Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PSYC-2920 > Chapter 12: Antipsychotic drugs > Flashcards

Chapter 12: Antipsychotic drugs Flashcards

1
Q

Delusions

A

beliefs that have no basis in reality, or that do not make sense.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Positive symptoms of schizophrenia

A

symptoms that are not usually present in normal people. feelings of grandeur, delusions, auditory or visual hallucinations, irrational beliefs, excessive motor activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Negative symptoms of schizophrenia

A

traits that are normally present in normal people, but absent in psychotic people.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

affective flatenning

A

an example of a negative symptom. where the person’s face is immobile and unresponsive, limited range of overt emotion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

anhedonia

A

an example of a negative symptom. state where a person feels no pleasure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

algoia

A

an example of a negative symptom. impoverished speech, where replies are brief and uncommunicative and seem to reflect diminished thinking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

avolition

A

an example of a negative symptom. inability to inititiate or engage in goal-related activity. Includes lack of ability to eat, clean oneself etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

T/F men have higher chances of being schizophrenic than women

A

false. men and women are equally affected by schizophrenia, but men often are affected at an earlier age than women.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

T/F schizophrenia is genetic

A

true, people who’s siblings are schizophrenic may have chances 10 times higher than a normal person of having schizophrenia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which genes are involved in the vulnerability of onset schizophrenia

A

genes that are involved in neuronal migration, neuronal differentiation and growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What issues in pregnancy affect risks of schizophrenia?

A

1) virus in mother
2) lack of oxygen during childbirth
3) lack of vitamin D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what system in the brain causes the positive symptoms of schizophrenia?

A

overactive mesolimbic dopamine system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what system in the brain causes the negative symptoms of schizophrenia?

A

degeneration and lessening of pfc activity, increasing hypoactivity at the mesoCORTICAL dopaminergic syapses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what part of the brain is twice as large in people with schizophrenia compared to “normal” people?

A

they have enlarged ventricals, fluid filled portions of the brain. indicates tissue loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

T/F: people affected by schizophrenia have less brain tissue than nonschizophrenics

A

true. individuals with schizophrenia have less brain tissue volume in up to 50 different brain regions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what parts of the brain are most largely subject to deterioration?

A

large parts of the

  • corpus callosum,
  • the cerebellum
  • areas of the frontal and temporal lobes
  • limbic system (amygdala, hippocampus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

deterioration of which part of the brain is responsible for decreased cognitive functioning and deficits in working memory in indivduals with schizophrenia

A

deterioration of the prefrontal cortex and hippocampus is associated with deficits in working memory and impaired cognitive function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

T/F: brain deteriorations in individuals with schizophrenia may happen even before birth

A

true. children who later have schizophrenia or have a parent with schizophrenia often showed delayed speech development, lack of motor coordination, problems with socializing, and poor short term and verbal memory deficits.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is synaptic pruning

A

where weak and unused synapses are pruned out and strong frequently used synapses remain and grow stronger.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what happens to synaptic pruning in individuals wtih schizophrenia? which synapses are most largely affected?

A

pruning may be exaggerated in individuals with schizophrenia, too many synapses may be degenerated. most synapses are dopaminergic and glutaminergic neurons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what brain regions are involved in the nigrostriatal dopamine pathway? Why is this pathway important? How do antipsychotics affect this pathway?

A

nigrostriatal pathway circulates dopamine from the substantia nigra to the striatum in the basal ganglia. this is important because activation of this symptoms allows smooth movements. antipsychotics work to decrease dopamine in the brain to avoid the positive symptoms of schizophrenia, but it also affects the nigrostriatal pathway, which is why people on antipsychotic medication may exhibit parkinsonian-like symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what brain regions are involved in the mesocortical dopamine pathway?

A

dopamine neurons run through the cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the dopamine hypothesis?

A

the hypothesis that schizophrenia results from excessive dopamine activity in the brain, specifically at D2 receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

outline an antipsychotics therapeutic effects and its relaitonship with bindinf afinity

A

drugs that can bind to dopamine receptors more readily (higher binding affinity) need to take less of a dose than drugs with weaker binding affinities in order to produce a therapeutic affect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

diathesis stress model

A

the idea that an individual is more likely to have schizophrenia if the mother has a stressed pregnancy (gets sick, troubles in labour leading to less oxygen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

affinity to which type of dopamine receptor is an indicator of antipsychotic potency?

A

affinity to the D2 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

the extrapyramedal motor system is invovled in which dopmanergic pathway?

A

the nigrostriatal pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

which brain regions are invovled in the mesolimbic dopamine system?

