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Neuroscience > neuropyschopharmacology > Flashcards

neuropyschopharmacology Flashcards

1
Q

What is Bipolar 1

A

at least 1 manic episode, impairment functioning, duration 1 week

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2
Q

What is Bipolar 2

A

at least 1 hypomanic episode, no severe impairment, duration 4 days

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3
Q

what is the criteria for mania?

A

1 week elevated/irritable mood, 3+(grandiosity, decr sleep, racing thoughts, distractibility, agitation etc), impaired functioning

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4
Q

what is involved in bipolar disorder with psychotic symptoms

A

hallucinations, delusions, grandiose/depressed mood, formal thought disorder

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5
Q

what is the epidemiology of bipolar

A

1% (adult)

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6
Q

what is the gender distribution of bipolar

A

equal in men and women

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7
Q

half of bipolar patients are diagnosed before what age?

A

25

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8
Q

what are the causes of bipolar

A

environmental and genetic- polygenetic

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9
Q

what are some diseases coexisting with bipolar?

A

substance abuse, ADHD, anxiety, thyroid disease, migraine, heart disease etc

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10
Q

What would you use antidepressant alongside?

A

mood stabiliser as need to be taken with caution

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11
Q

what drugs can be used prophylactically to prevent relapse

A

lithium, valproate, carbamazepine, olanzapine, risperidone

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12
Q

how does lithium work?

A

affects cation transport, monoaminergic transmission, cholinergic transmission, affects second messengers, has some neuroprotective functions

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13
Q

how does lithium affect cation transport?

A

increase Na+/K+ ATPase pump, neurotransmitter release

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14
Q

how does lithium affect NA and 5HT function

A

increases their functions

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15
Q

How does lithium affect cholinergic activity

A

increases it

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16
Q

what Is the effect of lithium on second messengers in the brain

A

inhibits cAMP, limits IP3 formation

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17
Q

How does lithium lead to neuroprotection

A

increased neuronal growth factors, makes neurones more resilient to stress

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18
Q

side effects of lithium

A

early- polyuria, dry mouth, weak; late- fine tremor, hair loss, thyroid enlargement; toxic- nausea, vomiting, confusion, convulsions

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19
Q

what do you need to monitor in lithium treatment

A

plasma monitoring- therapeautic window; TFTs; u and es

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20
Q

what is the problem with lithium and pregnancy

A

teratogen

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21
Q

what else is used in the treatment of bipolar (psychosocial)

A

CBT, psychoeducation

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22
Q

what is the definition of psychosis?

A

mental state dysfunction of behaviour, perception and thought processes

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23
Q

what is the definition of delusions

A

abnormality in the content of thought, not explained by cultural background

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24
Q

definition of hallucination

A

false perception without external stimulus present

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25
Q

what is the difference between true hallucinations and illusions?

A

illusions are the misperception of an external stimulus whereas hallucinations don’t have an external stimulus

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26
Q

what are the disorganised symptoms associated with schizophrenia

A

symptoms of the thought process- impairment to think properly, making up words, altered sense of self, changes in emotion and movements and behaviour

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27
Q

what is needed for the diagnosis of schizophrenia (at least one)

A

delusions of thought, delusions of control, voices in 3rd person, persistent delusions completely impossible

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28
Q

what is needed for the diagnosis of schizophrenia (at least 2)

A

persistent hallucination, formal thought disorder, catatonic behaviour, negative symptoms, change in overall quality of behaviour

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29
Q

what are the positive symptoms of schizophrenia

A

delusions, hallucinations, thought disorder

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30
Q

what are the negative symptoms of schizophrenia

A

decrease reactivity/range of emotions, poverty of speech/thought, apathy

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31
Q

what is the most reported symptom in schizophrenia

A

lack of insight (95%), then auditory hallucinations (74%)

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32
Q

how is the onset of schizophrenia

A

gradual

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33
Q

how is the outcome of schizophrenia

A

1/3s- good, intermediate, poor

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34
Q

what is a common clinical feature of schizophrenia

A

depression

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35
Q

what is the lifetime risk of having schizophrenia

A

1%

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36
Q

what is the peak age group of schizophrenia

A

20-24 (males), 25-29 (female)

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37
Q

what is enlarged in schizophrenia

A

lateral ventricles

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38
Q

what is a hypothesis in schizophrenia

A

dopamine hypothesis- mesolimbic dopamine overactivity

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39
Q

what is a limitation of the dopamine hypothesis in schiz

A

doesn’t explain the negative symptoms

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40
Q

what are the alternate hypotheses

A

glutamate, serotonin, and non neurochemical hypotheses

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41
Q

what are short term and long term medical treatments of schiz

A

short term- tranquilisers. long term- antipsychotics

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42
Q

how long is the delay of the antipsychotics in schizop

A

2-4 weeks

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43
Q

what are the 4 pathways associated with dopamine?

