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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
basal ganglia
group of nuclei at base of forebrain influence motor cortex via direct/indirect pathways through thalamus make/prevent movement
26
what are the components of the basal ganglia
``` striatum globus pallidus caudate nucleus subthalamic nucleus substantia nigra ```
27
where does the striatum (basal gnaglia) receive input signals from
thalamus | cortex
28
outline mechanism of direct pathway
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
29
receptors in direct pathway
D1
30
effect of dopamine on direct pathway
binds to D1 recepors increases direct pathway stimulates movement
31
differences between indirect pathway and direct
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
32
outline mech of indirect pathwya
cortex excites striatum striatum inhibits globus pallidus external inhibits subthalamic nucleus excites globus pallidus internal and substantia nigra
33
receptors for dopamine in indirect pathway
D2
34
anticipation
as a genetic disorder is passed on each generation, the symptoms become more apparent earlier in life and often more severe
35
huntingtons disease
HTT gene trinucleotide repeat level of disorder depends on number of repeats
36
causes of protein misfolding
improper interactions - proteins stuck in intermediate/non-active state environmental condiitons - extreme temp/oxidative stress
37
effects of protein misfolding
protein can become toxic loss of normal function cause disease - proteopathies
38
examples of proteopathies
alzheimers | parkinsons
39
proteopathy
when protein misfolding causes disease prevented by chaperones common in proteins containnig amino acid sequence repeats
40
identification of protein misfolds
tagged with ubiquitin and sent to protesome for degradation
41
ligand binding assays
to determine presence of ligand-receptor complezes | relies on binding of ligand molecules to antibodies
42
uses of ligand binding assays
measure rate and extent of binding measure number of binding sites measure affinity/accessibility for various drugs
43
use of ligand binding assays detection of disease
schizophrenia identification
44
IC50
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
ligand-binding assay graph
amount of radioligand plotted against log(concentration of competing ligand)
46
how do you calculate IC50
read off 50% of amount of ligand and go across to where it hits line will give you logIC50 as value
47
process of ligand binding assay
measure the binding of a labelled ligand (with a known conc) in presence of various concentrations of unlabelled ligands
48
epigenetics
the study of heritable changes in gene expression that do not chnage the underlying DNA sequence chnage in phenotype not genotype
49
types of epigenetic changes
DNA methylation histone modification non-coding DNA gene silencing
50
causes of epigenetic modification
naturally occuring influenced by age/environment disease mutations
51
how do you test for dna methylation
bisulphate sequencing compare to untreated sequence unmethylated cytosine will be converted to uracil
52
how do you test for histone modifications
chromatin immunoprecipitation finds DNA regions associated with proteins Next Gen Seq techniques
53
siRNA =
small interfering RNA
54
effects of siRNA
binds to mRNA causes degradation of mRNA reduced gene expression
55
uses of siRNA
treatment of parkinsons | knock down gene encoding a-synuclein
56
process of siRNA
``` 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
deep brain stimulation
neurosurgical procedure that stimulates brain to treat parkinsons
58
where is deep brain stimulation carried out
specific movement related regions of the brain - thalamus - globus pallidus - subthalamic nucleus
59
process of deep brain stimulation
``` electrodes implanted attached to pulse generator via wires HFS stimulated to target area neuro - electrical signals altered symptoms decrease ```
60
advantages of deep brain stimulation
non-destructive surgery - no part of brain is destroyed | effects are reversible
61
MAO inhibitors
inhibit monoamine oxidase enzymes A and B | antidepressants
62
effect of MAO inhibitors
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
tyramine metabolism
broken down in small intestine and liver by MAO A
64
MAO A
gut
65
MAO B
brain
66
MAOs cheese effect
MAO inhibitors prevent breakdown of tyramine in gut tyramine present in tissues cause hypertension/stroke
67
L-Dopa importance
increases dopamine in brain | dopamine cannot cross BBB
68
why cant dopamine cross BBB
lipophilic
69
peripheral dopa decarboxylase inhibitor
important so L-dopa not converted to dopamine in periphery | maintains concentration gradient
70
dopa decarboxylase
breaks down L-dopa to dopamine once crossed BBB into brain
71
uses of L-dopa
treat parkinsons disease | increase dopamine in brain following death of dopaminergic neurons
72
COMT inhbitors
inihbit COMT enzyme | maintains concentration gradient between periphery and break
73
COMT enzyme
breaks down L-dopa into non-dopamine stuff
74
uses of COMT
controls symptoms between doses of L-dopa | reduces amount of L-dopa needed
75
example of dopa decarboxylase inhibitor
carbidopa
76
anticholinergics
block Ach binding | prevent activation of ACh receptors
77
uses of anticholinergics
anaesthetics - produce paralysis | treat parkinsons to reduce tremours
78
3 classes of anticholinergics
antimuscarinic ganglionic neuromuscular
79
antimuscarinic anticholinergic
drug that blocks the activity of muscarinic Ach receptors
80
ganglionic anticholinergic
durg that blocks ACh activity between pre and post-ganglionic receptors
81
neuromuscular anticholinergic
blocks Ach activity at NMJ
82
anti-psychotic drugs
use dopaminergic pathways to decrease dopamine concentration typical or atypical
83
uses of anti-psychotics
treat symptoms of schizophrenia | sedatives
84
typical antipsychotic - 1st generation
D2 receptor antagonism- blocks D2 receptors in meso-limbic and meso-cortical pathways EPS symptoms high potency or low potency
85
EPS
extra pyramidal symptoms e..g acute dyskinesia
86
high potency typical anti-psychotic
slightly anticholinergic minimally sedating more weight gain high risk EPS
87
low potency typical antipsychotic
more sedating more anticholinergic low risk EPS
88
atypical antipsychotic - 2nd gen
block serotonin receptors as well as dopamine receptor s less severe side effects less EPS

DDT (12 decks)

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