Drugs Flashcards
Benserazide (Indication + Mechanism)
I: With L-Dopa in Parkinsons disease
M:Inhibits DDC (Dopamine decarboxylase) so stopping decarboxylation of Levodopa (L-Dopa) before it crosses the BBB
Name two MOA-B inhibitors and a common problem with prescribing them
Seregiline and Rasagiline. Can’t be eaten with cheese/ wine etc as it prevents them being broken down so causes massive hypertensive crisis
Name two COMT inhibitors, what is their MOA?
Tolcapone and Entacapone. They inhibit catechol-O-methyltransferase which slows L-Dopa breakdown
Levodopa (I, M, S.E). What is the problem taking Levodopa long term?
I: For Parkinsons disease
M: Is L-Dopa (the amino acid precursor to dopamine which can cross BBB)
S.E: Dyskinesia, hypotension, nausea, extreme emotion
Caution: After prolonged use its effects are lowered and side effects increase
Name two dopamine agonists?
Pramipexole (oral) and ropinirole (patch)
What is Apomorphine, when would it be given and how?
Dopamine agonist which acts rapidly, given via subcutaneous injection. Often for ‘rescue therapy’ when SE’s of Parkinsons have had an acute flare up
Why must Levodopa be taken at least 40min before meals and why should protein rich meals be avoided?
L-Dopa competes with protein from the meals for transport across the BBB
What are the NICE guidelines for early Parkinsons treatment?
1st Line: Levodopa > dopamine agonist > MOABI
2nd Line: Anticholinergic/ B-Blocker/ Amantadine
Amantadine (I,M)
M: Levodopa induced dyskinesia
M: Blocks NMDA receptor so is glutamate antagonist (blocks striatum inhibition of GPi- therefore increased wanted movement, decreased unwanted)
Phenylephrine (I,M,CI, SE)
I: Dilates the pupil, also used as a decongestant (vasoconstrictor)
M: Alpha 1 adrenoceptor agonist
CI: Angle closure glaucoma
SE: Photophobia/ blurred vision
Tropicamide (I, M, CI)
I: Pupil dilation (mydrasis)
M: Anticholinergic (Blocks M4 receptor- so stops PNS constricting pupil)
CI: Angle closure glaucoma
Pilocarpine (I, M, CI)
I: Pupil constriction/ treat glaucoma/ increase saliva production (to treat dry mouth)
M: M3 receptor agonist (So boosts PNS constrictive action)
CI: Don’t give systemically if have asthma/ COPD (due to bronchoconstriction)
Beta Interferons (I, M, SE's) (Betaferon, avonex, rebif, extavia)
I: Treatment of RRMS
M: Bind to type 1 interferon receptors, changing expression of immunomodulatory proteins in the brain, lowering inflammation
SE’s: Skin reaction at injection site, flu like symptoms for 24hrs
Fingolimod (I, M, SE’s)
I: Treating RRMS
M: Binds to Sphingosine (S1) receptor, this blocks lymphocytes from leaving lymph nodes (so less in CNS and less inflammation)
SE: Headahce, fatigue, bradycardia, macular oedema
Amitryptiline (I, M, SE’s)
Also applies to Trimpramine and Amoxapine
I: TCA Last choice treatment of MDD/ Anxiety
M: Blocks 5-HT and NA reuptake channels in pre-synaptic membrane
SE’s: Dry mouth, blurred vision, drowsiness, weight gain
(Side effects due to additional blocking of histamine and muscarinic ACh receptors)
Name 5 drugs you could prescribe to help with nerve pain:
Gabapentin, pregabalin, caramazepine, TCA’s, opioids
What is the NICE recommended treatment pathway for MDD?
