Week 1-Anxiety and Schizophrenia Flashcards

Question

What does Benzodiazephine do to the amygdala?

Answer 1

Benzodiazepines work by increasing GABA activity BENZODIAZEPINES REDUCE AMYGDALA ACTIVITY Benzodiazepines work by increasing GABA activity?

Answer 2

* Now, drug treatment has shifted away from benzodiazepines due todependence concerns (addictive) * Selective Serotonin Reuptake Inhibitors (SSRIs) increase levels of the neurotransmitter serotonin, and are now the first choice of treatment for most anxiety disorders SRIs are drugs that increase serotonin levels Why do SSRIs work in anxiety disorders? - a single dose of SSRIs DECREASES amygdala activation to fear faces stimulus. -SSRI treatment reduces amygdala activation in anxious patients *Also REDUCES hippocampal activityunder stress conditions

Answer 3

-Over-activation in amygdala disappears after therapy in phobic patients -Increased activity in frontal cortex after exposure therapy:cognitive control of fear response

Answer 4

1%- 1 in 100 people will be diagnosed in their lifetime. | Late adolescence or early 20s esp males

Answer 5

•Schizophrenia was first described as ‘dementia praecox’and popularized by Emil Kraepelin in 1893 • Eugen Bleuler was the first to coin the term schizophrenia in 1908 • Some psychiatrists believe Vincent Van Gogh suffered from schizophrenia, with his paintings inspired by his hallucinations..

Answer 6

Schizophrenia is NOT ‘split/multiple personality’ disorder! .. It’s actually a very complex and heterogeneous disorder –considerable variability between cases, in terms of symptoms, severity,course, and response to treatment (different symptoms and severity-mild or severe) .. It has serious consequences: People with schizophrenia are sometimes unable to be part of society and need to be INSTITUTIONALIZED

Answer 7

1) Positive Symptoms: PRESENCE of symptoms - Delusions (e.g., grandeur-special powers or paranoia) - Hallucinations (perceptual disturbances, often auditory: “Hearing voices”) - Disorganised speech → Nonsense sentences or no logical connections 2) Negative Symptoms: ABSENCE of response - Reduced expression of emotion(lack of emotion in facial expression ;hand gestures; emorion) - Poverty of speech(hard to intiate and carry on convo) - Difficulty in initiating goal-directed behaviour(difficulty in daily activities) - Neglect of personal hygiene

Answer 8

DSM-V CRITERIA Two or more of the following 5 symptoms present for AT LEAST 1 MONTH At least one of these must be 1, 2, or 3: 1. *Delusions 2. *Hallucinations 3. *Disorganised speech 4. Disorganised or catatonic behaviour 5. Negative symptoms **Social/occupational dysfunction(impairment of day to day life) Continuous signs of illness for at least 6 months (with at least 1 month of active symptoms)

Answer 9

• Positive and negative symptoms seem to worsen and improve in cycles known as relapses and remissions • A period of intense positive symptoms = “psychotic episode” • Cognitive Symptoms(more stable-present across the illness) also a core feature of Schizophrenia-IMPAIRMENTS OVER COGNITIVE DOMAINS • Attention: poor ability to maintain attention when doing a task • Working memory: verbal WM particularly impaired • Executive function: ‘inflexible’ thinking style • Unlike other symptoms, these are relatively stable overmthe course of the illness

Answer 10

``` • Schizophrenia is a complex disorder with no single ‘cause’ • Genetics and environment interact to increase risk • We’ll look at: • 1. Genetics • 2. Neurodevelopmental factors • 3. Brain abnormalities • 4. Neurotransmitters ```

Answer 11

• Twin, adoption and family studies provide consistent evidence that genetic factors are important. (STRONG GENETIC INFLUENCE of Schizophrenia) • Schizophrenia has a high heritability • ***The child of someone with schizophrenia is 13x more likely than average to develop it** • There is a 48% chance that the identical twin of someone affected also has schizophrenia

Answer 12

* A large number (>100) ‘high-risk’ genes have been identified * Some overlap with other disorders (e.g. autism) * Includes the dopamine receptor D2 gene (links to treatment) * But these explain less than half the genetic variance * Gene mutations also have a role * Increased paternal (father)age at conception (more mutations) =increased schizophrenia risk * Could explain why schizophrenia still present in 1% of the population (quite a large proportion), despite patients not living as long/less likely to reproduce

Answer 13

Genetics only explains some of the risk: 85% of individuals with schizophrenia have no first-degree relative with the illness • Environment also important? Gene-environment interactions: Environmental factors can affect gene expression and/or Genes make a person more vulnerable to develop the disease when exposed to certain environmental factors. STUDY: Adopted children with a biological schizophrenic mother but no schizophrenia in the adopting family Probability for developing schizophrenia is slightly higher,but this effect is greatly magnified if the adopting family is dysfunctional.

Answer 14

NEURODEVELOPMENTAL FACTORS may cause Schizophrenia -Prenatal factors=> seem to be the most important e.g. infections during pregnancy(influenza, rubella), low birth weight. These might affect neurodevelopment with the results only showing later in life. -Some evidence that cannabis use in adolescence increases risk,particularly in those with genetic risk.

Answer 15

• On average, people with schizophrenia have larger than average ventricles (fluid-filled spaces in the brain), reduced brain volumes, and less brain connectivity

Answer 16

DOPAMINE HYPOTHESIS-Excess dopamine release causes Schizophrenia • .. Says that schizophrenia results from excess dopamine activity: Neurons release dopamine faster than they should • Evidence? • Genetics: 4 of the top 10 gene variants (high risk genes) most strongly associated with schizophrenia are directly involved in dopamine pathways • Some dopaminergic recreational drugs (e.g., cocaine, amphetamine) can cause hallucinations and delusions

Answer 17

--->All ANTIPSYCHOTIC drugs BLOCK dopamine receptors (D2-receptors) ---->D2 receptor Antagonists ----->leads to improved positive symptoms ----->Higher dopamine receptor blocking= larger effect on symptoms There seems to be a threshold amount of D2 binding needed for the treatment to work Side effects: extrapyramidal symptoms (motor restlessness/rigidity)

Answer 18

• Typical antipsychotics (developed in 1950s), act on D2 receptors • Otherwise known as ‘first’generation antipsychotics (or Neuroleptics) • High incidence of side-effects on motor control (EPS, or extrapyramidal symptoms) * Atypical (‘second’ generation) antipsychotics (developed in 1990s) * Reduced risk of these side effects on motor system. Act on several dopamine receptors(e.g., D2, D3, D4) and serotonin pathway * Have other side effects: e.g. Drowsiness; weight gain

Answer 19

• Treatment resistance: (1/3 don’t respond to antipychotics, though might respond to clozapine which has only weak D2 affinity) • There may be a ‘non-dopaminergic’ subtype of schizophrenia? • Antipsychotics have only LIMITED effects on cognitive impairments and negative symptoms • Not all patients show higher dopamine levels

Answer 20

➢ Glutamate hypothesis:- schizophrenia is due to NMDA receptor (asubtype of glutamate receptor) dysfunction ➢ Evidence?-Recreational drugs affecting NMDA receptor ➢ NMDA receptor antagonists, including phencyclidine (PCP) and ketamine have psychological effects which resemble positive, negative and cognitive symptoms ➢ These drugs make symptoms worse in schizophrenia patients ➢ But - trials of glutamatergic treatments have not been successful ➢ But some researchers think that NMDA dysfunction might contribute to the negative symptoms.. ➢ And have knock-on effects on dopamine

Week 1-Anxiety and Schizophrenia Flashcards

(44 cards)