Drugs Flashcards
(218 cards)
1
Q
What are the main clinical uses of methylphenidate?
A
Treatment of attention-deficit hyperactivity disorder (ADHD) and narcolepsy.
2
Q
What is the mechanism of action of methylphenidate?
A
It blocks the reuptake of noradrenaline and dopamine into presynaptic neurons, increasing their levels in the synaptic cleft, enhancing attention, reduces impulsivity, and improves focus and behaviour.
3
Q
What are the common side effects of methylphenidate?
A
Insomnia, reduced appetite, abdominal pain, nausea, headache, and dry mouth.
4
Q
Why must cardiac history be considered before prescribing methylphenidate?
A
It can increase heart rate and blood pressure, posing a risk in patients with underlying heart conditions.
5
Q
Is methylphenidate a controlled drug?
A
Yes, it is classified as a Schedule 2 controlled drug due to its potential for abuse and dependence.
6
Q
What important interactions does methylphenidate have?
A
It can interact with MAO inhibitors, increasing the risk of hypertensive crisis, and with drugs lowering the seizure threshold.
7
Q
What are the main clinical uses of amfetamines?
A
Treatment of ADHD, narcolepsy, and (rarely) severe obesity.
8
Q
What is the mechanism of action of amfetamines?
A
They increase synaptic concentrations of noradrenaline and dopamine by promoting their release and blocking reuptake.
9
Q
What are common side effects of amfetamines?
A
Insomnia, reduced appetite, weight loss, dry mouth, headache, and anxiety.
10
Q
What are serious adverse effects of amfetamines?
A
Cardiovascular events (e.g., hypertension, arrhythmias), psychosis, aggressive behavior, and growth retardation in children.
11
Q
Are amfetamines controlled substances?
A
Yes, they are Schedule 2 controlled drugs due to high abuse and dependence potential.
12
Q
What important drug interactions do amfetamines have?
A
Risk of hypertensive crisis with MAO inhibitors, and additive effects with other sympathomimetics.
13
Q
What advice should patients be given regarding alcohol and amfetamines?
A
Avoid alcohol as it can enhance CNS side effects and mask intoxication.
14
Q
What is the main difference between amfetamines and methylphenidate?
A
Amfetamines mainly promote neurotransmitter release; methylphenidate mainly blocks reuptake.
15
Q
What is memantine used for?
A
Memantine is used to treat moderate to severe Alzheimer’s disease and can also be used in some cases of Parkinson’s disease dementia and vascular dementia.
16
Q
How does memantine work in the brain?
A
Memantine is an NMDA receptor antagonist, meaning it binds to and blocks the NMDA receptor, which is a type of glutamate receptor.
Glutamate is an excitatory neurotransmitter that plays a crucial role in learning and memory, but excessive glutamate activity can lead to neuronal excitotoxicity and cell damage.
By blocking NMDA receptors, memantine helps to regulate glutamate activity and potentially protects nerve cells from damage.
17
Q
When is memantine typically prescribed for Alzheimer’s disease?
A
Memantine is prescribed for moderate to severe Alzheimer’s disease. It may also be added to acetylcholinesterase inhibitors like donepezil in moderate to severe cases.
18
Q
What are some side effects of memantine?
A
Common side effects include dizziness, headache, constipation, and confusion. Rare side effects may include hallucinations or delusions.
19
Q
What are acetylcholinesterase inhibitors (AChEIs)?
A
Acetylcholinesterase inhibitors are a class of medications that increase levels of acetylcholine in the brain by inhibiting the enzyme acetylcholinesterase, which breaks down acetylcholine. They are used to treat Alzheimer’s disease and other types of dementia.
20
Q
Name some commonly used acetylcholinesterase inhibitors for treating Alzheimer’s disease.
A
Common AChEIs include Donepezil, Rivastigmine, and Galantamine.
21
Q
How do acetylcholinesterase inhibitors help in Alzheimer’s disease?
A
AChEIs increase acetylcholine levels in the brain, which can help improve or stabilize cognitive function and memory in patients with mild to moderate Alzheimer’s disease.
22
Q
What are the first-line treatments for mild to moderate Alzheimer’s disease?
A
The first-line treatments for mild to moderate Alzheimer’s disease are acetylcholinesterase inhibitors such as Donepezil, Rivastigmine, and Galantamine.
23
Q
What are some side effects of acetylcholinesterase inhibitors?
A
Common side effects include nausea, vomiting, diarrhea, muscle cramps, and fatigue. These side effects are usually mild and tend to decrease over time.
