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805 > Lecture 16 (Cut off for Exam 4) > Flashcards

Lecture 16 (Cut off for Exam 4) Flashcards

Depression/Mania/SCZ

1
Q

Major Unipolar Depression

A
  • Changes in mood
  • Not related to life experiences usually
  • Cannot experience pleasure, loss of interest in normal activities, insomnia, loss (or sometimes gain) of appetite
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2
Q

Unipolar Depression Screening

A 
SALSA
S - Sleep disturbance (insomnia with 2-4 AM waking)
A - Anhedonia
LS - Low Self Esteem
A - Appetite Decreased
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3
Q

Mania

A
  • Elevated euphoria, self esteem, and grandiosity
  • Restlessness with high energy and activity levels
  • Hypomania = less severe form of mania
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4
Q

Manic-Depression Disorder

A
  • Aka Bipolar Disorder
  • Bipolar I - Mania and major depression
  • Bipolar II - Hypomania and major depression
  • Cyclothymic - Hypomania and mild to moderate depression
  • Dysthymic - Mild to moderate depression most of the time with not discrete episodes
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5
Q

Monoamine Theory of Depression

A
  • Depression due to lack of 5-HT (Serotonin) and NE
  • Reserpine depletes biogenic amines and induces depression
  • B-Blockers have high lipid solubility and cause depression as a side effect
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6
Q

Effective Antidepressants

A

Increase 5-HT or NE Levels

  1. TCA
  2. SSRI
  3. MAOI - Monoamine Oxidase Inhibitors
  4. Drugs that increase 5-HT or NE release

Require 2-6 weeks of chronic treatment to reap the benefits

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7
Q

Neurogenesis Theory of Depression

A
  • Stress-induced decrease of hippocampal neurogenesis that leads to depression
  • Increased neurogenesis via antidepressants can take weeks
  • Stress, genetics, and growth factors all effect this
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8
Q

BDNF

A

Neuropeptide that regulates growth, survival, and differentiation of neurons for synaptic plasticity

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9
Q

Depression Facts

A
  • Affects ~19 million Americans
  • Affects women more than men
  • Genetics - you are 2-3x more likely to develop depression if a close relative also has depression
  • 76% of identical twins both had depression in a study
  • About 50% of those with bipolar disorder have a clinically depressed parent
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10
Q

Antidepressants (6)

A
  1. TCA - Amitriptyline (Elavil)
  2. SSRI - Similar efficacy and better side effect profile, Citalopram, Sertraline, Fluoxetine, Lexapro, Paxil
  3. SNRI - similar efficacy, Atomoxetine (Strattera), Venlafaxine, Duloxetine
  4. MAOI - tyramine interaction, do not combine with TCA or SSRI. Phenylzine (Nardil)
  5. Increase 5-HT or NE levels - Trazodone & Mirtazapine
  6. Electroconvulsive Therapy - most rapid and effective in severe, suicidal depression
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11
Q

Mood Stabilizers for Bipolar Disorder (3)

A
  1. Lithium - prevents manic and depressive phases
  2. Anticonvulsants - Gabapentin, Topiramate, Lamotrigine, Valproic Acid (Depakote)
  3. Antipsychotics - Quetiapine, Risperidone, Abilify, Olanzapine (Zyprexa)
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12
Q

Psychoses

A
  • Disorders of Thought
  • Impaired behavior with inability to think coherently or comprehend reality
  • May include hallucinations and delusions
  • Most telling symptom is “lack of insight”
  • People are unaware that they are acting unusually not matter how outrageous their delusion may be
  • Lack of insight varies from patient to patient and doesn’t occur in everyone
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13
Q

Disorders + Psychoses (7)

A
  1. Brain Damage
  2. Alzheimer’s Disease
  3. Bipolar Disorder
  4. Mania
  5. Schizophrenia
  6. Parkinsons on high dose L-DOPA
  7. Amphetamine and cocaine psychoses
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14
Q

Best Psychoses Treatment

A
  • Antipsychotics
  • Best choice no matter what the cause may be
  • May need to use in conjunction with antidepressant, anticonvulsants, or other drugs
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15
Q

Drug Induced Psychoses

A
  • Causes from overstimulation of brain by stimulants (amphetamine or cocaine)
  • Can experience excitation after withdrawal from a strong sedative
  • Treat with Benzos, though antipsychotics are also effective
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16
Q

Schizophrenia History

A
  • Documented back to 3000 BC - possessions and exorcisms, some of which were drilling holes in head
  • “Bedlam” hospital in 1330 London held lunatics and you could pay a penny to watch them in their cells (“Show of Bedlam”)
  • Dr. Emile Kraepelin - named it a discrete mental illness in 1887, termed “dementia praecox” (early dementia) and believed it to be a disease of the brain
  • Term “Schizophrena” coined by Dr. Eugen Bleuler in 1911
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17
Q

Schizophrenia Epidemiology

A
  • Global prevalence is ~1%
  • Men and women have it in equal frequency
  • Men show in late teens or early twenties, women show in late twenties or early thirties
  • Higher comorbid incidences including hypertension, diabetes, cardiac concern, STDs, smoking etc. with Schizophrenic patients
  • Increases the natural causes of death in these patients linked to these other disease states, possibly due to reduced use of medical services, disorganized behavior, or drug therapy utilized
  • Mortality is higher in this disease state, 10% incidence of suicide
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18
Q

Schizophrenia (SCZ)

A

Characterized by delusions, hallucinations, disorganized speech and behavior, and other symptoms

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19
Q

SCZ Diagnosis

A

States by APA - Diagnostic Manual of Mental Disorders

  • Disorder lasts at least 6 months
  • Includes at least 1 month of active-phase symptoms
  • Should have at least two of characterized symptoms
  • Subtypes no longer identified
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20
Q

