Disorders of thought, memory, mood and sleep Flashcards
(110 cards)
1
Q
What is a dyssonmia?
A
- difficulty in sleeping
- excessive sleepiness
2
Q
What are the five types of dyssomnias?
A
- circadian rhythm disorders
- insomnia
- narcolepsy
- restless leg syndrome
- obstructive sleep apnea
3
Q
What is an example of a circadian rhythm disorder?
A
- jet lag
- meds are not needed, can take supplements
- no strong evidence based reason to treat these disorders
4
Q
What is insomnia?
A
difficulty sleeping when the opportunity for sleep is present
- most common sleep disorder
- more common in women than man
- increases with age and health problems
5
Q
What are the two types of insomnias?
A
acute and chronic
6
Q
What is acute insomnia? what are the causes?
A
Acute insomnia lasts one night to a few weeks
- causes: emotional and physical discomfort (too excited, too sad, too happy = emotional, physical = environment change i.e. not in your own bed)
7
Q
What is chronic insomnia? what are the causes?
A
- happens three times a week for a month minimum before it can be classified as chronic
- Causes: medical/psychiatric disorders (pain, hormonalchanges) drugs (caffeine, nicotine, alcohol)
8
Q
What are the consequences of both types of insomnia?
A
sleepiness, fatigue, negative mood (irritability, depression), impaired performance, impaired concentration
9
Q
Why is it not beneficial to pull an all nighter before an exam?
A
Because you will perform poorly because sleep is important for cognitive performance and concentration
10
Q
If you are not sleeping well the week of final exams you would be classified as suffering from?
a. acute insomnia
b. chronic insomnia
c. sleep deprivation
A
C. because you cannot afford the time to sleep and in acute insomnia you have the opportunity to sleep but can’t, and chronic insomnia is over a month
11
Q
What is narcolepsy?
A
- daytime sleep attacks with cataplexy, hallucinations, sleep paralysis
- boring sedentary situations relieved by movement (shouldn’t drive a long time without getting up to move)
- no amount of night time sleep produces alertness or relief
12
Q
Who is more likely to suffer insomnia?
A
men
13
Q
What causes insomnia?*******
A
Unknown but there is a genetic link with HLA DQB1-0602
(human leukocyte antigen: DQB1-0602
14
Q
What is cataplexy?
A
muscle weakness, sudden loss of muscle tone, brought about by simple day to day life conditions: laughter, anger, fear
i.e. scare someone really bad they lose muscle tone and fall to the ground
15
Q
What stage of sleep do you go to when having a narcoleptic attack?
A
REM - causing hallucinations and sleep paralysis - oss of muscle tone and dreaming
16
Q
What are ways to treat narcolepsy?
A
with stimulants: methylphenidate and methamphetamine
17
Q
What is restless leg syndrome?
A
A neurological disorder, strong urge to move the legs due to creeping/crawling/uncomfortable sensation, worsens during inactivity
18
Q
What may be the causes of RLS?
A
We thin genetics may play a role because it seems to run in families
- iron deficiency -> pregnancy
- spinal cord lesions
19
Q
What is obstructive sleep apnea?
A
a life threatening disorder, sleep apnea/ breathing cessation
- an insufficient amount of air flow through the nose or mouth
20
Q
What is the cause of obstructive sleep apnea in most cases?
A
upper airway obstruction, snoring, disrupted sleep
21
Q
What are symptoms of obstructive sleep apnea/ what does it cause?
A
persistent daytime sleepiness, morning headache, memory/ judgement problems, irritability, difficulty in concentration, etc
22
Q
Which gender is obstructive sleep apnea more prevalent?
A
males
23
Q
What factors increase risk of obstructive sleep apnea?
A
- male
- increases with age
- increases with obesity (larger people with shirt collar size more than 40cm or 18 inches)
- increases with alcohol use/ abuse
24
Q
How do you treat obstructive sleep apnea?
A
- treat obese by weight loss
- decrease alcohol intake
- put appliances in nose or mouth
- no drugs used for this method- no pharmacological methods
25
What are disorders of perception? what is an example?
- common symptoms of many psychiatric disorders are hallucinations and delusions
ex: schizophrenia bipolar
26
What are hallucinations in perception disorders?