24
Q
What is the difference between Rivastigmine and Donepezil?
A
Rivastigmine can be administered as a patch, offering an alternative for patients who have trouble taking oral medications. Donepezil is taken orally and is known for its longer half-life, allowing for once-daily dosing.
25
How do SSRIs (selective serotonin reuptake inhibitors) work?
They selectively inhibit the reuptake of serotonin (5-HT) in the synaptic cleft, increasing its availability to fill up nerve receptors.
26
How do SSRIs compare to tricyclic antidepressants (TCAs)?
SSRIs have similar efficacy but fewer adverse effects and are safer in overdose.
27
Name common adverse effects of SSRIs.
GI upset, appetite/weight changes, skin rash, hyponatraemia, suicidal thoughts, lowered seizure threshold, QT prolongation, bleeding risk, serotonin syndrome, withdrawal symptoms.
28
What is serotonin syndrome?
A triad of autonomic hyperactivity (e.g. tachycardia, pounding headache), altered mental state, and neuromuscular excitation.
29
What can happen with sudden withdrawal of SSRIs?
GI upset, flu-like symptoms, neurological issues, and sleep disturbance.
30
In which patients should SSRIs be used cautiously?
Those with epilepsy, peptic ulcer disease, hepatic impairment, and young people (due to suicide risk).
31
Why should SSRIs be prescribed carefully in young people?
Poor efficacy and increased risk of self-harm/suicidal thoughts—should be initiated by specialists.
32
What drugs should SSRIs not be combined with due to risk of serotonin syndrome?
Monoamine oxidase inhibitors (MAOIs).
33
What combination increases the risk of GI bleeding?
SSRIs with aspirin, NSAIDs or anticoagulants; gastroprotection should be considered.
34
What types of drugs should not be combined with SSRIs due to QT prolongation risk?
Antipsychotics and other QT-prolonging drugs.
35
Do all SSRIs cause QT prolongation?
While not all SSRIs cause QT prolongation to the same extent, they are generally considered to increase the risk. Citalopram and escitalopram are particularly associated with a higher risk.
36
Why are lower doses used in elderly patients?
Increased sensitivity and risk of adverse effects.
37
How long should a patient continue SSRIs after feeling better?
At least 6 months (2 years for recurrent depression).
38
What should patients be told about treatment onset?
Symptom improvement may take a few weeks, especially sleep and appetite.
39
What should patients be warned about stopping SSRIs suddenly?
It can cause withdrawal symptoms—taper gradually over 4 weeks.
40
Which SSRIs are preferred in polypharmacy due to fewer interactions?
Citalopram and escitalopram.
41
What are the common indications for SNRIs?
Major depressive disorder, generalized anxiety disorder (GAD), panic disorder, and sometimes neuropathic pain (e.g. duloxetine).
42
How do SNRIs work?
They inhibit the reuptake of both serotonin (5-HT) and noradrenaline (NA) from the synaptic cleft, increasing their levels and enhancing neurotransmission.
43
How do SNRIs differ from SSRIs?
SNRIs also act on noradrenaline reuptake, which may offer additional benefit for some patients, particularly those with fatigue or pain symptoms.
44
What is noradrenaline?
Noradrenaline acts as a chemical messenger in the brain, influencing mood, attention, arousal, and memory.
45
What are common adverse effects of SNRIs?
GI symptoms (nausea, constipation), dry mouth, headache, increased blood pressure, insomnia, sexual dysfunction, and sweating.
45
What cardiovascular effect is particularly associated with SNRIs?
Dose-dependent increase in blood pressure and heart rate, especially with venlafaxine.
46
What withdrawal symptoms can occur when stopping SNRIs abruptly?
Dizziness, irritability, insomnia, sensory disturbances ("electric shock" sensations), and flu-like symptoms.
47
In which patients should SNRIs be used with caution?
Those with hypertension, cardiac disease, seizure disorders, narrow-angle glaucoma, or hepatic/renal impairment.
48
What should be monitored regularly during SNRI therapy?
Blood pressure and heart rate—especially at higher doses of venlafaxine.
49
Which drugs should SNRIs not be combined with due to risk of serotonin syndrome?
Monoamine oxidase inhibitors (MAOIs), triptans, SSRIs, and other serotonergic agents.
50
Why must caution be used with NSAIDs or anticoagulants?
SNRIs may increase the risk of bleeding, especially gastrointestinal bleeding.
51
Do SNRIs cause QT prolongation?
While most SNRIs are generally considered safe with regards to QT prolongation, venlafaxine is a notable exception. The risk of QT prolongation is generally low for other SNRIs like duloxetine.
