Pharmacology Flashcards
(238 cards)
1
Q
Definition of physiochemical drug interactions?
A
How different drugs interact with each other
2
Q
Definition of pharmacodynamic drug interactions?
A
How a drug affects the body
3
Q
Definition of pharmacokinetic drug interactions?
A
What the body does to the drug (eg. whether it’s absorbed)
4
Q
What is the physiochemical way of drug interaction?
A
Adsorption - solutes absorbed by solid or liquid surfaces
5
Q
What is summative/additive pharmacodynamics?
A
Two drugs have the same effect, so the total effect is the sum of 2 drugs put togehter (with the same effect as a single drug would)
6
Q
What is synergism in pharmacodynamics?
A
Putting two drugs together has a bigger effect than individual effects predicted. Eg. paracetamol and morphine
7
Q
What is antagonism/blockade in pharmacokinetics?
A
Drugs that block the effects of each other, eg. beta-blockers
8
Q
What is potentiation in pharmacokinetics?
A
Adding two drugs together and just one of the drugs having an increase in effect, the other drug isn’t affected
9
Q
What is ADME in pharmacokinetics?
A
Absorption, Distribution, Metabolism, Excretion
10
Q
Is the time of absorption quicker intravenously or orally?
A
intravenously
11
Q
Definition of bioavailability?
A
How much drug is available over a given time in the systemic circulatuon (usually measuring oral in comparison to IV)
12
Q
What are 3 factors that affect absorption of drugs?
A
- motility in the gut - if gut has slowed digestion, drugs won’t work as well
- acidity - whether ionised or unionised, pH and pKa interactions
- physiochemical - solubility and complex formation
13
Q
How can drugs be distributed?
A
Into proteins, tissues, or effect sites
14
Q
How does protein binding of drugs work?
A
A drug that is bound to a protein doesn’t have an effect because it’s stuck. So when 2+ drugs are given that are protein bound, one will be free and EXTRA ACTIVE
Eg. warfarin and amiodarone
15
Q
What does protein binding depend on?
A
Albumin levels
16
Q
Where are drugs usually excreted?
A
Renally and is pH dependent - weak bases cleared faster if urine is acidic and vice versa
17
Q
What is used to prevent aspirin overdose?
A
Bicarb because it forces aspirin to remain in collecting system
18
Q
Where are majority of drugs metabolised and excreted?
A
hepatically metabolised, renally excreted
19
Q
Definition of a drug?
A
A medicine or other substance which has a physiological effect when ingested or introduced to the body
20
Q
Definition of druggability?
A
Describes a biological target that is known or predicted to bind with hgh affinity to a drug
21
Q
What is a drug 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
22
Q
What can drug receptor ligands be?
A
Exogenous (drugs) or endogenous (hormones, neurotransmitters)
23
Q
What types of drug chemicals use receptors?
A
Most - neurotransmitters (ACh, seratonin), autacoids (cytokines, histamine), hormones (testosterone, hydrocortisone)
24
Q
What are some examples of chemical imbalances leading to pathology?
A
allergy - increased histamine
parkinson’s - reduced dopamine
myasthenia gravis - loss of ACh receptors
25
What are ligand-gated ion channels?
Pore-forming membrane proteins that allow ions to pass through
26
What form do drug receptors mostly come in?
proteins
27
How do ligand-gated ion channels work?
cause a shift in charge distribution which is mediated by influx of cation (+ve) or efflux of anion (-ve)
28
Example of a ligand-gated ion channel?
nicotinic ACh receptors
29
What is the largest group of membrane receptors?
G protein coupled receptors
30
What type of ligands do G protein coupled receptors use?
Light energy, peptides, lipids, sugars, proteins
31
What do G protein coupled receptors transmit signals from?
GPCRs
32
How is activity of G protein coupled receptors regulated?
Factors control ability to bind and hydrolyse guanosine di/triphosphate - these act as switches
33
Example of G protein couple receptor?
Beta-adrenoceptors
34
What are kinase linked receptors?