Try each step for 10wks then increase:
Computerised CBT > CBT > SSRI > SNRI > TCA > MAOI
(Recurrence of depression is the norm, 73% over 15yrs)
Propofol (I,M,SE)
I: Induction and maintenance of anaesthesia
Given IV as a bolus- Induce in 45sec (one arm brain time)
M: Positive allosteric modulator of GABA A receptor
SE: Low BP, post operative seizures
Isoflurane (I,M,SE)
Or Enflurane
I: Induction and maintenance of anaesthesia
Given inhaled (Small and lipid soluble so crosses alveolar membrane)
M: Reduces GAP junction conduction
SE: Low BP (vasodilation), mucus membrane irritation
Name a common GA given a) IV and b) Inhaled
What is a common side effect of GA’s?
a) Propofol
b) Isoflurane
Low BP
Suxamethonium (I,M,SE)
I: Short term (4min) muscle relaxant, use for intubation
M: Depolarising, nicotinic ACh receptor agonist
SE: Muscle pain, hyperkalemia, hyperthermia
Atracurium (I,M,SE)
I: (non depolarising) muscle relaxant
M: Cholinergic ACh receptor antagonist (no ACh activating motor end plate)
SE: Low BP, flushing
Good as naturally hydrolysis in blood (on stable in acid) so doesn’t need healthy kidneys)
Fentanyl (I,M)
100x more potent than morphine
I: Opioid analgesic
M: Binds to u opioid receptors (inhibitory G-proteins which hyperpolarise via blocking of Ca and opening of K)
Neostigmine (I,M,SE)
I: Reverse muscle relaxants
M: Reversibly inhibits acetyl-cholinesterase so raises synaptic ACh conc
SE: Blurred vision and bradycardia
Glycopyrrolate (I,M)
I: Dry secretions, slow HR
M: Muscarinic antagonist (relaxes smooth muscle and reduces secretions)
Used with neostigmine to reverse some of the side effects of increased ACh neostigmine causes
Mannitol (I,M)
I: Diuretic, reducing intercranial pressure (ICP), treat cerebral oedema
M: Osmotic diuretic, elevates blood plasma osmolarity, drawing fluid out of tissues (also reducing water and Na re uptake in kidney)
Paracetamol (M, SE)
M: Inhibition of COX-2 (stopping prostaglandin formation)
SE: Renal failure in chronic high dose use
Hepatotoxicity, leading to failure within 48hrs in doses over 150mg/kg (21 tablets in 70kg person)
Sodium Valproate (I, M, SE) Brand name: Depakote
I: Treat seizures/ mood stabiliser (i.e. bipolar)
M: Inhibits GABA transaminase so increases synaptic GABA conc, so more GABA inhibition
SE: Weight gain, dyspepsia, dizziness, drowsiness, NTD in pregnancy (TERATOGEN)
Ibuprofen (M, SE, I)
M: NSAID. Non selective COX inhibitor (COX2= decreased prostaglandins, COX1= unwanted GI side effects)
SE: Nausea, dyspepsia, GI ulcer/ bleeds
I: Beta blockers, anticoag, alcohol
Gabapentin (I,M,SE)
I: Neuropathic pain
M: Amino acid analogue of GABA, binds to Ca gated channels and reduces Ca entry, reducing excitability
SE: Dizziness, weight gain, drowsiness, depression, fatigue
Lidocaine (I,M,SE)
I: Local anaesthetic (approx 90min)
M: Blocks fast gated sodium channels (prevents depolarisation)
SE: Parasthesia (pins and needless). Dizziness and drowsiness if injected too quick
What is the mechanism of opioid analgesics?
Binds to mew, delta and K receptors on CNS neurons
Close pre-synaptic VG Ca channels (less NT release)
Open post-synaptic K channels (hyperpolarise)
What are the effects of opioid’s on the body?
Analgesia, euphoria, respiratory depression, nausea, constipation, vomitting, depression renal function, pupil constriction, drowsiness
TOLERANCE AND DEPENDENCE
Tricyclic Antidepressants (M, SE) (Amitriptiline, amoxapine, trimipramine)
M: Block 5-HT and noradrenaline reuptake transporters, increasing synaptic conc
SE: Dry mouth, blurred vision, weight gain
(SE Due to additional blocking of post synaptic histamine and muscarinic ACh receptors)
Ketamine (I, A)
I: Analgesic or anaesthetic
A: Acts on NMDA receptors, also stimulates cardiovascular system
Beta-interferons (I,M,SE)
Avonex, Rebif, Betaferon, Extavia
I: Treatment of relapsing- remitting MS (INJECTION)
M: Bind to type 1 interferon receptors, changing expression of immunomodulatory proteins in brain (reduces inflammation)
SE: Skin reaction at injection site, flu sympt for 24hrs
Nataluzimab (I, M, SE)
I: Treatment of MS or crohns
M: Monoclonal antibody for alpha4beta1 integrin (which normally allows lymphocytes to move into organs)
SE: Opportunistic John Cunningham Virus infection, causing multifocal encephalopathy
Baclofen (I, M)
I: To help relieve spasticity in MS
M: Agonist at GABA B receptor (GABA inhibits)
Methylprednisalone (I,M)
Prednisalone derivative given IV
I: Acute inflammation episodes (such as MS)
M: Binds to intracellular receptors and modifies transcription and protein synthesis (Prostaglandins and leukotienes)
Co-Beneldopa (What disease and what drug combination?)