52
Name the SSRIs prescribed in the UK.
The SSRIs prescribed in the UK are:
fluoxetine (brand names Prozac, Oxactin)
paroxetine (Seroxat)
citalopram (Cipramil)
escitalopram (Cipralex)
sertraline (Lustral)
fluvoxamine (Faverin)
53
Name SNRIs prescribed in the UK.
The SNRIs prescribed in the UK are:
venlafaxine - brand names:
Bonilux
Depefex
Foraven
Politid
Venlalic
Winfex
Efexor
duloxetine - brand names
Cymbalta
Yentreve
54
What symptoms should patients report during treatment?
Agitation, suicidal thoughts, increased blood pressure, or signs of serotonin syndrome.
55
What is a tip when prescribing SNRIs for patients with comorbid chronic pain?
Duloxetine may be especially beneficial due to dual action on mood and pain.
56
Why is duloxetine used for neuropathic pain over venlafaxine?
Duloxetine is often preferred over venlafaxine for neuropathic pain due to its more balanced serotonin and norepinephrine reuptake inhibition, potentially leading to fewer side effects.
57
What are the common indications for tricyclic antidepressants (TCAs)?
Second-line treatment for moderate-to-severe depression when SSRIs are ineffective; also used for neuropathic pain (off-label).
58
What is the mechanism of action of TCAs?
Inhibit reuptake of serotonin and noradrenaline from the synaptic cleft, increasing neurotransmission.
59
Which receptors do TCAs block, leading to many adverse effects?
Muscarinic, histamine (H1), α-adrenergic (α1, α2), and dopamine (D2) receptors.
60
What are the cardiovascular risks associated with TCAs?
Arrhythmias, QT and QRS prolongation, and severe hypotension.
61
Why are SSRIs preferred in overdose risk?
SSRIs are associated with fewer toxic effects.
62
Why are TCAs dangerous in overdose?
They can cause coma, respiratory failure, severe arrhythmias, hypotension—potentially fatal.
63
In which patient populations should TCAs be used with caution?
Elderly, those with cardiovascular disease, epilepsy, prostatic hypertrophy, constipation, or raised intraocular pressure.
64
What kind of drugs can worsen TCA side effects?
Drugs with antimuscarinic, sedative, or hypotensive properties.
65
How quickly can symptom relief begin with TCAs?
Evidence shows improvement can begin in the first week, though full effect takes longer.
66
Names TCAs prescribed in the UK.
Amitriptyline, clomipramine, dosulepin, imipramine, lofepramine and nortriptyline.
67
What is the mechanism of action of mirtazapine?
Antagonist of presynaptic α2-adrenoceptors, enhancing release of serotonin and noradrenaline.
68
Names of tetracyclic antidepressants.
Mirtazapine.
69
What are common side effects of mirtazapine?
Dry mouth, increased appetite, weight gain, sedation, abnormal dreams, dizziness.
70
What class of antidepressant is reboxetine?
Selective noradrenaline reuptake inhibitor (NARI).
71
What is amantadine primarily used for?
Parkinson’s disease and drug-induced extrapyramidal symptoms
Influenza A (less common now due to resistance)
72
What is the mechanism of action of amantadine in Parkinson’s disease?
It increases dopamine release and blocks dopamine reuptake in the brain.
It is a weak dopamine agonist.
73
What are common side effects of amantadine?
Dizziness
Insomnia
Dry mouth
Nausea
Peripheral edema
74
How is amantadine excreted from the body?
Primarily renal excretion – dosage must be adjusted in renal impairment.
75
What are contraindications or cautions with amantadine use?
Seizure disorders
Renal impairment
Elderly patients (risk of confusion)
76
What are the main dopaminergic drugs used in Parkinson’s disease?
Levodopa (with carbidopa or benserazide: co-careldopa, co-beneldopa)
Dopamine agonists: ropinirole, pramipexol
77
When are dopamine agonists typically preferred?
In early Parkinson’s disease, especially to delay the need for levodopa.
78
What is levodopa and how does it work?
Levodopa is a dopamine precursor that crosses the blood–brain barrier and is converted to dopamine in the brain.
79
Why is levodopa combined with carbidopa or benserazide?
To prevent peripheral conversion of levodopa to dopamine, reducing side effects and increasing brain availability.
80
What is the 'wearing-off effect' with levodopa?
Symptoms return before the next dose as the drug effect diminishes over time.
81
What is the 'on–off effect'?
