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Psychopharmacology > Final > Flashcards

Final Flashcards

1
Q

What is the definition of Schizophrenia?

A

a sever, lifelong mental illness consisting of distrubed thinking, abnormal behavior, an inability to understand what is real, and impaired processing of emotions

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2
Q

What are positive symptoms in schizophrenia?

A

presence of abnormal behaviors (hallucinations, delusions, thoughts of persecution)

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3
Q

What are negative symptoms of schizophrenia?

A

reduction in normal behaviors (reduced emotional responsiveness, social withdrawal, reduced movemet, lack of motivation)

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4
Q

How long must the schizophrenic symptoms be present in order to be diagnosed?

A

6 months

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5
Q

What are the five types of schizophrenia?

A
  1. paranoid- prominent positive symptoms
  2. catatonic- predomininant negative symptoms
  3. disorganized- silly or immature emotional responses
  4. undifferentiated- does not appropriately fit these categories
  5. residual- now present less symptoms than they did in the past
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6
Q

What percent of patients exhibit chronic symptoms of schizophrenia? The remaining percent exhibit….

A

50-70% of patients exhibit chronic symptoms…the remaining 30-50% exhibit residual features

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7
Q

What is treatment resistant schizophrenia? How many patients exhibit this?

A

exhibit minimal or no improvements afer two trails with either typical or atypical antipsychotic drugs… 1/3 qualify.

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8
Q

When are benzodiazepines prescribed to patients with schizophrenia? What causes the reason?

A

those with catatonia (negative symptoms)

may be caused by depression, alcohol withdrawal, AIDS

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9
Q

Nearly all patients with schizophrenia have deficits in…

A

cognitive functioning (working memory, reference memory, attention, executive function)

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10
Q

People with schizophrenia often have poor functional outcomes, what does this mean?

A

patients inclusion in a community, behaving normally in social situations, successful psychosocial skills are all impraied

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11
Q

What is a sensory gating deficit? What test is used to test for this?

A

low capacity to filter out unimportant stimuli in the enviornment (misinterpretation of the enviornment…can lead to delusional behavior)
test used: prepulse inhibition procedure…schizophrenia patients have a diminished ability to inhibit a startle response

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12
Q

What is cognitive dysmetria?

A

abnormalties in processing, coordinating, and responding to information

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13
Q

When is schizophrenia usually first diagnosed?

A

late teens/early 20s (never really before puberty or after 40)

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14
Q

How many people does schizophrenia affect?

A

1% of world population (~3 million in the US)

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15
Q

How does schizophrenia affect men and women

A

equal prevalence in both, but earlier onset in males (18-25) later in women (25-35)
-men will prematurely have poor socail functioning, whereas women portray fewer schizotypal traits
men show more negative symptoms, more withdrawn and passive…women have pos. symptoms (hallucinations and paanoia, more emotional and impulsive–easier to treat)

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16
Q

What happens in the prodromal phase of schizophrenia?

A

pre-schizophrenia signs characterized by less frequent and less severe symptoms…attention impairment most predictive
exhibit reduced volume of cortical gray matter

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17
Q

What does schizophrenia derive from?

A

genetic abnormalities, reduced volume of brain structure, and abnormal connectivity among brain structures

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18
Q

most evidence of the derivation of schizophrenia is found in what gene? and what does this gene code for?

A

disrupted SIDC1 gene (gene codes for a protein important in signaling event that occur within neurons, development of neurons, and cell migration)

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19
Q

What is the most consistent observation in schizophrenic brains?

A

reduced volume sizes of structures in the left hemisphere and temporal lobe
–also fine decreased volume of frontal lobe, reduced connectivity from thalamus to cerebellum

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20
Q

What is found in the cognitive dysmetria theory?

A

dysfunctions in connectivity between thalaus and cerebellum…and thalamus and cerebral cortex
leads to abnormal sensory processings, timing functions, and error processings

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21
Q

What is found in the brain during auditory hallucinations, memory tasks, and rest in schizophrenia?

A

abnormal levels of activity in the hippocampus

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22
Q

What is the neurodevelopmental hypothesis?

A

abnormal nervous system develoopment leads to irregular neuronal signaling in the brain
–genetics impacts synaptogenesis and myelination

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23
Q

What did early treatments of schizophrenia include?