Enzymes that catalyse the transfer of phosphate groups between proteins (phosphorylation)
35
When are kinase-linked receptors activated?
when binding of extracellular ligand causes enzymatic activity on intracellular side
36
Example of kinase-linked receptors?
Receptors for growth factors
37
How do cytosolic/nuclear receptors work?
Modify gene transcription
38
Example of cytosolic/nuclear receptors?
Steroid receptors
39
Definition of an agonist?
A compound that binds to a receptor and activates it
40
What is the two state model of receptor activation?
Describes how drugs activate receptors by inducing or supporting confirmatinal change of the receptor
41
How is drug potency measured?
logarithmic curve
42
What is EC50?
The concentration that gives half the maximal response
43
Definition of efficacy?
(intrinsic activity) - ability of a drug-receptor complex to produce a maximum functional response
44
Definition of an antagonist?
A compound that reduces the effect of an agonist - doesn't activate receptors but reverses agonist effect
45
What is the difference between competitive and non-competitive antagonism?
competitive binds to the same site so is selective, non-competitive binds to an allosteric site on the receptor
46
Cholinergic receptor characterisation?
1. agonist = muscarine, antagonist = atropine, receptor = mAChR
2. agonist = nicotine, antagonist = curare, receptor = nAChR
47
Definition of affinity? (ligands)
Describes how well a ligand binds to the receptor
48
Does affinity apply to agonists or antagonists?
both
49
Definition of efficacy? (ligands)
describes how well a ligand activates the receptor
50
Does efficacy apply to antagonists or agonists?
agonists
51
What is receptor reserve for agonists?
some FULL agonists only need to activate a small amount of receptors to produce maximal response (reserve can be small or large)
52
What is signal transduction of drugs?
Signalling cascade that causes conversion of a signal from outside the cell to a functional change within the cell
53
What is signal amplification of drugs?
Increasing strength of a signal
54
What is allosteric modulation?
allosteric ligand binds to a different site on the molecules and prevents it from being transmitted
55
What is inverse agonism?
When a drug binds to the same receptor as an agonist but induces pharmacological response opposite to agonist
56
Defintion of drug tolerance?
reduction in agonsit effect over time due to continuous/repeated/high concentrations of the drug
57
Definition of desensitisation of drugs?
Complete changes in receptors due to uncoupled, internalised, degraded
58
Difference between tolerance and desensitisation?
tolerance is a slow process, desensitisation is fast
59
Definition of enzyme inibition?
A molecule that binds to an enzyme and decreases its activity by preventing substrate from binding to active site and catalysing
60
What are the two types of enzyme inhibition?
Irreversible inhibitors and reversible inhibitors?
61
What is the difference between irreversible and reversible inhibitors?
Irreversible react with enzyme and change it chemically (eg. via covalent bond formation), whereas reversible inhibition has different types depending on whether the inhibitor binds to the enzyme, enzyme-substrate complex, or both (non-covalent)
62
How are statins an example of enzyme inhibitors?
They block the rate limiting step in the cholestrol pathway to reduce levels of LDLs
63
What happens whenangiotensin converting enzyme (ACE) inhibited?
Reduces angiotnesin II production so blood pressure is reduced
64
How is parkinson's treated?
with multiple enzymatic inibitor drugs
65
How does peripheral DDC inhibitor increase dopamine in parkinson's?
blocks DDC in periphery which means more is available in the CNS
66
How does peripheral COMT inhibitor increase production of L-DOPA in parkinson's?
Prevents breakdown of L-DOPA so more available in CNS
67
How do central COMT inhibitors help in parkinson's?
maintain dopamine levels in CNS
68
How does mono amine oxidase B inhibitor help parkinson's?
prevents dopamine breakdown in CNS so increases availability
69
Difference between passive and active ion transport?
passive uses symporters and channel proteins, active uses carrier proteins and ATPases
70
How do uniporters work?
use energy from ATP to pull molecules in
71
How do symporters work?
use movement of one molecule to pull in another molecule against its concentration gradient
Eg. Na-K-Cl (NKCC) cotransporter
72
What is an antiporter?