- sensory perceptions occurring without external stimulation
27
How are hallucinations different from illusions?
Illusions are misinterpreted sensory perceptions stimulated by actual external stimuli?
28
What are two types of hallucinations?
Visual: i.e. migraine you see stars or flashing lights that aren't there but you can still see them
Auditory hallucination: when you are trying to sleep but a dog is barking next door or a child is crying ... even though the sound stops you still hear them or feel like the noise is repeating in your ears ... even though you know it is not happening
29
What is a delusion?
false belief: persistent and unshakable (grandeur/possession)
incorporate from multiple sensory systems
30
How do delusions and hallucinations differ?
hallucinations may be only one stimuli (visual or auditory)
| Delusions are from every stimuli around them
31
Train tracks meeting together at a horizon is an example of:
a. hallucination
b. illusion
c. delusion
Illusion
32
What are most delusions caused from?
grandeur/possession - people think they are Jesus Christ or King Arthur but you cannot argue with them because they will not understand or believe you
33
What is schizophrenia?
splitting of the mind: disconnection between thought and language
- people may think one thing but say something else
- too much dopamine activity
34
What is the onset for schizophrenia in males? Females?
males: 17-25
females: 25-35
35
What is the prevalence of schizophrenia between genders?
The incidence is the same between men and women
36
How common is schizophrenia?
1% of the general population has it
37
What plays a role in schizophrenia?
family history
38
What is the requirement from the diagnostic statistical manual to be diagnosed with schizophrenia?
must have two or more of the positive symptoms and one negative symptom
39
What are positive symptoms of schizophrenia?
presence of abnormal behaviors:
disorganized/ incomprehensible speech (neoglisms, derailment, tangentiality, incoherence, word salad), delusions, hallucinations, disorganize/ cationic behavior
40
what are neoglisms?
invented words i.e. someone talking to you isnt using real words
41
what is derailment?
making associations that aren't present/valid - not strong
42
What is tangentiality?
can't stick to specific point of what they started talking about - lose track
43
what is incoherence?
loss of logical connections - speech
44
What is a word salad?
a person is using real words jumbled together, the order they are speaking in doesn't make any sense
45
What are the negative symptoms of schizophrenia?
absences of normal social/ interpersonal behaviors:
| - alogia, avolition, apathy, affective flattening, anhedonia, decreased pain response
46
What is alogia
little speech
47
what is avolition?
lack of motivation
48
what is affective flattening?
lack of emotions
49
What is anhedonia?
inability to enjoy activities (pleasurable activities or experience pleasure)
50
Schizophrenics lose the ability to interpret incoming stimuli, what does this cause?
Sensory overload
the loss of ability to interpret incoming stimuli impairs the ability toe respond appropriately to the environment causing sensory overload
51
What causes schizophrenia (etiology)?
- abnormalities in brain structure enlarged ventricles, smaller hippocampus and thalamus, left hemisphere smaller and smoother, reduced metabolic activity - cannot treat these issues
- new hypothesis is that its because nerurons are all over the place (not vertically aligned)
- dopaminergic hypothesis
52
What is the dopaminergic hypothesis of the etiology of schizophrenia?
drugs blocking dopamine receptors are helpful because schizophrenia is increased dopamine activity, while drugs enhancing dopamine activity worsens symptoms, increase D2- like receptors
*Drugs treat chemical imbalance
53
If people use drugs that increase dopamine activity what may happen?
They may resemble schizophrenic patients
54
What happens to serotonin activity (5-HT2a) in schizophrenic patients?
5- HT2a is a serotonin receptor which is decreased in schizophrenic patients so there are less serotonin NTs
= too little serotonin activity
55
If there are too many receptors for NTs what happens?
the same amount of NT can bring about enhanced activity
56
If there are too few receptors for NTs?
the same amount of NT can't stimulate receptors to a greater extent, therefore reduced activity
57
In schizophrenic patients what happens to the glutamate activity?
it decreases, it is too little - i.e. there are too few NMDA receptors
58
What is the goal of drugs used to treat schizophrenia?
to block dopamine receptors, increase serotonin and increase NMDA receptor activity
59
What is the prevalence of depression?
very common, about 20% of the general population have been diagnosed, yet it is still under diagnosed/ under treated
60
What is the DSM criteria for depression?
