BIO T9 Flashcards
What is the issue surrounding construct validity and the use of animal research in psychopathology?
- Injecting animals with a known genetic mutation linked to the disease → not possible
- Altering the expression of proteins hypothesised to lead to disease pathogenesis → lack of human evidenceExposure to validated environmental risk factors → not as straightforward
- how penetrant a given genetic variant is in producing a disorder/ how clearly linked; lack of human evidence for common genetic variants being irrefutably linked to mental health conditions*
antidepressant that blocks the reuptake of catecholamines and serotonin by presynaptic terminals
tricyclic
antidepressant that blocks the reuptake of serotonin in the presynaptic terminal
SSRI
antidepressant that blocks the reuptake of serotonin and norepinephrine
SNRI
antidepressant that blocks a presynaptic terminal enzyme that metabolizes catecholamines and serotonin into inactive forms
MAOI
drug that mimics or increases the effects of a neurotransmitter
agonist
affinity
tendency of a drug to bind to a receptor
efficacy
drug’s tendency to activate the receptor
brain area that is rich in dopamine and is central to the brain’s reinforcement system
nucleus accumbens
craving
insistent search for something
tolerance
decreased effect of a drug after repeated use
withdrawal
effect of drug cessation
antabuse
drug that antagonizes the effects of acetaldehyde dehydrogenase by binding to its copper ion
methadone
drug similar to heroin and morphine that is taken orally
SAD
seasonal affective disorderdepression that recurs during a particular season, such as winter
mania
condition characterized by restless activity, excitement, laughter, self-confidence, rambling speech, and loss of inhibitions*
lithium
element often used as therapy for bipolar disorder
presence of behavior not seen in normal people
positive symptom
negative symptom
absence of behavior ordinarily seen in normal people (e.g., lack of emotional expression)
concordance
similarity, such as having the same disorder as someone else*
differential diagnosis*
one that rules out other conditions with similar symptoms
DISC1 (disrupted in schizophrenia 1)
gene that controls production of dendritic spines and generation of new neurons in the hippocampus
chemical family that includes antipsychotic drugs that relieve the positive symptoms of schizophrenia*
phenothiazinechemical family that includes antipsychotic drugs that relieve the positive symptoms of schizophrenia
dopamine hypothesis of schizophrenia
idea that schizophrenia results from excess activity at dopamine synapses in certain brain areas
movement disorder characterized by tremors and other involuntary movements*
tardive dyskinesia
second-generation antipsychotic
drug that alleviates schizophrenia with less likelihood of movement problems
drug that inhibits the NMDA glutamate receptors*
phencyclidine (PCP)
Which of the following statements is MOST true regarding the brains of severely depressed patients?
a. Severely depressed patients’ brains show increased hippocampal volumes as compared to controls.
b. Severely depressed patients’ brains have a lower hippocampal function as compared to healthy individuals.
c. Severely depressed patients’ brains havehigher concentrations of 5-HT and catecholamines.
d. Severely depressed patients’ brains are characterised by up-regulated adult neurogenesis.
B
Which of the following is a TRUE DISADVANTAGE of Electroconvulsive therapy in depression?
a. It is only used as a supplement to other treatments rather than a therapy by itself.
b. The probability of a quick relapse is high.
c. It takes longer than anti-depressant drugs to provide improvements in the treatment of depression.
d. It is not effective in patients with severe depression.
B
Which of the following is the MOST accurate regarding the role of the allele polymorphism for the serotonin transporter in depression?
a. Stressful life experiences increase the likelihood of depression in people with the shortgene for the serotonin transporter.
b. People with the long form of the gene for the serotonin transporter have a higher increased probability of depression in response to stressful experiences.
c. People with the short and long forms of the gene for the serotonin transporter have an equal probability of depression in reaction to stressful events.
d. The serotonin transporter is not related to depression.
A
Which of the following is MOST TRUE regarding the course of the illness for patients with depression?
a. The majority of patients have a long depressive episode and never experience symptoms again.
b. The majority of patients have an episodic illness course and they feel well between acute episodes during their lifetimes.
c. The majority of patients do not recover and experience depression symptoms continuously during their life.
d. The majority of patients have a long depressive episode in their mid-40s.
B
What is the MAIN mechanism of action of antidepressant drugs?
a. Inhibition of acetylcholinesterase
b. Inhibition of 5-HT and norepinephrine storage in vesicles of presynaptic nerve endings.
c. Blocking serotonin and norepinephrine reuptake transporters.
d. Stimulation of dopamine receptors.
