Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Neuropsychopharmacology > Lecture 16: Treatment of CNS Degenerative Disorders > Flashcards

Lecture 16: Treatment of CNS Degenerative Disorders Flashcards

(66 cards)

Start Studying
1
Q

movement disorder

A

neurological condition causing abnormal voluntary or involuntary movements

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

hypokinetic movement disorders

A
  • parkinson disease
  • parkinson plus
  • secondary parkinsonism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

hyperkinetic movement disorders

A
  • tremor-essential tremor
  • chorea-huntington disease
  • dystonia
  • tics-tourette
  • wilson disease
  • myoclonus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

direct dopamine pathway function

A

facilitates movement via DA activation of D1 (stimulatory) receptors

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

indirect DA pathway function

A

inhibits movement (DA activation of D2 (inhibitory) receptors

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

function of direct & indirect DA pathways together

A

help brain initiate & sustai purposeful movememtn

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

pathology of hyperkinetic disorders

A
  • degeneration of striatal neurons part of indirect pathway –> reduced inhibitory control over thalamus & motor cortex –> excessive movements due to unopposed activation of motor programs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

essential tremor

A

common movement disorder: involuntary shaking of body

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

Tourette syndrom

A

ticks

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

Dopamine blocker

A

Aripiprazole

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

Aripiprazole function

A
  • partial agonist at D2 & 5-HT1A receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

treatment for tics

A
  • alpha-2 adrenergic agonists
  • antipsychotics
  • VMAT2 inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

drugs used for comorbid ADHD + tics

A
  • stimulants
  • non-stimulants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what converts L-DOPA to DA

A

aromatic L-amino acid decarboxylase

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

what blocks DATs

A

reserpine

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

what drug antagonizes DA membrane carrier protein

A

cocaine

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

what can degrade DA

A

MAO & COMT

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

synthesis of DA

A

tyrosine -> DOPA (via tyrosine hydroxylase) –> DA (via DOPA decarboxylase)

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

best treatment for Tourettes syndrome

A

acetylleucine

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

what is Huntington’s disease

A

progressive, inherited neurodegenerative disorder caused by 36+ CAG trinucleotide repeat expansion in HTT gene

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

structural changes in HD

A

destruction of the head of the caudate nucleus

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

when do symptoms onset for HD

A

30 - 50 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

HD diagnosis steps

A
  1. clinical evaluation
  2. genetic testing
  3. imaging studies (supportive)
  4. other assessments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

HD motor symptoms

A
  • chorea
  • dystonia (sustained muscle contractions)
  • bradykinesia (slowness of voluntary movements)
  • gait instability
  • dysarthria (slurred speech)
  • dysphagia (difficulty swallowing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
cognitive symptoms of HD
- executive dysfunction - memory impairment - attention deficits - perseveration - dementia
26
psychiatric symptoms of HD
- depression - irritability - obsessive-compulsive behaviors - psychosis - apathy & social withdrawal
27
stages of HD
presymptomatic -> early stage -> middle stage -> late stage -> end stage
28
presymptomatic HD
genetic mutation present, no symptoms
29
early stage HD
onset of mild motor & psychiatric symptoms
30
middle stage HD
worsening motor & cognitive decline
31
late stage HD
severe disability & dependence
32
end stage HD
full care required
33
pharmacological treatments for chorea
- VMAT2 inhibitors that reduce DA release - antipsychotics
34
treatments for psychiatric symptoms
- SSRIs - atypical antipsychotics
35
non-pharmacological management
- physical therapy - speech therapy - occupational therapy - psychotherapy & counseling
36
what is PD research focused on
1. mechanisms responsible for neuronal death 2. pharmacological approaches to prevent neuronal loss 3. pharmacological approaches to compensate for neuronal loss
37
pathological hallmark of PD
loss of pigmented, DA neurons of SNpc, with the appearance of Lewy Bodies
38
Lewy bodies
intracytoplasmic eosinophilic inclusions primarily composed of misfolded alpha-synuclein
39
4 cardinal features of PD
- bradykinesia - muscular rigidity - resting tremor - impairment of postural balance leading to disturbances of gait & falling
40
central symptoms of PD
- depression - anxiety - decline in intellectual functioning - dizziness or fainting
41
systemic symptoms of PD
- tremor & slowness - impaired coordination - small handwriting - sleepiness - trouble moving or walking
42
drug treatments for PD
- amantadine - carbidopa & L-DOPA combination therapy
43
what is the 1st line therapy for PD
Levodopa
44
why does levodopa have therapeutic effects
decarboxylation of levodopa --> DA
45
what is levodopa always administered alongside
carbidopa
46
what is carbidopa
peripherally acting inhibitor of L-amino acid decarboxylase
47
what symptoms does levodopa treat
all of them
48
49
where does levodopa with carbidopa get metabolized
equally in the GI tract & peripheral tissues, with 10% --> brain
50
advantages of dopamine receptor agonist drugs
1. enzymatic conversion not required for activity 2. functional capacity of nigrostriatal neurons not required
51
example of dopamine receptor agonist
Bromocriptine
52
adverse effects of D2 receptor agonists
- compulsive behaviors - nausea & vomiting - psychiatric disturbance
53
high risk genes for PD
- SNCA - LRRK2 - PARK2, PINK1, DJ-1
54
environmental risk factors for PD
pesticide exposure, rural living, heavy metals, TBI
55
protective factors against PD
caffeine intake, physical activity, smoking
56
links b/w DA & depression
1. anhedonia 2. motivation & goal-directed behavior 3. cognitive impairment 4. stress & DA
57
type of hallucinations in PD
primarily visual
58
type of hallucination in schizophrenia
primarily auditory
59
insight into hallucinations in PD
often preserved; patient knows hallucinations aren't real
60
insight into hallucinations in schizophrenia
usually lost - hallucinations are believed to be real
61
delusions in PD
typically absent or mild
62
delusions in schizophrenia
often present, bizarre, or persecutory
63
thought disorder in PD
absent
64
thought disorder in schizophrenia
priminent- disorganized speech, tanchentiality
65
onset of PD
late in life, especially in patients on dopaminergic therapy or w/ cognitive decline
66
onset of schizophrenia
early adulthood

Neuropsychopharmacology (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions