Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuropharmacology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

How many standard deviations lower is the IQ of patients with schizophrenia?

A

2 SD

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

What are the main symptoms of schizophrenia?

A

Cognitive impairments

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

What is the prevalence of schizophrenia?

A

1.1% (1/3 of homeless population)

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

What are the positive symptoms of schizophrenia?

A

Hallucinations, feelings of persecution/grandeur, bizarre behavior

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

What are the negative symptoms of schizophrenia?

A

Social withdrawal, anhedonia, decreased movement, reduced motivation

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

What tract modulates positive symptoms of schizophrenia?

A

Mesolimbic tract

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

What tract modulates negative and cognitive symptoms?

A

Mesocortical tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the dopamine hypothesis?

A

Overactivation of mesolimbic tract leads to positive symptoms. Control with D2 receptor blockers (antipsychotics).

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

What is the revised dopamine hypothesis?

A

Hypoactivation of mesocortical tract leads to negative/cognitive symptoms.

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

What is the glutamate hypothesis?

A

Because symptoms of PCP use are similar to +/- schizo symptoms, hypofunction of NMDA receptors could be a cause

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

How does the glutamate hypothesis account for positive symptoms of schizo?

A

Normally mesolimbic DA neurons are inhibited by glutamate neurons from the frontal cortex. But hypofunction of NMDA receptors on GABA interneurons leads to overactivity in the VTA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does the glutamate hypothesis account for negative symptoms of schizo?

A

Normally mesocortical DA neurons are excited by glutamate neurons from the frontal cortex. Hypofunction leads to hypoactivity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is another glutamate-related hypothesis for schizo?

A

Excitotoxicity leads to neurodegeneration causing malfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a developmental hypothesis for schizo?

A

Mutation in certain proteins (BDNF, neuregulin) or environmental challenges

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

What could cause predisposition to schizophrenia?

A

Birth trauma, viral infections, maternal stress

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

What genes could be the cause of schizophrenia?

A

Neuregulin 1, COMT, DISC1

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

What are some noticeable brain abnormalities with schizophrenia?

A

Enlarged ventricles, disordered neuronal organization, loss of gray matter

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

What is the model of typical antipsychotics?

A

D2 antagonist to reduce positive symptoms

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

What is the model of atypical antipsychotics?

A

5-HT2A antagonist to improve negative symptoms

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

What are side effects of antipsychotics?

A

EPS, constipation, blurred vision, dry mouth, drowsiness, weight gain, dizziness

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

What is the bottom line of current schizophrenia treatment?

A

They are inadequate, no change in symptoms

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

What are some motor features of Parkinson’s Disease?

A

Resting tremor, akinesia, bradykinesia, rigdity

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

Parkinson’s Disease Dementia is characterized by what?

A

Cognitive impairments that interfere with daily life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the pathology of Parkinson’s Disease?

A

Degeneration of brain areas starting in the vagus/olfactory areas and working back to sensory motor areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What contributes to neuronal degeneration?

A

Mitochondrial dysfunction, oxidative stress, inflammation, excitotoxicity, protein misfolding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What do neuronal degeneration mechanisms form?

A

Lewy bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the evidence for mitochondrial dysfunction?

A

MPTP is used to model PD in animals. Converted to MPP+ in neurons and accumulates in mitochondria, blocking respiration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the evidence for protein aggregation?

A

Presence of Lewy bodies formed by α-synuclein and other proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How are animal models used to simulate PD?

A

Administration of rotenone, use of reserpine to deplete DA, lesion models

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the limitation of animal models of PD?

A

They are not progressively degenerative like PD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the five categories of PD drugs?

A

1) Prevent clinical progression of disease
2) Symptomatic monotherapies
3) Adjunct treatments to L-DOPA therapy
4) Drugs that prevent motor complications
5) Drugs that treat motor complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is Levodopa?

A

Most common treatment of PD and precursor to DA, but causes motor fluctuations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are other treatments for PD that increase DA signaling?

A

MAO inhibitors, COMT inhibitors, DA receptor agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are additional treatments for PD?

A

Amantadine (NMDA antagonist) and statin drugs to lower cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is Alzheimer’s disease?

A

Chronic, progressive dementia disorder that is more widespread than PD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the prevalence of AD?

A

10% in patients over 65, 50% over 85

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is AD preceded by?

A

Mild cognitive impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the cellular pathology of AD?

A

Formation of amyloid plaques and neurofibrillary tangles lead to cell degneration and synapse loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What causes the formation of amyloid plaques?

A

Accumulation of beta-amyloid protein between neurons instead of being degraded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the types of amyloid plaques?

A

1) Core of amyloid surrounded by abnormal neurites
2) Focal diffuse deposits of amyloid w/ no neurites around core
3) Dense form w/o neurites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are neurofibrillary tangles?

