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topic 7 Flashcards

1
Q

what percentage of the EU population suffer from a mental disorder?

A

38.2%

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2
Q

what are the most common mental disorders?

A 
anxiety
insomnia
major depression
drug and alcohol dependence
adhd
dementia
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3
Q

what are the 3 symptom domains of schizophrenia?

A

positive (psychosis), negative (asociality, unmotivated) , cognitive

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4
Q

what is the incidence rate of schizophrenia

A

1%

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5
Q

what neurotransmitter is implicated in schizophrenia

A

overactivity of dopamine

also evidence for the involvement of glutamate and serotonin

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6
Q

what is the dopamine hypothesis of schizophrenia

A
  • an increase in dopaminergic neurotransmission in the mesolimbic pathway
  • this leads to abnormally high levels of dopamine in the nucleus accumbens and striatum
  • this is thought to underlie the positive symptoms of psychosis
  • there is also thought to be a decrease in dopamine transmission in the mesocortical pathway, projecting from the VTA to cerebal cortex
  • this is associated with the negative and cognitive symptoms
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7
Q

what are the 3 categories of antipsychotics

A

Typical/1st generation
Atypical/2nd generation
partial agonists

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8
Q

what is the distinction between different types of antipsychotics based on?

A

receptor binding profile
incidence of extrapyramidal symptoms
efficacy against negative symtpoms
efficacy in treatment resistant patients

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9
Q

what symptoms do antipsychotics treat

A

positive symptoms

not generally effective at negative or cognitive symptoms

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10
Q

what is treatment faliure?

A

loss of efficacy over time

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11
Q

how do most antipsychotic drugs work?

A

most are antagonists or partial agonists at D2 dopamine receptors - thought to determine potency

there is also activity at some other receptors such as muscarinic receptors - thought to determine side effect profile

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12
Q

how many dopamine d2 receptors must be blocked for the maximum therapeutic effect of antipsychotics

A

60-80%

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13
Q

what are extrapyramidal symptoms of antipsychotics

A

diskinesia and other movement disorders

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14
Q

what are 3 antipsychotic side effect clusters

A

sedation
metabolic
extrapyramidal (motor side effects)

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15
Q

what does it mean when an affective disorder is unipolar

A

mood swings are in the same direction

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16
Q

what proportion of major depression cases are reactive or endogeneous (genetic)

A

75% reactive

25% endogeneous

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17
Q

what is the monoamine theory of depression?

A
  • depression results from functional deficit in monoamine neurotransmitters (dopamine, noradrenaline, serotonin)
  • mania results from an excess in monoamine neurotransmitters
  • tricyclic antidepressent drugs are effective and boost monoamine neurotransmisison
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18
Q

what are two categories of antidepressant drugs?

A

slow acting anti depressants and fast acting antidepressants

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19
Q

what are 3 categories of slow acting antidepressants?

A

monoamine uptake inhibitors
monoamine oxidase inhibitors
atypical antidepressants

20
Q

what are 3 rapid action antidepressants?

A

ketamine
scopolamine
pscilocybin

21
Q

how do tricyclic antidepressants work

A

they non selectively inhibit both NA and Serotonin reuptake into nerve terminals

22
Q

what are side effects of tricyclic antidepressants

A 
sedation
postural hypotension
dry mouth, blurred vision, constipation
occasional mania
risk of cardiovascular side effects
23
Q

why might SNRI’s be better than SSRIs

A

fewer side effects

24
Q

What are side effects of SSRIs

A

nausea
insomnia
sexual dysfunction

25
Q

what is the difference between SSRis and SNRis

A

ssris block serotonin reuptake

snris block noradrenaline reuptake

26
Q

are monoamine oxidase ihibitors irreversible or reversible

A

most of the time the monoamine oxidase inibition is irreversible

27
Q

what are the main side effects of monoamine oxidase ihibitors

A

postural hypertension
weight gain
restlessness

28
Q

how do MAO inhibitors work

A

inhibit monoamine oxidase
these are ezymes that degrade monoamines
this increases ctyosolic stores of 5HTP and NA in nerve terminals

29
Q

describe atypical antidepressants

A
  • refer to a heterogeneous group of drugs that are known to improve mood but have no common mechanism of action
  • they mainly act at presynaptic receptors, perhaps to enhance monoamine release
30
Q

describe lithium as a mood stabilizer

A
  • lithium is an inorganic ion taken as lithium carbonate
  • 2 possible mechanisms of action:
    1. interference with inositol phsophate formation
    2. interferance with cAMP formation
  • it has a long plasma half life
  • side effects are common
31
Q

what are 3 categories of CNS stimulants

A
  1. convulsants and respitory stimulants - little effect on mental function
  2. psychomotor stimulants - alter mental function and behaviour
  3. psychotomimetric drugs - alter perception and cognition
32
Q

what are 3 proposed mechanisms for amphetat=mine

A
  • inhibition of dopamine reuptake by acting as a competitive antagonist of dopamine transporters
33
Q

how does cocaine work?

A

inhibits dopamine reuptake

34
Q

how do psychedelic drugs work

A

5HT21 agonism

35
Q

what are the 5 main types of drugs that are abused

A 
narcotic analgesics (e.g morhpine)
general cns depressents
anxiolytic drugs (e.g benzodiazepines)
psychomotor stimulants (e.g amphetimines)
psychotominetric drugs (psychedelic)
36
Q

what are the common features of abused drugs

A

all produce rewarding effects that lead to stimulants

they are accompanied by habituation/adaptatio when used repeatedly

37
Q

what is the dual diagnosis for substance abuse?

A

there is a statistically significant overlap between genes that confer risks for schizophrenia and drug dependence

38
Q

how many pharmocologically active cannaboids are in cannabis?

A

over 60

39
Q

what are the best known constituents of cannabis

A

THC and CBD

40
Q

how do cannoboids work

A

they act on cannaboid receptors

CB1 receptor activation reduces neuronal activity

41
Q

what are the endogenous ligands of cannaboid receptors?

A

anandamide and 2-AG (released from the post synaptic terminal, travelling to the pre)

functions in memory, synaptic depression, immune system, sleep, stress response, pain relief

42
Q

what are the two cannaboid receptors

A

CB1 receptors are abundant in the hippocampus, cerebelleum, substantia nigra, mesolimbic dopamine pathway and the cortex

CB2 receptors are in the peripheral lymphoid system (potential immune role?)

  • they are both g protein coupled receptors
  • they are present in the presynaptic neurons (retrograde messengers)
43
Q

where is the expression of CB1 receptors highest?

A

prefrontal cortex, amygdala, hippocampus,
all thought to be involved in cognition

there is also expression in the meso-corticolimbic system thought to be associated with its rewarding effects

44
Q

what are 3 effects of cannabis exposure in the CNS?

A
  • increased dopamine released
  • reduces GABA and Glutamate release in nucleus accumbes
  • increases opiod peptide release in the nucleus accumbens
45
Q

what is it thought that the disruptions in cognition due to cannabis are due to

A
  • Decrease ACh release in the hippocampus and the prefrontal cortex
  • reduced GABA release and increased Glutamate release in the prefrontal cortex
  • increased NA release in HIPP and frontal cortex
46
Q

what are some adaptive changes due to chronic cannabis exposure in the CNS

A
  • decreased regional cannabis receptor 1 expression
  • deficiets in cortical and hippocampus CBR1 associated with impaired memory and cognition
  • disruption of reward related signalling associated with reduced DA cell density and firing in the VTA and reduced dopamine release in the nucleus accumbens
  • these effects are more prominent in those meeting the criteria for dependence

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