A

the vta and nucleus accumbens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

a molecule that binds really tightly to the d2 receptor will have a _____ dissociation constant

A

a low dissociation constant. (not likely to be dissociated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

which dopaminergic system is overactive? which dopaminergic system in underactive? what symptoms does this trigger?

A

the mesoLIMBIC dopamine system is overactive in a person with schizophrenia, triggering POSITIVE symptoms. the mesoCORTICAL pathway (PFC) is less active (HYPOFRONTALITY), and does not have a lot of dopamine, triggering cognitive deficits.

31
Q

how did researchers come up with the glutamate theory of schizophrenia?

A

they realized that individuals on PCP and ketamine, which antagonize NMDA receptors, showed aspects of positive and negative schizophrenia symptoms

32
Q

glutaminergic thoery

A

the theory that dopamine dysfunction is caused by glutamine dysfunction.

33
Q

which glutamate receptors are antagonized? are agonized? during the glutamate theory of sschizophrenia

A

the glutamate theory of schizophrenia believes that schizophrenia arises from NMDA receptor HYPOactivity and AMPA receptor HYPERactivity.

34
Q

How does NMDA hypoactivity (blockade) trigger AMPA receptor Hyperactivity?

A

Because blocking of NMDA receptors on GABA interneuron prevents GABA from being released into the cortex, activating glutamate release via the stimulation of AMPA receptors that are no longer inhibited by GABA.

35
Q

Why can’t you just give a schizophrenic NMDA agonists so that their GABA interneurons work?

A

because over stimulation of NMDA receptors will cause GABA cell death, aka excitotoxicity

36
Q

in schizophrenia, the mesocortical dopamine pathway is ____, producing negative symptoms, and the mesolimbic pathway is ____, producing positive symptoms.

A

in schizophrenia, the mesocortical dopamine pathway is UNDERACTIVE, producing negative symptoms, and the mesolimbic pathway is OVERACTIVE, producing positive symptoms.

37
Q

other transmitters that may be involved in schizophrenia?

A

serotonin, acetyl choline and histamine

38
Q

T/F: there is a similar effect in chemistry with anti-psychotics and benzodiazepines

A

false. the chemistry and effects are completely different between anti-psychotics and anti-anxiety medication.

39
Q

What does neuroleptic mean? What do neuroleptic drugs do?

A

neuroleptic: neuron claspers. These drugs cause extrapyramedal symptoms, such as rigidity or parkinsonian like symptoms.

40
Q

typical vs atypical antipsychotics

A

typicals are older than atypicals

41
Q

typical antipsychotics typically block ____ receptors, and only treat ____ symptoms of schizophrenia.

A

typical antipsychotics typically block D2 receptors, and only treat positive symptoms of schizophrenia.

42
Q

major side effect of typical antipsychotics

A

EPS. some patients on typical antipsychotics get severe parkinsonian like symptoms

43
Q

Typical drugs would most likely have a ____ dissociation constant to the D2 receptors

A

most likely have a low dissociation constant, meaning it would bind readily to the D2 receptors.

44
Q

A typical drugs have low affinities for the ___ receptors, and high affinities for ____

A

low affinities for D2 receptors, unlike typical anti-psychotics, and high affinities for 5-HT2a receptors, blocking the serotonin receptors.

45
Q

why do atypical antipsychotics not cause EPS like typical antipsychotivs?

A

because they do not bind to the D2 receptors in the basal ganglia, and thus they are not blocking dopamine in the nigrostriatal system. People will parkinsons do not have enough dopamine in the nigrostriatal system, and thus get shaky. People on atypical antipsychotics do not get a decrease in dopamine in the nigrostriatal pathway, preventing EPS symptoms.

46
Q

what kind of dopamine receptors to atypical antipsychotics bind to rather than D2?

A

they bind to D3 and D4 receptors, which are NOT located in the motorsystems, preventing EPS. although they bind to these receptors, the most well known difference is due to atypicals ability to bind and block excitatory 5HT2a receptors.

47
Q

relationship between LSD and atypical antipsychotics

A

LSD agonizes 5-HT2a, causing an increasing in positive schizophrenic symptoms like hallucinations, whereas atypical antipsychotics bind and block 5-HT2a receptors, decreasing positive side effects of schizophrenia.

48
Q

what symptoms do atypical antipsychotics mainly prevent?

A

mainly prevent negative symptoms, and they have a greater effect on reversing hypofrontality. (mesocortical system
hypoactivity)

49
Q

T/F: Schizophrenia drugs always and only bind to either D2 or 5-HT2a receptors

A

FALSE. these are not “clean” drugs. they effect a multitude of systems and effect glutamate, gaba, histamine and acetylcholine receptors and transmitters as well.