C
A man has been suffering from severe depression and suicidal ideations after being treated for a year with cognitive-behavioural therapy and multiple antidepressant medication trials. His doctor will now MOST likely prescribe:
a. Monoamine therapy.
b. Electroconvulsive therapy.
c. Psychosurgery
d. Antipsychotic therapy
B
Which of the following hypotheses BETTER explain the antidepressant drug effectiveness?
a. Antidepressant drugs increase monoamine oxidase activity.
b. Antidepressant drugs lead to increased levels of a neurotrophin (BDNF) important for hippocampal neuronal proliferation and learning.
c. Antidepressant drugs decrease the effects of serotonin and norepinephrine in the brain.
d. Antidepressant drugs lead to neuronal loss and hyperactivity in the right prefrontal cortex
B
K.S. has been diagnosed with major depression. During her EEG scan, her doctor observes:
a. Hyperactivation of her right prefrontal cortex.
b. Hypoactivation of her right prefrontal cortex.
c. No changes in her prefrontal cortex activation.
d. None of the above.
A
How is Schizophrenia diagnosed?
At least two symptoms, being oneof them: delusions, hallucinations, ordisorganized speech. Ongoing for 6 months(at least 1 month of delusions/hallucinations)
When is the usual onset of schizophrenia
The usual onset of schizophrenia is in late adolescence to early adulthood, typically between 16–30 years old. It rarely develops before age 13 or after 40
What is the risk level for schizophrenia amongst MZs?
48%
What does schizophrenia affext in the brain?
ventricles are enlarged<img></img>
Environmental risk factors of schizophrenia?
Environmental risk factors:
* Living in cities vs. rural areas
* Childhood trauma
* Autoimmune diseases
* Cannabis use
What is the neurodevelopmental hypothesis of schizophrenia?
prenatal or neonatal influences produce abnormalities in the developing brain
* Prenatal or childhood infection with the parasite toxoplasma gondii
* Poor nutrition or stress exposure of the mother;season-of-birth effect (winter and early spring)<img></img><img></img>
What are the brain abnormalities of schizophrenia and how can they be tracked?
pet scan* <img></img>*
* Enlarged ventricles
* Reduced white matter
* Abnormalities in subcortical areas
* Reduced grey matter specially in hippocampus, amygdala, thalamus
* Decreases in brain volume(about 5%)
* Abnormalities visible in blood vessels of the retina
* Dorsolateral prefrontal cortex anatomically affected
What is early onset schizophrenia?
Comparison of three-dimensionalmaps derived from MRI scans revealsthat, compared with healthy teenagersaged 13 to 18 (left), patients withchildhood-onset schizophrenia (right)have widespread loss of gray matteracross the cerebral hemispheres* <img></img>
What are the chemical treatments?
*Phenothiazines (e.g., chlorpromazine)
* Butyrophenones (e.g., haloperidol - tradename Haldol)
* These drugs block dopamine type D2synapses
Which pathway is responsible for positive symptoms?
Mesolimbic pathway| increased DA relese in NAc
Which pathway is responsible for negative symptoms?
Mesocortical| decresed DA release in prefrontal cortex leads to negative cognitive sym
What is the glutamate hypothesis of schizophrenia?
schizophrenia results from deficient activity atglutamate synapses in PFC* <img></img>* <img></img>
Wht are the class of symptoms of depression?
<img></img>* At least five symptoms, being at least oneof them a fundamental one, nearly everyday during a 2-week period. Thesymptoms are clearly different from theindividual´s previous general functioning.
Persistent depressive disorder
Moderate depression that persists for morethan 2 years (American PsychiatricAssociation, 2013), with at least two of thefollowing symptoms: difficulty with decisionmaking and concentration, feelings ofhopelessness, low appetite or overeating,fatigue, low self-esteem, problems with sleep
Which neurochemical systems of depression?
<img></img>
What is the pathology of depression?
results from a deficit of one of theseNT: serotonin and noradrenaline (Monoaminehypothesis)
How do stress and depression intersect?
elevatedlevels of circulating cortisol –>; failure of negativefeedback mechanisms* <img></img><img></img>of glucocorticoidsalter the serotonin,norepinephrine, and dopaminesignaling systems
What happens to the brain in bipolar disorder?
gray matter losse anterior insula,prefrontal córtex (ventrolateral,ventromedial, dorsomedia), andsubgenual cingulate cortex.<img></img>
What is the inflammatory hypothesis of depression?
Cytokines pass the blood brain barrier andstimulate the release of CRH and interactwith noradrenaline, dopamine andserotonin signaling pathways due to infection which influences the BDNF
What do these scans of one individual’s brain show?
A bipolar brain
When is the usual onset of schizophrenia
Which neurochemical systems of depression?
