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DDT > 10 - psychiatric/movement disorders > Flashcards

10 - psychiatric/movement disorders Flashcards

1
Q

function of noradrenaline

A

stimulates adrenoreceptors
fight/flight
triggers glucose release into blood
a1 adrenoreceptor - vasoconstriction

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2
Q

effects of noradrenaline

A

increased blood pressure
increased systemic vascular resistance
peripheral vasoconstriction
increased myocardial O2 consumption

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3
Q

a1 adrenoreceptor

A

inreased BP

vasoconstriction

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4
Q

a2 adrenoreceptor

A

SM contraction

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5
Q

B1 adrenoreceptor

A

increased heart rate

increased contractility

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6
Q

B2 adrenoreceptor

A

smooth muscle dilation

e.g. bronchioles in lungs

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7
Q

what is 5-HTP

A

decarboxylated to 5-HT (serotonin)
can cross BBB unlike 5-HT
works on brain/cns to increase serotonin production

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8
Q

association of 5-HT to depression

A

decreased 5-HT (serotonin) receptors leads to depression

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9
Q

selective serotonin reuptake inhibitors

A

antidepressant drug
increase extracellular serotonin concentration
more serotonin can bind to post synaptic

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10
Q

signalling pathways caused by dopamine

A

D1 and D5 are couples via g proteins to Gas signalling

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11
Q

amphetamines

A

stimulate dopamine release from dopamine-secreting neurons

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12
Q

where is dopamine most abundant

A

corpus striatum

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13
Q

too much dopamine caused by and effects

A

cocaine/amphetamines

drug-induced psychosis/schizophrenia and paranoia

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14
Q

too little dopamine caused by and effects

A

death of dopaminergic neurons in substantia nigra

parkinsons

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15
Q

ADHD and dopamine

A

ADHD has increased dopamine transporters so dopamine signalling is reduced

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16
Q

4 dopaminergic pathwasy

A

nigro-striatal
meso-limbic
meso-cortical
tubulo-infundibular

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17
Q

nigro-striatal pathway from and to

A

substantia nigra to basal gangla/corpus striatum

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18
Q

nigro-striatal involved in

A

movement - motor neurons

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19
Q

meso-limbic from and to

A

VTA to nucleus accumbens/limbic system

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20
Q

meso-limbic involved in

A

reward

+ve symptoms of schizophrenia

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21
Q

meso-cortical from and to

A

vta to cortex

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22
Q

meso-cortical involved in

A

motivation and emotion

-ve symptoms of schizephrenia

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23
Q

tubulo-infundibular from and to

A

hypothalamus to posterior pituitary

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24
Q

what is tubulo-infundibular involved in

A

hyperprolactinemia
hormone regulation

dopamine release inhibits prolactin release

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25
Q

basal ganglia

A

group of nuclei at base of forebrain
influence motor cortex via direct/indirect pathways through thalamus
make/prevent movement

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26
Q

what are the components of the basal ganglia

A 
striatum
globus pallidus 
caudate nucleus
subthalamic nucleus
substantia nigra
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27
Q

where does the striatum (basal gnaglia) receive input signals from

A

thalamus

cortex

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28
Q

outline mechanism of direct pathway

A

signals from cortex excite striatum
signals from striatum inhibit internal globus pallidus and substantia nigra
these signals inhibit thalamus
thalamus sends excitatory signals to cortex

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29
Q

receptors in direct pathway

A

D1

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30
Q

effect of dopamine on direct pathway

A

binds to D1 recepors
increases direct pathway
stimulates movement

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31
Q

differences between indirect pathway and direct

A

indirect takes longer route to get to substantia nigra and globus pallidus internal
indirect goes via globus pallidus external and subthalamic nucleus first

when dopamine binds, indirect pathway signalling is reduced
muscle movement is reduced

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32
Q

outline mech of indirect pathwya

A

cortex excites striatum
striatum inhibits globus pallidus external
inhibits subthalamic nucleus
excites globus pallidus internal and substantia nigra

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33
Q

receptors for dopamine in indirect pathway

A

D2

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34
Q

anticipation

A

as a genetic disorder is passed on each generation, the symptoms become more apparent earlier in life and often more severe

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35
Q

huntingtons disease

A

HTT gene
trinucleotide repeat
level of disorder depends on number of repeats

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36
Q

causes of protein misfolding

A

improper interactions - proteins stuck in intermediate/non-active state
environmental condiitons - extreme temp/oxidative stress

37
Q

effects of protein misfolding

A

protein can become toxic
loss of normal function
cause disease - proteopathies

38
Q

examples of proteopathies

A

alzheimers

parkinsons

39
Q

proteopathy

A

when protein misfolding causes disease
prevented by chaperones
common in proteins containnig amino acid sequence repeats

40
Q

identification of protein misfolds

A

tagged with ubiquitin and sent to protesome for degradation

41
Q

ligand binding assays

A

to determine presence of ligand-receptor complezes

relies on binding of ligand molecules to antibodies

42
Q

uses of ligand binding assays

A

measure rate and extent of binding
measure number of binding sites
measure affinity/accessibility for various drugs