Uses energy from second substrate moving down its gradient to move another substance against its concentration gradient
73
What are the different types of ion channels used in passive transport of drugs?
epithelial, voltage-gated, metabolic, receptor activated
74
What is an epithelial ion channel and what does it transport?
apical membrane bound heterotrimeric ion channel. selectively permeable to Na+ so is often used in heart failure
75
What is a voltage gated ion channel?
in membranes of excitable cells so closed at resting membrane potential and activated during an action potential
76
What does activation of calcium voltage-gated channel result in?
muscular contraction and excitation of neurons
77
What does a sodium voltage gated channel result in?
increases Na+ into the cell and has 3 conformational states - closed, open, inactivated
78
What are calcium/sodium voltage-gated channels used to treat?
nerve arrhythmias
79
What is a receptor activated ion channel?
igand-gated ion channel that allow ions to pass through the membrane in response to binding to a chemical messenger
80
Example of a receptor activated ion channel?
GABA inhibitory neurotransmitter inhibits GABA A which causes hyperpolarisation - eg. chloride in epilepsy
81
How are sodium pumps (active) used to decrease heart rate?
inibition causes increase in intracellular Na which also increases intracellular Ca, increasing length of cardiac action potential
82
How are proton pumps (active) used to treat acidifcation of the stomach?
proton-pump inhibitors are irreversible and inhibit acid secretion
83
What does drug metabolism occur through?
specialised enzymatic systems and biotransformation
84
What determines the duration and intensity of a drug's pharmacologic action?
rate of metabolism
85
What does drug metabolism and biotransformation do?
generates compounds that are more readily excretable
86
What is the main enzyme involved in drug metabolism?
CYPs (CYP450)
87
How do CYPs help metabolise drugs?
deactivates or bioactivates drugs, either directly or by facilitated excretion
88
What are the different types of opioids and examples of each? (x4)
- naturally occuring, eg. morphine
- simple chemical modifications, eg. diamorphine
- synthetic opioids, eg. pethidine
- synthetic partial agonists, eg. buprenorphine
89
What are some routes of administration of drugs?
- oral (bioavailability)
- parenteral - subcutaneous, IV, IM, IA
- inhalational
- topical
- sublingual
- rectal
- intrathecal
- IV patient controlled analgesia
- epidural into CSF
- trans-fermal patches
- first pass metabolism by the liver
90
What is first pass metabolism by the liver?
Eg. 50% oral morphine metabolised by first pass so needs to be halved if giving IV
91
How long does a single dose of morphine last?
3-4 hours but can be slow release twice a day in palloative patients
92
What existing pain modulation systems do opioids use?
- G protein couple receptors and act via second messengers
- descending inhibition of pain, produces fight or flight response rather than sustained activation
93
What do opioids inhibit?
pain transmitters at spinal cord and midbrain
94
How do opioids modulate pain perception in higher centres?
change emotional perception of pain (euphoria)
95
What type of receptors do opioids use?
μ receptors. Also: delta, kappa, nociception opioid-like receptors
96
What is the definition of drug potency?
Whether a drug is strong or weak relates to how well the drug binds to the receptor
97
Definition of opioid drug efficacy?
Concept of full or partial agonists and maximal response with the drug
98
Difference between tolerance and dependence?
tolerance occurs when there's a downregulation of receptors with prolonged use, requiring higher doses to achieve the same effect. Dependence is a physiological response of craving and euphoria
99
When does withdrawal from opioids start, and how long does it last?
starts within 24 hours and lasts about 72 hours
100
Why do we get side effects from opioid use?
Side effects happen because opioid receptors exist outside the pain system (eg. digestive tract and respiratory control centre) and opioids are usually delivered systemically
101
Why should you start with a small dose of opioids and titrate up?
Different patients have a range of sensitivity
102
What complication can arise from overusing opioids?
Respiratory depression
103
What are the side effects of respiratory depression?
sedation, nausea, vomiting, constipation, itching, immune suppression
104
What is the medical response for respiratory depression?
Help --> ABC --> naxolone IV
105
What is antagonist of opioids?