50
Q

What is akathesia? What drug is this sideeffect associated with?

A

Akathesia is uncontrolled restless ness and compulsive movements. this is caused by compensatory mechanisms of the body after prolonged use of TYPICAL antipsychotics. when on typical antipsychotics that are blocking D2 receptors (and causing EPS), the body is upregulating D2 receptors. Once someone is off the drug, there is a lot of D2 receptors and the person may display uncontrolled restlessness because of the overactive D2 receptor firings.

51
Q

what are side effect profiles?

A

side effects of antipsychotic drugs. side effects are usually caused by the fact that atypical and typical anti-psychotics effect other neurotransmission systems like acetyl choline and histamine.

52
Q

tardive dyskensia

A

a side effect of antipsychotics that results in the presentation of repetitive and involuntary purposeless movement like lip smacking. Usually the effects of an TYPICAL antipsychotic. Due to over sensitization of the EXTRAPYRAMIDAL MOTOR SYSTEM and compensatory mechanism and response to DA blockage.

this is usually seen when the antipsychotic is withdrawn and there is nothing blocking hte upregulated amount of dopamine receptrs. Opposite of parkisons. Parkisons prevents movement, while patients with tardive cannot stop moving.

53
Q

are antipsychotics absorbed in the digestive system?

A

yes

54
Q

why do antipsychotics have long half lives?

A

because they are quickly bound to blood proteins which cannot be excreted in the urine. they also have a tendency to stay in body fat,

55
Q

what is agranulocytosis?

A

fatal loss of white blood cells and decline in the immune system function due to suppression of bone marrow activity.

56
Q

what brain region is responsible for problems of temperature regulation in patients on antipsychotics?

A

dopamine D3 receptors are blocked in the isles of Calleja, which is responsible for temperature regulations.

57
Q

what’re some symptoms of antipsychotics as a result of their anticholinergic effects?

A

dry mouth, impaired Vision and constipation.

58
Q

T/F Antipsychotics alter sleep cycles and rem sleep

A

false.

59
Q

T/F you must be very careful taking antipsychotics because it is really easy to overdose

A

false. these drugs are not lethal and have an extremely high LD50

60
Q

T/F moving through molasses is commonly said to be a subjective effect of antipsychotics

A

true

61
Q

plastic immobility

A

antipsychotics suppress SMA in nonhumans, effectively rendering the animals immobile

62
Q

effects on antipyschotics on conditioned behavior

A

drugs cause a decreas in response rate on schedules maintained by positive reinforcement.

drugs will decrease avoidance but have no effect on escape from shock.

63
Q

problems with dissociation?

A

sometimes people will not remember what they had learned before they were on the drug, or sometimes they will only remember things if they are on the antipsychotic.

64
Q

Typicals will ____ to other typicals.

A

typicals will generalize to other antipsychotics

65
Q

T/F: typicals can generalize to antidepressants and benzodiazepines

A

false, they don’t realyl generalize to anything besides other typicals.

66
Q

do atypicals generalize to typicals

A

No.

67
Q

why don’t antipsychotics generalize to other drug classes?

A

because antipsychotics overall block D2 receptors, while other drugs like alcohol and antidepressents and meth increase the release of D2

68
Q

T/F: antipsychotics are positive reinforcers

A

false. they are not self administered. in fact, they are avoided.

69
Q

cognitive deficits with acute administration?

A

yes, but they build up tolerance after 2 weeks.

70
Q

5-HT2a receptors are ____ while 5-HT1a receptors are ____

A

2a= excitatory, 1a= inhibitory.

71
Q

atypical antipsychotics typically block ___

A

5-HT2a receptors, but there is variability in their actions on 1A.

72
Q

How do antipsychotics increase activity in the frontal cortex to account for efficacy against both negative and positive symptoms?

A

atypical antipsychotics increase activity via 5ht2A (excitatory) ANTAGONISM (BLOCK) and 5HT1a AGONISM on GABA-containing neurons (1a is inhibitory, therefore, gaba is inhibited therefore MORE dopamine in the mesocortical pathway (less negative symptoms), and also decrease DA activity in the mesolimbic pathway, accounting for less positive symptoms.

73
Q

5HT1a ____ improves cognitive function. 5HT2a ____ improves cognitive function.

A

5HT1a AGONISM improves cognitive function. 5HT2a ANTAGONISM improves cognitive function.

74
Q

how is sensorimotor gating in animal models tested?

A

through pre pulse inhibition

PSYC-2920 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions