Final Exam Flashcards
(124 cards)
1
Q
How many standard deviations lower is the IQ of patients with schizophrenia?
A
2 SD
2
Q
What are the main symptoms of schizophrenia?
A
Cognitive impairments
3
Q
What is the prevalence of schizophrenia?
A
1.1% (1/3 of homeless population)
4
Q
What are the positive symptoms of schizophrenia?
A
Hallucinations, feelings of persecution/grandeur, bizarre behavior
5
Q
What are the negative symptoms of schizophrenia?
A
Social withdrawal, anhedonia, decreased movement, reduced motivation
6
Q
What tract modulates positive symptoms of schizophrenia?
A
Mesolimbic tract
7
Q
What tract modulates negative and cognitive symptoms?
A
Mesocortical tract
8
Q
What is the dopamine hypothesis?
A
Overactivation of mesolimbic tract leads to positive symptoms. Control with D2 receptor blockers (antipsychotics).
9
Q
What is the revised dopamine hypothesis?
A
Hypoactivation of mesocortical tract leads to negative/cognitive symptoms.
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
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.
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.
13
Q
What is another glutamate-related hypothesis for schizo?
A
Excitotoxicity leads to neurodegeneration causing malfunction
14
Q
What is a developmental hypothesis for schizo?
A
Mutation in certain proteins (BDNF, neuregulin) or environmental challenges
15
Q
What could cause predisposition to schizophrenia?
A
Birth trauma, viral infections, maternal stress
16
Q
What genes could be the cause of schizophrenia?
A
Neuregulin 1, COMT, DISC1
17
Q
What are some noticeable brain abnormalities with schizophrenia?
A
Enlarged ventricles, disordered neuronal organization, loss of gray matter
18
Q
What is the model of typical antipsychotics?
A
D2 antagonist to reduce positive symptoms
19
Q
What is the model of atypical antipsychotics?
A
5-HT2A antagonist to improve negative symptoms
20
Q
What are side effects of antipsychotics?
A
EPS, constipation, blurred vision, dry mouth, drowsiness, weight gain, dizziness
21
Q
What is the bottom line of current schizophrenia treatment?
A
They are inadequate, no change in symptoms
22
Q
What are some motor features of Parkinson’s Disease?
A
Resting tremor, akinesia, bradykinesia, rigdity
23
Q
Parkinson’s Disease Dementia is characterized by what?
A
Cognitive impairments that interfere with daily life
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
25
What contributes to neuronal degeneration?
Mitochondrial dysfunction, oxidative stress, inflammation, excitotoxicity, protein misfolding
26
What do neuronal degeneration mechanisms form?
Lewy bodies
27
What is the evidence for mitochondrial dysfunction?
MPTP is used to model PD in animals. Converted to MPP+ in neurons and accumulates in mitochondria, blocking respiration.
28
What is the evidence for protein aggregation?
Presence of Lewy bodies formed by α-synuclein and other proteins
29
How are animal models used to simulate PD?
Administration of rotenone, use of reserpine to deplete DA, lesion models
30
What is the limitation of animal models of PD?
They are not progressively degenerative like PD
31
What are the five categories of PD drugs?
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
32
What is Levodopa?
Most common treatment of PD and precursor to DA, but causes motor fluctuations
33
What are other treatments for PD that increase DA signaling?
MAO inhibitors, COMT inhibitors, DA receptor agonists
34
What are additional treatments for PD?
Amantadine (NMDA antagonist) and statin drugs to lower cholesterol
35
What is Alzheimer's disease?
Chronic, progressive dementia disorder that is more widespread than PD
36
What is the prevalence of AD?
10% in patients over 65, 50% over 85
37
What is AD preceded by?
Mild cognitive impairment
38
What is the cellular pathology of AD?
Formation of amyloid plaques and neurofibrillary tangles lead to cell degneration and synapse loss
39
What causes the formation of amyloid plaques?
Accumulation of beta-amyloid protein between neurons instead of being degraded
40
What are the types of amyloid plaques?
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
41
What are neurofibrillary tangles?
Fibrous inclusions in neuron cytoplasm, associated with the tau protein
42
What are some risk factors of AD?