A

confinement, induced fevers, convulsive shock therapies, and frontal lobotomies

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24
Q

What drug did Dr. Henri Laborit administer in 1952 which showed a reduction in psychotic symptoms?

A

preanesthetic agent: chlorpromazine

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25
Q

Most neurotransmission theories in schizophrenia consider abnormalities in what neurotransmitters?

A

dopamine and glutamate

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26
Q

Positive symptoms in schizophrenia arise from what

A

increased dopamine release in the LIMBIC SYSTEM

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27
Q

antispcyhotic drugs act as agonists/antagonists on what receptors? resulting in..

A

antipsychotics act as antagonists on D2 receptors (dont trigger postsynaptic response)…releases dopamine–positive symptoms

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28
Q

what effect does amphetamine have on schizophrenia

A

causes psychotic symptoms through the increase of dopamine release

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29
Q

What does an increase in dopamine release from mesolimbic dopaminergic neurons result in? where do they terminate?

A

results in positive symptoms–terminates in nucleus accumbens

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30
Q

What is the glutamate hypothesis?

A

there is a decreased release of glutamate throughout the cerebral cortex and limbic system

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31
Q

What was the first typical antipsychotic drug?

A

chlorprozamine

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32
Q

are typical antipsychotics better at treating negative or positive symptoms?

A

positive symptoms…have a weak efficacy for negative symptoms and cognitive impairement

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33
Q

What are extrapyramidal side effects?

A

adverse effects consisting or tremor, msucle rigidity, and involuntary movements associated with TYPICAL antipsychotic drugs
in many ways, EPS resemble Parkinsons

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34
Q

What causes EPS?

A

antagonism of D2 receptors in the basal ganglia (typical antipsychotics)

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35
Q

are atypicals or typicals better at reducing negative symptoms and cognitive impairment?

A

atypicals

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36
Q

What’s the difference of the mechanism of action of typical and atypical antipsychotics?

A

typical: mainly through blockade of D2 receptors
atypical: through bloackade of D2 receptors and 5HT2A receptors

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37
Q

Today, if typical antipsychotics are prescribed, what is also prescribed with it?

A

muscarinic receptor agonist to reduce EPS severity (Benztropine)
but this further impairs cognitive functioning

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38
Q

What is tardive dyskinesia?

A

a motor disorder affects mainly facial muscles–adverse effects may not occur until a patient stops taking medications but can still persist for a long time after discontinuation

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39
Q

what is neurolepic malignant syndrome?

A

resembles flu-like symptoms and bloop pressure changes…ANS changes and EPS

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40
Q

what is hyperolactinemia?

A

occurs from high prolactin in the blood…decreases lactionation and libido…erectyle dysfunction. D2 receptor regulates prolactin from anterior hypothalamus

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41
Q

What are antiemetic effects?

A

reduce nausea and vomiting.

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42
Q

nausea and vomiting occur from activtion of where?

A

chemoreceptor trigger zone (area in medulla unprotected by the blood brain barrier)…sends signals to area postrema which elecits vomiting

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43
Q

What effect does 5HT3 antagonism have?

A

linked to antiemetic effects

some typical antipsychotics have this effect

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44
Q

What is the first line treatment for schizophrenia?

A

atypical antipsychotic drugs

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45
Q

which drug was the first atypical antisychotic?

A

clozapine (Clozaril)

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46
Q

Why was clozapine declared as the first atypical antipsychotic?

A

there was a lack of EPS…led to the development of olanzapine and risperidone

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47
Q

What effect do atypical antipsychotic drugs have on schizophrenia?

A

reduce positive and negative symptoms and lower the risk of EPS…may improve cognitive functioning…may reduce depression

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48
Q

What adverse effects do atypical antipsychotics carry?

A

EPS at HIGH doses, risk of neuroleptic malignant syndrome, may produce hyperolactinemia
-significant increases in body weight, risk of type II diabetes
QT interval prolongation-cardiac arrest

have lower risk but not absence of adverse risks than typicals

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49
Q

what adverse effects could clozapine cause?

A

slight risk of agranulocytosis (low WBC count)

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50
Q

Which atypical antispychotic is preferred to be used as an antiemetic?

