
19
Q
Types of receptor
A
- Ligand-gated ion channels
- G-protein coupled receptors
- Kinase-linked receptors
- Cytosolic or nuclear receptors
20
Q
Agonist and antagonist of muscarinic receptors
A
Agonist is muscarine. Antagonist is atropine.
21
Q
Agonist and antagonist of nicotinic receptors
A
Agonist is nicotine. Antagonist is curare.
22
Q
Define affinity
A
How well a ligand binds to the receptor
23
Q
Define efficacy
A
How well the ligand activates the receptor
24
Q
Describe an antagonist’s affinity and efficacy
A
Antagonists have some affinity but NO EFFICACY.
25
Describe signal transduction
A basic process involving the conversion of a signal from outside the cell to a functional change within the cell
26
Purpose of signal amplification
To increase the strength of a signal (duh)
27
Describe allosteric modification
When an allosteric ligand binds to a different site on the molecule and prevents the signal from being transmitted (non-competitive inhibition)
28
Describe tolerance
Reduction in drug effect over time at same dose. Caused by repeated high concentrations of that drug
29
Molecular reasons for someone becoming desensitised to a drug
Uncoupling of receptor-ligand relationship
Internalised receptor due to conformational change
Receptor degradation
30
Define adherence
The extent to which a patient follows agreed recommendations
31
Define necessity beliefs
A patient's perceptions of personal need for treatment (including concerns about side-effects)
32
What does patient centeredness encourage
Holistic view of patient care
| Shared control of consultation with patient
33
Impacts of good Dr-patient communication
Better health outcomes
Higher adherence!
Higher patient and clinician satisfaction
Decrease in risk of malpractice
34
Key principles of patient centred care
```
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)
```
35
What is concordance?
Extension of patient centred medicine (patients are equals and involved in care)
36
Barriers to concordance (not exhaustive)
Increased worry
Patients want the doctor to just tell them what to do
Communication skills
Patient choice vs evidence
37
Ethical considerations of concordance
Mental capacity
Decision that may be harmful to patient or others
When patient is a child (Gillick)
38
Describe drug ionisation
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
Obstacles for oral absorption into circulation
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
Describe intradermal and subcutaneous absorption
Limited by blood flow so only a small volume can be given. Used for local effect or to limit rate of absorption
41
Describe intramuscular absorption
Depends on blood flow and water solubility of drug. Can make a depot which release drug over days/weeks.
42
Describe inhalational absorption
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
Most common reversible protein binding of drugs in blood
Good ole Albumin
| binding creates a depot
44
Where do lipid soluble drugs readily pass?
Blood to brain
| Across placenta
45
What is bioavailability?
The fraction of the administered drug that reaches the systemic circulation unaltered.
46
What is clearance?
The volume of bloods cleared of a drug per unit time
47
What is the apparent volume of distribution?
The total amount of drug in the body / plasma concentration (that is a division btw)
48
What is the relationship of clearance and apparent volume of distribution?
They are inversely proportional (K=CL/Vd)
49
What is steady state?
A balance between drug input and elimination (rate of infusion/CL)
50
What is the antagonist to opioids?
NALOXONE
51
Some examples opioids
Morphine, Codeine, Oxycodone, Fentanyl, Alfentanil etc.
52
What are the four opioid receptors and which one is acted on by all the drugs used?
MOP (mu), KOP (kappa), DOP (delta) and NOP (nociception).
All the drugs used are mu agonists (MOP)
53
Define potency of a drug
How well the drug binds to a receptor (affinity)
54
Define tolerance
Down regulation of receptors with prolonged use. Need higher doses for same effect
55
When does opioid withdrawal start and how long does it last?
Starts around 24 hours after last dose, lasts around 72 hours
56
Side effects of opioids
```
Respiratory depression
Sedation
Nausea
Constipation
Itching
Immune suppression
Endocrine effects
```
57
Metabolism of morphine
Metabolised to morphine-6-glucuronide. Excreted renally and can build up in renal failure.
58
What do sympathetic and parasympathetic fibres from the CNS release to what receptors on the ganglia they synapse with?
Acetylcholine to nicotinic receptors
59
What neurotransmitter do sympathetic fibres release at the effector and to what receptors?
Noradrenaline to adrenergic receptors
60
What neurotransmitter do parasympathetic fibres release at the effector and to what receptors?
Acetylcholine to muscarinic receptors
61
Difference between ganglia in sympathetic and those in parasympathetic systems
Sympathetic = ganglia near spinal cord
Parasympathetic = ganglia near targets
62
What type of receptors are muscarinic receptors?
G-protein-coupled receptors (GPCRs)
63
How many types of muscarinic receptors are there and where are they?
5
```
M1 = brain
M2 = heart
M3 = glands and smooth muscle
M4/5 = CNS
```
64
Side effects of anti-cholinergics
```
Worsen memory
Confusion
Constipation
Dry mouth
Blurred vision
Worsening of glaucoma
```
65
What do alpha agonists cause?
Alpha 1 = raise BP (vasoconstriction)
Alpha 2 = lower BP
(alpha blockers do the opposite)
66
What do beta agonists cause?
Beta 1 = increased heart rate and chronotropic effects
Beta 2 = smooth muscle cells in asthma (bronchodilation)
Beta 3 = reduce over-active bladder symptoms
67
What to beta blockers do?
LOWER BP
Reduce cardiac work and can treat arrhythmias
68
Uses for beta blockers
Angina
MI prevention
High BP
Heart Failure
69
Side effects of beta blockers
Fatigue
Bronchoconstriction
Bradycardia
Cardiac depression
70
Define druggability
The ability of a protein target to bind small molecules with high affinity
71
Recombinant proteins in clinical use
```
Insulin
Erythropoietin
GH
IL-2
Gamma interferon
IL-1 receptor
```
72
What is an adverse drug reaction?
Unwanted or harmful reactions following administration of drugs under normal conditions of use
73
Difference between adverse drug reaction and side effect
Something CAN be both.
| Adverse drug reactions are always bad but side effects can be beneficial.
74
What are hyper-susceptibility effects?
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
What are toxic effects?
When a very high dose of a drug (beyond therapeutic range) causes damage.
76
Example of a collateral effect ADR
Beta blockers can cause bronchospasm as a secondary adverse effect
77
Describe Type A Rawlins Thompson Classification
Augmented
predictable, dose dependent and common
78
Describe Type B Rawlins Thompson Classification
Bizarre
unpredictable, not dose dependent (e.g. anaphylaxis and penicillin)
79
Describe Type C Rawlins Thompson Classification
Chronic
Osteoporosis and steroids
80
Describe Type D Rawlins Thompson Classification
Delayed
Malignancies after immunosuppression
81
Describe Type E Rawlins Thompson Classification
End of treatment
After abrupt drug withdrawal
82
Describe Type F Rawlins Thompson Classification
Failure of therapy
e.g. failure of contraceptive pill in presence of enzyme inducer
83
Causes of ADRs
Pharmaceutical variation, receptor abnormality, abnormal biological system unmasked by drug, drug-drug interaction etc.
84
When to suspect an ADR
Symptoms soon after starting a new drug, after an increase in dose, disappear when drug is stopped and reappear when restarted.
85
What to include on a yellow card
Suspected drug and reaction. Patient and reporter details.
86
When should the yellow card scheme be used?
All reactions with herbal medicine or black triangle drugs. Reported on any serious reaction with any drugs.