Advancing age, obesity and unhealthy lifestyle, head trauma, genetic contribution
43
What are some deterministic genes for AD?
1) Genes for APP on chromosome 21
2) PS-1
3) PS-2
44
What is the greatest gene risk for AD?
Mutation of ApoE gene, which carries very low density lipoprotiens (VLDLs)
45
What risk does Down Syndrome carry for AD?
AD is linked to trisomy 21, 3 copies of APP gene
46
How is AD diagnosed?
Cannot be diagnosed after death, only rule out other sources of dementia
47
What are some animal models for AD?
Mice with APP mutations form Aß plaques, aged beagles, rabbits on high cholesterol diets
48
What are the two categories of AD treatment?
Cholinesterase inhibitors and NMDA receptor antagonists
49
What are new approaches to AD therapy?
Epothilone D (reduces tau in NFTs), antibodies, spin-labeled fluoren compounds to prevent plaque formation, vaccine to target Aß buildup
50
What is Huntington's Disease?
Neurodegerative disorder with singular genetic cause
51
What is the genetic cause of Huntington's Disease?
~35 trinucleotide repeats to activate huntingtin gene
52
What does the number of repeats correlate with?
Penetrance, age of onset
53
What are symptoms of HD?
Reduced ability to suppress unwanted movement, difficulty with higher-order functions
54
What is comorbid with HD?
OCD, bipolar disorder, depression
55
What are treatments of HD?
Nothing can alter course of disease, but use of tetrabenazine reduces symptoms
56
What are anxiety disorders?
Umbrella term that covers several disorders characterized by excessive rumination, worrying, uneasiness, and apprehension
57
How is anxiety both good and bad?
Anxiety is important to survival in cavemen and can enhance performance in small doses but high anxiety damages performance
58
What are the three components of anxiety?
Emotions, behavior, and physiology
59
What is the amygdala responsible for?
Emotion processing and coordinating complex emotional and physiological responses
60
What is the difference between anxiety and fear?
Fear is immediate danger, anxiety is apprehension of future events
61
What part of the amygdala controls anxiety?
Bed nucleus stria terminalis (BNST)
62
What changes occur in the amygdala in response to anxiety?
Increases dendritic length and branching of neurons in BNST
63
What role does the amygdala play in memory formation?
Formation and consolidation of emotional memories
64
How does the amygdala interact with the PFC?
Cognitive control over emotional responses?
65
How does corticotrophin-releasing hormone modulate anxiety?
Released in response to stress peripherally and used as a NT centrally (pro-anxiety)
66
How can CRF modulated anxiety be treated?
CRF antagonist to prevent/attenuate anxiety
67
How does norepinephrine contribute to anxiety?
Also a pro-anxiety NT that increases firing of locus coeruleus
68
How can NE modulated anxeity be treated?
Clonidine, α2 agonist
69
What role does NE play in memory formation?
Formation of emotional memories
70
What role does GABA play in anxiety?
Has an inhibitory influence on anxiety
71
How can GABA be modulated to treat anxiety?
Use of benzodiazepenes reduce anxiety by positively modulating GABAa
72
What role does serotonin play in anxiety?
Antianxiety effects and by enhancing 5-HT function anxiety can be reduced
73
What role does dopamine play in anxiety?
Modulates activity and is released during stress to permit expression of anxiety
74
What developmental factors can contribute to anxiety?
Genes (CRF gene polymorphism) and environment (early exposure to stress)
75
What are the 5 main types of anxiety disorders?
1) Generalized anxiety disorder (GAD)
2) Panic disorder
3) Phobias
4) PTSD
5) OCD
76
How is GAD characterized?
Constant worry and continuously predicting, anticipating, or imagining dreadful events
77
What are the symptoms of panic disorder?
Acute fear reaction (panic attack) triggered by environmental cues. Leads to both panic attacks and anticipatory anxiety of attacks.
78
What are phobias?
Persistent fear of an object or situation.
79
What is a treatment of phobias?
Behavioral desensitization by presenting the stimulus in gradual increments
80
What is the most common phobia?
Social anxiety disorder, fear of being criticized by other
81
What is posttraumatic stress disorder?
