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Brain and Behaviour 2 PBL > PBL 1 > Flashcards

PBL 1 Flashcards

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1
Q

define mad-par

A

benserazide (Dopa decarboxylase inhibitor) and levodopa is contained inside it, it forms the drugs that make up antiparkinsons agents

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2
Q

define rotigotine

A

– this is a dopamine agonist used in Parkinson’s disease, can be used in a transdermal patch which is useful in the later stages of the disease

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3
Q

define selegilline

A

this is an MAO inhibition that works by slowing the breakdown of substances such as dopamine, noradrenaline and serotonin

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4
Q

define micrographic

A

this is the progression to progressively smaller handwriting, it is associated with neurodegenerative disorders of the basal ganglia

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5
Q

define vitamin E

A

vitamin that dissolves it fat, it is found in many foods including vegetable oils, cereals, meat, poultry, eggs, fruits, and vegetables – it can cause nerve problems

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6
Q

define cogwheel Rigidity

A

– this is muscular rigidity in which passive movements of the limbs causes a ratchet like start and stop movements through the range of motion of a joint

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7
Q

describe what the cause of Parkinson’s is due to

A
  • Due to loss of dopaminergic neurones in the substanita nigra pars compacta which usually project and innervate the caudate and putamen
  • 80% of dopamine neurones have to degenerate before the clinical symptoms manifest themselves
  • Causes a shift towards the indirect pathway
  • Shows both motor and non motor conditions
  • Associated with the SNCA gene which codes for protein alpha synuclein – this increase the risk of developing Parkinson’s significantly
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8
Q

describe the motor and non motor characteristics of Parkinson’s

A

Characteristics

  • Resting tremor
  • Slowness of movement (bradykinesia)
  • Muscular rigidity
  • Minimal facial movements

Non motor characterstics (usually precede motor functions by 12-15 years)

  • Olfactory dysfunction
  • Sleep disturbance
  • Depression
  • Autonomic dysfunction
  • Dementia (late phase)
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9
Q

describe the histology of Parkinson’s

A
  • Loss of dopaminergic cells in substantia nigra pars compacta
  • And presence in neurones of Lewy bodies ( these are intracellular formation that are enriched in the protein alpha-synuclein)
  • These Lewy bodies are also presence in other conditions such as dementia
  • There are also losses of cells throughout the nervous system
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10
Q

describe the drug Madopar

A
  • This is L dopa with a peripheral decarboxylase inhibitor (Benserazide) this prevents the conversion of L dopa to dopamine in the periphery which can cause nausea and vomiting, this means that L dopa is only converted to dopamine once past the blood brain barrier
  • L-dopa is converted to dopamine via dopa decarboxylase and this increases the concentration of dopamine present
  • Beneserazide inhibits the conversion of L dopa to dopamine in the periphery
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11
Q

describe L dopa and its side effects

A
  • After a few years use the efficacy of L dopa tends to wear off
  • The effects of the Parkinson’s comes back worse than before even with increased dose
  • This is an on off effect of L dopa where there is dramatic fluctuations in performance due to the intake of L dopa
  • In patients with this effect L dopa is combined with benserazide or carbidopa both peripherally acting dopa decarboxylases
  • Side effects include: nausea and vomiting, postural hypotension, psychosis, impuslve control disorders, excessive day-time sleepiness
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12
Q

describe dopamine agonists

A
  • These include ropinirole, pramipexole, rotigotine, pergolide, bromocriptine, cabergoline
  • Rotigotine - dopamine agonist which can be used as transdermal patch – important as the disease progresses and they can no longer swallow
  • Dopamine agonist usually less efficious than L dopa but they have fewer side effect
  • Prescribed before
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13
Q

describe MOA inhibitors

A

MAOB inhibitors (protect residual dopamine against oxidation)

   - rasagiline, selegiline - this prevents the breakdown and oxidation of dopamine
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14
Q

describe the prescribing hierarchy

A
  • L dopa - increases motor system control most 0 increase risk of motor complications and other adverse events
  • dopamine agonists - increases motor system control the 2nd most - decrease risk of motor complications but has other adverse effects
  • MAOb inhibitors - increases motor system control the least - decrease risk of motor complications but has other adverse effects
    • mild motor disability and no cognitive impairment - begin MAOb inhibitor
    • mild/moderate motor disability and no cognitive impairment - begin dopamine agonist
    • moderate/severe disability and age 70-75+ years or with significant comorbidity including cognitive impairment - begin L Dopa and plus or minus COMT inhibitor
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15
Q

describe the new treatments available for parkinsns

A
  • Vitamin E – vitamin E is an antioxidant and there is increased idea that there is a lot of oxidation in parkinsons and this can reduce this
  • long term survivial of human embryonic mesencephalic graft in parkisnons disease, - the graft is functional and releases dopamine (after administration of metamphetamine) the dopamine released by the graft can displace the radioalabelled raclopride
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16
Q

describe the link between parkinsons, depression and memory

A
  • depression and dementia are co-morbidities of parkisnons
  • might be that drugs that treat depression can cause parkinsons disease
  • can be decreased levels of serotonin present in the brain
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17
Q

describe the nuclei of the basal ganglia

A
  • Input nuclei – caudate nucleus and putamen
  • Intrinsic nuclei – external globus pallidus, subthalamic nucleus, pars compact of the substantia nigra
  • Output nuclei – internal globus pallidus, pars reticulata of the substantia nigra
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18
Q

what do the globes pallidus and putamen form

A
  • Globus pallidus and putamen for the lentiform nucleus
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19
Q

What does the caudate and putamen form

A

corticostriatium

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20
Q

describe the substantial nigra

A
  • Divides in pars compacta and pars reticulata
  • Pars compacta – cells produce dopamine, these are the cells that are broken down in Parkinson’s disease and are degenerated
  • Pars reticulata – receives input from the striatium but sends it outside the basal ganglia to control head and eye movement
21
Q

describe where the sub thalamic nuclei are

A
  • Inferior to the thalamus and right above the substanita nigra
22
Q

describe the globes palladium

A
  • Made out of the internal and external segment
  • Intenral segmenet sends output to the thalamus
  • External segement relays information between other basal ganglia nuclei and the globus pallidus internal segement
23
Q

describe the blood supply to the basal ganglia

A

Caudate

  • Middle cerebral artery (body)
  • Anterior cerebral artery (anterior)

Putamen

  • Middle cerebral artery
  • Anterior cerebral artery (anterior)

Globus pallidus

  • Middle ceberal artery
  • Anterior choroidal

Internal capsule

  • Middle cerebral artery (middle)
  • anterior cerebral artery (anterior limb)
  • anterior choroidal (posterior limb)
24
Q

What is the function of the basal ganglia

A
  • Initiation of movement
  • Together with the cerebellum the basal ganglia modify movement on a minute to minute basis
  • Process information relaying to emotion, motivation and cognition
25
Q

describe the direct pathway

A
  • D1 via the substantial migration pars compacta activates the striatum via dopamine
  • striatum consist of the caudate and putamen
  • the striatum sends an inhibitory signal to the globes pallidus internal segment and the substantial nigra pars reticulate via GABA
  • these both send negative signals to the thalamus nuclei
  • there is disinhibition of the thalamus (VA/VL nuclei) which leads to increased excitatory of the frontal motor cortex via glutamate
26
Q

describe the indirect pathway

A

neurones in the subtanita migration pars compacta are expressed D2

  • D2 gives an inhibitory signal tot he striatum (putamen and caudate`0
  • this gives an inhibitory signal via GABA to the globes pallidus external
  • GABA again gives an inhibitor signal to the sub thalamic nucleus
  • this gives a excitatory signal to the globes pallidus internal via glutamate
  • which gives an inhibitory signal tot he thalamus via GABA
  • this leads to a less excitatory signal in the motor cortex and inhibits the motor cortex instead of disinhibition as seen in the direct pathway
27
Q

when do patients experience complications with L dopa

A

within 5 years = mainly due to disease progression

28
Q

name the 3 effects to do with L dopa

A
  • on off effect = motor fluctuations
  • dyskinesia
  • neuropsychiatric problems
29
Q

describe the on off effect experienced in L dopa

A

 In this scenario Louis experiences: normal mobility (on) and then freezing (off).

 End-of-dose deterioration: wearing-off clinical benefit that increases after years of usage.
o Often due to change in sensitivity of dopamine receptors.

30
Q

in patients with motor fluctuations what is L dopa better combined with

A

L-DOPA/benserazide

L-DOPA/carbidopa.

these are peripheral dopa decabroyxlase inhibitors

31
Q

what are two types of dyskinesia

A
  • chorea like movement

- dystonias

32
Q

describe the two type of dyskinsia movement

A

Chorea-like movements: hyperkinetic, purposeless dance-like movements.

Dystonias: intense and sustained muscle contractions.

 Peak-dose dyskinesia and wearing-off dystonias are due to fluctuations in the level of dopamine
produced intracerebrally after each dose of L- Dopa.

33
Q

what are the future drug treatments used to treat speicifcly L dopa induced dyskinesia

A

 Alpha2-receptor antagonists.
 Glutamate receptor antagonists.
 5-HT1A receptor agonists.

34
Q

what do COMT inhibitors do to L dopa

A

use of L-DOPA combined with entacapone (inhibitor of enzyme catechol-O-methyl-
transferase/COMT) may alleviate dystonias and motor fluctuations in long-term management.

 COMT inhibitors prolong the effect of L-DOPA.

35
Q

when are dopamine agonists prescribed

A

 Less efficacious than L-DOPA

 Often prescribed before prescription of L-DOPA.

36
Q

what are non motor complications of L dopa

A

Tingling, pain, akathisa, autonomic dysfunction.

37
Q

what are neuro-psychiatric complications of L dopa

A

Hallucinations, mood changes, hypersexuality, nightmares.

38
Q

name two common co morbidities to do with parkinsons

A

Depression: common to develop in patients with

Parkinson’s Disease.
Dementia: often a co-morbidity with Parkinson’s’.

39
Q

name the anticholinergic side effects

A
  • dry mouth
  • constipation
  • confusion
  • blurred vision
40
Q

what is the intimal treatment for Parkinson

A
  • start with dopamine agonists to delay the introduction of L dopa which will lead to motor complications
41
Q

what treatment is used for mild symptoms

A

 Selegiline or a newer drug Rasagiline (MAOb Inhibitor). OR

 Anticholinergic drug= used for tremor (e.g. Orphenadrine,
Procyclidine, Trihexyphenidyl.
o Dry mouth, constipation, confusion, blurred vision
(important to know side effects!)

 Drugs that released dopamine.
These drugs are less efficacious than L-DOPA, and are used as ADJUNCTIVE THERAPHY.

42
Q

what treatment is used for severe treatments

A

Severe Symptoms
 Use of L-DOPA, however leads to symptoms described above.

 Studies have shown that addition of selegiline/rasagiline to L-DOPA improves motor fluctuations and
allows for a reduction of L-DOPA dose by 20-30%.
o Benefit is short lived and only works in ½ patients.

 Can also be combined with entracapone/tolcapone (COMT inhibitors).
o Enhances effects of L-DOPA

43
Q

what surgical procedures can be used

A

Pallidotomy/deep brain stimulation of the subthalamic nucleus can alleviate symptoms.
o Not available on a large scale.
o Patients must adhere to certain criteria.
 Depression and dementia make it unsuited.

  • or you can use a human embryonic mesencephalic graft
44
Q
  1. Name the neurotransmitters released by the corticostriatal and striatopallidal pathways. (1 mark)
A

corticostriatal = glutinate

striatopallidal = GABA

45
Q
  1. Describe the effects of D1 receptor activation on striatal efferent circuitry. (2 marks)
A 
D1 receptor activation causes the activation of the direct pathway (½ mark) by which the internal GP is
inhibited (½ mark). This causes the disinhibition of the thalamus (½ mark) and consequently the activation of
the cortex (½ mark).
46
Q
  1. What is alpha-synuclein, where is it found in the brain and what is its genetic link with Parkinson’s
    disease? (2 marks)
A

Alpha-synuclein is a protein found in Lewy bodies in neurons (½ mark); Lewy bodies are a major
histopathological feature of Parkinson’s disease (½ mark).
The gene for alpha-synuclein is the SNCA gene; mutations associated with this gene (e.g. PARK1/4) have been
identified as a genetic risk factor for Parkinson’s disease (1 mark).

47
Q
  1. List and briefly describe three long-term complications of L-DOPA therapy. (3 marks)
A

Motor fluctuations: include “on-off” phenomenon in which sudden and dramatic fluctuations of motor
performance occur; periods of normal mobility (on) followed by sudden ‘freezing’ (off). End of dose
deterioration and delayed (or ‘no on’- freezing) responses also occur (1 mark).

Dyskinesia’s: include choriform movements (purposeless involuntary dance-like movements) and dystonias
(sustained intense muscle contractions) (1 mark).

Neuro-psychiatric problems: hallucinations, delirium, mood changes, sleep disturbance and nightmares (1
mark).

48
Q
  1. What is rotigotine and what is its route of administration? (2 marks)
A

Dopamine receptor agonist (non-selective agonist); high affinity for the dopamine D1, D2, D3 receptors, and to
a lesser extent D4 and D5 receptors (1 mark)
It is applied transdermally as a patch. (1 mark)

Brain and Behaviour 2 PBL (6 decks)

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