Topic 3 Flashcards

1
Q

Parts of NT system

A

1) Metabolic enzyme that synthesis the NT
2) Vesicle transporter to package the NT
3) The receptor that they bind to
4) The transporter protein that is involved in their re-uptake
5) metabolic enzyme that degrades them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Glutamate

A

Excitaory - causes cation channels to open letting cations in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

GABA

A

Inhibitory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Neuropharmacology

A

Drugs that alter the functions of the nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Enhancer

A

doesn’t directly bind to receptor but enhances it’s affects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Antagonists

A

Binds directly to receptor and blocks it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Agonist

A

Mimics NT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ionotropic receptor

A

embedded in the membrane
Let ions pass through
NT attaches to the outside which will either activate or deactivate it
generally fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ionotropic receptor structure

A

5 subunits of protein are put together to form a pentameric structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Metabotropic receptor

A

uses G-proteins as a second messenger system to activate channel/ response
slower, but longer lasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

G-protein subunits

A

G-alpha
G-beta,gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Activation of G-protein

A

1) G-protein is freely floating around
2) NT binds to the Metabotropic receptor, then G-protein binds, then GDP turns into GTP
3) G -protein subunits split and do their own thing
4) GTP is phosphorylated back to GDP
5) Subunits reattach at messenger system stops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Push pull mechanism

A

push - message flows down system
pull - message stops and G-protein tells everybody else to stop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Signal amplification

A

When multiple G-proteins attach and amplify the signal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Convergence

A

One NT activates more than one receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Divergence

A

Different NT can act on the same receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Glutamate

A

Amino Acid NT
Inotropic and metabotropic
cognitive function, synaptic plasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Glutamate inoptropic receptors

A

AMPA
NDMA
Kainate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Glutamate Metabotropic receptors

A

mGluRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

AMPA and NMDA

A

often found together and working together, NDMA will often experience a magnesium block at -65mv
therefore AMPA has to do all the work

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

GABA

A

synthesised from glutamate
by GAD (GLUTAMIC ACID DECARBOXYLASE)
Action is terminated by takeup by GABA transporter and is then degraded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

GABA receptors

A

Alpha - ionotropic
Beta - metabotropic - Ggamma binds to k+ channels - lowering membrane making it harder for an action potential to occur

23
Q

Benzodiazapene (valium)

A

Anxiety Medication
increase the frequency of GABAalpha receptors opening

24
Q

Barbituates

A

Act on GABAalpha receptors - keep gates open for longer
sedating affect

25
Q

Glycine

A

only inotropic
inhibitory
caffeine is an antagonist for it
abundant in brainstem and spinal cord

26
Q

Acetylcholine

A

Ach
neuromuscular junction
Activates muscle contraction
Excitatory
synthesized from Acetyl CoA and choline
degraded by acetylcholinesterase in synaptic cleft - reuptake of choline is the limiting reagent

27
Q

ACh Receptors

A

Nicotinic
ionotropic
activation causes skeletal muscle to contract
Curare is antagonist for this

Muscaronic
Metabotropic
Found in the heart
Activates heart, GIT, bladder
Atropine is an antagonist

28
Q

Acetylcholinesterase Inhibitor

A

Leaves ACh in the synaptic cleft for longer as it prevents it degradation

29
Q

Reversible AChE inhibtiors

A

Neostigmine - treat Mystania Gravis and Alzheimers

30
Q

Irreversible AChE Inhibitors

A

not clinically used
organophosphates, pesticides

31
Q

Catecholamines

A

Dopamine, noradrenaline, adrenaline
movement, mood regulation, attention
all synthesised from tyrosine
hydroxylase converts tyrosine to dopamine
dopamine hydroxylase then onverts it to noradredaline

32
Q

Catecholamine Receptors

A

All metabortropic

33
Q

Termination of catecholamines

A

Dopamine is taken up by dopamine transport
noradrenaline - taken up by noradredaline transporter
both are then degraded in presynaptic terminal

34
Q

Serotonin

A

Acts only on metabotropic receptors
AKA 5HT
comes from the amino acid tryptophan
tryptophan - hydroxylase- 5HT - decarboxylase to Serotonin
Mood, sleep, emotional behaviour
terminated by re-uptake of serotonin transporter

35
Q

SSRI

A

Selective Serotonin reuptake inhibitor
stops the reuptake of serotonin so it stays in synaptic cleft for longer
used to treat depression

36
Q

Endocannaboids

A

Retrograde messenger
go from post synaptic to pre synaptic
bind to their own cannaboid receptors but can affect GABA, glycine and glutamate receptors

37
Q

Myasthina Gravis

A

Autoimmune disease
affects skeletal muscle
B-cells bind to nictonic recepetors, preventing ACh from binding

38
Q

MG symtoms

A

Fatigue that worsens throughout the day or with exercise
droopy eyelids (affects extra occular muscle)
weaker doing repetitive movements
muscle weakness
tiredness that improves with rest

39
Q

Types of MG

A

ocular MG - only affects the extraocular eye muscles

Generalised MG

40
Q

MG Diagnosis

A

Tensilon test - given ultra short acting AChE to see if it stops the droopy eyes
Nerve conduction
Anitbody test

41
Q

MG treatment and prognosis

A

AchE inhibtors
corticosteroids
plasmaphoresis

42
Q

Hyperklexia

A

Exaggerated startle response
all muscles stiffen then the person faints but remains consciousness
drop seizures
caused by a gentic mutation in the glycine receptor

43
Q

Hyperklexia Treatment

A

no cure
give benzodiazapene

44
Q

Classifying Sezuires

A

1) generalised or focal
2) if patient still has awareness
3) Degree of motor involvment

45
Q

Focal seziure

A

Only affects one portion of the brain
whatever portion is affect the symptoms will manifest accordingly

two types
focal aware
focal dyscognitive - loss of awareness

46
Q

Genralised

A

When multiple areas of the brain are affected

47
Q

Tonic - clonic

A

Tonic - all muscles contract and patient fall with teeth clenched and eyes open
clonic - convulsions

48
Q

Absence Seizure

A

Short period of impaired conscouiness
zoned out

49
Q

Atonic seizure

A

All muscles contract and the patient falls to the ground but they still fully aware

50
Q

Myoclonic

A

Myo - muscle
clonic - contract
muscle contraction / jerks can be one muscle or multiple
patient is fully aware

51
Q

Status Epilepticus

A

a series of seizure where there is no regain of consciousness

52
Q

Epilepsy Diagnosis

A

EEG
Medical History
MRI
genetic testing

53
Q

Treatment

A

Phenytoin - stops repetitive activation of sodium channels
Valproate - unclear mechanism of action