Naxolone - short half life so weary of overdose
106
What are the disadvantages of using opioids in chronic non-cancer pain?
- lose effectiveness quickly
- addiction to drug leads to manipulative behaviour, easy to start, difficult to stop
107
What needs to happen to codeine and tramadol in order for them to work?
They need to be metabolised by cytochrome CYP2D6 to morphine
108
What does morphine have to be metabolised to in order to be excreted?
morphine 6 glucuronide which is more potent and renally excreted
109
What patients do you have to be careful in giving morphine to?
Those with renal failure - it can build up and cause respiratory depression
110
What is drug development?
Process of bringing a new pharmaceutical drug to the market
111
What are the 4 steps of drug discovery?
1. lead compound identification
2. pre-clinical development
3. clinical development and trials
4. regulatory approval and marketing
112
What have drugs been commonly developed from?
plants (morphine), organic chemistry (choloroform, anaesthetics), inorganic chemistry (anti-cancer), sulphonamide nucleus (hypertensives, diabetes), bacteria/mold/fungi
113
What are stereoisomers?
Same molecular formula but with different orientation in space - cause differentpotencies in drugs
114
What types of antibodies are used in immunotherapy?
Polyclonal and monoclonal
115
How are recombinant proteins used clinically?
DNA enclosed protein inserted into plasmid vector and into bacteria to produce protein. Grown and purified --> used as therapeutic agent
116
WHat other proteins are used in recombinant therapy?
insulin, erythropoietin, growth hormone, interleukin 2, gamma interferon
117
Examples of drugs developed to target DNA?
methotrexate and protein kinase inhibitors (eg. vemurafenib)
118
What is gene therapy in drug development?
Experiemental technique that uses genes to treat or prevent disease
119
How can genes be used to prevent disease?
- replacing mutated gene with healthy copy
- inactivating mutated gene
- introducing new gene to help fight disease
120
How does high throughput screening help in drug discovery
Provides starting points for drug design and for understanding the interaction or role of a particular biochemical process
121
What is rational drug design?
The process of finding new medications based on the knowledge of a biological target
122
WHat type of drugs are commonly used in rational drug design?
organic small molecules that activate or inhibit function of a biomolecule
123
Why does rational drug design use drugs that are complementary in shape to biomolecular target?
So that they will interact and bind
124
What does rational drug design rely on?
computer modelling techniques and knowledge of 3D structure of biomolecular target
125
What is drug selectivity?
The degree to which a drug acts on a given site relative to other sites
126
What is drug specificity?
The measure of a receptors ability to respond to a single ligand
127
What is the principle of the pain analgesic ladder?
medications used in incremental fashion according to the patient's reported pain intensity
128
Why is the pain ladder unhelpful for persistant pain?
substantial reduction in pain is rarely achievable and requires other control methods
129
Should the stepped pain ladder be used to make medication choices?
Can be considered but should ultimately aim to start with non-opioid drugs
130
When can paracetamol overdose occur?
When patients take other drugs containing paracetamol without realising, eg. cocodamol
131
What must most drugs do in order to enter general circulation?
Cross at least one membrane barrier from site of generation
132
What are the different ways drugs can pass across membranes?
- passive diffusion through lipid layer
- diffusion through pores or ion channels
- carrier mediated processes
- pinocytosis
133
What are ionizable groups essential for?
mechanism of action of most drugs because ionic forces are part of ligand receptor interaction
134
What type of drugs is ionisation a basi property of?
drugs that are either weak acids or weak bases
135
Which forms (ionised or unionised) are water soluble and lipid soluble?
ionised = water soluble
unionised = lipid soluble
136
What feature of the small intestine allows rapid and complete absorption of oral drugs?
Large surface area and high blood flow
137
What do drugs need to be in order to be absorbed from the gut?
lipid soluble
138
Why do some drugs have to be given by an alternative route?
If unstable at low pH or in presence of digestive enzymes
139
Why do some drugs have a capsule or coating?
