Drugs Flashcards

1
Q

Benserazide (Indication + Mechanism)

A

I: With L-Dopa in Parkinsons disease
M:Inhibits DDC (Dopamine decarboxylase) so stopping decarboxylation of Levodopa (L-Dopa) before it crosses the BBB

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2
Q

Name two MOA-B inhibitors and a common problem with prescribing them

A

Seregiline and Rasagiline. Can’t be eaten with cheese/ wine etc as it prevents them being broken down so causes massive hypertensive crisis

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3
Q

Name two COMT inhibitors, what is their MOA?

A

Tolcapone and Entacapone. They inhibit catechol-O-methyltransferase which slows L-Dopa breakdown

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4
Q

Levodopa (I, M, S.E). What is the problem taking Levodopa long term?

A

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

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5
Q

Name two dopamine agonists?

A

Pramipexole (oral) and ropinirole (patch)

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6
Q

What is Apomorphine, when would it be given and how?

A

Dopamine agonist which acts rapidly, given via subcutaneous injection. Often for ‘rescue therapy’ when SE’s of Parkinsons have had an acute flare up

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7
Q

Why must Levodopa be taken at least 40min before meals and why should protein rich meals be avoided?

A

L-Dopa competes with protein from the meals for transport across the BBB

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8
Q

What are the NICE guidelines for early Parkinsons treatment?

A

1st Line: Levodopa > dopamine agonist > MOABI

2nd Line: Anticholinergic/ B-Blocker/ Amantadine

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9
Q

Amantadine (I,M)

A

M: Levodopa induced dyskinesia
M: Blocks NMDA receptor so is glutamate antagonist (blocks striatum inhibition of GPi- therefore increased wanted movement, decreased unwanted)

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10
Q

Phenylephrine (I,M,CI, SE)

A

I: Dilates the pupil, also used as a decongestant (vasoconstrictor)
M: Alpha 1 adrenoceptor agonist
CI: Angle closure glaucoma
SE: Photophobia/ blurred vision

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11
Q

Tropicamide (I, M, CI)

A

I: Pupil dilation (mydrasis)
M: Anticholinergic (Blocks M4 receptor- so stops PNS constricting pupil)
CI: Angle closure glaucoma

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12
Q

Pilocarpine (I, M, CI)

A

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)

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13
Q
Beta Interferons (I, M, SE's)
(Betaferon, avonex, rebif, extavia)
A

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

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14
Q

Fingolimod (I, M, SE’s)

A

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

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15
Q

Amitryptiline (I, M, SE’s)

Also applies to Trimpramine and Amoxapine

A

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)

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16
Q

Name 5 drugs you could prescribe to help with nerve pain:

A

Gabapentin, pregabalin, caramazepine, TCA’s, opioids

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17
Q

What is the NICE recommended treatment pathway for MDD?

A

Try each step for 10wks then increase:
Computerised CBT > CBT > SSRI > SNRI > TCA > MAOI

(Recurrence of depression is the norm, 73% over 15yrs)

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18
Q

Propofol (I,M,SE)

A

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

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19
Q

Isoflurane (I,M,SE)

Or Enflurane

A

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

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20
Q

Name a common GA given a) IV and b) Inhaled

What is a common side effect of GA’s?

A

a) Propofol
b) Isoflurane
Low BP

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21
Q

Suxamethonium (I,M,SE)

A

I: Short term (4min) muscle relaxant, use for intubation
M: Depolarising, nicotinic ACh receptor agonist
SE: Muscle pain, hyperkalemia, hyperthermia

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22
Q

Atracurium (I,M,SE)

A

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)

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23
Q

Fentanyl (I,M)

A

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)

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24
Q

Neostigmine (I,M,SE)

A

I: Reverse muscle relaxants
M: Reversibly inhibits acetyl-cholinesterase so raises synaptic ACh conc
SE: Blurred vision and bradycardia

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25
Q

Glycopyrrolate (I,M)

A

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

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26
Q

Mannitol (I,M)

A

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)

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27
Q

Paracetamol (M, SE)

A

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)

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28
Q
Sodium Valproate (I, M, SE)
Brand name: Depakote
A

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)

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29
Q

Ibuprofen (M, SE, I)

A

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

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30
Q

Gabapentin (I,M,SE)

A

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

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31
Q

Lidocaine (I,M,SE)

A

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

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32
Q

What is the mechanism of opioid analgesics?

