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ÉRS And NS > NS > Flashcards

NS Flashcards

1
Q

Structure of Na VGC

A

Consist of alpha and beta subunits
Alpha subunit consist of 4 domain and each domain contains S1-S6 (six segments) with each domain linked by an amino acid chain

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2
Q

Function of beta subunits in Na VGC

A

Fine tuning properties on channels - it helps channel inactivation to occur faster

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3
Q

Can the Na VGC inactivate on its own With only alpha subunits?

A

Yes, beta subunits accelerate channel inactivation

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4
Q

In the ball and chain model for Na VGCs, whereabouts is this chain in the channel?

A

The amino acid chain between domain III and IV

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5
Q

S4 domain of the Na VGC does what to activate channel

A

Move towards the EXtracellulat side of the membrane as it is positively charged

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6
Q

Size difference between Na and K VGC

A

Na VGC is 4x larger than K+ VGC

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7
Q

How do we inactivate S type K channels

A

Delete the first 20 aminoacid at N terminal

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8
Q

Function of AKC is to

A

Delay onset and frequency of AP to allow variability in AP pattern

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9
Q

When does AKC open and how

A

AKC opens during depolarisation phase and closes later in the same phase as MP increases.
It requires hyperpilarisation in order to be activated again hence often fire after repeated firing or after inhibitory neurones activation

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10
Q

AKC is coded by

A

Shaker B

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11
Q

Structure of K delayed channels

A

4 alpha subunits consisting of 1 domain each come together without any physical linkage

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12
Q

TTX blocks

A

Na VGCs

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13
Q

TEA blocks

A

K+ VGC

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14
Q

APV blocks

A

NMDA channels

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15
Q

What blocks both Na and K channels

A

Lidocaine

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16
Q

Where is the primary cortex located

A

In the precentral gyrus - area 4

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17
Q

What Cortex are responsible for planning movements

A

Supplementary and pre-motor cortex in area 6

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18
Q

What’s a basal ganglia

A

A functional unit in the brain that consist of a group of associated subcortical nuclei

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19
Q

What’s the function of BG

A

Integrates sensory and motor input from cortex and modulate response via the promotors cortex via ventrolateral thalamus
Also selects and initiate voluntary movement

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20
Q

Disorders of basal ganglia is associated with

A

The inability to suppress unwanted movements - often present with dyskinesia

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21
Q

df. Of dyskinesia

A

Unwanted uncoordinated involuntary movements

Diminished voluntary movement

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22
Q

Pathological cause of Parkinson’s

A

Degeneration of dopaminergic neurones in the Nigro-striatal pathway which leads to the overactivaion of the SNc/GPi thereby constantly inhibiting the ventrolateral thalamus

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23
Q

Does patient with Parkinson’s always have uncontrolled movement?

A

No, if they are doing things or moving, the disinhibition of thalamus is released and hence the motor signals will override the default control

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24
Q

The limbic region includes

A

Anything that is associated with emotion regulation

  • hippocampus
  • amygdala
  • neocortex
  • thalamus (ATN)
  • hypothalamus (PVN)
  • ant. Pit.
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25
Q

Why do we need emotion

A

To communicate better

Helps learning and memory retention by giving relavence to the memory

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26
Q

The ANS symptoms exhibited in anxiety patients is due to

A

Increase activity of the hypothalamus as it is the centre of ANS control

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27
Q

Disease / disorders of the Amgdala

A

Kluver-Bucy syndrome
- range of behavioural abnormalities mostly characterised by decease in fear and lack of emotions
Urbach-Wiethe disease
-natural degeneration of amgdala
-patients unable to recognise facial expression
-sometimes patients can get TLE

28
Q

what part of brain is related to the sense of pleasure

A

The orbitofrontal cortex

29
Q

Mesolithic pathway

A

Runs via the medial forebrain bundle Via the VTA (ventral tegmemtal area ) to the nucleus accumbens and limbic area n the midbrain

30
Q

What is the amgdala associated with

A

Fear and aggression

31
Q

Patients with PTSD shows increase activity in the amygdala. Apart from SSRIs, what other methods can we use to treat these patients (surgical procedure)

A

Deep brain stimulation or removal of the amygdala

32
Q

Drugs for treating anxiety

A
  • think calming
  • BDZ, 5-HT1A partial agonist (Buspirone)
  • SSRI, a AR antagonist (symptomatic relief
33
Q

The use of BDZ along with ethanol and opioids put patient in risk of

A

Severe respiratory depression
Unconsciousness (excessive sedation)
And potentially coma snd death

34
Q

What happens to the hypothalamus if patient has chronic depression

A

Volume (size) of hypothalamus decreases

But reversible with use of drug

35
Q

How does psychotherapy helps with anxiety or depression

A

Alter neurotransmitters transmission
Alter neuronal circuitry via change in synaptic plasticity
Desensitisation/habituation if phobic anxiety

36
Q

Structure of GABAa receptor

A

5subunits - ABAB-gamma
Channel pore allows Cl- influx
GABA binding site is between AB whilst BDZ allosteric binding site is at A-gamma

