Psychological Disorders Flashcards
1
Q
Drugs either facilitate or inhibit transmission at:
A
Synapses.
2
Q
What is an antagonist?
A
A drug that blocks a neurotransmitter.
3
Q
What is an agonist?
A
A drug that mimics or increases the effects of a neurotransmitter.
4
Q
What is a mixed agonist-antagonist?
A
An agonist of some effects of the neurotransmitter and an antagonist for others, or an agonist at some doses and an antagonist at others.
5
Q
Explain affinity.
A
A drug has an affinity for a receptor if it binds to it.
6
Q
Explain a drug’s efficacy.
A
Its tendency to activate the receptor.
7
Q
Who discovered the effects of dopamine and norepinephrine?
A
Olds and Milner.
8
Q
What is the nucleus accumbens central for?
A
Reinforcing experiences of all types.
9
Q
What do addictive drugs do to the nucleus accumbens?
A
They release dopamine or norepinephrine.
10
Q
How do stimulant drugs affect dopamine?
A
They block reuptake of dopamine or reverse the dopamine transporter so it releases dopamine instead of producing reuptake.
11
Q
What is the effect of opiates on the brain?
A
Inhibiting GABA, and increasing dopamine release.
12
Q
What is GABA?
A
A neurotransmitter that inhibits the firing of dopamine neurons.
13
Q
Name some things that release dopamine in the nucleus accumbens.
A
Sexual excitement, music, sugar, and imagining something pleasant.
14
Q
Explain craving.
A
An insistent search for the activity.
15
Q
Give some genetics predispositions for addiction.
A
A gene that controls variations in the dopamine 4 receptor. making it less sensitive, and the COMT enzyme that breaks down dopamine after its release.
16
Q
Name the two types of alcoholism.
A
Type A/I and Type B/II.
17
Q
What is type B alcoholism?
A
Rapid onset, usually before age 25.
18
Q
What is type A alcoholism?
A
Developing alcohol problems gradually, usually after age 25.
19
Q
Alcoholism is more likely among tose who were described in childhood as:
A
Impulsive, sensation-seeking, risk taking, easily bored, and outgoing.
20
Q
What is contingency management?
A
A version of therapy that includes rewards for remaining drug-free.
21
Q
What toxic substance does the liver convert ethyl alcohol to?
A
Acetaldehyde.
22
Q
What converts acetaldehyde to acetic acid?
A
Acetaldehyde dehydrogenase.
23
Q
What does disulfiram do?
A
Antagonises the effects of acetalhyde dehydrogenase by binding to its copper ion.
24
Q
What do naxolone and naltrexone do?
A
Block opiate receptor and thereby decrese the pleasure from alcohol.
25
Give three drugs used to treat heroin addiction.
Methadone, buprenorphine and levomethadyl acetate.
26
How does propranolol reduce cravings?
Reconsolidation requires protein synthesis, and propranolol interferes with protein synthesis and therefore prevent reconsolidation.
27
Give some characteristics of major depression.
Feeling sad most of the day for weeks at a time, don't enjoy anything, lack of energy, feeling worthless, suicidal ideation, insomnia, poor concentration.
28
The ___ form of the serotonin transporter gene increase the risk of a depressive reaction to major stressors.
Short.
29
Most people with depression have decreased activity in the ___ prefrontal cortex and increased activity in the ___ prefrontal cortex.
Left, right.
30
Give some types of antidepressants.
Triyclics, selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, and atypical antidepressants.
31
How do tricyclic antidepressants work?
They block transporter proteins that reabsorb serotonin, dopamine and norepinephrine into the presynaptic neuron after release.
32
What do tricyclics block?
Histamine and acetylcholine receptors, and sodium channels.
33
What are four issues with tricyclic antidepressants?
They produce drowsiness, difficulty urinating, dry mouth, and heart irregularities.
34
How do monoamine oxidase inhibitors work?