Fluctuations between dyskinesia ("on") and bradykinesia ("off"), typically after long-term levodopa use.
82
What are the common side effects of dopaminergic drugs?
Nausea
Drowsiness
Confusion
Hallucinations
Hypotension
Dyskinesia (especially with levodopa)
83
In which patients should dopaminergic drugs be used cautiously?
Elderly
Cognitive or psychiatric disease
Cardiovascular disease (risk of hypotension)
84
What drugs should be avoided with dopaminergic therapy?
Antipsychotics (especially first-generation)
Metoclopramide (both block dopamine receptors)
85
What is a key risk of abruptly stopping dopaminergic therapy?
It may trigger neuroleptic malignant syndrome – a potentially life-threatening condition.
86
What is an alternative route for dopaminergic therapy if oral administration is not possible?
Transdermal dopamine agonists (e.g. rotigotine patch)
87
What are the two main indications for quinine?
Nocturnal leg cramps (when non-drug methods fail)
Plasmodium falciparum malaria (first-line treatment)
Drug class - antimalarials.
88
What is quinine’s mechanism of action?
Leg cramps - It reduces the excitability of the motor end plate to acetylcholine, decreasing muscle contraction frequency.
Malaria - Rapid killing of P. falciparum in the schizont blood stage (mechanism not fully understood).
89
What is the recommended dose of quinine for leg cramps?
200–300 mg at night for oral use.
90
Name three serious adverse effects of quinine.
Tinnitus, deafness, or blindness (may be permanent)
QT prolongation → arrhythmias
Hypoglycaemia (especially in malaria)
91
Why is quinine contraindicated in the first trimester of pregnancy?
It is teratogenic—may harm the fetus. Use only if benefits outweigh risks (e.g. severe malaria).
92
Why should quinine be avoided in G6PD deficiency?
It can cause haemolysis (destruction of red blood cells) in these patients.
93
Name five drug classes that interact with quinine due to QT prolongation risk.
Amiodarone
Antipsychotics
Quinolones
Macrolides
SSRIs
94
What advice should be given to patients starting quinine for cramps?
It's a 4-week trial
Stop if no improvement
Report symptoms like hearing loss, visual disturbance, or palpitations immediately
If continued - Re-review at 3 months and consider stopping to avoid long-term use.
95
What is the primary indication for carbocisteine?
It is used as a mucolytic to reduce the viscosity of sputum in respiratory conditions such as COPD, bronchiectasis, and thick saliva in motor neurone disease.
96
What are common side effects of carbocisteine?
Gastrointestinal upset (nausea, diarrhoea)
Skin rash (rare)
Possible gastric bleeding (rare)
97
What are the main indications for baclofen?
Treatment of spasticity from multiple sclerosis, spinal cord injury, or motor neurone disease
Used off-label for muscle cramps and spasms
98
What is the mechanism of action of baclofen?
It is a GABA-B receptor agonist that inhibits excitatory neurotransmitter release, leading to muscle relaxation.
99
What is the usual starting dose of oral baclofen in adults?
Usually 5 mg three times daily, gradually increased according to response and tolerability.
100
Name common side effects of baclofen.
Drowsiness
Dizziness
Weakness
Nausea
Confusion (especially in elderly)
101
What are serious side effects or risks with baclofen?
Seizures (especially with withdrawal)
Respiratory depression
Hypotension
Psychiatric effects (hallucinations, depression)
102
How should baclofen be discontinued?
Taper slowly—sudden withdrawal can lead to seizures, hallucinations, or rebound spasticity.
103
What are the two main lithium salts used in clinical practice?
Lithium carbonate and lithium citrate.
104
Are lithium salts interchangeable?
No. Lithium carbonate and lithium citrate are not directly interchangeable. The dose and formulation must be prescribed by brand due to differences in bioavailability.
105
What are the brand names of lithium carbonate and lithium citrate?
Lithium carbonate: Priadel®, Camcolit®, Liskonum®
Lithium citrate (liquid): Li-Liquid®
106
What are the main indications for lithium therapy?
Prophylaxis and treatment of mania
Treatment and prophylaxis of bipolar disorder
Recurrent unipolar depression (in some cases)
Aggressive or self-harming behaviour (off-label)
107
How should lithium be started?
Start low and titrate up, based on serum lithium levels, aiming for a therapeutic range after steady state (usually 5–7 days after starting).
108
What is the target serum lithium level for maintenance therapy?