A

Olanzapine–antagonisitc actions at D2 and 5HT3 receptors

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51
Q

what is the serotonin dopamine hypothesis?

A

drug effects derive from preferntial antagonism of 5HT2A receptors compared to D2 receptors

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52
Q

What is the fast D2-off hypothesis?

A

rapid dissociation of a drug from a D2 receptor

typicals SLOWLY dissociate, atypicals don’t block D2 receptors for as long a time

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53
Q

What other receptors do antipsychotic drugs bind to other than dopamine and serotonin?

A

alpha 2 (combined with D2 antagonist–> atypical antipsychotic effects)
clozapine: antagonism of histamine H1 receptor (causes drowsiness)
H1+5HT2C: weight gain and increased risk of diabetes

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54
Q

What are third-generation antipsychotic drugs?

A

drugs that produce antipscyhotic effects through mechanisms of action different from those of typical and atypical antipsychotic drugs

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55
Q

What is the best known third-generation antipsychotic drug? and what is its mechanism of action?

A

Aripiprazole (Abilify) is a wek partial agonist for D2 receptors
shares antagonistic effects at 5HT2A (similar to atypicals)
unlikely to produce EPS…less effective than olanzapine for treating schizophrenia but might offer less risk of type II diabetes

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56
Q

What is an antipsychotic depot injection?

A

provides a slow release of antipsychotic drug, over the course of weeks, after a single injection
-preferred in situations when patients do not comply with their prescribed treatment regime

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57
Q

definition of autism

A

neurodevelopmental disorder conssisting of social impairments, verbal and nonverbal language difficulties, irritability and repetitive behaviors

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58
Q

what are the genetic links found in autism?

A
  • usually found in both twins
  • abnormalities in chromosomes 4 and 7…causes abnormal connectivity in prefrontal cortex, which may have implications in cognitive, social, and emotional features; visual system may be out of sync with activity in motor system
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59
Q

What medicines can be given to people with autism? What are the risks?

A

aripiprazole and risperidone…reduce autism-related irritability
risks: weight gain, fatigue, EPS–> more common in children than adults

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60
Q

In schizophrenia, where is dopamine high/low according to the glutamate hypothesis?

A

low in cortical, high in limbic system

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61
Q

What do low levels of dopamine in the prefrontal cortex result in?

A

cognitive impairment and negative symptoms

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62
Q

What increases dopamine concentration in the prefrontal cortex?

A 
atypical antipsychotics (not typical)
clozapine and risperidone increase DA concentration
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63
Q

What is the result of diminished dopamine release in the prefrontal cortex? (next step)

A

fails to excite glutamate neurons

negative symptoms

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64
Q

What does diminished glutamate release result in? (Next step)

A

fails to excite mesocortical dopamine neuron activity

and fails to excite GABA neurons (negative symptoms)

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65
Q

What does diminished GABA release result in? (next step)

A

fails to diminish mesolimbic dopamine activity

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66
Q

What happens when no gaba can diminish the mesolimbic dopamine activity ? (next step)

A

excess dopamine release occurs in the nucleus accumbens (positive symptoms)

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67
Q

Does haloperidol have an impact on dopamine levels in the prefrontal cortex?

A

no. it is a typical antipsychotic (D2 agonist) and does not have an effect on dopamine levels unless is it combined with a 5HT2A agonist

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68
Q

What effect does 5HT2A receptor have on dopamine?

A

dopamine brake.when serotonin is released onto the postsynaptic 5HT2A receptor, dopmine neuron is inhibited

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69
Q

What effet does the 5HT1A receptor have on dopamine?

A

5HT1A is an autoreceptor which inhibits serotonin release…so when ligand binds, cannot be activated nd the dopamine brake is NOT applied.
dopamine neurons lose inhibition of action of 5HT via 5HT2A receptors (disinhibition)
–there is an increase in dopamine

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70
Q

How does 5HT2A antagonism make an antipsychotic atypical?

A

stimulates dopamine release…receptor brake is disrupted by the antagonist, which disinhibits dopamine neuron and increases dopamine release

reduces EPS and reduces negative symptoms

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71
Q

What effect does 5HT1A agonism have on glutamate?