Treatment of Parkinsons
Combination of L-Dopa (levodopa) and benserazide
Selegiline (I,M,SE, Caution)
alternative: rasagiline
I: Slow Parkinson’s progression
M: MAO-B inhibitor
SE: Hypersexuality
Caution: Can’t take with cheese or wine!
Pramipexole and Ropinirole (I, M)
I: Treatment of parkinsons
M: Dopamine agonists
Entacapone/ Tolcapone (I,M)
I: Treatment for late stage parkinsons
M: COMT (Catechol-o-methyl transferase) inhibitor so slows levodopa breakdown
Risperidone (I, M, SE)
I: Atypical antipsychotic (Pyschosis, schizophrenia, mania)
M: Blocks D2 receptors in limbic system (lowers +ve sympt)
Blocks 5-HT2 receptors in mesocortical tract (lowers -ve sympt)
SE: Hyperprolactinaemia, weight gain (60-75% blockade for theraputic dose)
SNRI (I, M, SE)
Venlafaxine, Duloxetine
I: Depression, anxiety, neuropathic pain
M: Inhibits serotonin and noradrenaline reuptake
SE: Headache, insomnia, nausea, sexual dysfunction
Diazepam (valium)- I, M, SE
Also lorazepam, chlordiazepoxide
I: Benzodiazepine (Short term anxiety, insomnia, anticonvulsant, muscle relaxant)
M: Positive allosteric modulator of GABAA receptor
SE: Drowsiness, dizziness, reduced coordination and alertness
Mirtazapine (I, M, SE)
I: Anti-depressant (MDD)
M: Blocks alpha2 adrenoceptors, blocking -ve feedback, increasing synaptic conc
SE: Inc appetite, dry mouth, post hypotension, peripheral oedema
Give 3 examples of MAO-A inhibitors?
What is a problem prescribing them?
Phenelzine, tranylcypromine, moclobomide
(Stop serotonin and noradrenaline breakdown)
Can’t break down tyramine protein (cheese and wine)- Hypertensive crisis
SSRI’s (Examples, M, SE)
Fluoxetine, sertraline, paroxetine, fluvoxamine
M: Stop serotonin reuptake
SE: Nausea, headache, drowsiness, sexual dysfunction
INCREASED risk of depression and suicide in children!!!
Alteplase (I, M, SE)
I: Thrombolysis (t-pa)
M: Blinds to thrombus, converts plasminogen to plasmin which degrades the fibrin matrix
SE: Bleeds
Lots of complications so give ideally within 3hours, can give upto 4.5hrs. Benefits tail off after 1.5hrs.
Pancuronium (I, M)
I: Long acting muscle relaxant in surgical procedures
M: Non depolarising ACh blocker at motor end plate
Metabolised by liver and excreted by kidneys so clearance can be affected by hepatic or renal function
Carbamazepine (I, M, SE)
I: Anticonvulsant (also for nerve pain or bipolar)
M: Sodium channel blocker
SE: Sedation, ataxia, blurred vision, water retention
The elimination of Atracurium from the body is slowed by?
Respiratory acidosis
Sodium Thiopental (I, M, SE)
I: Given IV for short term induction (15min) of anaesthesia
M: Binds to Cl ionopore at GABA-A receptor, opening GABA for longer, causing inhibition (of brain stem resp centre)
SE: Slow recovery time (so not given for maintainance)
Potassium Chloride (I and effect on cardiac muscle)
I: Electrolyte replacement and treating hypokalemia
Depolarises cardiac muscle cells and stops them firing AP’s
What is the difference between typical and atypical antipyschotics?