0.4–1.0 mmol/L (usual maintenance: 0.6–0.8 mmol/L)
Higher end (0.8–1.0 mmol/L) used for acute mania or relapses
Elderly or those with adverse effects: aim for 0.4–0.6 mmol/L
109
When should lithium levels be checked after starting or changing the dose?
5–7 days after starting or dose change, then weekly until levels are stable.
110
Once stable, how often should serum lithium levels be monitored?
Every 3 months normally
Every 6 months in well-controlled, low-risk patients
More frequently if intercurrent illness, kidney impairment, or drug interactions
111
What other tests are required before and during lithium therapy?
Before starting: U&Es, eGFR, TFTs, weight/BMI, ECG if CV risk
Every 6 months: U&Es, eGFR, TFTs, weight/BMI
Annually: Calcium levels and mental health review
112
What are early signs of lithium toxicity?
Tremor, nausea, vomiting, diarrhoea, drowsiness, confusion, ataxia - poor muscle control.
113
What are serious complications of lithium toxicity?
Seizures
Coma
Arrhythmias
Renal failure
Can be fatal if not managed urgently
114
What should be done if lithium toxicity is suspected?
Stop lithium immediately
Check serum lithium level urgently
Refer for hospital assessment ± dialysis if severe
115
Name drugs that increase the risk of lithium toxicity.
ACE inhibitors / ARBs
NSAIDs (except aspirin)
Diuretics (especially thiazides)
Metronidazole
SSRIs / Antipsychotics (↑ risk of neurotoxicity)
116
How do diuretics affect lithium levels?
Thiazide diuretics reduce sodium reabsorption, leading to increased lithium retention and toxicity.
117
Can lithium be used in pregnancy?
Generally avoided due to teratogenic risk, especially in the first trimester
May be continued if the risk of relapse outweighs the risk, but under specialist supervision
118
What should be done if the patient develops diarrhoea, vomiting, or sweating excessively?
Stop lithium temporarily and seek medical advice, as dehydration increases risk of toxicity.
119
What are the two main forms of valproate used in bipolar disorder?
Sodium valproate
Valproic acid as semisodium valproate (Depakote®).
Different formulations are not interchangeable - they have different pharmacokinetics. Use the same brand/formulation consistently, and changes should be made under specialist supervision.
120
What are the indications for valproate in mental health?
Acute mania (short-term)
Prophylaxis of bipolar disorder if lithium is not tolerated or ineffective
Adjunct in schizoaffective or resistant cases (off-label)
121
What is the usual starting dose of sodium valproate in adults for bipolar disorder?
Typically 750 mg daily in divided doses
Titrate according to response
Usual maintenance: 1–2 g/day (max: 2.5 g/day)
122
Should valproate be prescribed by brand?
Yes, especially with modified-release (MR) formulations. Prescribe by brand to avoid variation in blood levels.
123
What baseline monitoring is required before starting valproate?
Liver function tests (LFTs)
Full blood count (FBC)
Urea and electrolytes (U&Es)
BMI / weight
Pregnancy status (for women of childbearing potential)
124
What symptoms should trigger urgent LFTs during treatment?
Abdominal pain, nausea, vomiting, jaundice, lethargy, loss of seizure control.
125
What are common side effects of valproate?
Weight gain
Tremor
Hair loss
Nausea
Sedation
Thrombocytopenia.
126
What serious adverse reactions can occur?
Hepatotoxicity (especially in first 6 months)
Pancreatitis
Encephalopathy (hyperammonaemia)
Bone marrow suppression
Severe skin reactions (e.g. SJS)
127
Why is valproate contraindicated in pregnancy?
It is highly teratogenic – linked to:
Neural tube defects (e.g., spina bifida)
Facial and cranial abnormalities
Neurodevelopmental disorders (in up to 30–40% of children exposed in utero)
128
What are the MHRA regulatory requirements for prescribing valproate to women of childbearing potential?
Enrol in a Pregnancy Prevention Programme (PPP)
Use reliable contraception
Annual specialist review confirming no alternative is suitable
Risk acknowledgment form signed by both patient and clinician
129
What about men taking valproate?
MHRA advises:
Use effective contraception
Specialist review by two clinicians to document that no better alternative exists
130
If a woman is already on valproate and is of childbearing potential, what is recommended?
Do not stop abruptly
Gradual withdrawal over 4–6 weeks, unless urgently needed
Discuss risks of foetal harm and consider switching to safer alternatives
131
What should patients be told when starting valproate?
Take with or after food
Report symptoms like abdominal pain, jaundice, bleeding, or confusion
Avoid alcohol
Do not stop abruptly
Pregnancy prevention is essential for women and advised for men
Be aware of weight gain and regular blood tests
132
Is valproate safe in breastfeeding?