A

mesolimbic, mesocortical, nigrostriatal, tuberoinfundibular

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44
Q

what is the key action of antipsychotics but why are they ‘dirty’

A

blockade of D2 receptor. dirty as they bind other receptors- cholinergic, histaminic, adrenergic

45
Q

what are the problems with conventional antipsychotics

A

extra pyramidal side effects

46
Q

which conventional antipsychotics have more EPSEs?

A

high potency (low potency have less EPSE)

47
Q

example of high potency conventional antipsych

A

haloperidol

48
Q

example of low potency conventional antipsych

A

chlorpromazine, thioridazine

49
Q

what are some side effects of conventional antipsychs

A

hyperprolactinaemia, tardive dyskinesia (involuntary movements), neuroleptic malignant syndrome, nigrostriatal blockade- EPSE, parkinsonism, rigidity, tremor, bradykinesia, acute dystonia, akathisia (inner restlessness)

50
Q

what are the advantages of newer atypical antipsychotics

A

don’t cause EPSEs, less D2 blockade

51
Q

examples of atypical antipsychotics

A

clozapine, olanzapine, risperidone, quetiapine

52
Q

what are other side effects of atypical antipsych

A

weight gain, lipid, diabetes

53
Q

what is the annual prevalence of unipolar depression

A

3-10% (lifetime 10-20%)

54
Q

what classifies as a major depressive ep

A

> 5 of following- depressed mood; diminished interest; insomnia/hypersomnia; retardation; feeling worthless; suicidal; loss concentration

55
Q

what are the biological symptoms of depression

A

mood worse in mornings, sleep disturbance, loss libido, appetite changes, psychomotor agitation

56
Q

what is decreased (neurotransmitters) in depression

A

decrease 5HT and NA. (monoamine hypothesis of depression)

57
Q

what endocrine abnormalities are associated with depression

A

hypercortisolaemia

58
Q

what % of depressions are heritable

A

30%-males, 40%- females

59
Q

what is hyperactive in depression

A

hypothalamic- pituitary- adrenal axis

60
Q

what does hypercortisolaemia lead to

A

shrinkage of the hippocampus

61
Q

what drugs are used in the treatment of depression

A

SSRIs (fluoxetine, citalopram); TCA (imipramine); MAOI (phenelzine); SNRIs (serotonin noradrenaline reuptake inhibitors- venlafaxine)

62
Q

what are the causes of dementia

A

alzheimers (50%), vascular dementia (25%), mixed alzheimers/vascular dementia (25%), Lewy body (15%), others- frontotemporal,subcortical, secondary causes eg lesions (5%)

63
Q

what is aphasia

A

difficulty in speech, communication, writing

64
Q

what is agnosia

A

loss of ability of recognition

65
Q

what is apraxia

A

can’t execute motor actions even though have ability in the muscles

66
Q

what protein is involved in alzheimers

A

apolipoprotein E4

67
Q

brain volume reduces but where is there more atrophy in the brain in alzheimers

A

in frontoparietal and temporal lobes

68
Q

what pathology is found in alzheimers

A

neuritic plaques (amyloid B); neurofibrillary tangles (phosphorylated tau)

69
Q

what are the main neurotransmitters in alzheimers

A

ach and glutamate

70
Q

what happens to cholinergic innervation in alzheimers

A

loss of neurones from the nucleus of Meynert (cholinergic nucleus). neocortical cholinergic innervation lost due to amyloid plaque.

