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Pharmacology > Drugs for personality disorders > Flashcards

Drugs for personality disorders Flashcards

1
Q

what is the single most important diagnostic feature of schizophrenia?

A

hallucination

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2
Q

what is schizophrenia ALWAYS accompanyed by?

A

decline in cognitive function

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3
Q

what are the features of Type1 schizophrenia?

A

auditory hallucinations
thought disorders
delusions
thought broadcasting

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4
Q

what are the features of Type 2 schizophrenia?

A

loss of drive
motor disturbances (catatonia)
social withdrawal

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5
Q

what evidence is there to support the dopamine theory of schizophrenia?

A

the use of D2 antagonists - helps reduce auditory hallucinations

the use of amphetamine, which causes an increase in dopamine, is associated with exacerbating schizophrenia

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6
Q

what evidence is there to support the 5HT theory of schizophrenia?

A

all drugs which cause hallucinations bind to the 5HT2A receptors

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7
Q

give an example of a typical drug?
advantages and disadvantages

how does it work?

A

chlorpromazine and halopiridol

they are D2 receptor antagonists: therefore reduce Dopamine affects in the nucleus accumbens, thereby reducing hallucinations

advantages:

  • works to eliminate positive features
  • have profound sedation

negatives:

  • do not solve the negative features
  • cause extra-pyrmidal side effects
  • saliohorrea
  • aplastic anaemai
  • hyperprolactinaemia
  • tardative dyskinesia (particularly of face) does not resolve even when drug is withdrawn
  • malignant neuroleptic syndrome
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8
Q

what are some of of the pharmcokinetic aspects of phenothiazines

metabolism and other receptor actions

A

they have enterohepatic circulation, so take up to 4-6 weeks to be excreted from body - therefore must be very careful to not overdose

they have actions on H1 receptors - sedation
on A1 receptors - hypotension
on M receptors - ameliorate the EPS effects, infact they have less EPS than other typicals because of this

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9
Q

give an example of an atypical drug?
how does it work?
what are its side effects? and advantages

A

example: clozapine

drugs work by:

  • antagonises 5HT2A/C receptors
  • 5HT1/A agonist
  • alpha 2 adrenoreceptor and muscurinic antagonists (associated with reduced EPS symptoms)

positive effects:

  • effect both positive and negative symptoms of schizophrenia
  • lower incidence of EPS and tardative dyskinesia
  • can relief psychosis resistant to typical neuroleptics

relief of negative symptoms associated with 5HT1A agonist activity - increased dopamine release to mesocortical pathways

negative effects:

  • weight gain, but in visceral fat (link to type II diabetes)
  • weight gain associated with 5HT2A antagonism
  • prolonged QT interval
  • agranulocytosis
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10
Q

aripiprazole - what is its mechanism of action in schizophrenia?

A

3rd generation neuroleptic drug shows:
- D2 partial antagonism (less hallucinations)
- 5HT2A antagonism (less hallucinations)
5HT1 agonists (increased dopamine release in mesocortical pathway/less negative symptoms)

positive effects:
- little effect on QT interval 
reduced EPS (As much as placebo)
- reduced weight gain 
- safe in overdose

negative effects:

  • hyperprolactinamia
  • hypercholisternamiea
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11
Q

what is the treatment for bipolar disorder? side effects of treatment

A

the only present effective treatment is lithium salts
problem is large plasma concentration required, by low therapeutic index

side effects:

  • nephrotoxicity
  • hypothyrodism
  • culumination in CNS causes coma and death
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12
Q

give an example of a
phenoxthiazine
butyrphenone
thioxanthes

A
  • chlorpromazine
    haloperiodal
    flupenthixol
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13
Q

what is thioridizine?

A

this is a phenoxthiazine:

  • has moderate sedation effects-
  • the most anti-muscraninc (least EPS incidence)
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14
Q

what is chlorpromazine/

A

this is a phenoxthiazine:

  • has profound sedation
  • causes hypotension
  • some anti-muscuranic action?
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15
Q

why does halperidol cause the most EPS?

A
  • because it binds to D2 receptors with the highest affinity
  • has no anti-muscaranic actions
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16
Q

when are the atypicals used, and why?

A

they’re only used when the patient is not responsive to the typicals, and this is because of the fact that they can cause agranulocytosis?

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17
Q

what are some EPS side effects?

A
  • tardative dyskinsia (Which can persist after drug withdrawal)
  • dystonia
  • akathisia
  • pseudo-parkinosnism
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18
Q

what is the biggest problem with hypnotic drugs

A

they carry a risk of dose escalation and dependance over long term use

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19
Q

which GABA binding pocket do barbiturates bind to?

A

A1/B2

B2/Y2

20
Q

what is phenobarbitrone used for?

A

an anti-convulstant

21
Q

what is pentobarbitorone used for?

A

used as an anxiolytic and for sedation

22
Q

what is thiopentone used for?

A

used for Induction anaesthesia

23
Q

what is the mechanism of action of barbiturates

A

so they bind to their specific binding pocket on the GABAa receptor, and they increase the time GABA is bound to the receptor, thereby increase the mean time of Cl-channel opening. at higher concentrations the barbiturates directly open the chloride channels - and this causes hyper polarisation

24
Q

why do barbiturates induce dose tolerance?

A

because they induce the P450 enzymes in the liver, which increases drug metabolism, therefore higher concentration of the drug is required each time to produce the same therapeutic effects

25
Q

what is the single best reason the BZP are better than the barbiturates?

A

the BZP are safe in overdose, meaning the maximal affect of their dose-response curve is loss of consciousness, for the barbiturates it is respiratory depression and cardiovascular collapse leading to death.

furthermore, the BZP do not syngerise with other CNS depressants, but the barbiturates do.

26
Q

what is meprobamate?

A

this is an anxiolytic at non-sedative dosages.

can induce dependance with withdrawal syndrome. it is used as a muscle relaxant

27
Q

what binding pockets do the BZP bind to, which alpha subunits do they not bind to?

A

BZP bind to A1/Y2

they do not bind to GABAa receptors with the alpha 4 subunit

28
Q

what is the mechanism of action of the BZP?

A

They’re positive allosteric modulators of the GABAa receptor, so they increase GABA binding to the receptor, this increases the frequency of channel opening of the chloride channels (but does not affect the duration at which the chloride channels are open for)

29
Q

what is the action of the BZP dependant on?

A

it is dependant on the GABAa receptor composition

30
Q

what is the extent of CNS depression brought about by the BZP dependant on?

A

dependant no receptor occupancy. but anxiolytic and anti-convulstant effects of the BZP are brought at much lower receptor occupancies than those required for sedation and hypnosis (80%)

31
Q

what is the main difference between the BZP

A

They differ in their duration of action and rate of onset

32
Q

what is the main difference between the BZP

A

They differ in their duration of action and rate of onset

33
Q

what is diazepam used for? what type of BZP is it?

A

diazepam is a long acting BZP with a half life os 32 hours.

used as an anxiolytic - reduces risk of rebound anxiety.
has an active metabolite with a much longer half life

34
Q

what is clonazepam used for?

A

it is a long acting BZP. used for anti-convulsants. not really used as an anxiolytic because produces anti-convulstant effect before anti-anxiety effect. because it has a long half life provides a sustained anti-convulstant effect with a little risk of rebound convulsants

35
Q

what type of drugs are triazolam and temazepam?

A

those are intermediate acting BZP and they’re used as hypnotic drugs, they’re important to have a short acting effect to reduce residual day time hangover

36
Q

what is midazolam?

A

this is a short acting BZP, used in dental surgery to induce amnesia and anxiolysis

37
Q

how are BZP excreted and why?

A

they must be first conjugated in the liver (because otherwise too lipid soluble to be excreted) active or non-active metabolites need to be conjugated.

clonazepam is not conjugated, but metabolised differently in the liver

38
Q

what us B-carboline?

A

this is ah negative allosteric modulator at the BZp receptor site, meaning it binds to BZP site, but induces the complete opposite effects of the drug. it is used in cases of overdose

39
Q

what is fluemazemil used for?

A

this is an antagonist at the BZP receptor site, used for overdose

40
Q

what is fluemazemil used for?

A

this is an antagonist at the BZP receptor site, used for overdose

41
Q

what is the mechanism of action of busiprone as an anxiolytic?

A

5HT-1A receptor agonist reduces 5HT release, which is increased in anxiety

  • has a full agonist activity at pre-synaptic receptors, and only partial activity at the post-synaptic receptors
42
Q

what is the mechanism of clonidine as an anxiolytic?

A

A2 agonist- reduces nor-adrenaline release which is increased in anxiety

43
Q

when is propanolol used as an anxiolytic?

A

only in situational anxiety

44
Q

when is propanolol used as an anxiolytic?

A

only in situational anxiety

45
Q

what is zopiclone?

A

a BZP agonist (but a non-benzodiazapene hypnotic) - used in patients with insomnia- but disturbes sleep arhcitetucre causing REM deficiency

46
Q

what’s the single best cause for the relief of the negative symptoms of schiz?

A

this is binding to the 5HT1A receptors, which is thought to increase dopamine release in the mesocortical pathway

3rd generation - full agonist
atypicals - partial agonists

47
Q

what is the proof that antagonising the D2 receptors is not essential for an anti-pyscotic effect?

A

this is due to the fact that the atypicals and the 3rd generation drugs only show weak binding actions to those receptors

Pharmacology (17 decks)

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