Generally considered compatible, but monitor infants for drowsiness or liver issues.
133
What drugs interact with valproate?
Inhibits metabolism of lamotrigine → risk of skin rash
Increased CNS effects with benzodiazepines, antipsychotics, alcohol
Levels altered by enzyme inducers (e.g., carbamazepine, phenytoin)
May potentiate effect of anticoagulants
134
What is a common use of gabapentin and pregabalin in epilepsy?
They are used for focal epilepsies (with or without secondary generalisation), usually as add-on treatments.
135
Are gabapentin and pregabalin mechanisms related to GABA?
Despite structural similarity to GABA, their mechanism appears unrelated; they act by binding voltage-sensitive calcium channels to inhibit neurotransmitter release.
136
What are the most common side effects of gabapentin and pregabalin?
Drowsiness, dizziness, and ataxia - poor muscle control.
137
What should be done with the dose in patients with renal impairment?
The dose should be reduced.
138
Compared to other antiepileptic drugs, what is notable about gabapentin and pregabalin regarding interactions?
They have relatively few drug interactions.
139
What is the mechanism of action of Tramadol?
Tramadol is a centrally acting analgesic that works as a weak μ-opioid receptor agonist and also inhibits reuptake of noradrenaline and serotonin.
140
Name two contraindications for Tramadol use.
Acute intoxication with alcohol, hypnotics, or other opioids.
Uncontrolled epilepsy.
141
What are some common side effects of Tramadol?
Nausea, dizziness, headache, constipation, dry mouth, and drowsiness.
142
What serious adverse effect is associated with serotonergic activity in Tramadol?
Serotonin syndrome, especially when combined with SSRIs, MAOIs, or other serotonergic drugs.
143
What is the BNF warning about Tramadol and dependence?
Tramadol may lead to dependence and withdrawal symptoms—caution is advised with long-term use.
144
What are signs of Tramadol overdose?
Respiratory depression, seizures, coma, vomiting, tachycardia, and CNS depression.
145
What is the risk of seizures with Tramadol?
Tramadol lowers the seizure threshold, especially at high doses or when combined with other medications like antidepressants.
146
What is the mechanism of action of Triptans?
Triptans are 5-HT₁B/₁D receptor agonists that constrict cranial blood vessels and inhibit release of pro-inflammatory neuropeptides, relieving migraine symptoms.
147
What are the main indications for Triptans?
Acute treatment of migraine (with or without aura); sumatriptan also licensed for cluster headaches.
148
Name at least three Triptans available in the UK.
Sumatriptan
Zolmitriptan
Rizatriptan
149
How are Triptans administered?
Orally (tablets, melts), nasal spray, or subcutaneous injection (e.g., sumatriptan).
150
When should a Triptan be taken during a migraine?
As soon as possible after the onset of headache pain (not during aura phase alone).
151
What is the maximum dose of Sumatriptan (oral) in 24 hours?
300 mg (usually 50–100 mg dose, can repeat after 2 hours if needed).
152
Name three common side effects of Triptans.
Tingling or warm sensations
Heaviness or pressure (often in chest or limbs)
Dizziness or drowsiness
153
What serious cardiovascular adverse effects are associated with Triptans?
Coronary vasospasm, myocardial infarction, and hypertension (rare but serious).
154
What are the main contraindications for Triptan use?
Ischaemic heart disease or previous MI
Uncontrolled hypertension
History of stroke or TIA
Severe hepatic impairment
Use within 24 hours of ergotamine or other triptans
155
What is the BNF advice on repeat dosing of Triptans?
If the first dose is ineffective, a second dose should not be taken for the same attack. If symptoms return after improvement, a second dose may be used (timing and max dose vary by agent).
156
What is the mechanism of action of capsaicin cream?
Capsaicin depletes substance P from sensory nerve endings, reducing the transmission of pain signals.
157
How often should capsaicin cream be applied?
Usually 3–4 times daily, depending on formulation and indication.
158
What is the main side effect of capsaicin cream?
Local burning or stinging sensation at the application site, especially initially.
159
What patient advice should be given about capsaicin application?
Do not apply to broken or inflamed skin
Wash hands thoroughly after use (unless treating hands)
Avoid contact with eyes, mouth, and mucous membranes
Heat (e.g., showers or heating pads) can intensify burning
160
Is capsaicin cream available over the counter (OTC)?
Some low-strength formulations (e.g., 0.025%) may be available OTC, but higher strengths typically require prescription.