one must have 5 of the depression symptoms for more than two weeks
61
What are the symptoms seen in depression?
depressed mood, anhedonia, feelings of worthlessness/guilt, decreased concentration, dyssomnia, decreased libido, change in weight or appetite, ideas about death or suicide
62
What two things play a major role in depression?
family history (genetics must be involved) and environment (seasonal affective disorder i.e. winter)
63
What are the two types of depression?
unipolar and bipolar
64
What is unipolar depression
Persistent, unpleasant mood, 2 times more common in women than men
- don't want to go anywhere, see anyone, do anything
- major depression
65
What is bipolar depression?
alternating periods of depression and mania
- same prevalence in men and women
- very happy, confident, idea jumping (buy and sell cars to buying hospitals) - manic episode = exact opposite of depressed
66
In bipolar depression why is extreme happiness a problem?
It is often followed by severe depression which may result in suicide
67
What is the etiology of depression?
- decrease volume of gray matter in prefrontal cortex, decrease activity in these areas
- biogenic amine hypothesis
- disturbances in hypothalmic-pituitary-adrenal (HPA) axis: erratic cortisol levels
- disturbances in circadian rhythm (seasonal affective disorder - SAD): winter, long nights, little daylight
68
What is the biogenic amine hypothesis?
decrease levels of 5-HT (serotonin), NE (norepinephrine), and DA (dopamine) in the synapse, drugs depleting these neurotransmitters worsen symptoms because these biologic amines are already decreased in depressed patients, drugs that increase these amines help them overcome the depressed episode
69
How prevalent are anxiety disorders?
affect 15% of general population
| - more often in women than men
70
What are the five major types of anxiety disorders?
```
Panic Disorder
Generalized Anxiety disorder
Obsessive compulsive disorder
Social anxiety disorder
PTSD
```
71
What is panic disorder?
increased fearfulness
| - something happens I'll die, these patients find the quickest way out
72
What is generalized anxiety disorder?
prolonged, excessive worry
73
What is obsessive compulsive disorder?
repeated thoughts and actions
- wash hands continuously
74
What is social anxiety disorder?
intense, irrational, persistent fear of being scrutinized/negatively evaluated by others
75
What is PTSD?
anxiety experienced due to trauma, activation of stress response
- replay scene over and over, it still seems real
- often people feel guilt ( why did I survive but they didn't?
Treat by increased serotonin
76
What is dementia?
syndrome of intellectual deterioration that interferes with occupational/social performances involving disturbances in memory, language, perception, motor skills, solve problems, think abstractly and make judgements
- disturbances in more than just memory
77
What causes dementia?
damaged association areas (higher order thinking)
78
What are the types of dementia?
Alzheimer's disease
| Other dementias - huntington's disease
79
When does alzheimers disease occur?
in middle/late life
80
What is the prevalence of alzheimers? What are risk factors?
~ 6 million americans have it
| - risk increases with age, genetic influence
81
What are the manifestations of alzheimers disease?
loss of short-term memory and denial of such memory loss, with eventual disorientation, impaired abstract thinking, changes in personality, three stages
82
What is the pathophysiology/ reasons alzheimers occurs?
- cortical atrophy and loss of neurons, enlarged ventricles
- presence of amyloid containing neuritic plaques and neurofibrillary tangles in hippocampus (where memory formation occurs)
- decrease in level of choline acetyl-transferase which synthesizes Ach
83
What is the etiology of alzheimers?
idopathic in most cases:
- old age is a risk factor (10% of population greater than 65
severe dimentia
84
How is alzheimers treated?
With drugs that try to increase Ach levels
- recently people have tried to target plaques but we don't know if the disease causes the formatioin of plaques or if the plaques form and cause the disease
85
Is APP a protein or an enzyme?
protein
86
Are PS1 and PS2 proteins or enzymes?
enzymes
87
How do senile plaques form?