37
Q

Is depression or mood or thought disorder

A

Depression is a mood disorder

Thought disorder is the disorder of the mind - hence refer to psychosis such as schizophrenia

38
Q

Definition of anxiety

A

An inappropriate manefiststion of fear response to a stressor which can be present or absent

39
Q

Drugs treatment for depression

A
  • atypical depressing man invites SIRI for Tea
  • atypical neuroleptic
  • MAOI
  • SSRI
  • TCA
40
Q

Phenelzine is what type or class of drug

A

Non selective MAOI that blocks breakdown of Monoamine in mitochondria
Increase intracrllulwr and intrasynaptic monoamine levels

41
Q

TCA such as amitriptyline and imipramine MoA and s/e

A

They are dirty drugs
Mainly block reuptake of 5-HT and NA
But because they are dirty drugs - give sedative effect (H1R antagnism

42
Q

Fluroxetine and paroxetine are what class of drugs

A

SSRIS

43
Q

Visual input travel up which fibre to the cerebellum

A

Climbing fibre

44
Q

Reserpine, an neuroleptic that is often used as an depressant/hypotensive agent works by

A

Blocking presynaptic Mg/ATP dependent transport of amines from being packaged into vesicles
-deplete NA levels

45
Q

What is the basis of learning and memory

A

LTP - the modification of synaptic transmission and connection

46
Q

Potentiarion of the cell requires

A

Strong activation of synapses and synchronised firing of neurones

47
Q

NMDA is a ________________ receptor that only opens when _______?

A

NMDA is a coincidence receptor that only opens when postsynaptic membrane depolarises in response to presynaptic firing

48
Q

Process of LTP

A

Glutamate release and bind to both AMPA and NMDA receptor. However NMDA is blocked due to Mg+. The AMPA opening allows Ca/Na influx and K+ efflux. Further depolarisation of membrane results in repel of the Mg which opens up NMDA, allowing further depolarisation. Increase [Ca] cause activation of CAMKII (which is activated by CA-CAM). This will Pi AMPA which increase Na conductance, further depolarising membrane. Also drives gene transcription of more AMPA for insertion - mediated by SNARE. Ca also trigger retrograde signals which further stimulate presynaptic membrane, enhance synapse via neurotrophin release( BDNF)

49
Q

How does LTD occur

A

If Ca influx is slow, it will activate Ca dependent dephosphorylation cascade which results in decreased signalling in post synaptic membrane and hence decrease insertion of AMPA

50
Q

Plaques is formed by aggregation of

A

APP (amyloid precursor protein) that is important in neuronal repair and growth

51
Q

What are sutures

A

Immovable joints in the skull (fibrous joints)

52
Q

The sutures have zig zag patterns, what do they do

A

For stabilisation of bones
Hard to dislocate
The only way to break is to crush the bone

53
Q

3 sutures

A

Saggital
Coronal
Lambdoid (parieto-occipital)

54
Q

Where is the Calvaria

A

Top of skull bone above orbital bone (eye socket)

55
Q

Middle cranial fossa contains a big hole where the brain stem passes through, what is that called

A

Foramen magnum

56
Q

Technically the skull is composed of which two main compartment

A

Skull and the mandible bone connected by sphenoid bone

57
Q

What does the subarachnoid space contain

A

Blood vessels
CSF
Nerves
Arachnoid granulation where CSF drains into superior saggital sinuses (in between the two dura mater later

58
Q

Why do we need delayed AP firing

A

1) distinguish info from one stimuli from another
2) to generate patterns that allows complex behaviour
3) to hold back excitatory response
- protective sense
- can cause seizure/epilepsy if over fire

59
Q

Flumazenil is what type of drug

A

Competitive antagonist of BDZ

Short acting

60
Q

Barbiturates and BDZ increases what properties of the GABA Channels

A

Both barbiturates and BDZ binds to the GABA channel at dif allosteric sites
Barbiturates increases the duration of channel opening whilst BDZ increase GABA affinity thereby affecting the FREQency of channel opening

61
Q

Lorazepam is amnestic and usually used for what Tx

A

Hypnotic drug for sleeping

- short acting agents

62
Q

TCA drugs MoA

A

Serotonin dopamine reuptake inhibitor but also inhibit receptors such as H1R, mAChR causing serious S/E

63
Q

SSRI MoA

A 
Block SERT (5HT reuptake) 
More selective
64
Q

UMN lesion results in

A

Movement deficit (not quite muscles)
Muscle wasting due to lack of use/disuse
Hypertonicity in muscles (spasticity)
Positive banbinski sign (abnormal > 1 yr)

65
Q

Banbinski sign only exist normally in healthy babies under 1yr
Why is that

A

Corticospinal cord not fully developed so reflex will overpower the motor control

66
Q

LMN lesion will cause

A

Individual/groups of muscles tonne affected
Pronounced Muscle wasting/atrophy
Flaccid/hypotonic muscles

67
Q

Levetiracetam MoA

A

Block SV2A on vesicular membrane to inhibit release of excitatory NTR
Anticonvulsant

ÉRS And NS (2 decks)

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