They block the enzyme monoamine oxidase, a presynaptic enzyme that metabolises catecholamines and serotonin into inactive forms.
35
What do people taking monoamine oxidase inhibitors have to avoid?
Foods containing tyramine (cheese, raisins, etc) as the combination raises blood pressure.
36
People with depression have lower levels of what neurotransmitter?
Brain-derived neurotrophic factor.
37
What is brain-derived neurotrophic factor important for?
Synaptic plasticity, learning, and proliferation of new neurons in the hippocampus.
38
Why do people with depression have a smaller hippocampus, impaired learning, and redued production of hippocampal neurons?
Low BDNF (brain-derived neurotrophic factor).
39
Give a problem with the Hamilton Depression Rating Scale.
It is less reliable at lower levels of depression.
40
What is the simplest, least expensive anti-depressant treatment?
A program of regular, moderate-intensity exercise.
41
What is the most common side effect of ECT?
Memory loss.
42
How does sleep deprivation relieve depression?
Its causes astrocytes to release adenosine, which has anti-depressant effects.
43
Explain unipolar depression.
People with unipolar depression vary between normality and depression.
44
Explain bipolar disorder.
People alternate between depression and mania.
45
Give another name for bipolar disorder.
Manic-depressive disorder.
46
What characterises mania?
Restless activity, excitement, laughter, excessive self-confidence, rambling speech, and loss of inhibitions.
47
Explain bipolar I disorder.
Fully fledged manic episodes.
48
Explain bipolar II disorder.
Mild or hypomanic episodes.
49
Name the first treatment for bipolar disorder.
Lithium salts.
50
Who discovered the effectiveness of lithium salts in combating bipolar disorder?
Cade.
51
Name two effective drugs in treating bipolar disorder, besides lithium salts.
Valproate and carbamazepine.
52
How do lithium salts, valproate and carbamazepine affect the brain? (2)
They decrease the number of AMPA types glutamate receptors in the hippocampus, and block the synthesis of arachidonic acid.
53
What foods can prevent bipolar disorder and how?
Seafood, as omega-3 fatty acids counteract the effects of arachidonic acid.
54
What is seasonal affective disorder?
Depression that recurs during a particular season, like winter.
55
In what environment is SAD most common?
Near the poles, where winter nights are longer.
56
How does SAD differ from depression?
Patients with SAD have phase-delayed sleep and temperature rhythms, and therefore become sleepy and wakeful later than normal.
57
What was schizophrenia originally called?
Dementia praecox.
58
What did Bleuler mean by the term schizophrenia?
A split between the emotional and intellectual aspects of intelligence.
59
Give the DSM-5's list of symptoms for schiophrenia.
Delusions, hallucinations, disorganised speech, grossly disorganised behaviour, and weak or absent signs of emotions, speech, and socialisation.
60
What are the cognitive symptoms of schizophrenia?
Limitations of thoughts and reasoning that are common in schizophrenia, like difficulty understanding and using abstract concepts and difficulty maintaining attention.
61
What could be the central symptom of schiophrenia?
Memory impairment, specifically to working memory.
62
Give five conditions that resemble schizophrenia.
Substance abuse, brain damage, Huntington's disease, nutritional abnormalities, and undetected hearing deficits.
63
What is a differential diagnosis?
A diagnosis that rules out other conditions with similar symptoms.
64
Give three explanations for the higher incidence of schizophrenia in cities compared to rural area.
More exposure to toxic substances, less social support, and less exposure to the sun, resulting in less absorption of vitamin D.
65
What kind of diet aggravates schizophrenia?
One high in sugar and saturated fat.
66
How does schizophrenia relate to diabetes?
It is less common in people with type I diabetes, than in type II adult-onset diabetes.
67
Explain schizophrenia's connections to cancer.
People with schizophrenia have a higher than average risk of colon cancer, but less risk of other types of cancer, rheumatoid arthritis, and allergies.