Beta amyloid percursor protein (APP) is a transmembrane protein containing Abeta peptide, which is normally cleaved by alpha secretase to soluble products
- if a mutation occurs (environmental factors?): cleavage by beta secretase and gamma secretase to Abeta1-40/Abeta1-42 -> aggregate causing senile plaques
88
What is the issue of senile plaques?
they exert a neurotoxic effect causing neuronal cell death
89
What are normal functions of APP?
still unknown
90
Why is a 42 aa peptide worse than a 40 aa peptide?
a 40 aa peptide is slightly more soluble because of size
91
Which of the following are the bad guys in Alzheimers?
a. APP
b. beta amyloid 1-40
c. beta amyloid 1-42
b and c
92
What is tau?
- microtubule (provide stability to axon) associated protein in neuronal axons
- responsible for tubulin polymerization and microtubule stabilization
- normally phosphorylated at 2-3 sites (addition of phosphate group)
93
How do genetic issues/ environmental factors affect tau?
they cause it to become hyperphosphorylated at 6-8 sites (instead of 2-3)
- either kinases (which add phosphate groups) are over active or phosphatases (which remove phosphate groups) are underactive
94
What happens when tau is hyperphosphorylated?
it causes dissociation from microtubules, relocalization and self aggregation into paired helical fragments causing neuronal cell death
95
What is the role of apolipoprotein E4 (genetic) in alzheimers disease?
- there are three major alleles: apoE2, apoE3, and apoE4
- apoE4: heightened risk and severity for suffering from alzheimers disease
- earlier age onset
- lower survival
96
What are the physiological functions of apoEs?
- blood transport of cholesterol and triglycerides (outside nervous system)
- salvage and reutilization of membrane lipide after nervous tissue damage (inside nervous system)
- inhibitors of amyloid fibril formation (apoE4 least effective)
- inhibitors of tau phosphorylation (apoE4 least effective)
97
What is worse being homozygous or heterozygous for apoE4?
homozygous because guaranteed earlier onset and lower survival of alzheimers disease
98
How may glutamate excitotoxicity effect alzheimers diesase?
- the glutamate transporter is downregulated ( usually on astrocytes or presynaptic nerve terminals: responsible for taking up glutamate, if downregulated glutamate concentration is increased outside the cell leading to problems
- increased synaptic glutamate and glutamate receptor activity
99
What is the effect of beta amyloid on glutamate>
it inhibits glutamate uptake and enhances glutamate release
100
What does the excitotoxicity of glutamate increase?
levels of APP
101
What does increased NMDA-receptor activity increase?
tau phosphorylation
102
What is Huntington's disease?
a hereditary disorder with late onset
- chronic progressive chorea (choreographic movements, rigidity and akinesia(loss of voluntary movement)) psychological changes (depression, personality changes), dementia (memory loss(
- localized death of brain cells in basal ganglia leading to decreased GABA (inhibitory transmitter) and Ach, imbalance with dopamine
103
What are the genetic factors of huntington's disease?
- inherited as autosomal dominant neurodegenerative disorder
- Huntingtin (Htt) protein from HD which normally contains 11-34 CAG glutamine repeats
- more than 40 CAG repeats abnormal, HD earlier onset correlates with increased repeats
- expanded huntingtin (Httexp): abberant and or novel protein interactions
104
What is normal Htt responsible for?
- functioning of nuclear organelles: transcriptional regulation
- membrane, vesicular and intracellular trafficking:
- cytoskeletal organization
105
What are mechanisms of Httexp toxicity?
Transcriptional upregulation: caspases
| - role of ubiquitin proteasome pathway
106
What are caspases involved in?
apoptosis: programmed cell death
107
What happens to proteins tagged with ubiquitin?
they go through a proteasome pathway and get destroyed
108
What is the problem with Httexp?
the Htt is not destroyed so accumulation leads to activation of caspases which lead them to cell death
109
In Httexp glutamate receptor excitotoxicity, what is a possible target?
mGluR5 - metaboloc glutamate receptor 5
110
What are the mechanisms of mitochondrial trafficking?
immobilization of mitochondrial trafficking:
- mitochondrial trafficking is essential in dendrites and axons of neurons to provide energy and upregulate calcium levels, recycle damaged ones
- Httexp forms cytoplasmic protein aggregates ( interact with cytoskeletal components and molecular motors, act as physical roadblocks to impair mitochondrial movement)
- damaged mitochondria release ROS and cytochrome c causing apoptosis
- inhibition of mitichondrial respiration bu increasing ROS leads to decreased energy levels
