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Years 1+2 > S3C7 (2.0) > Flashcards

S3C7 (2.0) Flashcards

1
Q

What is SPECT scanning?

A 
Three-dimensional (tomographic) images of the distribution of radioactive tracer molecules
Gamma emitting radioisotope
Cheap
Convenient
Poor spatial resolution
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2
Q

What is PET scanning?

A

Positron emitting radioisotopes
Expensive
More effort
Good spatial resolution

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3
Q

What is CT scanning?

A 
X-rays round body
Quick
Cheap
Convenient
Involves radiation
Poor quality
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4
Q

What is MRI scanning?

A 
Magnetic donut
Slow
Expensive
More effort
No radiation
High quality
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5
Q

What is the epidemiology of parkinsons?

A

Male predominance
Prevalence increases with age
Onset ~60 yo

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6
Q

What is parkinsonism?

A

A syndrome featuring bradykinesia and either resting tremor or rigidity (or both)

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7
Q

What are the risk factors for Parkinson’s?

A 
Familial history - 10-15% cases
Environmental factors - e.g. Exposure to manganese
Diet/ metabolism
	Low levels Vit D
	High iron intake
	Obesity
Structural damage
	History of traumatic brain damage
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8
Q

What medication can cause secondary parkinsonism?

A 
Familial history - 10-15% cases
Environmental factors 
	E.g. Exposure to manganese
	Diet/ metabolism
	Low levels Vit D
	High iron intake
	Obesity
Structural damage
	History of traumatic brain damage
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9
Q

What metabolic disorders can cause parkinsonism?

A

Wilson disease - an autosomal recessive metabolic disorder of copper (due to ATP7B gene mutation) in which both impaired binding to its transporter protein (ceruloplasmin) and biliary excretion increase free serum copper, leading to accumulation in the body

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10
Q

What is the pathophysiology of parkinsons?

A

Progressive dopaminergic neuron degeneration in the substantia nigra and the locus coeruleus
Dopamine deficiency at the respective receptors of the striatum with interrupted transmission to the thalamus and motor cortex

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11
Q

What causes the depressive symptoms of parkinsons?

A

Serotonin and noradrenaline depletion (in the Raphe nuclei)

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12
Q

What causes the dyskinesia in parkinsons?

A

Acetylcholine surplus in nucleus basalis of Meynert

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13
Q

What causes lewy bodies ?

A

Aggregates of misfolded α-synuclein and hyaline eosinophilic globules

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14
Q

What is the pathogenesis of cell death?

A 
Oxidative stress
Intracellular calcium accumulation with excitotoxicity
Inflammation
Mitochondrial dysfunction (apoptosis)
Proteolytic stress
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15
Q

What are the clinical features of parkinson’s?

A

Unilateral onset with persistently asymmetrical course but may progress on the contralateral side
Bradykinesia/ akinesia
Resting tremor (4-6Hz)
Rigidity

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16
Q

What frequency is the resting tremor?

A

4-6Hz

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17
Q

What is the tremor like in parkinsons?

A 
Pill rolling tremor that subsides with voluntary movements but increases with stress
Typical in hands
May involve
	Legs
	Jaw
	Lips
	Tongue
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18
Q

What is bradydiadochokinesia?

A

Alternating antagonistic movements are conducted unusually slowly

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19
Q

What is rigidity?

A

Increased and persistent resistance to passive joint movement that is independent of speed of movement

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20
Q

What is the froment maneuver?

A

Facilitates the evaluation of rigidity, especially in early stages

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21
Q

What is cogwheel rigidity?

A

Most likely caused by the overlay of increased muscle tonus and tremor in PD patients
Muscles in an extremity give way in successive jerks when passively move

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22
Q

What is the parkinsonian gait?

A

Shuffling gait with quickened and shortened steps

5-8 extra steps to turn around

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23
Q

What is the glabellar reflex?

A

Primitive reflex elicited by tapping of the glabella, the area between the eyebrows, causing the subject to close his or her eyes
positive in PD patients and babies

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24
Q

What causes bradykinesia?

A

Increased inhibitory output to central pattern generators in brainstem
Increased inhibitory output to thalamus and motor cortex
Abnormal 20 Hz (β band) oscillations in basal ganglia circuit

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25
Q

What causes peripheral rigidity?

A

Reduced inhibition from type Ib fibres
Overactive type II fibres
Increased activity due to peripheral stimulation

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26
Q

What causes central rigidity?

A

Altered activity in GABA and Ach interneurones
Altered inhibition in indirect pathway
Increased responsiveness of STN/GPi firing to peripheral stimulation

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27
Q

What % of PD patients do not have a tremor?

A

30%

28
Q

What drugs can be used to treat PD?

A

Levodopa
Dopamine Agonists
MAO-B Inhibitors

29
Q

What surgery can be used for PD?

A

Bilateral subthalamic nucleus (STN) or globus pallidus interna (GPi) stimulation may be used.

30
Q

What is co-beneldopa made of?

A

Levodopa

Benserazide

31
Q

What is benserazide?

A

a peripherally-acting DOPA decarboxylase inhibitor.
This is combined with levodopa to reduce peripheral side effects.
Benserazide cannot cross the BBB and so doesn’t prevent the effects of levodopa in the brain.

32
Q

What is Levodopa?

A

A precursor of dopamine

Crosses BBB and is decarboxylated into dopamine

33
Q

What are the two main side effects of L-dopa?

A

Involuntary writhing movements (dyskinesia)

Rapid fluctuations in clinical state

34
Q

What is selegiline?

A

MAO-B inhibitor
Inhibition of MAO-B protects dopamine from extraneuronal degradation.
Combination of selegiline and levodopa is more effective than levodopa alone in relieving symptoms and prolonging life.

35
Q

What is the striatum comprised of?

A 
Caudate and putamen in primates
Medium spiny neurones
	96% striatal neurones
	GABAergic +/- neuropeptides
Interneurons
	GABAergic
	Cholinergic (large aspiny neurones)
36
Q

What neurotransmitter is used in the corticostriatal pathway?

A

Glutamate

37
Q

What is the role of the

direct dopamine pathway?

A

D1 receptor
Dynorphin precursor (PPE-B)
Facilitation of desired movements

38
Q

What is the role of the indirect dopamine pathway?

A

D2 receptors
Enkephalin precursor (PPE-A)
Inhibition of unwanted movements

39
Q

Which dopamine pathway prefers tonic dopamine release?

A

D2R

40
Q

Which dopamine pathway prefers phasic dopamine release?

A

D1R

41
Q

Where is ACh found?

A 
NMJ
Preganglionic autonomic synapses
Postganglionic parasympathetic synapses
Various sites in CNS
	Basal nucleus of Meynert
Ganglia of visceral motor system
42
Q

How is ACh made synthesised?

A

Synthesised in nerve terminals from acetyl CoA and choline

Catalysed by choline acetyltransferase

43
Q

How is ACh broken down?

A

hydrolysed by acetylcholinesterase at the synpatic cleft into acetate and choline
Choline is taken up into cholinergic neurons by a high-affinity Na+/choline transporter

44
Q

What are the 2 types of ACh receptor?

A

Nicotinic

Muscarinic

45
Q

What is a nicotinic ACh receptor?

A

Nonselective cation channels
Generate excitatory postsynaptic responses
Found at ganglion between pre and postganglionic nerve

46
Q

What is a muscarinic ACh receptor?

A

Metabotropic
Mediate most of the effects of Ach in the brain
Highly expressed in the striatum
Found at the presynaptic membranes after the postganglionic nerve

47
Q

Can glutamate cross the BBB?

A

Nope

48
Q

What can glutamate be synthesised from?

A

Glucose

Glutamine

49
Q

How is glutamate synthesised from glutamine?

A

Glutamine is released by glial cells
Taken up into presynaptic terminals
Metabolised into glutamate by glutaminase

50
Q

What happens to glutamate once its been released?

A

Released glutamate is taken up by glial cells and converted into glutamine
Enzyme - glutamine synthetase
Glutamine is then transported out of glial cells and into nerve terminals

51
Q

What generate an excitatory response with glutamate?

A

All ionotropic glutamate receptors (NMDA, AMPA, kainite)

Allow passage of Na+, K+ and Ca2+

52
Q

What does Ca2+ concentration act as?

A

A second messenger to activate intracellular signalling cascades

53
Q

What blocks the NMDA receptor channel when hyperpolarised?

A

Mg2+

54
Q

What is required to push Mg2+ out of the NMDA pore?

A

Depolarisation and glycine

55
Q

What is the difference is synaptic currents between NMDA and AMPA?

A

Synpatic currents produced by NMDA receptors are slower and longer-lasting that AMPA/kainate receptors

56
Q

What does activation of metabotropic glutamate receptors mean?

A

Leads to inhibition of postsynaptic Ca2+ and Na+ channels

Cause slower postsynaptic responses that can either in crease or decrease the excitability of postsynaptic cells

57
Q

Where is glycine abundant?

A

The spinal cord grey matter of the ventral horn

58
Q

What is GABA formed from?

A

Glutamate

59
Q

Where is glycine abundant?

A

The nigrostriatal system

60
Q

What catalyses the conversion of glutamate to GABA?

A

Glutamic acid decarboxylase - found almost exclusively in GABAergic neurons

61
Q

What is most GABA converted into?

A

Succinate by GABA transaminase

62
Q

What are the 3 postsynaptic GABA receptors?

A

GABAa - ionotropic
GABAb - metabotropic
GABAc - ionotropic

63
Q

Where can GABA-c receptors be found?

A

Retina

64
Q

What happens during ionotropic GABA receptor activation?

A

GABA binds between the α and β subunits, causing Cl- ions to flow into the neuron, leading to a decreased chance of action potential (hyperpolarisation)

65
Q

What happens when GABA-b receptors are activated?

A

Due to the activation of K+ channels and inhibition of Ca2+ channels which tends to hyperpolarise postsynaptic cells

66
Q

What is dopamine?

A

A catecholamine dervied from dopa

Produced by action of DOPA decarboxylase on L-DOPA

67
Q

What happens once dopamine is released?

A

Once released, dopamine acts exclusively by activating G-protein-coupled receptors.
Most dopamine receptor subtypes act by either activating or inhibiting adenylyl cyclase.
Activation and inhibition of these receptors generally contribute to complex behaviours, depending on the receptor subtype being activated.

Years 1+2 (21 decks)

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