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Flashcards in Drugs Deck (82)
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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