Experience of severely traumatic events leads to nightmares and flashbacks (strong genetic contribution)
82
What is OCD?
Recurring, persistent, intrusive thoughts (obsessions) and compulsions relieve anxiety generated by obsessions
83
What are the categories of people with OCD?
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
What circuitry is involved in OCD?
Basal ganglia, frontal lobe, thalamus, anterior cingulate cortex
85
What are drugs relieve anxiety?
Anxiolytics
86
What is a good anxiety drug?
Relieves anxiety with minimal side effects
87
What is the primary mechanism of anxiety medication?
Enhances GABA transmission
88
What is the oldest sedative-hypnotic?
Barbituates (significant side effects)
89
What are benzodiazepenes?
Similar to barbiuates
90
What is the mechanism of action for benzodiazepenes?
Enhance the effects of GABA, but do not open channels without GABA present
91
What are second-generation anxiolytics?
Fewer side effects than BDZs (i.e. Buspirone) and are 5-HT1a partial agonists
92
How are antidepressants used to treat anxiety?
Enhance 5-HT function by blocking reuptake and alleviating anxiety
93
What characterizes affective disorders?
Extreme and inappropriate exaggeration of mood
94
What are the two main types of affective disorders?
Major depression and bipolar disorder
95
What is reactive depression?
State of sadness in response to situations
96
How many DSM IV described symptoms indicate pathological depression?
5
97
What are symptoms of pathological depression?
```
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
How long must symptoms persist for MDD?
Minimum 2 weeks
99
What distinguishes bipolar disorder from MDD?
Manic episodes in combination with depression
100
What disorders are comorbid with depression?
Anxiety and alcohol dependence
101
What genetic factors contribute to depression?
Being a woman also being an identical twin
102
What environmental factors contribute to depression?
Environmental stress and anxiety
103
What hormone is abnormally secreted in patients with depression?
Cortisol
104
How are sleep patterns altered with depression?
Sleep is delayed and REM periods get shorter
105
How is depression modeled in animals?
Forced swim test, chronic mild unpredictable stress, maternal separation
106
How is bipolar disorder modeled in animals?
Sleep deprivation
107
What is the monoamine hypothesis of depression?
Reduction of DA, NE, and 5-HT leads to depressive symptoms
108
How was the monoamine hypothesis first observed?
Using reserpine lead to depressive symptoms
109
What is evidence for the serotonin hypothesis of depression?
Rats with low 5-HT are irritable, low 5-HT metabolites in suicide victims, low Trp blood levels in depressed patients
110
What is the tryptophan depletion challenge?
Consume tryptophan deficient cocktail that reduces 5-HT levels in the brain
111
What were the results of the tryptophan depletion challenge?
Patients who had been depressed or had family history of depression exhibited depressive symptoms
112
What genes contribute to depression vulnerability?
SERT short allele, 5-HT2 upregulation
113
What areas of the brain show increased flow in patients with depression?
Orbitofrontal cortex and amygdala
114
What is the serotonin-norepinephrine hypotheis of depression?
Dysregulated functional interactions between NE and 5-HT systems
115
What is the glucocorticoid hypothesis of depression?
High levels of CRF found in depressed patients
116
What is the neurotrophic hypothesis?
Low BDNF due to stress can reduce neurogenesis
117
What are issues with current affective disorder therapies?
Requires chronic administration to work
118
What is the function of MAO inhibitors? What is the downside?
Increases amount of monoamines for release by inhibiting breakdown. However, takes weeks to be effective.
119
What are side effects of MAOi's?
Drug interactions that increase NE function as well as tyramine buildup that can dangerously increase BP
120
What is the function of tricyclic antidepressants?
Blocks SERT and NET
121
What are side effects of TCAs?
Histamine blockade causes sedation, anticholinergic effects, α1 blockade which can be dangerous for the heart, TCAs have low therapeutic index
122
What is the benefit of second-generation antidepressants?
More selective, fewer side effects?
123
What is an example of a second-generation antidepressant?
SSRIs
124
What is the current therapy for bipolar disorder?
Lithium carbonate, helps reduce suicide
