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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
what is the difference between SSRis and SNRis
ssris block serotonin reuptake | snris block noradrenaline reuptake
26
are monoamine oxidase ihibitors irreversible or reversible
most of the time the monoamine oxidase inibition is irreversible
27
what are the main side effects of monoamine oxidase ihibitors
postural hypertension weight gain restlessness
28
how do MAO inhibitors work
inhibit monoamine oxidase these are ezymes that degrade monoamines this increases ctyosolic stores of 5HTP and NA in nerve terminals
29
describe atypical antidepressants
- 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
describe lithium as a mood stabilizer
- 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
what are 3 categories of CNS stimulants
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
what are 3 proposed mechanisms for amphetat=mine
- inhibition of dopamine reuptake by acting as a competitive antagonist of dopamine transporters
33
how does cocaine work?
inhibits dopamine reuptake
34
how do psychedelic drugs work
5HT21 agonism
35
what are the 5 main types of drugs that are abused
``` narcotic analgesics (e.g morhpine) general cns depressents anxiolytic drugs (e.g benzodiazepines) psychomotor stimulants (e.g amphetimines) psychotominetric drugs (psychedelic) ```
36
what are the common features of abused drugs
all produce rewarding effects that lead to stimulants | they are accompanied by habituation/adaptatio when used repeatedly
37
what is the dual diagnosis for substance abuse?
there is a statistically significant overlap between genes that confer risks for schizophrenia and drug dependence
38
how many pharmocologically active cannaboids are in cannabis?
over 60
39
what are the best known constituents of cannabis
THC and CBD
40
how do cannoboids work
they act on cannaboid receptors CB1 receptor activation reduces neuronal activity
41
what are the endogenous ligands of cannaboid receptors?
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
what are the two cannaboid receptors
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
where is the expression of CB1 receptors highest?
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
what are 3 effects of cannabis exposure in the CNS?
- increased dopamine released - reduces GABA and Glutamate release in nucleus accumbes - increases opiod peptide release in the nucleus accumbens
45
what is it thought that the disruptions in cognition due to cannabis are due to
- 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
what are some adaptive changes due to chronic cannabis exposure in the CNS
- 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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