test 2 Flashcards

1
Q

What is considered a negative symptom of Schizophrenia?

A

Negative symptoms are considered a reduction in normal functions: The five As- Alogia, affective blunting or flattening, asociality, anhedonia, avolition.

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2
Q

What percent of the population is has Schizophrenia?

A

0.5-1%

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3
Q

What are the five As and what do they mean?

A
  1. Alogia- dysfunction of communication; restriction in the fluency and productivity of thought and speech.
  2. Affective blunting or flattening- restrictions in the range and intensity of emotional expression.
  3. Asociality- reduced social drive and interaction.
  4. Anhedonia- reduced ability to experience pleasure.
  5. Avolition- reduced desire, motivation or persistence; restrictions in the initiation of goal-directed behavior.
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4
Q

What can potentially happen as side effects in using antipsychotic drugs long term?

A

Antipsychotic drugs cause an increased incidence of obesity and diabetes. Also cardiovascular disease is inferred.

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5
Q

What do all known antipsychotics capable of treating positive symptoms block?

A

All known antipsychotic drugs capable of treating positive psychotic symptoms are blockers of the dopamine D2 receptor.

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6
Q

Know about the mesolimbic dopamine pathway.

A

Hyperactivity in the mesolimbic dopamine pathway hypothetically accounts for positive psychotic symptoms.
The mesolimibic dopamine pathway, which projects from the ventral tegmental area in the brainstem to the nucleus accumbens in the ventral striatum is involved in regulation of emotional behaviors and is believed to be the predominant pathway regulating positive symptoms of psychosis. Specifically, hyperactivity of this pathway is believed to account for delusions and hallucinations.

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7
Q

What is Glutamate?

A

Glutamate or glutamic acid is a neurotransmitter which is an amino acid. Its predominant use is not as a neurotransmitter but as an amino acid building block for protein biosynthesis. Glutamate is the major excitatory neurotransmitter in the central nervous system and sometimes considered to be the “master switch” of the brain, since it can excite and turn on virtually all CNS neurons.

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8
Q

Know what Stahl says about neurodevelopment and schizophrenia.

A

Schizophrenia may be caused by neurodevelpmental abnormalities in the formation of glutamate synapes at a specific site: namely at certain GABA interneurons in the cerebral cortex. Something appears to be wrong with the genetic programming of those particular GABA interneurons that can be identified in prefrontal cortex as containing a calcium binding protein called parvalbumin. Theses parvalbumin containg GABA interneurons appear to be faulty postsynaptic partners to incoming glutamate input from pyramidal neurons in prefrontal cortex, and to form defective NMDA receptor containing synaptic connections with incoming pyramidal neurons . Just read the section starting on page 108

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9
Q

How are genes turned on and off by the environment?

A

a person may have multiple genetic risk factor and exposed to life stresses (abusive childhood, virus or toxin, marijuana, traumatic life events) that change the “biased” circuit. This leads to decompensation and the circuit becomes hypoactivated with unsuccessful compensation. This leads to several symptoms: hallucinations, delusions, thought disorder. page 118

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10
Q

What are atypical antipsychotics approved to treat?

A

schizophrenia, manic and depressed phases of bipolar disorder, augmenting agents for treatment resistant depression.

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11
Q

What happens when a substantial number of D2 receptors are blocked in the brain?

A

Psychomotor slowing, emotional quieting, and affective indifference—Neuroleptsis
EPS is also caused by blocking D2 receptors.

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12
Q

Know the various brain pathways that are affected by treatment in schizophrenia.

A

The mesolimbic dopamine pathway of untreated schizophrenia is hypothesized to be hyperactive and is targeted in schizophrenia treatment.

The mesocortical, nigrostiatal and tuberoinfundibular D2 receptor pathways are impacted negatively with conventional antipsychotic symptoms.

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13
Q

What is Tardive Dyskinesia?

A

Tardive Dyskinesia is a hyperkinetic movement disorder causes facial and tongue movements, such as constant chewing, tongue protrusions, facial grimacing, and also limb movements that can be quick, jerky or choreiform (dancing). About 5% of patients maintained on conventional antipsychotics will develop tardive dyskinesia every year (about 25% every five years).

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14
Q

Know about extrapyramidal symptoms.

A

EPS is motor symptoms that occur from blocking D2 receptors in the nigrostriatal pathway which is part of the extrapyramidal nervous systems. Patients who develop EPS early in conventional antipsychotic symptoms are twice as likely to develop tardive dyskinesia if treatment persists.