161
What is the proposed mechanism of action of paracetamol?
Weak COX inhibitor, particularly COX-2 in the CNS, increasing pain threshold and reducing PGE2 in the hypothalamus (thermoregulation).
162
What serious toxicity occurs with paracetamol overdose?
Liver failure due to accumulation of toxic metabolite NAPQI.
163
How is hepatotoxicity from paracetamol overdose treated?
With acetylcysteine, a glutathione precursor that detoxifies NAPQI.
164
What is the mechanism of action of NSAIDs?
NSAIDs inhibit cyclooxygenase (COX), preventing the synthesis of prostaglandins from arachidonic acid.
165
What is the difference between COX-1 and COX-2 enzymes?
COX-1: Constitutive; protects gastric mucosa, maintains renal perfusion, and prevents thrombus formation
COX-2: Inducible; promotes inflammation and pain
Therapeutic effect: Mainly via COX-2 inhibition
Adverse effects: Mainly via COX-1 inhibition
166
What are some hypersensitivity reactions linked to NSAIDs?
Bronchospasm and angioedema
167
When should NSAIDs be avoided?
In patients with severe renal impairment, heart failure, liver failure, or known NSAID hypersensitivity
168
Why might COX-2 inhibitors not always be preferred despite lower GI risk?
They have a higher risk of cardiovascular events compared to non-selective NSAIDs
169
Which NSAIDs can be used in heart failure if needed?
Low dose ibuprofen, Naproxen
AVOID - cox 2 inhibitors (etoricoxib, celecoxib), indomethacin and diclofenac.
170
What are common adverse effects of codeine/dihydrocodeine?
Nausea, constipation, and drowsiness.
171
What must be considered when prescribing opioids to elderly or renally/hepatically impaired patients?
Dose reduction is necessary due to impaired drug clearance.
172
What is breakthrough analgesia and how is it calculated?
Extra doses for pain spikes; typically 1/6th of the total daily dose.
173
What should be co-prescribed with regular opioids?
A laxative and possibly an antiemetic.
174
Why might codeine be ineffective in some people?
About 10% of Caucasians have a CYP2D6 polymorphism, impairing codeine metabolism.
175
What are the common indications for valproate use?
Epilepsy (especially generalised and absence seizures, and focal seizures) and bipolar disorder (acute manic episodes and prophylaxis).
176
How does valproate work to control seizures?
It stabilises neuronal membranes by weakly inhibiting sodium channels and increases brain GABA levels.
177
What are the common dose-related adverse effects of valproate?
GI upset (nausea, diarrhoea), tremor, ataxia, behavioural changes, thrombocytopenia, and raised liver enzymes.
178
What rare but serious adverse effects are associated with valproate?
Liver failure, pancreatitis, bone marrow failure, antiepileptic hypersensitivity syndrome.
179
What unusual side effect can affect hair?
Hair loss with regrowth that may be curlier.
180
How does valproate interact with drugs metabolised by cytochrome P450 enzymes?
It inhibits these enzymes, increasing levels and toxicity of drugs like warfarin.
181
Which drugs reduce valproate levels and may increase seizures?
Cytochrome P450 inducers (e.g. phenytoin, carbamazepine) and carbapenems.
182
Name a drug that displaces valproate from protein binding sites and increases its effects.
Aspirin.
183
What drug classes may reduce antiepileptic efficacy by lowering the seizure threshold?
SSRIs, tricyclic antidepressants, antipsychotics, tramadol.
184
What is the usual starting dose of valproate for epilepsy?
600 mg/day in 1–3 divided doses.
185
What is the typical maximum daily dose of valproate?
1–2 g/day.
186
What symptoms should prompt urgent medical review?
Lethargy, appetite loss, vomiting, abdominal pain, bruising, mouth ulcers, high temperature.
187
Are valproic acid and semisodium valproate different in their mechanism of action from sodium valproate?
No, valproic acid and semisodium valproate work in the same way as sodium valproate. They are similar in action and used for similar clinical purposes.
188
What is the mechanism of action of phenytoin?
Phenytoin binds to neuronal sodium (Na⁺) channels in their inactive state, prolonging their inactivity and preventing Na⁺ influx. This inhibits the spread of seizure activity.
189
What cardiac effect is related to phenytoin's action on Purkinje fibers?
Its effect on cardiac Purkinje fibers may explain both antiarrhythmic and cardiotoxic effects.
Purkinje fibers are specialized conductive fibers located in the inner walls of the heart's ventricles. They allow the heart's conduction system to create synchronized contractions of its ventricles and are essential for maintaining a consistent heart rhythm.