68
How does schizophrenia related to gender at birth?
Women with a schizophrenic breakdown during pregnancy give birth to girls, while those that give birth to sons usually have a breakdown shortly after.
69
What chemical causes the distinctive body odour in schizophrenics?
Trans-3-methyl-2-hexenoic acid.
70
What does the gene DISC1 control? (3)
Differentiation and migration of neurons in brain development, production of dendritic spines, and the generation of new neurons in the hippocampus.
71
Explain the neurodevelopmental hypothesis.
Prenatal or neonatal influences produce abnormalities that leave the developing brain vulnerable to other disturbances later in life, which results in mild abnormalities in brain anatomy and major disorders of behaviour.
72
What did Torrey find regarding schizophrenia?
One of the highest risk factors for schizophrenia is having a parent or sibling with schizophrenia.
73
Name some of Torrey's intermediate risk factors for schizophrenia.
Having a father over age 55, living in a crowded city, and prenatal or childhood infection with the parasite toxoplasma gondii.
74
Give some of Torrey's low risk factors for schizophrenia.
Poor nutrition of the mother during pregnancy, premature birth, low birth weight, complications during delivery, the mother being exposed to extreme stress early in pregnancy, prolonged illness of the mother during pregnancy, and head injuries in early childhood.
75
How does a baby's Rh-positive blood factor potentially lead to schizophrenia?
If the mother is Rh-negative the baby may be immunologically rejected.
76
Explain the season of birth effect.
The tendency for people born in the winter to have a slightly greater probability of developing schizophrenia.
77
What may account for the season of birth effect?
Viral infection.
78
How does viral infection of the mother impair foetal development? (2)
Excessive cytokines may cross the placenta and impair brain development, and fever may slow the development of foetal neurons.
79
What is different about a schizophrenic person's grey and white matter?
There is less than average.
80
What is abnormal in the prefrontal cortex regarding schizophrenics? (2)
There are weaker than average connections from the dorsolateral prefrontal cortex to other brain areas, and less than normal activity in this area during tasks requiring attention and memory.
81
What kind of brain damage to people with schizophrenia emulate?
Damage to the prefrontal or temporal cortex, resulting in deficits in memory and attention.
82
What task tests for damage in the prefrontal cortex?
The Wisconsin Card Sorting Test.
83
How does laterisation differ in people with schizophrenia?
Most people have a larger planum temporale in the left hemisphere, but in people with schizophrenia, the planum temporale in the right hemisphere is equal or larger.
84
What does chlorpromazine do?
Relieves the positive symptoms of schizophrenia in most patients.
85
Explain the dopamine hypothesis of schizophrenia.
Schizophrenia results form excess activity at dopamine synapses in certain brain areas.
86
Where is dopamine activity increased in schizophrenic people?
The basal ganglia.
87
What evidence supports the dopamine hypothesis of schizophrenia?
Extensive abuse of amphetamine, methamphetamine or cocaine induces substance-induced psychotic disorder, which results in the positive symptoms of schizophrenia (hallucinations, delusions).
88
Explain the glutamate hypothesis of schizophrenia.
The problem relates to deficient activity at glutamate synapses in the prefrontal cortex.
89
What is phencyclidine?
A drug that inhibits NMDA glutamate receptors.
90
What does phencyclidine produce at low doses?
Intoxication and slurred speech.
91
What does phencyclidine produce at high doses?
Positive and negative symptoms of schizophrenia.
92
What is the mesolimbocortical system?
Neurons that project from the midbrain tegmentum to the limbic system and prefrontal cortex.
93
How do drugs that block dopamine produce their effects?
They act on neurons in the mesolimbocortical system.
94
What produces tardive dyskinesia?
The effect of drugs that block dopamine synapses on neurons in the mesostriatal system.
95
What is tardive dyskinesia characterised by?
Tremors and other involuntary movements that develop gradually.