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15
Q

What is neuroleptic malignant syndrome?

A

Neuroleptic malignant syndrome is associated with extreme muscular rigidity, hegh fevers, coma, and even death and possibly related in part to D2 receptor blockade in the nirostriatal pathway can also occur with conventional antipsychotic agents.

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16
Q

What causes hyperprolactinemia?

A

Dopamine D2 receptors in the tuberinfundibular DA pathway are also blocked by conventional antipsychotics and this causes plasma prolactin concentrations to rise. A condition called hyperprolactinememia. It is associated with galactorrhea (breast secretions) amenorrhea, fertility problems, and possibly bone demineralization in older woman not on estrogen.

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17
Q

What are the side effects of anticholinergic agents?

A

Constipation, blurred vision, dry mouth, drowsiness

read page 139 for what happens with antichlinergic agents.

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18
Q

What makes an antipsychotic atypical?

A

They are atypical from what is expected of conventional antipsychotics. They have a clinical profile of equal positive antipsychotic actions but low EPS and hyperprolactinemia symptoms.

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19
Q

Know the side effects when medicines work on histamine H1 receptors, alpha 1 aderenergic recptors and muscarinic receptors.

A

Weight gain and drowsiness is side effects with the histamine receptors.
Cardiovascular disease and orthostatic hypotension are side effects of the alpha 1 aderenergic receptors.
Blocking muscarinic receptors cause dry mouth, blurred vision, constipation, and cognitive blunting.

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20
Q

What is the abbreviation for Serotonin?

A

5-hydroxytryptamine, 5HT

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21
Q

Blocking which receptor improves learning and memory in experimental animals?

A

5HT6

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22
Q

What is a partial agonist?

A

A partial agonist binds in an intermediary manner. It binds “just right” not to hot or to cold. THey are sometimes called “goldilocks drugs.

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23
Q

Which two atypical antipsychotics have the highest metabolic risk?

A

Clozapine, olanzapine

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24
Q

What is metabolic syndrome?

A

Increased appetite and weight gain. Progresses to obesity, insulin resistance and dyslipidemia with increases in fasting triglyceride levels. Ultimately, heyperinsulinemia advances to pancreatic Beta cell failure, prediabetes, and then diabetes.

25
Q

What two receptors associated with increased weight?

A

H1 histamine receptor and the 5HT2c serotonin receptor

26
Q

Stahl tells us it is best practice to monitor which of the following parameters in patients taking atypical antipsychotics?

A

Weight (BMI), fasting triglycerides, fasting glucose, and blood pressure. Before start of treatment and during switches.

27
Q

Stahl reminds us that we cannot change a patient’s genetic makeup or age, but we can encourage patient’s to do which of the following to prevent metabolic syndrome?

A

Good diet and exercise habits

28
Q

How do you switch antipsychotics?

A

Cross titration over days to weeks (clozapine 4weeks or more). Increase new drug, decrease old drug and continue until old drug is stopped. Do not continue both drugs if they improve in the middle. read charts on 218, 219,220, 221

29
Q

What must an antipsychotic do to decrease positive symptoms and violence?

A

target >60% D2 receptor occupancy

30
Q

What are being studied for their potential role in the treatment of schizophrenia?

A

Novel glutamatergic treatments for schizophrenia: Direct acting glycine site agonist and glycine transporter on glial cells
AMPAkines, mGluRpresynaptic antagonist/postsynaptic agonists, glycine agonist, GlyT1 inhibitors

31
Q

What is affect?

A

external display of mood

32
Q

A switch so fast between mania and depression, is called ?

A

rapid cycling

33
Q

What do postmortem studies consistently show in the frontal cortex of patients who commit suicide?

A

serotonin 2 receptors

34
Q

What plays a role in the proper growth and maintenance of neurons and neuronal connections?

A

Stress
Brain derived neurotrophic factor (BDNF) Normally, BDNF sustaings the viability of brain neurons but under stress the gene for BDNF can be repressed.

35
Q

Know about women abused as children vs. never-abused women in relation to depression.

A

depression in woman abused as children can be found up to four times more often than in never abused woman.

36
Q

Know about the s genotype of SERT

A

The s variant leads to an excessive reaction of the amygdala to fearful faces. People with the s genotype of SERT are more likely to develop an affective disorder when exposed to multiple life stressors. They may have more hippocampal atrophy, more cognitive symptoms, and less responsiveness or tolerance to SSRI/SNRI treatment. More likely to develop major depression as an adult.