A

reduces it. reduces positive symptoms

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72
Q

definition of fear

A

negative emotion caused by a real or perceived imminent danger/threat

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73
Q

defiintion of anxiety

A

worry and distress concerning potential events or outcomes

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74
Q

what is a specific phobia?

A

anxiety provoked by exposure to specific objects/situations

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75
Q

what is panic disorder?

A

consists of repeat occurrences of panic attacks

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76
Q

what is agorophobia?

A

profound fear of being in a situation from which escape is difficult or embarrassing

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77
Q

what is the prevalence of anxiety disorders?

A

7.3% worldwide, 2x as common in females

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78
Q

what is the most associated factor with developing anxity?

A

childhood abuse

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79
Q

what is the amygdala responsible for?

A

a critical structure for fear and anxiety (increased activity)…less involved in OCD
-relating stimuli or events to fear and for mediating the physiological and psychological response to fear

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80
Q

Where is there abnormal functioning in OCD?

A

thalamus, cingulate cortex, preforntal cortex, basal ganglia, and nucleus accumbens

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81
Q

in the nervous system, the what brain structure sends sensory information to the amygdala?

A

the thalamus

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82
Q

what is the thalamo-amygdala pathway

A

sends unprocesses sensory info directly to amygdala “short route”
provides only basic features of the stimulus

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83
Q

what is the thalamo-cortical-amygdala pathway?

A

information is processed in the cebreal cortex “long route”
info about stimulus
if context of environment is important, then info sent from hippocampus
prefrontal cortex can reduce amygdala activity

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84
Q

what is the early immediate gene?

A

a gene rapidly activated in response to stimuli

  • c-fos becomes activated in response to stimuli
  • channelrhodopsin…used to demonstrate how activation of appropriate neurons led to fear response even in places the animals had never been fear conditioned
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85
Q

When the amygdala receives fear-related stimulus, where does it send output signals to?

A

prefrontal cortex, hyppothalamus, and locus coeruleus

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86
Q

what does the prefrontal cortex play a role in?

A

in determining how we behave in a fearful situation

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87
Q

what do the hypothalamus and locus ceroulus play a role in?

A

facilitate physiological reactions to fear…activated sympathetic nervous system>release of epinephrine from adrenal gland

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88
Q

what is the general adaptation syndrom?

A

stress syndrome occurring in three progressive phases: alarm, resistance, and exhaustion

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89
Q

what is the alarm stage of the general adaptation syndrome?

A

increased physiological arousal in preparation for an emergency situation…hypothalamus activates sympathetic nervous system

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90
Q

what is the resistance stage of the general adaptation syndrome?

A

sustained level of physiological arousal…hypothalamus elicits the release of ACTH from pituitary gland; adrenal gland releases cortisol

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91
Q

what is the exhaustion phase of general adaptation syndrome?

A

fatigue, suceptibility to disease…immune system and metabolic activity of organs throughout the body are underactive

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92
Q

What can prolonged increases in cortisol lead to?

A

damage to the hippocampus…impairments in memory

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93
Q

what is the tonic phase?–cortisol

A

baseline state…altered cortisol levels before event or during normal day

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94
Q

what is the phasic phase of cortisol

A

occurs during a stressful event

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95
Q

what were the first anxioltyic drugs made

A

barbiturates

96
Q

what were barbiturates made for

A

sleep, nervousness. other uses: anesthesia and reduced seizures

97
Q

what are long acting barbiturates

A

take an hour to take effect but produce effects for 10-12 hours. have poor lipid solubility and slow metabolism

98
Q

what are ultra-short acting barbiturates?

A

produce effects within 10-20 seconds but effective for only about a half hour. hhighly soluble in lipids, quickly store in fats, rapid metabolize

99
Q

what functional group is found in anesthesia (barbiturates)?

A

ether…activates GABA a receptors

100
Q

examples of barbiturates having an addicting effect?

A

produced feelings of well-being, lowered inhibitions, primates self-administer, participants prefer just as well as morphine

101
Q

what do deaths from overdose of barbiturates occur from?

A

respiratory depression…has memory-impairing effects also so some people forget that they have already taken the pill

102
Q

what is barbiturate abstinence syndrome?

A

anxiety, muscle weakness, and abdominal pain caused by abrupt cessation of barbiturate use

103
Q

where is the barbiturate binding site found?

A

on GABA A receptors

104
Q

what are barbiturates effect on GABA A?

A

positive modulators so it enhances the INHIBITORY effects of GABA

105
Q

when barbiturates enhance the inhibitory effects of GABA, what parts of the brain are inhibited?

A

amygdala activity, thalamic and cortical activity, and medulla

106
Q

when the thalamic and cortical activity are reduced, what does this have an effect on?

A

seizures, memory, attnetion, cognitive functions

107
Q

what is a sedative hypntic?

A

drugs that are calming or sleep inducing

108
Q

what happens when the medulla is inhibited

A

lower respiratory function

109
Q

what are the most common benzodiazepines?

A

librium and valium. less sedative than barbiturates

110
Q

what are two short-acting benzodiazepines? What is their half-life?

A

alprozolam and clonezepam…these take 1-2 hours to produce effect and have a 12-24 hour elimination half life

111
Q

Do long or short lasting benzodiazepines metabolize to other benzo;s?

A

long lasting

112
Q

What is benzodiazepine withdrawal syndrome?

A

a physiological form of dependence characterized by anxiety, mania, suicidality, convulsions after abrupt withdrawal

113
Q

benzodiazepines are a positive modulator for what binding site?

A

GABA A

114
Q

Where is the higher affinity for benzo’s in a GABA A receptor?

A

contained within an alpha 1 subunit

115
Q

where is there a lower affinity for benzo’s in a GABA receptor?

A

alpha 2,3,or 5 subunits. bind even poorer to alpha 4 and 6

116
Q

what is the BZ1 binding site? where are these found

A

high affinity–> alpha 1. found in cerebellum and thalamus

117
Q

What is a BZII binding site? where are these found?

A

low affinity for benzo’s –> alpha 2, 3, 5. found in amygdala and hypothalamus

118
Q

What are endozepines?

A

endogenous substances which bind to benzo sites…released from astrocytes, serve as negative GABA A modulators (also called gliotransmitterS)
they play a role in promoting neuronal proliferation by preventing GABA-induced inhibition

119
Q

What are Z-drugs

A

non-benzodiazepine hypnotics

sleep aids

120
Q

where do Z drugs bind?

A

BZ 1 sites

121
Q

What are some common z-drugs?

A

zolpidem (ambian) and zopiclone

122
Q

Where do Z drugs have a high binding affinity?

A

GABA A @ alpha 1 subunit

123
Q

why do z drugs produce hypnotic effects?

A

positive modulation of alpha 1 GABA A and others from BZ II sites

124
Q

How do anticonvulsant drugs work?

A

they facilitate neurotransmission of GABA

125
Q

What is the drawback in using antidepressants for anxiety?

A

1/3 of patients dont respond

126
Q

What is buspirone?

A

partial agonist for 5HT1A…antianxiety med
no abuse potential
takes several weeks to become effective
rapidly breakdown in stomach

127
Q

how do antidepressants reduce anxiety?

A

block serotonin membrane transporters–> prevent reuptake of serotonin to increase levels in the synapse

128
Q

what do antidepressants cause desnsitization of?

A

5HT1A somatodendritic autoreceptors

alpha 2 receptors (less inhibition to serotonin neurons increases 5ht levels in the synapse)

129
Q

antidepressants cause in increase of serotonin binding where?

A

at 5HT1A postsynaptic receptors

130
Q

what is a mental disorder?

A

impairment in normal behavioral , cognitive, or emotional functioning

131
Q

how is someone diagnosed with a mental disorder?

A

must experience significant dysfunction and stress from the disorder and that it doesnt arise frome a medical condition

132
Q

what is major depressive disorder

A

characterized by at least 5 symptoms occurring within the same 2-week period

133
Q

what are some symptoms of depression?

A

depressive modd, lack of interest or pleasure in activities, change in body weight, change in sleep patterns, fatigue, feeling of worthlessness, difficulty concentrating, thoughts of suicide

134
Q

what is persistent depressive disorder (dysthmia)

A

milder form of depressed mood that occurs nearly everyday for at least two years (must have at least 2 symptoms)

135
Q

depression is the ___ leading cause of diability worldwide

A

4th. 16.6% during a lifetime. higher in university students

136
Q

what is vascular depression

A

depressed symptoms associated with poor blood flow to the brain…more common in the elderly and people with Alzheimers

137
Q

what happens in the amygdala during depression

A

increased activity

138
Q

what happens in the hippocampus during depression?

A

reduced volume

139
Q

what happens in the prefrontal cortex during depression?

A

reduced activity

140
Q

what happens in the nucleus accumbens during depression?

A

reduced volume and decreased activity

141
Q

what happens in the basal ganglia in depression?

A

reduced volume

142
Q

what was the first antidepressant drug?

A

iproniazid…first developed for the treatment of terberculosis found to reverse sedation and depressive symptoms

143
Q

what is resperine

A

an antidepressant drug which depletes brain of monoamine oxiade by irreversible blocking transporters

144
Q

what is the monoamine hypothesis of depression

A

a monoamine neurotransmitter deficiency causes depressive mood

145
Q

where is MAO A found?

A

brain, peripheral nervous system, intestinal tract

resides in dopamine and norepinephrine neurons

146
Q

whre is MAO B found?

A

found mainly in the brain. resides in serotonin and norepinerphrine neurons

147
Q

what are mao inhibitors?

A

produce antidepressant effects by binding to MAO and preventing it from breaking down neurotransmitters

148
Q

what is an irreversible mao inhibitor?

A

drug never releases from MAO. to make up for the loss of functional MAO enzymes, neurons synthesize more MAO

149
Q

what is a reversible mao inhibitor?

A

drug either temporarily binds MAO or other compounds such as tyramine to displace drug from MAO

150
Q

what is the cheese reaction?

A

overactivated sympathetic nervous system functioning because of MAO inhibition that leads to increased heart rate, hypertension, sweating

151
Q

in the cheeese reaction, inhibition y MAO increases…

A

levels of NE and tyramine

152
Q

what are selective MAOB inhibitors?

A

greater affinitity for MAOB–mostly act through brain

153
Q

what are reversible inhibitors of MAO A (RIMA)?

A

selectively inhibit MAOA by allowing the displacement by tyramine

154
Q

what are tricyclic antidepressant drugs

A

antidepressants that inhibit the reuptake of norepinepherine and serotonin and function as antagonists for various receptors

155
Q

mechanism of action for TCA

A

achieve high serotonin and NE by inhibiting reuptakes at MEMBRANE TRANSPORTERS rather than catabolism of NTS as MAOIs do

156
Q

what are some adverse effects of TCAs?

A

antagonist for cholinergic muscarinic recpetors: dry mouth, eyes, constipation
block alpha1: vasodilation, low BP
H1 antagonists-sedative
weight gain

157
Q

what is fluoxetine (prozac)

A

an SSRI

158
Q

what is serotonin syndrome?

A

life threatening condition which causes agitation, restlessness, impaired cognitive function, possible hallucinations

159
Q

what is serotonin discontinuation syndrome?

A

abrupt withdrawal ssris causing sensory disturbances, sleep disturbances, flulike symptoms, gastrointestinal effects

160
Q

what is an SNRI

A

enhance levels of serotonin and NE by blocking membrane transporters

161
Q

what was the first SNRI

A

effexor…then cymbalta

162
Q

SNRIs were origanlly used to treat

A

fibromyalgia syndrome- musculoskeletal disorder characterized by widesread pain occuring as muscle tenderness as well as other symptoms

163
Q

what is an atypical antidepressant drug?

A

reduce depression through mechanisms that differ from those of other antidepressants

164
Q

what is bupropion (wellbutrin)?

A

an atypical antidepressant. reuptake inhibit for NE and DA (lack of serotonin elevation)
no risk for sexual side effects

165
Q

What are some limitations in antidepressant drug effectiveness and devlopement?

A

length of response time, treatment resistance, placebo effects

166
Q

what are combination strategies when using antidepressants?

A

augmentation strategy- used to boost the effects of a medication
add-on treatments- used to adjust the effects of one medication using another
off-label- the drug is being used in a nonapproved way

167
Q

The benefits of combining psychotheraphy and pharmacotherapy may depend on…

A

the drug type and/or the severity of depression

168
Q

most antidepressants increase which neurotransmitter?

A

serotonin

169
Q

Which serotonin receptors play a role in depression?