A

Fibrous inclusions in neuron cytoplasm, associated with the tau protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are some risk factors of AD?

A

Advancing age, obesity and unhealthy lifestyle, head trauma, genetic contribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are some deterministic genes for AD?

A

1) Genes for APP on chromosome 21
2) PS-1
3) PS-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the greatest gene risk for AD?

A

Mutation of ApoE gene, which carries very low density lipoprotiens (VLDLs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What risk does Down Syndrome carry for AD?

A

AD is linked to trisomy 21, 3 copies of APP gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How is AD diagnosed?

A

Cannot be diagnosed after death, only rule out other sources of dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are some animal models for AD?

A

Mice with APP mutations form Aß plaques, aged beagles, rabbits on high cholesterol diets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the two categories of AD treatment?

A

Cholinesterase inhibitors and NMDA receptor antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are new approaches to AD therapy?

A

Epothilone D (reduces tau in NFTs), antibodies, spin-labeled fluoren compounds to prevent plaque formation, vaccine to target Aß buildup

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is Huntington’s Disease?

A

Neurodegerative disorder with singular genetic cause

51
Q

What is the genetic cause of Huntington’s Disease?

A

~35 trinucleotide repeats to activate huntingtin gene

52
Q

What does the number of repeats correlate with?

A

Penetrance, age of onset

53
Q

What are symptoms of HD?

A

Reduced ability to suppress unwanted movement, difficulty with higher-order functions

54
Q

What is comorbid with HD?

A

OCD, bipolar disorder, depression

55
Q

What are treatments of HD?

A

Nothing can alter course of disease, but use of tetrabenazine reduces symptoms

56
Q

What are anxiety disorders?

A

Umbrella term that covers several disorders characterized by excessive rumination, worrying, uneasiness, and apprehension

57
Q

How is anxiety both good and bad?

A

Anxiety is important to survival in cavemen and can enhance performance in small doses but high anxiety damages performance

58
Q

What are the three components of anxiety?

A

Emotions, behavior, and physiology

59
Q

What is the amygdala responsible for?

A

Emotion processing and coordinating complex emotional and physiological responses

60
Q

What is the difference between anxiety and fear?

A

Fear is immediate danger, anxiety is apprehension of future events

61
Q

What part of the amygdala controls anxiety?

A

Bed nucleus stria terminalis (BNST)

62
Q

What changes occur in the amygdala in response to anxiety?

A

Increases dendritic length and branching of neurons in BNST

63
Q

What role does the amygdala play in memory formation?

A

Formation and consolidation of emotional memories

64
Q

How does the amygdala interact with the PFC?

A

Cognitive control over emotional responses?

65
Q

How does corticotrophin-releasing hormone modulate anxiety?

A

Released in response to stress peripherally and used as a NT centrally (pro-anxiety)

66
Q

How can CRF modulated anxiety be treated?

A

CRF antagonist to prevent/attenuate anxiety

67
Q

How does norepinephrine contribute to anxiety?

A

Also a pro-anxiety NT that increases firing of locus coeruleus

68
Q

How can NE modulated anxeity be treated?

A

Clonidine, α2 agonist

69
Q

What role does NE play in memory formation?

A

Formation of emotional memories

70
Q

What role does GABA play in anxiety?

A

Has an inhibitory influence on anxiety

71
Q

How can GABA be modulated to treat anxiety?

A

Use of benzodiazepenes reduce anxiety by positively modulating GABAa

72
Q

What role does serotonin play in anxiety?

A

Antianxiety effects and by enhancing 5-HT function anxiety can be reduced

73
Q

What role does dopamine play in anxiety?

A

Modulates activity and is released during stress to permit expression of anxiety

74
Q

What developmental factors can contribute to anxiety?

A

Genes (CRF gene polymorphism) and environment (early exposure to stress)

75
Q

What are the 5 main types of anxiety disorders?

A

1) Generalized anxiety disorder (GAD)
2) Panic disorder
3) Phobias
4) PTSD
5) OCD

76
Q

How is GAD characterized?

A

Constant worry and continuously predicting, anticipating, or imagining dreadful events

77
Q

What are the symptoms of panic disorder?

A

Acute fear reaction (panic attack) triggered by environmental cues. Leads to both panic attacks and anticipatory anxiety of attacks.

78
Q

What are phobias?

A

Persistent fear of an object or situation.

79
Q

What is a treatment of phobias?

A

Behavioral desensitization by presenting the stimulus in gradual increments

80
Q

What is the most common phobia?

A

Social anxiety disorder, fear of being criticized by other

81
Q

What is posttraumatic stress disorder?

A

Experience of severely traumatic events leads to nightmares and flashbacks (strong genetic contribution)

82
Q

What is OCD?

A

Recurring, persistent, intrusive thoughts (obsessions) and compulsions relieve anxiety generated by obsessions

83
Q

What are the categories of people with OCD?

A

Washers (contamination), checkers (check things), doubters and sinners (if everything isn’t right they’ll be punished), counters and arrangers (obsessed with order/symmetry), an hoarders (can’t throw things away)

84
Q

What circuitry is involved in OCD?

A

Basal ganglia, frontal lobe, thalamus, anterior cingulate cortex

85
Q

What are drugs relieve anxiety?

A

Anxiolytics

86
Q

What is a good anxiety drug?

A

Relieves anxiety with minimal side effects

87
Q

What is the primary mechanism of anxiety medication?

A

Enhances GABA transmission

88
Q

What is the oldest sedative-hypnotic?

A

Barbituates (significant side effects)

89
Q

What are benzodiazepenes?

A

Similar to barbiuates

90
Q

What is the mechanism of action for benzodiazepenes?

A

Enhance the effects of GABA, but do not open channels without GABA present

91
Q

What are second-generation anxiolytics?

A

Fewer side effects than BDZs (i.e. Buspirone) and are 5-HT1a partial agonists

92
Q

How are antidepressants used to treat anxiety?

A

Enhance 5-HT function by blocking reuptake and alleviating anxiety

93
Q

What characterizes affective disorders?

A

Extreme and inappropriate exaggeration of mood

94
Q

What are the two main types of affective disorders?

A

Major depression and bipolar disorder

95
Q

What is reactive depression?

A

State of sadness in response to situations

96
Q

How many DSM IV described symptoms indicate pathological depression?

A

5

97
Q

What are symptoms of pathological depression?

A 
Depressed mood
Loss of interest (anhedonia)
Significant weight change
Change to appetite
Difficulty sleeping
Slow or agitated behavior
Thoughts of worthlessness or guilt
Loss in cognitive ability
Contemplating suicide/death
98
Q

How long must symptoms persist for MDD?

A

Minimum 2 weeks

99
Q

What distinguishes bipolar disorder from MDD?

A

Manic episodes in combination with depression

100
Q

What disorders are comorbid with depression?

A

Anxiety and alcohol dependence

101
Q

What genetic factors contribute to depression?

A

Being a woman also being an identical twin

102
Q

What environmental factors contribute to depression?

A

Environmental stress and anxiety

103
Q

What hormone is abnormally secreted in patients with depression?

A

Cortisol

104
Q

How are sleep patterns altered with depression?

A

Sleep is delayed and REM periods get shorter

105
Q

How is depression modeled in animals?

A

Forced swim test, chronic mild unpredictable stress, maternal separation

106
Q

How is bipolar disorder modeled in animals?

A

Sleep deprivation

107
Q

What is the monoamine hypothesis of depression?

A

Reduction of DA, NE, and 5-HT leads to depressive symptoms

108
Q

How was the monoamine hypothesis first observed?

A

Using reserpine lead to depressive symptoms

109
Q

What is evidence for the serotonin hypothesis of depression?

A

Rats with low 5-HT are irritable, low 5-HT metabolites in suicide victims, low Trp blood levels in depressed patients

110
Q

What is the tryptophan depletion challenge?

A

Consume tryptophan deficient cocktail that reduces 5-HT levels in the brain

111
Q

What were the results of the tryptophan depletion challenge?

A

Patients who had been depressed or had family history of depression exhibited depressive symptoms

112
Q

What genes contribute to depression vulnerability?

A

SERT short allele, 5-HT2 upregulation

113
Q

What areas of the brain show increased flow in patients with depression?

A

Orbitofrontal cortex and amygdala

114
Q

What is the serotonin-norepinephrine hypotheis of depression?

A

Dysregulated functional interactions between NE and 5-HT systems

115
Q

What is the glucocorticoid hypothesis of depression?

A

High levels of CRF found in depressed patients

116
Q

What is the neurotrophic hypothesis?

A

Low BDNF due to stress can reduce neurogenesis

117
Q

What are issues with current affective disorder therapies?

A

Requires chronic administration to work

118
Q

What is the function of MAO inhibitors? What is the downside?

A

Increases amount of monoamines for release by inhibiting breakdown. However, takes weeks to be effective.

119
Q

What are side effects of MAOi’s?

A

Drug interactions that increase NE function as well as tyramine buildup that can dangerously increase BP

120
Q

What is the function of tricyclic antidepressants?

A

Blocks SERT and NET

121
Q

What are side effects of TCAs?

A

Histamine blockade causes sedation, anticholinergic effects, α1 blockade which can be dangerous for the heart, TCAs have low therapeutic index

122
Q

What is the benefit of second-generation antidepressants?

A

More selective, fewer side effects?

123
Q

What is an example of a second-generation antidepressant?

A

SSRIs

124
Q

What is the current therapy for bipolar disorder?

A

Lithium carbonate, helps reduce suicide

Neuropharmacology (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions