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Mental health- PA30324 > Drugs > Flashcards

Drugs Flashcards

1
Q

Triptans (Sumatriptan etc)

A

Used to treat migraines

They are selective 5HT1B/5HT1D agonists

5HT1B receptors are on smooth muscle and voasconstriction

5HT1D lies on trigeminal nerve terminals and blocks release of vasoactive peptides from trigeminal nerves

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2
Q

What drugs are used in the prophylaxis of migraine?

A

B-blockers (bisoprolol, propanolol etc)

Antiepileptic drugs (gabapentin, pregabalin etc)

Antidepressants (Amitriptyline etc)

Calcium channel blockers (Nifidipine etc)

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3
Q

Tissue plasminogen activator (tPA)

A

Used to treat ischaemic stroke only

Disperses thrombus and restores blood flow

Must be administered in 3 hours for maximum effect

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4
Q

Stroke prophylaxis

A

Antihypertensives

Statins (reduces risk of thrombus formation but also contraindicated in haemorrhagic stroke)

Antiplatelets (Aspirin, clopidogrel)

Anticoahulants (Warfarin)

Compression stockings

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5
Q

Orlistat

A

Only centrally acting licensed drug in the UK for obesity

Acts as a lipase inhibitor and prevents the breakdown of dietary fats to fatty acids as well as decreasing the absorption of fats by 30%

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6
Q

Side effects of orlistat

A

Oily stools, abdominal cramps, flatus with discharge

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7
Q

Anti epileptics (VGSC blockers)

A

Phenytoin, Carbamazepine, Lamotrigine, Sodium Valproate

Keeps the VGSC in an inactivated state allowing it to produce 1 AP but not many successive AP’s

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8
Q

Anti-epileptics (VGCC blockers)

A

Ethosuxamide, Gabapentin, phenytoin

Allows for AP causes by VGSC but does not allow it to be propagated by VGCC’s

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9
Q

Levetiracetam

A

Anti epileptic that directly reduces vesicle fusion hence there is less Glu release therefore less neuronal excitation

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10
Q

Vigabatrin

A

Anti-epileptic that increase GABA synthesis causing more inhibition of neurones

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11
Q

Tigabine

A

Anti-epileptic that reduces the reuptake of GABA allowing for inhibition of neurones

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12
Q

How do benzodiazepines and barbituates help with epilepsy?

A

They increase the effectiveness of GABAa receptors which are Cl- channels which will prolong channel open time

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13
Q

Felbamate

A

Anti-epileptic that blocks NMDAr’s thereby reducing AP’s

However very hepatotoxic

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14
Q

Topiramate

A

Anti-epileptic that blocks AMPA/Kainate receptors thereby reducing AP’s

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15
Q

Retigabine

A

Anti-epileptic that activates K+ channels and makes the neurone less excitable both pre/post synaptically

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16
Q

Lesigamane

A

Anti-epileptic that blocks low threshold Na currents which decreases the propagation of AP’s

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17
Q

L-DOPA

A

Aimed at replacing the lost DA in Parkinson’s

L-DOPA is converted to DA by DOPA decarboxylase thereby causing increased DA synthesis

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18
Q

Carbidopa/bensarzide

A

Co-administered with L-DOPA to as a peripheral DA blocker to reduce the peripheral side effects of L-DOPA

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19
Q

Selegiline

A

MAO inhibitor to reduce degradation of DA

20
Q

Baclofen

A

Used for antispasticity

Targets and reduces motor output in the spinal cord

21
Q

Z-drugs (Zopiclone, zolpidem, zolepton)

A

Non-benzo’s which bind to GABAa receptors

Has a short duration of action

Less likely than benzo’s to cause rebound insomnia

Can cause dependence

22
Q

Typical antipyschotics (1st gen)

A

Eg Chlorpromazine, Haloperidol

High affinity D2 antagonists

Effective against the +ve symptoms of Schizophrenia via D2 blockade in the mesolimbic pathway

Around 80% block required for antipsychotic effects to occur

23
Q

Extrapyramidal side effects of 1st gen antipsychotics

A

Acute dystonias (Parkinson like)

Tardive dystonias (Huntingtons like)

Galctorrhea caused by increased prolactin release due to D2 block in TI pathway

Decreased pleasure due to inhibition of mesolimbic pathway

24
Q

Non dopamine related side effects of typical antipsychotics

A

Antipsychotics are also antagonists at other GPCR’s

Can cause sedation (H1)

Hypotension (alpha adrenergic receptors)