Means they dissolve more slowly and are resistant to the acidity of the stomach
140
What are the 4 metabolic barriers drugs have to pass in first pass metabolism?
intestinal lumen, intestinal wall, liver, lungs
141
When are drugs given intradermally/subcutaneously?
allows small volume to be given, used for local effect, used to deliberately limit rate of absorption, avoids stratum corneum barrier
142
What is intradermal/subcutaneous absorption limited by?
blood flow
143
What does intramuscular absorption depend on?
blood flow and water solubility because increasing either can enhance drug removal
144
What is a pro for inhalational absorption of drugs?
large SA and blood flow
145
What are cons for inhalational absorption?
- risks of toxicity to alveoli
- largely restricted to volatiles, eg. anaesthetics and bronchodilators
- asthma drugs non-volatile so have to be made aerosol
146
Which type of drugs can readily cross placenta and BBB?
lipid soluble
147
What is elimination of drugs?
Removal of drugs activity from the body which may involve metabolism or excretion
148
Why are drugs converted to water soluble products to be excreted?
Lipid soluble would get reabsorbed
149
Difference between phase 1 and phase 2 metabolism?
phase 1 - transformation to more polar metabolite, add functional group using CYP
phase 2 - formation of covalent bond between drug and endogenous substrate so more readily excreted
150
What different forms are drugs excreted in?
1. fluids - sweat, tears, breast milk
2. solids - faecal elimination
3. gases - expired air
151
Difference between first order and zero order metabolic pharmacokinetics?
1st Order: decline is exponential, constant fraction of drug is eliminated per unit of time
Zero Order: once saturated, rate of removal is constant and unaffected by increase in concentration
152
What is the half life of a drug?
time taken for a concentration of a drug to reduce by half
153
How is the apparent volume of distribution measured?
total amount of drug in body/plasma concentration
154
What does a water soluble vs lipid soluble drug rate of distribution depend on?
water = rate of passage across membranes
lipid = blood flow to tissues
155
What is the rate of elimination inversely proportional to?
volume of distribution
156
What is drug clearance?
volume of blood or plasma cleared of a drug per unit of time
157
What does it mean when a drug is in a steady state?
there is a balance between input and elimination of a drug
158
What is most long term drug administration by?
Oral route - doses are intermittent so have peaks and troughs
159
Difference between adrenergic and cholinergic?
adrenergic: relating to adrenaline or noradrenaline
cholinergic: relating to acetylcholine
160
Difference between neuron chain of somatic and autonomic?
somatic - single neuron between CNS and skeletal muscle
autonomic - two neuron chain separated by autonomic ganglion
161
Difference between somatic and autonomic innervation?
somatic - innervates skeletal muscle = excitation
autonomic - innervates smooth muscle = excitation or inhibiton
162
What neurotransmitters and receptors do sympathetic NS use?
preganglionic: ACH on nicotine receptors
postganglionic: Nordadrenaline on alpha/beta receptors
163
What neutrotransmitters and receptors do parasympathetic NS use?
preganglionic: ACh on nicotine receptors
postganglionic: ACh on muscarinic receptors
164
Are muscarinic receptors adrenergic or cholinergic?
cholinergic
165
Where are muscarinic receptors found and what do they activate?
found outside cell - M1 (brain), M2 (heart). activate intracellular processes though G proteins
166
How do M2 receptors affect SA and AV node?
At SA: decrease heart rate
At AV: decrease conduction velocity and induce AV node block by increasing PR interval
167
Where are M3 receptors activated?
resp system: produce mucus and induce bronchoconstriction
GI: increase saliva and gut motility
Skin: sweating
168
Symptoms of muscarine poisoning?
blurred vision, hypersalivation, bronchoconstriction, bradycardia, diarrhoea, polyuria, hyperhidrosis (excessive sweat)
169
Example of a muscarinic agonist?
pilocarpine eye drips increase drainage of aqueous humour to reduce pressure
170
Example of muscarinic antagonists?
atropine eye drops dilate pupils and can also be used IV to increase HR
171
What does local delivery of inhaled antimuscarinics result in?
bronchodilation
172
Examples of M3 antimuscarinics in bladder and gut?
