PBL 1 Mr Body Flashcards

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1
Q

define resting tremor

A

Involuntary, rhythmic muscle contractions causing oscillational movements at rest

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2
Q

what is Madopar?

A

Tablet containing levodopa and benserazide

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3
Q

What is cogwheel rigidity?

A

Combination of lead-pipe rigidity and tremor

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4
Q

What is lead-pipe rigidity?

A

Sustained resistance to passive movement due to increased muscle tone

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5
Q

What is clasp-knife reflex?

A

Rapid decrease in resistance to passive movement

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6
Q

What is micrographia?

A

Patient’s writing becomes smaller and more difficult to read - associated with neurodegenerative disease of basal ganglia such as PD

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7
Q

What is rotigotine

A

dopamine agonist

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8
Q

What is selegiline

A

MAOb inhibitor

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9
Q

What forms the dorsal striatum?

A

Caudate nucleus

Putamen

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10
Q

What are the input nuclei

A

Dorsal Striatum

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11
Q

What are neurones of the basal ganglia?

A

Medium spiny

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12
Q

What is the ventral striatum?

A

Accumbens nucleus

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13
Q

What do the putamen and globus pallidus together form?

A

Lentiform nucleus

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14
Q

What does the caudate nucleus curve around?

A

Lateral wall of lateral ventricles

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15
Q

Where does caudate nucleus end?

A

Temporal lobe

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16
Q

What separates the putamen from caudate nucleus?

A

Grey matter

Internal capsule

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17
Q

What is the output nuclei of the basal ganglia?

A

Globus pallidus
Substantia nigra pars reticula
subthalamic nuclei

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18
Q

Where do the output nuclei project out to?

A

VA and VL regions of the thalamus

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19
Q

What makes up the substantia nigra?

A

Pars compacta

Pars reticula

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20
Q

What is the pars compacta?

A

Cells that produce dopamine

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21
Q

Where do neurones in pars compacta project to?

A

Basal ganglia

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22
Q

What happens when pars compacta cells degenerate?

A

Parkinsons Disease

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23
Q

Where does Pars reticula receive input from?

A

Basal ganglia

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24
Q

Where does pars reticula project out to?

A

Motor thalamus

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25
Q

The pars reticula neurones are what?

A

GABA inhibitory

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26
Q

What does pars reticula do?

A

Control of head and eye movements

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27
Q

What supplies basal ganglia?

A

Striate arteries from the M1 branch of the MCA

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28
Q

What does basal ganglia control?

A

Initiation and stopping of movements

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29
Q

What are the 3 neurotransmitters?

A

Glutamate
GABA
Dopamine

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30
Q

Where is glutamate used?

A

Corticostriatal pathway

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31
Q

Where is GABA used?

A

Striato-pallidal pathway

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32
Q

Where is dopamine used?

A

Nigrostriatal pathway

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33
Q

Where does the cortex project neurones to?

A

Striatum

34
Q

Whre does the striatum project neurones to?

A

GP

35
Q

Where does substantia nigra pars compacta project neurones to?

A

Striatum

36
Q

What converts L-tyrosine into DOPA

A

Tyrosine hydroxylase

37
Q

What is L-tyrosine converted into?

A

DOPA

38
Q

What is DOPA converted into?

A

Dopamine

39
Q

What converts DOPA into dopamine?

A

DOPA decarboxylase

40
Q

What breaks down dopamine into DOPAC?

A

MAO

41
Q

What converts DOPAC into homovanillic acid?

A

COMT

42
Q

What is DOPAC converted into?

A

Homovanillic acid

43
Q

What are the two main dopamine receptors?

A

D1 and D2

44
Q

Where are D1 and D2 receptors found?

A

GABAergic neurones in basal ganglia

45
Q

What does D1 do?

A

Increase function of GABAergic neurones, increased inhibition

46
Q

What does D2 do?