71
Q

what is glutamate involved in and what happens in alzheimers

A

main of neocortical and hippocampal pyramidal neurones. involved in higher functions such as cognition and memory. die due to the neurofibrillary tangles

72
Q

what treatments are used in alzheimers and examples

A

ACHEIs (donezepil, rivastigmine) and NMDA receptor antagonist (memantine)

73
Q

when are ACHEIs used in alzheimers

A

mild to moderate. (NMDA antagonist used in moderate to severe)

74
Q

what are the 3 symptoms in dementia with Lewy Bodies

A

fluctuating cognitive impairment; parkinsonism; visual hallucinations

75
Q

what is the pathology in Lewy Body dementia

A

cortical atrophy, ventricular enlargement, Lewy bodies in cortex

76
Q

what neurochem abnormalities are present in Lewy Body

A

cholinergic, disruption dopaminergic input to striatum

77
Q

what does vascular dementia co exist with?

A

multi infarct dementia (problem in blood supply to the brain), small vessel disease (leading to subcortical changes), subtypes include post stroke dementia

78
Q

what is the onset of multi infarct dementia

A

abrupt onset

79
Q

what occurs in multi infarct dementia

A

emotional and mood changes, insight may be retained for longer, epilepsy more common

80
Q

what is a common history for someone with multi infarct dementia

A

prev strokes and TIA

81
Q

how many people with dementia develop at least one behavioural and psychological symptom of dementia (BPSD)

A

90% (85% of these are serious)

82
Q

what are the main 3 syndromes associated with BPSD

A

agitation, psychosis, mood disorders

83
Q

what pharmacological treatments are given to those with dementia

A

antidepressants, anticonvulsants, antipsychotics

84
Q

what is the volume of distribution calculated by

A

total amount of drug/concentration in plasma

85
Q

what is the rate of elimination calculated by?

A

clearance x concentration in the blood

86
Q

why would you need to give drugs at a higher concentration

A

if they undergo first pass metabolism

87
Q

is lithium metabolised?

A

no, relies entirely on excretion

88
Q

what can affect the excretion of lithium

A

dehydration/overhydration; alcohol; diuretics; renal insufficiency; polyuria

89
Q

what are the dopamine tracts and associated conditions

A

nigrostriatal (parkinsons); mesocortical and mesolimbic (schizophrenia); and tuberoinfundibular (prolactin release control)

90
Q

what is the precursor of serotonin and enzymes involved

A

trytophan (tryptophan hydroxylase)

91
Q

what is the precursor of dopamine and enzymes involved

A

tyrosine (tyrosine hydroxylase)

92
Q

precursor of NA and enzyme involved

A

dopamine. dopamine B oxidase

93
Q

precursor of Ach metabolised by what enzyme

A

choline. choline acetylcholinesterase

94
Q

what is NA involved in

A

attention

95
Q

what is involved in alzheimers

A

Ach

96
Q

where are amino acid neurotransmitters contained (GABA, glutamate)

A

astrocytes and interneurones

97
Q

what is a benzo commonly used in anxiety

A

alprazolam, lorazepam

98
Q

what benzo is used in insomnia

A

temazepam

99
Q

what benzos are not metabolised in the liver and so can be considered in liver failure

A

LOT- lorazepam, oxazepam, temazepam

100
Q

what are the types of adrenoceptors and which are excitatory

A

alpha and beta. alpha 1- excitatory. alpha-2 inhibitory. b1,2,3 stimulatory

101
Q

what blocks muscarinic ACHRs

A

atropine

102
Q

what effects do muscarinic ACHrs have

A

increase sweating, decrease HR,bp; bronchoconstriction, contraction of pupils; increase motility of GI

103
Q

what effects do nicotinic ACHRs have

A

symp and para effects

104
Q

what are the side effects of anti cholinergic

A

tachycardia, dry mouth, blurred vision, urinary retention

105
Q

what are the side effects of anti adrenergic

A

hypotension, arrhythmia, tachycardia

106
Q

what are effects of dopamine blockade

A

EPSE- tardive dyskinesia, akithesia, acute dystonia, hyperprolactinaemia, anhedronia

107
Q

anti histaminic side effects

A

sedation, weight gain

108
Q

is glutamate increased or decreased in mood disorders, shizophrenia

A

increased

109
Q

is GABA increased or decreased in mood disorders, schizo, epilepsy

A

decreased

Neuroscience (8 decks)

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