Blurred vision, dry mouth, constipation (Muscarinic)

Sexual dysfunction (muscariinic, adrenergic and dopaminergic)

25
Q

Atypical antipsychotics (2nd gen)

A

Eg Clozapine, Olanzipine, Rispiredone, aripiprazole

Low affinity D2 block so causes partial block of D2 but also of 5HT2 recepetors

5HT2 blockade reduces inhibition of DA neurons in mesocortical pathway and nigrostriatal pathway as they don’t appear elsewhere

This reduces treats the -ve symptoms and also reduces the motor side effects seen with typical antipsychotics

26
Q

Side effects associated with atypical antipsychotics

A

Weight gain and diabetes

Agranulo cytosis/leukopenia (rare and occurs moreoften with clozapine)

27
Q

Why is clozapine different to other atypicals?

A

The only antipsychotic shown to be clinically more effective than the others

However has serious side effects of agranulo cytosis/leucopenia and other blood dyscrasis

Only given if more than 2 other antipsychotics have been tried and were ineffective

28
Q

Cholinesterase inhibitors

A

Eg Donepazil, rivastigmine, galantamine

Used in treatment for alzheimers (Does not slow progression)

ACH is important in memory formation so these act to reduce ACh breakdown in synapses thereby enhancing levels of ACh

29
Q

Memantine

A

Non-competive NMDA receptor blocker

Is neuroprotective in some way or form and can cause slight cognitive improvement

30
Q

Irreversible MOAi

A

Eg Phenezine, Tranyleypromine, iproniazid

Used in treatment of depression

Irreversibly inhibits MAO which inactivates DA/NA/5HT

Problematic as consumption of cheese can result in gut MAO not metabolising tyramine due to block resulting in sympathomimetic side effects

31
Q

Moclobemide

A

Used in depression treatment

Safer to use than irreversible inhibitors as high concentrations of tyramine can overcome the block in the gut

Therefore there is much less chance of the cheese reaction occurring

32
Q

Long acting hypnotics

A

Flurazepam/Dalmane/Diazepam (2-keto metabolised in liver)

Long duration of action owed to active metabolites

Can result in a ‘hangover’ effect due to long duration of action

33
Q

Short acting hypnotics

A

Restoril/Tempazepam/Triazolam/Halcion (3-OH converted to glucaronide radicals)

Shorter half life and duration of action than 2- keto benzo’s

Little to no hangover effect

Rophynol is part of this class and is known as the date rape drug

34
Q

Herbal hypnotics

A

Valerian root

The active ingredients are suggested to bind to 5HT, GABA and adenosine receptors

35
Q

Benzodiazepines

A

Diazepam,

Binds to allosteric sites on GABAa receptors (CL- channels) increasing their activity

Binds between alpha/gamma subunits

36
Q

TCA’s

A

Tricyclic antidepressants eg imipramine, amitriptyline
Blocks the uptake of monoamines with preference for 5HT/NA over DA

Competitive and non selective

Blockade of histamine and ACh recpetors contributes to side effects

Major metabolites are also active

37
Q

Major side effects of MAOi’s

A

Hypotension
Atropine like effects
Hepatocellular jaundice

38
Q

Major side effects of TCA’s

A 
Sedation 
Atropine like effects 
Postural hypotension 
Mania and convulsions 
Dysrhythmia and heart block
39
Q

SSRI’s

A

Citalopram, Fluoxetine, Sertraline

Much more selective for 5HT receptors and so have less S/E from NA enhancement

Much safer in overdose as well

40
Q

Mirtazipine

A

Blocks alpha2 adrenceptors/5HT2C receptors causing enhanced NA/5HT release

41
Q

Trazodone

A

Blocks 5HT2A/2C and 5HT reuptake

42
Q

Mianserin

A

Blocks multiple 5HT receptors as well as alpha 1/2 adrenoceptors

43
Q

Agomelatine

A

Blocks melatonin receptors

Useful in depression that causes sleep disturbance

44
Q

Lithium

A

Reduces both mania and depressive phases
Possibly permeates through Na+ but doesn’t leave causing depolarisation of excitabel cells
Also inhibits IP3
>1.5mmol is toxic

45
Q

Lithium side effects

A 
Polyuria/Polydipsia (too much drinking/urinating)
Weight gain
Aggravation of skin disorders 
Tremors and muscle twitching 
GI symptoms 
Drowsiness 
Hyper-reflexia, Coma 
Huntington/Parkison like symptoms

Mental health- PA30324 (7 decks)

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