37
Q

Know about the l genotype of SERT.

A

The I genotype is more resilient genotype with less amygdala reactivity to fearful faces, less likelihood of breaking down into a major depressive episode when exposed to multiple life stresors, as well as more likelihood of responding to SSRIs/SNRIs.

38
Q

What are the three monoamines involved in mood regulation?

A

Norepinephrine, dopamine, and serotonin

39
Q

What is the goal of antidepressant therapy?

A

the goal of treatment is complete remission of symptoms and lack of relapse shortly after remission, nor does the patient have a recurrent episode in the future.

40
Q

What are the most common residual symptoms of depression?

A

insomnia, fatigue, painful physical complaints, problems concentrating, and lack of interest.

41
Q

When SSRI treatment is initiated, 5HT increases first where?

A

somatodendritic area in the midbrain raphe

42
Q

The additional benefit of 5HT2C antagonist properties with the SSRI Fluoxetine enhances release of both dopamine and norepinephrine, which in turn contributes to which of the following therapeutic actions?

A

5HT2C antagonism may be generally activating and people detect energizing and fatigue reducing effects from the first dose. It is best matched to patients with reduced positive affect, hypersomnia, psychomotor retardation, apathy, and fatigue. May also contribute to the anti-bulimia effect of higher doses.

43
Q

Which SSRI is preferred by many clinicians for patients with anxiety symptoms?

A

Paroxetine

44
Q

Which SSRI has a limited level for dose increase based on its side effect potential for QTc prolongation?

A

citalopram

45
Q

Which SNRI is known to help decrease vasomotor symptoms in perimenopausal women?

A

desvenlafaxine

46
Q

Which SNRI has slightly more potent SERT than NET inhibition which leads to efficacy in treating depression caused by pain?

A

Duloxetine

47
Q

Which antidepressant is generally activating or even stimulating, but does not appear to have sexual dysfunction, and as an added bonus often helps patients to stop smoking?

A

Bupropion

48
Q

Which selective norepinephrine reuptake inhibitor is marketed in the US as a treatment for ADHD?

A

Atomoxetine (strattera)

49
Q

Which antidepressant due to its H1 antihistaminic actions relieves insomnia at night and anxiety during the day?

A

mirtazapine and mianserin

50
Q

Which SARI antidepressant is often added to a psychotropic medication regimen at night at a low dose for its hypnotic effect of enhancing sleep?

A

Trazodone

51
Q

Which of the following antidepressants metabolize dopamine and tyramine?

A

MAOI

52
Q

Hypertensive crisis is a potentially fatal reaction that can occur with which antidepressant?

A

MAOI

53
Q

Know what to discuss with patients before prescribing a MAOI

A

The strict diet. No tyramine

54
Q

What does Stahl mention about various augmenting agents in the treatment of depression?

A

Psyuchotherapy, Deep brain stimulation, Tanscranial magnetic stimulation, thyroid, s-adnosy-methionine (SAMe), L-5-Methyltetrahydrofolate monoamine modulatot. pages 346-353

55
Q

Know the risks of both antidepressant use and non-use during pregnancy.

A

Damned if you do- congenital cardiac malformations, newborn persistent pulmonary hypertension, neonatal withdrawal syndrome, low birth weight/premature, long term neurodevelopmental abnormalities, increase suicide risk up to age 25, medical-legal risks of using,
Damned if you dont- relapse of major depression, increased risk of sucide, poor self care, poor motivation for prenatal care, disruption of maternal infant bonding, low birth weight, developmental delays in children, self harm, harm to infant, medical-legal risks of not using antidepressants.

56
Q

Can you treat bipolar disorder with more than one mood stabilizer?

A

yes

57
Q

What undesirable side effects can happen to a women if she takes valproate?

A

A syndrome of menstrual disturbances, hyperandrogenism, obesity, and insulin resistance.

58
Q

What are some of the special considerations and cautions when treating women with bipolar disorder?

A

more depressive in nature, more thyroid dysfunction, more suicide attempts, mixed mania, and rapid cycling. Comorbid anxiety and eating disorders are more common with women. Symptoms may worsen during PMS.

59
Q

Know about Lithium and its special effects.

A

effective for mania and recurrent mania, decreases suicide, treats depressive symptoms,