43
Q

use of ligand binding assays detection of disease

A

schizophrenia identification

44
Q

IC50

A

the concentration of inhibiting ligand which reduces 50% of the binding

conc of competing ligand which displaces 50% of the specific binding of radioligand

45
Q

ligand-binding assay graph

A

amount of radioligand plotted against log(concentration of competing ligand)

46
Q

how do you calculate IC50

A

read off 50% of amount of ligand and go across to where it hits line
will give you logIC50 as value

47
Q

process of ligand binding assay

A

measure the binding of a labelled ligand (with a known conc)
in presence of various concentrations of unlabelled ligands

48
Q

epigenetics

A

the study of heritable changes in gene expression that do not chnage the underlying DNA sequence

chnage in phenotype not genotype

49
Q

types of epigenetic changes

A

DNA methylation
histone modification
non-coding DNA gene silencing

50
Q

causes of epigenetic modification

A

naturally occuring
influenced by age/environment
disease
mutations

51
Q

how do you test for dna methylation

A

bisulphate sequencing
compare to untreated sequence
unmethylated cytosine will be converted to uracil

52
Q

how do you test for histone modifications

A

chromatin immunoprecipitation
finds DNA regions associated with proteins
Next Gen Seq techniques

53
Q

siRNA =

A

small interfering RNA

54
Q

effects of siRNA

A

binds to mRNA
causes degradation of mRNA
reduced gene expression

55
Q

uses of siRNA

A

treatment of parkinsons

knock down gene encoding a-synuclein

56
Q

process of siRNA

A 
dsRNA
DNA cleaved by dicer to form siRNA
formation of RISC complex
one strand is degraded
siRNA forms complex with mRNA
RISC cleaves mRNA 
mRNA fragments further degraded by exonucleases
57
Q

deep brain stimulation

A

neurosurgical procedure that stimulates brain to treat parkinsons

58
Q

where is deep brain stimulation carried out

A

specific movement related regions of the brain

  • thalamus
  • globus pallidus
  • subthalamic nucleus
59
Q

process of deep brain stimulation

A 
electrodes implanted 
attached to pulse generator via wires
HFS stimulated to target area
neuro - electrical signals altered
symptoms decrease
60
Q

advantages of deep brain stimulation

A

non-destructive surgery - no part of brain is destroyed

effects are reversible

61
Q

MAO inhibitors

A

inhibit monoamine oxidase enzymes A and B

antidepressants

62
Q

effect of MAO inhibitors

A

prevent loss/degradation of noradrenaline, serotonin and dopamine
more neurotransmitter available to effect cells impacted by depression
mood improved
panic reduced

increase blood pressure

63
Q

tyramine metabolism

A

broken down in small intestine and liver by MAO A

64
Q

MAO A

A

gut

65
Q

MAO B

A

brain

66
Q

MAOs cheese effect

A

MAO inhibitors prevent breakdown of tyramine in gut
tyramine present in tissues
cause hypertension/stroke

67
Q

L-Dopa importance

A

increases dopamine in brain

dopamine cannot cross BBB

68
Q

why cant dopamine cross BBB

A

lipophilic

69
Q

peripheral dopa decarboxylase inhibitor

A

important so L-dopa not converted to dopamine in periphery

maintains concentration gradient

70
Q

dopa decarboxylase

A

breaks down L-dopa to dopamine once crossed BBB into brain

71
Q

uses of L-dopa

A

treat parkinsons disease

increase dopamine in brain following death of dopaminergic neurons

72
Q

COMT inhbitors

A

inihbit COMT enzyme

maintains concentration gradient between periphery and break

73
Q

COMT enzyme

A

breaks down L-dopa into non-dopamine stuff

74
Q

uses of COMT

A

controls symptoms between doses of L-dopa

reduces amount of L-dopa needed

75
Q

example of dopa decarboxylase inhibitor

A

carbidopa

76
Q

anticholinergics

A

block Ach binding

prevent activation of ACh receptors

77
Q

uses of anticholinergics

A

anaesthetics - produce paralysis

treat parkinsons to reduce tremours

78
Q

3 classes of anticholinergics

A

antimuscarinic
ganglionic
neuromuscular

79
Q

antimuscarinic anticholinergic

A

drug that blocks the activity of muscarinic Ach receptors

80
Q

ganglionic anticholinergic

A

durg that blocks ACh activity between pre and post-ganglionic receptors

81
Q

neuromuscular anticholinergic

A

blocks Ach activity at NMJ

82
Q

anti-psychotic drugs

A

use dopaminergic pathways to decrease dopamine concentration
typical or atypical

83
Q

uses of anti-psychotics

A

treat symptoms of schizophrenia

sedatives

84
Q

typical antipsychotic - 1st generation

A

D2 receptor antagonism-
blocks D2 receptors in meso-limbic and meso-cortical pathways
EPS symptoms
high potency or low potency

85
Q

EPS

A

extra pyramidal symptoms

e..g acute dyskinesia

86
Q

high potency typical anti-psychotic

A

slightly anticholinergic
minimally sedating
more weight gain
high risk EPS

87
Q

low potency typical antipsychotic

A

more sedating
more anticholinergic
low risk EPS

88
Q

atypical antipsychotic - 2nd gen

A

block serotonin receptors as well as dopamine receptor s
less severe side effects
less EPS

DDT (12 decks)

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