A

5HT2C and 5HT1A

170
Q

chronic administrtation of antidepressants is associated with increased dopamine in the…

A

nucleus accumbens

171
Q

antidepressant treatment is associated with what general effect?

A

neuronal growth and production in the hippocampus

172
Q

what is a stable mood in bipolar disorder referred to as?

A

euthymia

173
Q

what is type I bipolar disorder?

A

involved alternations between depression and severe mania

174
Q

what is type II bipolar disorder?

A

involves alterations between depression and hypomania

175
Q

during manic episodes of bipolar disorder, where is there reduced activity?

A

right frontal and temporal lobes

176
Q

during depressive episodes of bipolar disorder, where is there reduced activity?

A

left hemisphere of the brain

177
Q

Where are there abnormalities in the brain in bipolar disorder?

A

white matter, cingulate cortex, neurons connecting the lateral prefrontal and orbitofrontal cortices

178
Q

what are drugs refferred to as when they are used to treat bipolar disorder?

A

mood stabilizers

179
Q

which drug is the oldest and most effective mood stabilizer?

A

lithium

180
Q

What are some facts about using lithium as a mood stabilizer?

A
  • has a narrow therapeutic index dose range
  • regular blood monitoring is necessary to carefully adjust doses to maintain efficacy and avoid adverse effects
  • lithium enters through Na+ channels and is involved in a variey of intracellular processes
  • lithim seems to inhibit glycogen synthase kinase 3, which promotes apoptosis and regulates inflammation
181
Q

what are anticonvulsant drugs mechanism of action when being used for bipolar disorder?

A

positive modulation of GABA A receptors, but they also inhibit Na+ channel function and GSK-3 activity

182
Q

genetic differences can affect what in treatment response in depression?

A

can affect the drug’s ability to cross the blood-brin barrier, the function of serotonin transporters, and the expression of neurotrophins

183
Q

What is pharmacokinetics?

A

refers to how drugs are absorbed by and pass through the body

184
Q

what is absorption?

A

the passage of a drug from the site of administration into the bloodstream

185
Q

What does the route of administration of a drug determine?

A

which membrane a drug must pass through to gain access to the bloodstream, and the speed with which this occurs

186
Q

most absorption occurs through what process? and how is this process affected?

A

passive diffusion–this process is affected by the drugs pKa as well as the pH of the environment in which the ddrug is going to be absorbed

187
Q

to be absorbed, drug molecules must undergo…

A

liberation from the pill or medium in which they are delivered

188
Q

how are most orally administered drugs absorbed?

A

thorugh the small intestine, but obviously, the drug needs to survive the acidic environemnt of the stomach to make this possible

189
Q

how are inhaled drugs absorbed?

A

by the lungs (and to some extent through the mucous membranes of the mouth, throat and nose)

190
Q

how are drugs administered intravenously absorbed?

A

they are introduced directly to the bloodstream

191
Q

what is distribution (of a drug)?

A

the passage of a drug from the bloodstream to various sites in the body

192
Q

what is bioavailability?

A

a drugs ability to reach its site of action

193
Q

what three properties make it possible for passive diffusion through the blood brain barrier?

A
  1. drugs that are fat soluble are more likely to pass
  2. drugs that are uncharged
  3. small molecules
194
Q

what is biotransformation?

A

drug metabolism- involves breaking a drug down into its metabolites via the activity of various enzymes

195
Q

what is phase I biotransformation?

A

norally involves P450 enzymes and produces water soluble metabolites

196
Q

What do competitive antagonists do?

A

bind the same site as a neurotransmitter to prevent the NT from binding to and activating the receptors

197
Q

what do noncompetitive antagonists do?

A

do not prevent NTs binding but they do prevent activation of the receptor

198
Q

what is positive modulation?

A

bind to allosteric sites on the receptor and increase the ability of a NT to bind to or activate the receptor

199
Q

what is a negative modulator?

A

bind to allosteric sites and decrease the ability of a NT to bind and activate the receptor

200
Q

what is a neurotoxin?

A

substance that cause damage to parts of the nervous system. can cause destruction of neurons, the destruction of the myelin sheath, destruction of axons, as well as damaging processes related to neurotransmission

201
Q

what is tolerance

A

occurs when increasing doses of a given drug must be taken in order to achieve the desired effects

202
Q

what is pharmacokinetic tolerance or drug dispositional tolerance?