Solifenacin: blocks M3 and inhibits smooth muscle contraction
Mebeverine: blocks M£ and slows gut contractility
173
Where is ACh used outside of the autonomic NS?
in CNS receptors and skeletal muscle
174
What is a side effect of anticholinergics being used in CNS?
memory problems
175
Botulinum toxin (BoTox) prevents ACh release - what does this cause?
flaccid paralysis and death from resp muscle involvement
176
What is the pathology of myasthenia gravis?
blockage of normal transmission of ACh --> causes muscle weakness
177
Are catecholamines present in cholinergic or adrenergic?
adrenergic
178
What does post-atonomic ganglion neurotransmission depend on?
catecholamines: noradrenaline, adrenaline, dopamine
179
What do alpha 1 receptors cause when activated?
vasoconstriction and contraction in smooth muscle of eye and blood vessels
180
What are examples of agonists for alpha 1 receptors?
noradrenaline (shock) and adrenaline (anaphyalxis)
181
Example of antagonist for alpha 1 receptors?
doxazosin and tamsulosin
182
Where are alpha 2 adrenoreceptors located?
In brain so have mixed effects on vascular smooth muscle
183
What effects do alpha 2 receptors have once activated?
reduce vascular tone and blood pressure
184
Where are beta 1 receptors located?
heart, kidneys, fat cells
185
What effects do agonists of beta 1 receptors cause?
tachycardia, increased SV, renin release, lipolysis, hyperglycaemia
186
What are antagonists of beta 1 receptors known as?
beta blockers, eg. propranolol
187
What effects do beta blockers have
reduce heart rate and SV, reduce oxygen demand and remodel in heart failure
188
Where are beta 2 receptors located?
bronchi (dilate), bladder (inhibits micturition), uterus (inhibits labour), skeletal muscle (more contraction), pancreas
189
Example of beta 2 agonists?
salbutamol use in asthma
190
What is the definition of an adverse drug reaction?
unwanted or harmful reaction following administration of drug under normal conditions of use, and is suspected to be related to the drug
191
What does a drug reaction have to be in order to be classed as adverse?
noxious and unintended
192
Difference between mild and severe ADRs?
mild = nausea, drowsiness, itchy rash
severe = resp depression, anaphylaxis, haemorrhage
193
How is a side effect different to an ADR?
unintended effect of drug related to its pharmacology and can include unexpected benefits of treatment. Side effects could be beneficial
194
What are the three types of effects of an ADR?
toxic (above therapeutic range), collateral (therapeutic range), hyper-susceptibility (below theraputic range)
195
When can toxic effects occur? Example?
When dose is too high or drug excretion is reduced by impaired renal/hepatic function. Eg. nephrotoxicity with high doses of aminoglycosides
196
Example of collateral ADR effect?
beta blockers causing bronchoconstriction
197
Example of hyper-susceptibility ADR effects?
penicillin and anaphylaxis
198
Common patient risk factors for ADRs? (7)
- gender F>M
- age (elderly and neonates)
- polypharmacy
- adherence problems
- genetic predisposition
- hypersensitivity
- hepatic/renal impairment
199
What are common drug risk factors for ADRs? (4)
- steep dose-response curve
- low therapeutic index so easily toxic range
- already causes adverse reactions
- prescriber risks
200
What can causes for ADRs be due to?
- pharmaceutical variation
- abnormal biological system unmasked by drug
- abnormalities in drug metabolism
- receptor abnormality
- drug-drug interaction
201
What are the time-dependent ADRs?
rapid, first dose, early, intermediate, late, delayed
202
What is the classification of ADRs?
A - augmented pharmacological
B - bizarre/idiosyncratic
C - chronic
D - delayed
E - end of treatment
F - failure of therapy
203
What are the main characteristics of a type A ADR?
predictable, dose dependent, common. high morbidity, low mortality
204
What is the difference between a primary and secondary type A ADR?
primary effect eg. is bradycardia and propranolol
secondary effect eg. bronchospasm and propranolol
205
What are main characteristics of type B ADR?
not predictable, dose dependent, not readily reversed, less common, low morbidity but high mortality
206
What is a type B ADR often due to? and give an example.
idiosyncrasy, allergy, hypersensitivity. Eg. anaphylaxis and penicillin
207
Common characteristics of type C ADR? and example.
uncommon, time related, related to cumulative dose. Eg. osteoporosis and steroids
208
Common charcateristics of type D ADR? and example.
uncommon, dose related, shows some time after use of drug. Eg. malignancies and immunosuppression
209
Characteristics of type E ADR? and example.
uncommon, occur after ubrupt drug withdrawal. Eg. opiate withdrawal
210
Characteristics of Type F ADR? and example.
common, dose related, caused by drug interactions. Eg. failure of contraceptive pill in presence of enzyme inducer
211
What does DoTS stand for?
DOse relatedness, Timing, patient Susceptibiltity
212
Wht does idiosyncrasy mean?
Inherent abnormal response to a drug
213
When should we suspect an ADR?
- symptoms soon after a new drug is started or dosage changed
- symptoms disappear when drug is stopped and reappear when restarted
214
What is the recommended response to an ADR?
assess if urgent reaction, take a history, review meds, review adverse effect profile of drug, modify or stop drug, report drug
215
What are some drugs that commonly cause ADRs?
antibiotics, anti-neoplastics, cardiovascular, hypoglycaemic, NSAIDs, CNS drugs
216
What bodily systems are commonly affected by ADRs?
GI, renal, metabolc, endocrine, dermatologic, haemorrhagic
217
What are common side effects of ADRs?
confusion, nausea, balance problems, diarrhoea, constipation, hypotension
218
What is the Medicines and Healthcare Products Regulatory Agency (MHRA) responsible for?
Approving medicines and devices for use
219
What is yellow card reporting?
voluntarily collects spontaneous reports and suspected ADRs
220
Why are ADRs reported?
patient safety, to identify ADRs missed in clinical trials, compare drugs in same therapeutic class,identify ADRs in risk groups
221
What should you report on a yellow card?
- all suspected reactions for herbal medicines and black triangle drugs
- all serious reactions for established drugs, vaccines, and interactions
222
What is the optimisation of medicines?
looks at the value of medications to make sure they are clinically and cost-effective. Ensures people get right choice of medicines at the right time.
223
Definition of adherence?
Extent to which patient's actions match agreed recommendation
224
Why is adherence better than compliance?
acknowledges importance of patients belief but recognises health professional is still expert
225
What is compliance?
An old term that assumes doctor knows best and the patient should be passive and follow orders.
226
Example of non-adherence?
not taking, taking smaller/bigger/more/less doses, stopping without finishing course
227
What are some unintentional reasons for non-adherence?
difficulty understanding instructions, problems using treatment, financial
228
What are some intentional reasons for non-adherence?
patient's belief about their health/treatments, personal preferences
229
What are necessity beliefs?
Perceptions of personal need for treatment and concerns about a range of potential adverse consequences.
230
What is the aim of patient-centeredness?
Shift in focus from treatment to the process of care
231
What does patient-centredness encourage?
- focus in consultation on patient as a whole with preferences and social context
- shared control and decisions about health management
232
What are the benefits of good doctor-patient communication?
better health outcomes, higher adherence, higher doctor-patient satisfaction, reduced risk of malpractice
233
How can communication be improved for drug adherence?
adapt consultation style to patient's needs and encourage them to ask Qs
234
How can patient involvement of treatment be increased?
- explain condition and pros/cons of treatment
- ideas, concerns and expectations
- record patients decision if choose not to take medicine
235
How can a doctor understand patient's perspective of their treatment?
Ask what they know and believe, and if they have any concerns
236
How can doctors increase adherence (3)?
- provide clear and individualised info
- assess adherence in non-judgemental way
- review medicines
237
What is concordance?
extension of patient-centered care that thinks of patients as equals who are expected to take part in treatments
238
Why my patients not want to work in concordance about their treatment?
Might worry them more or medical decisions may be too complex