A

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)

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33
Q

What are the effects of opioid’s on the body?

A

Analgesia, euphoria, respiratory depression, nausea, constipation, vomitting, depression renal function, pupil constriction, drowsiness
TOLERANCE AND DEPENDENCE

34
Q
Tricyclic Antidepressants (M, SE)
(Amitriptiline, amoxapine, trimipramine)
A

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)

35
Q

Ketamine (I, A)

A

I: Analgesic or anaesthetic
A: Acts on NMDA receptors, also stimulates cardiovascular system

36
Q

Beta-interferons (I,M,SE)

Avonex, Rebif, Betaferon, Extavia

A

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

37
Q

Nataluzimab (I, M, SE)

A

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

38
Q

Baclofen (I, M)

A

I: To help relieve spasticity in MS
M: Agonist at GABA B receptor (GABA inhibits)

39
Q

Methylprednisalone (I,M)

A

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)

40
Q

Co-Beneldopa (What disease and what drug combination?)

A

Treatment of Parkinsons

Combination of L-Dopa (levodopa) and benserazide

41
Q

Selegiline (I,M,SE, Caution)

alternative: rasagiline

A

I: Slow Parkinson’s progression
M: MAO-B inhibitor
SE: Hypersexuality
Caution: Can’t take with cheese or wine!

42
Q

Pramipexole and Ropinirole (I, M)

A

I: Treatment of parkinsons
M: Dopamine agonists

43
Q

Entacapone/ Tolcapone (I,M)

A

I: Treatment for late stage parkinsons
M: COMT (Catechol-o-methyl transferase) inhibitor so slows levodopa breakdown

44
Q

Risperidone (I, M, SE)

A

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)

45
Q

SNRI (I, M, SE)

Venlafaxine, Duloxetine

A

I: Depression, anxiety, neuropathic pain
M: Inhibits serotonin and noradrenaline reuptake
SE: Headache, insomnia, nausea, sexual dysfunction

46
Q

Diazepam (valium)- I, M, SE

Also lorazepam, chlordiazepoxide

A

I: Benzodiazepine (Short term anxiety, insomnia, anticonvulsant, muscle relaxant)
M: Positive allosteric modulator of GABAA receptor
SE: Drowsiness, dizziness, reduced coordination and alertness

47
Q

Mirtazapine (I, M, SE)

A

I: Anti-depressant (MDD)
M: Blocks alpha2 adrenoceptors, blocking -ve feedback, increasing synaptic conc
SE: Inc appetite, dry mouth, post hypotension, peripheral oedema

48
Q

Give 3 examples of MAO-A inhibitors?

What is a problem prescribing them?

A

Phenelzine, tranylcypromine, moclobomide
(Stop serotonin and noradrenaline breakdown)
Can’t break down tyramine protein (cheese and wine)- Hypertensive crisis

49
Q

SSRI’s (Examples, M, SE)

A

Fluoxetine, sertraline, paroxetine, fluvoxamine
M: Stop serotonin reuptake
SE: Nausea, headache, drowsiness, sexual dysfunction
INCREASED risk of depression and suicide in children!!!

50
Q

Alteplase (I, M, SE)

A

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.

51
Q

Pancuronium (I, M)

A

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

52
Q

Carbamazepine (I, M, SE)

A

I: Anticonvulsant (also for nerve pain or bipolar)
M: Sodium channel blocker
SE: Sedation, ataxia, blurred vision, water retention

53
Q

The elimination of Atracurium from the body is slowed by?

A

Respiratory acidosis

54
Q

Sodium Thiopental (I, M, SE)

A

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)

55
Q

Potassium Chloride (I and effect on cardiac muscle)

A

I: Electrolyte replacement and treating hypokalemia

Depolarises cardiac muscle cells and stops them firing AP’s

56
Q

What is the difference between typical and atypical antipyschotics?

A

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)

57
Q

What would the drugs orpenadrine and procyclidine be used for?

A

Anticholinergics

Balances cholinergic/ dopaminergic levels so therefore can reduce parkinsonian side effects

58
Q

Clozapine (I, M, SE)

A

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)

59
Q

Name 5 SSRI’s

A

Citalopram, fluoxetine, sertraline, paroxetine, fluvoxamine

60
Q

Name 3 SNRI’s

A

Venlafaxine, duloxetine, desvenlafaxine

61
Q

Pregablin (I, M)

A

I: Anticonvulsant for neuropathic pain and seizures
M: Binds to alpha 2 delta subunit on VGCa2+ channels to limit Ca influx

62
Q

Lithium (I, M)

A

I: Treating bipolar
M: Mood stabiliser, stabilises glutamate (not too much or too little) by acting on the GluR3

63
Q

Midazolam (I, M)

A

I: Induction of general anaesthesia
M: Positive allosteric modulator of GABA-A

64
Q

Lamotrigene (I, M)

A

I: For epilepsy, type 1 bipolar and depression
M: Blocks Na and Ca channels to inhibit glutamate release

65
Q

What is the most important caution for Semisodium Valproate in a F of childbearing age?

A

Causes folate anatagonism (glutamate formil transferase inhibition) therefore increasing risk of neural tube defects in pregnancy

66
Q

Etomidate (I, M)

A

I: Induction of general anaesthesia
M: Extends GABA-A opening time, so increases Cl in and causes hyperpolarisation (in reticular activating system)

67
Q

Tubocurarine (I, M)

A

I: Muscle relaxant for surgery (non-depolarising)
M: Antagonist for nicotinic ACh receptor

68
Q

Physostigmine (I, M)

A

I: Used to treat glaucoma
M: Inhibits acetylcholinesterase (increasing synaptic ACh)

69
Q

What are the general effects of benzodiazepines?

A

Enhance the effect of GABA at GABA-A receptor

Sedative, hypnotic (sleep inducing), anxiolytic (anti-anxiety), anti-convulsant and muscle relaxant

70
Q

In what circumstances is ibuprofen contra-indicated?

A

Allergies to NSAIDS
Stomach ulcers
Heart failure
Severe liver disease

71
Q

How is codeine different to morphine?

A

It is a pro-drug (metabolised to morphine)

72
Q

Clopidogrel (I, M, SE)

A

I: Antiplatlet (prophylactic post stroke etc)
M: ADP platelet membrane receptor antagonist
SE: Haemorrhage

73
Q

Flumazenil (I, M)

A

I: Treat benzodiazapine overdose
M: GABA-A receptor antagonist

NB: Has a v.short half life

74
Q

Naloxone (I, M)

A

I: Treat opioid overdose
M: Opioid receptor antagonist

75
Q

Name a drug which could be used to treat the mania phase of bipolar type 1?

A

Rispiridone

76
Q

Name 3 drug treatments which could be used for GAD

A

Citalopram (SSRI), Venlafaxine (SNRI), Pregablin

77
Q

Chlorpromazine (I, M)

A

I: Typical antipyschotic
M: Blocks D2 receptors only

78
Q

Amisulpride (I,M)

A

I: Atypical antipyschotic
M: Blocks D2 (in limbic striatum- +ve sympt) and 5-HT in mesocortical pathway -ve sympt)

79
Q

Haloperidol (I,M)

A

I: Atypical antipyschotic
Blocks D2 and 5-HT receptors
Schizophrenia, mania, pyschosis etc

80
Q

Reserpine (I,M)

A

I: Antipyschotic and antihypertensive
M: Reduces catecholamines by blocking ATP/Mg pump which puts them in vesicles

81
Q

Phenytoin (I, M)

A

I: Anti-convulsant
M: Blocks Na channels

82
Q

Ticlopidine (I, M)

A

I: Anti-platelet. Prevention of thrombosis
M: Blocks ADP receptor on platelets