A

involves pharmacokinetic adaptations that reduce the amount of drug reaching its site of action. often accomplished by changes in drug metabolism

203
Q

what is pharmacodynamic tolerance?

A

occurs when thre is reduced responsivemness as a drugs site of action. this often involves changes in the nuber of neurotransmitter receptors

204
Q

what is behavioral tolerane?

A

occurs when there is a reduced behavioral responsiveness to a drug’s effects

205
Q

what is conditioned (or contingent) tolerane?

A

occurs when stimuli normally associated with the use of a drug serve to counteract the drugs effects

206
Q

what is cross tolerance

A

can occur for drugs that have similar biological actions

207
Q

what is sensitization

A

occurs when chronic drug use leads to an increase in responsiveness to the drug

208
Q

when does drug dependence occur?

A

when a user needs a drug in order to functiono normally. this dependence is often made apparent durig the withdrawal syndrome experienced upon cessation

209
Q

what is first pass metabolism

A

drug metabolism may begin to occur before the drug has a chance to enter general crculation…occus in orally administered meds because they pass through the liver before being introduced in general ciculation and the stomach may also contribute to first-pass metabolism

210
Q

what is an active metabolite

A

when a drug gets metabolized into a drug that has its own physiological effects

211
Q

what is a prodrug

A

may be used because the metabolites produced from its breakdown are more active than the prodrug itself

212
Q

what is elimination rate

A

refers to the amount of drug that is removed from the body over time

213
Q

what does the elimnation rate for most drugs follow

A

first order kinects, which involves half lifes

214
Q

alcohol follows what type of elimination?

A

zero order kinetics, which means that a set amount of drug will be eliminated in a given period of time

215
Q

what is pharacodynamics

A

refers to a drugs mechanis of action

216
Q

what is an ionotropic receptor

A

ion channels that open once bound to a nt

217
Q

what is a metabotropic receptor

A

often associated with G proteins that recruit effector enzymes to activate second messenger systems

218
Q

what is a protein kinase

A

used to phosphorylate substrate proteins

219
Q

what are the catecholamines

A

dopamine, NE, epinephrine. synthesized fro phenylalanine

220
Q

dopamine is synthesized from

A

phenylalanine - is the rate limiting step

221
Q

dopamine receptors are metabotropic/ionotropic

A

metabotropic

222
Q

what is the d1 family of dopamine receptors?

A

consists of D1 and D5 receptors. generally associated with excitatory effects

223
Q

what is the D2 family of dopamine receptors

A

consists of D2,3,4 receptors. generally have inhibitory effects

224
Q

where do dopaminergic neurons arise from

A

ventral tegmental area and substantia nigra and the hypothalamus

225
Q

where do the mesolimbic and mesocortical dopamine pathways originate and terminate

A

originate in the ventral tegmental area and terminate in the nucleus accumbens and front cortex

226
Q

where does the nigrostriatal dopamine pathway orginiate and terminate

A

substantia nigra and basal ganglia

227
Q

where does the tubero infundibular dopamine pathway orinigate and terminate

A

hypothalamis and pituitary gland

228
Q

where do noradrenergic neurons oringinate

A

locus couerulus

229
Q

where does serotonin arise and terminate

A

raphe nuclei…involve enzymatic catabolism and reuptake

230
Q

opiods are hte most studied…

A

neuropeptide

231
Q

what is different about nitric oxide

A

cannot be stored in vescicles and is released as soon as it is synthesis. does not bind receptors…it acts by foring bonds with intracellular proteins

232
Q

what are neurotrophins

A

molecules that promote survival and growth of neurons…bind to receptor tyrosine kinases rather than G proteins

233
Q

what is oxytoin

A

a pituitary hormone that is important for uterine contraction and milk letdown

234
Q

what is vasopressin

A

the antidiuretic hormone that causes kidneys to absorb more water from the blood

235
Q

what is used in treating alzheimers in early stages?

A

acetylcholinesterase inhibitors or trying to eliminate excitotoxicity by using drugs that prevent activation of NMDA receptors for glutamate

Psychopharmacology (1 decks)

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