A

Decreases function of GABAergic neurones, decreased inhibition

47
Q

What are some signs and symptoms of Parkinson’s Disease?

A
Tremor at rest
Rigidity
Akinesia
Postural instability
Olfactory dysfunction
Sleep disturbances
Depression
Cognitive dementia
48
Q

What is Parkinson’s Disease?

A

Neurodegenerative disease of the CNS affecting motor abilities

49
Q

What is Parkinson’s Disease caused by?

A

Lack of dopaminergic cells in SNpc

50
Q

What does loss of dopamine cause to pathways?

A

Direct pathway inhibition

Indirect pathway activation

51
Q

Why is there a loss of dopaminergic cells?

A

Production of the neurotoxin MPP+

52
Q

What is MPP+ made from?

A

MPTP

53
Q

What makes MPP+?

A

MAOb

54
Q

What does MPP+ do?

A

Disrupt oxidative phosphorylation -> production of free radicals

55
Q

What is a classic characteristic of PD?

A

Lewy bodies

56
Q

What are Lewy body?

A

Aggregation of proteins in nerve cells

57
Q

What are lewy bodies made of?

A

Alpha-synuclein

58
Q

What is a risk factor for PD?

A

Mutation in Alpha-synuclein (PARK1- 4+SNCA gene)

59
Q

How is PD diagnosed?

A

History and signs and symptoms

60
Q

What drugs can be used for PD?

A

MAOb inhibitors
Dopamine receptor Agonist
L-DOPA
Anti-cholinergic drugs

61
Q

What is a MAOb inhibitor?

A

Prevents breakdown of dopamine

62
Q

What is used in catabolism of dopamine?

A

Monoamine oxidase

63
Q

Give exaples of MAOb inhibitors

A

Selegiline

Rasagiline

64
Q

What side effects of MAOb inhibitors?

A

No cheese or wine
Headache
Aching joints
Depression

65
Q

Give examples of Dopamine receptor agonists

A
Rotigotine
Pergolide
Cabergoline
Bromocriptine
Apomorphine
66
Q

Side effects of dopamine receptor agonists?

A

Drowsiness
Nausea
Psychosis
Constipation

67
Q

Why give L-DOPA instead of giving dopamine?

A

L-DOPA can pass BBB

68
Q

What are complications of long term used of L-DOPA

A

On/off phenomenon - unpredictable fluctuation of motor ability
hallucinations
Pain/tingling/autonomic dysfunction
Dyskinesia

69
Q

What is the bioavailability of L-dopa used alone?

A

5-10%

70
Q

What is benserazide?

A

Peripheral L-DOPA decarbxylase inhibitor which cannot pass the BBB, so allows more dopamine to be produced in the brain

71
Q

What else can L-DOPA be used with?

A

Tolcapone

Entacapone

72
Q

What is tolcapone and entacapone?

A

COMT inhibitor

73
Q

Why do anti-cholinergic drugs work?

A

Dopamine inhibits activity of Ach neurones so therefore there is hyperactivity of cholinergic fibres

74
Q

Give examples of anti-cholinergic drugs?

A

Amantadine
Benzhexol
Orphenadrine
Benztropine

75
Q

What does Amantadine do?

A

Prevents dopamine reuptake - is an NMDA and ACh receptor antagonist

76
Q

Give side effects of anti-cholinergic drugs

A
Dry mouth
Blurred vision
Confusion
Constipation
Memory Defects
77
Q

What surgical options are there for PD?

A

Deep brain stimulation of subthalamic nuclei
Pallidotomy
Destruction of GP to control dyskinesia

78
Q

What is Huntington’s Disease?

A

Loss of GABAergic cells when striatum degenerates

79
Q

What happens when striatum degenerates?

A

Reduced indirect pathway - hyperkinesia

80
Q

How is huntington’s disease inherited?

A

Autosomal dominant

81
Q

What chromosome gene does huntington’s affect?

A

4