Typical: Only block D2 (chlorpromazine)- SE’s include dry mouth, weight gain, drowsiness and lowered libido
Atypical: Block D2 and 5-HT (Rispiridone, clozapine, amisulpride)
What would the drugs orpenadrine and procyclidine be used for?
Anticholinergics
Balances cholinergic/ dopaminergic levels so therefore can reduce parkinsonian side effects
Clozapine (I, M, SE)
I: Antipyschotic (For treatment resistant schizophrenia)
M: Blocks D2 receptors in limbic system (+ve sympt)
Blocks 5-HT2 receptors in mesocortical tract (-ve sympt)
SE: Agranulocytosis (in ~1%, do regular WBC)
Name 5 SSRI’s
Citalopram, fluoxetine, sertraline, paroxetine, fluvoxamine
Name 3 SNRI’s
Venlafaxine, duloxetine, desvenlafaxine
Pregablin (I, M)
I: Anticonvulsant for neuropathic pain and seizures
M: Binds to alpha 2 delta subunit on VGCa2+ channels to limit Ca influx
Lithium (I, M)
I: Treating bipolar
M: Mood stabiliser, stabilises glutamate (not too much or too little) by acting on the GluR3
Midazolam (I, M)
I: Induction of general anaesthesia
M: Positive allosteric modulator of GABA-A
Lamotrigene (I, M)
I: For epilepsy, type 1 bipolar and depression
M: Blocks Na and Ca channels to inhibit glutamate release
What is the most important caution for Semisodium Valproate in a F of childbearing age?
Causes folate anatagonism (glutamate formil transferase inhibition) therefore increasing risk of neural tube defects in pregnancy
Etomidate (I, M)
I: Induction of general anaesthesia
M: Extends GABA-A opening time, so increases Cl in and causes hyperpolarisation (in reticular activating system)
Tubocurarine (I, M)
I: Muscle relaxant for surgery (non-depolarising)
M: Antagonist for nicotinic ACh receptor
Physostigmine (I, M)
I: Used to treat glaucoma
M: Inhibits acetylcholinesterase (increasing synaptic ACh)
What are the general effects of benzodiazepines?
Enhance the effect of GABA at GABA-A receptor
Sedative, hypnotic (sleep inducing), anxiolytic (anti-anxiety), anti-convulsant and muscle relaxant
In what circumstances is ibuprofen contra-indicated?
Allergies to NSAIDS
Stomach ulcers
Heart failure
Severe liver disease
How is codeine different to morphine?
It is a pro-drug (metabolised to morphine)
Clopidogrel (I, M, SE)
I: Antiplatlet (prophylactic post stroke etc)
M: ADP platelet membrane receptor antagonist
SE: Haemorrhage
Flumazenil (I, M)
I: Treat benzodiazapine overdose
M: GABA-A receptor antagonist
NB: Has a v.short half life
Naloxone (I, M)
I: Treat opioid overdose
M: Opioid receptor antagonist
Name a drug which could be used to treat the mania phase of bipolar type 1?
Rispiridone
Name 3 drug treatments which could be used for GAD
Citalopram (SSRI), Venlafaxine (SNRI), Pregablin
Chlorpromazine (I, M)
I: Typical antipyschotic
M: Blocks D2 receptors only
Amisulpride (I,M)
I: Atypical antipyschotic
M: Blocks D2 (in limbic striatum- +ve sympt) and 5-HT in mesocortical pathway -ve sympt)
Haloperidol (I,M)
I: Atypical antipyschotic
Blocks D2 and 5-HT receptors
Schizophrenia, mania, pyschosis etc
Reserpine (I,M)
I: Antipyschotic and antihypertensive
M: Reduces catecholamines by blocking ATP/Mg pump which puts them in vesicles
Phenytoin (I, M)
I: Anti-convulsant
M: Blocks Na channels
Ticlopidine (I, M)
I: Anti-platelet. Prevention of thrombosis
M: Blocks ADP receptor on platelets