190
What are some long-term adverse effects of phenytoin?
Skin coarsening, acne, hirsutism, gum hypertrophy, cerebellar toxicity (e.g., ataxia, nystagmus), cognitive impairment, folic acid and vitamin D deficiency (leading to haematological disorders and osteomalacia).
191
What serious toxicity can result from phenytoin overdose or rapid IV administration?
Cardiovascular collapse and respiratory depression, potentially fatal.
192
Why is phenytoin dosing difficult and risky?
It is metabolised with zero-order kinetics and has a narrow therapeutic index, so small changes in dose can lead to toxicity.
193
What are the risks of phenytoin exposure in utero?
Fetal hydantoin syndrome, including craniofacial abnormalities and reduced IQ.
194
Is phenytoin a CYP450 inducer or inhibitor, and what is the consequence?
Phenytoin is a CYP450 inducer, reducing plasma levels and efficacy of drugs like warfarin, oestrogens, and progestogens.
195
What is the target therapeutic range for plasma phenytoin concentration?
10–20 mg/L, measured just before the next dose.
196
What monitoring is needed during phenytoin therapy?
Seizure frequency, plasma drug levels, and vital signs during IV use. Wait 7 days after a dose change before rechecking levels.
197
What are the 3 common indications for carbamazepine?
Epilepsy – first-line for focal and some generalised seizures
Trigeminal neuralgia – to reduce pain frequency and severity
Bipolar disorder – as prophylaxis when resistant or intolerant to other meds
198
What is the mechanism of action of carbamazepine?
Inhibits neuronal sodium channels, stabilising resting membrane potentials and reducing excitability—similar to phenytoin.
199
What are the main dose-related adverse effects of carbamazepine?
Gastrointestinal upset (nausea, vomiting), dizziness, and ataxia - poor muscle control.
200
What type of skin reactions are associated with carbamazepine hypersensitivity?
Mild maculopapular rash, and serious conditions like Stevens–Johnson syndrome and toxic epidermal necrolysis.
201
What electrolyte disturbance is associated with carbamazepine?
Hyponatraemia, due to its antidiuretic hormone-like effect.
202
What are the teratogenic risks of carbamazepine during pregnancy?
Neural tube defects, cardiac/urinary tract defects, and cleft palate.
203
What is the usual starting dose and max dose for carbamazepine in epilepsy?
Start at 100–200 mg once or twice daily, increase to max 1.6 g/day in divided doses.
204
What contraception and pregnancy advice should be given to women on carbamazepine?
Discuss contraception and the need for high-dose folic acid before conception.
205
When and how should plasma carbamazepine levels be monitored?
Rarely needed, but if done, take immediately before next dose; therapeutic range is 4–12 mg/L.
206
When is steady-state plasma concentration achieved with carbamazepine?
2–4 weeks after starting, or 4–5 days after dose change.
207
What are some long-term complications of phenobarbital use?
Osteomalacia (due to vitamin D metabolism) - new bone not hardening the way it should after formation.
Cognitive impairment
Drug dependence (it is highly addictive)
208
Why is phenobarbital not a first-line treatment in most cases?
Due to its sedative effects, long half-life, dependence risk, and cognitive impairment.
209
What are common indications for topiramate?
Epilepsy (partial and generalised seizures)
Migraine prophylaxis
Occasionally used in bipolar disorder, obesity, and alcohol dependence
210
What are serious adverse effects of topiramate?
Nephrolithiasis (kidney stones)
Metabolic acidosis
Glaucoma
Oligohidrosis (↓ sweating, overheating in children)
211
What is a unique beneficial side effect of topiramate?
Weight loss
212
What must be monitored in patients on topiramate?
Serum bicarbonate (risk of acidosis)
Eye exam (for glaucoma)
Kidney function and hydration status
213
What are the main indications for lamotrigine?
Epilepsy (especially focal and generalised seizures)
Bipolar disorder (especially for depressive episodes)
214
What are common side effects of lamotrigine?
Headache, nausea
Dizziness, blurred vision
Sleep disturbances
215
What serious skin reactions are associated with lamotrigine?
Stevens–Johnson syndrome
Toxic epidermal necrolysis (especially if titrated too quickly or combined with valproate)
216
How is lamotrigine titrated?
Slowly over several weeks to reduce risk of serious rash. Dosage increases should follow strict protocols.
217
Which drug significantly increases lamotrigine levels and risk of rash?
Valproate – inhibits lamotrigine metabolism.