Delusions

A
  • Erroneous beliefs - involve misinterpretation of perceptions or experiences
  • Can be persecutory (tormented, spied on)
  • Alien thoughts placed into mind and judged to be bizarre
21
Q

Hallucinations

A
  • Auditory is most common
  • Voices distinct from person’s own thoughts
  • Hearing, seeing, feeling, and smelling something not there
22
Q

Disorganized Speech

A
  • Thinking as well
  • Conversations or thinking that slips off track
  • Loose associations, unrelated, disorganized
23
Q

Grossly Disorganized

A
  • Inability to function in society

- Restless, angry, agitated, disheveled, difficulties in daily activities, repeating the same activity

24
Q

Other Negative SCZ Symptoms (Four A)

A
  • Affective Flattening - unresponsive face and diminished emotions
  • Alogia - poverty of speech, brief & empty replies
  • Avolition - inability to initiate/persist in work/social activities
  • Anhedonia - without please, inability to experience pleasurable emotions from pleasurable activities
25
Q

SCZ Complexity

A
  • Combination of positive, negative, mood, and cognitive symptoms
  • Comorbid substance abuse
  • Combinations of these lead to disruptive everyday life (social and occupational)
26
Q

SCZ Etiology

A
  • Remains unknown, many theories
    1. Neurodevelopmental - fetal, childhood, adolescence, teens)
    2. Neurodegenerative - Progression over lifetime?
    3. Genetic Susceptibility - Multiple Alleles
27
Q

SCZ + Genetics

A
  • Risk of SCZ in general population is ~1%
  • ~10% if you have a first degree relative with SCZ
  • 48% of indentical twin pairs both will have SCZ

Must be pre/post natal environment, psychosocial, and/or physical environment factors as well

28
Q

Neurodevelopment Hypothesis of SCZ

A

Normal Brain Development

  • Newborn to adult: about a 50% decrease in neurons
  • On average, about 35% of dendrites at two years of age are pruned by mid-adolescence

Possible Development Problems

  • Fetal disturbance (infection, hypoxia, etc.) leads to abnormal neuron migration in developing brains
  • May be excessive pruning or excessive loss of neurons from start which would explain SCZ development
  • Development disturbances may lead to abnormal neuron migration and the pruning may lead to loss of neurons and could produce disorganization
29
Q

Neurodegenerative Hypothesis of SCZ

A
  • Progressive nature of illness - indicates that underlying cause isn’t static and previously completed pathological process
  • Excessive glutamate stimulation
  • May be a combination of theories, so it is recommended to start early, aggressive, sustained treatment from first break to keep disease under control
30
Q

Glutamate + SCZ

A
  • In excessive amounts, glutamate can cause excitotoxicity where the neurons are “excited to death”
  • Starts as a normal process, overstimulation of brain leads to first break damage
  • Calcium channels remain open and the influx of calcium causes the formation of free radicals that cause toxic actions on organelles and membranes which can lead to cell death
  • *NO GLUTAMATE ANTAGONISTS FOR SCZ, ONLY ALZHEIMER’S**
31
Q

SCZ + Lesions

A
  • May be connected to brain disease where lesions form on cortical areas of brain that may exhibit cortical thickness in enlarged ventricles
  • Lesions are disorganized neural networks that have fewer neurons and excess loss of cortical gray matter
  • Leads to overstimulation of brain, difficulty filtering out extraneous stimuli, and delusions/hallucinations
32
Q

SCZ + Surroundings

A
  • SCZ patients have a decreased capability to filter out unimportant environmental features
  • Attention is drawn impulsively and unpredictably to many details that others ignore
  • Can lead to misinterpretation of their environment and could cause hallucinations and/or delusions
33
Q

Course of Illness

A
  • Ideal - Initial psychotic episode is quickly detected and treated so that further illness can be prevented by prophylatic treatment
  • Chronic Relapsing - Each psychotic exposure decreases global function
34
Q

Neurochemical Circuits

A
  • Potential therapeutic sites for antipsychotic drugs

- Dopamine neurons in ventral tegmental area project nucleus accumbens which stimulate DA2 receptor

35
Q

Dopamine Agonism

A

Stimulant, Cocaine & Amphetamine

36
Q

Dopamine D2 Antagonist

A

First Generation (Haloperidol)

37
Q

D2 & 5-HT Antagonist

A

Second Generation (Olanzapine, Risperidone, Quetiapine, Ziprasidone)

38
Q

Dopamine Theory of Psychoses

A
  1. Psychoses is due to excessive dopamine activity in brain from things like cocaine, amphetamine, levodopa, and increased DA in brain
  2. DA antagonists are clinically effective antipsychotics
39
Q

Dopamine Regulation in SCZ & Antagonists

A
  1. Mesolimbic pathway - hyperactivity of DA neurons causes positive symptoms. Therapeutic D2 blockade
  2. Mesocortical pathway - negative symptoms, cognitive effects, increased DA levels. Therapeutic DA2 receptor blockers
  3. Nigrostriatal Pathway - regulates motor movement, side effects = pseudoparkinson
  4. Tuberoinfundibular pathway - regulates prolactin release, side effect = hyperprolactinemia
40
Q

SCZ Treatment Options

A
  • First Generation Antipsychotics (FGA) - typical antipsychotics, conventional agents, neuroleptics
  • Second Generation Antipsychotics (SGA) - atypical antipsychotics

ALL ARE DOPAMINE D2 RECEPTOR ANTAGONISTS

41
Q

D2 Receptor Antagonism + SCZ

A
  • Correlations between therapeutic potency of antipsychotics and their affinity for D1 or D2 binding
  • The higher the affinity the lower the dose and vice versa
42
Q

First Generation Antipsychotics

A
  • Phenothiazine - Chlorpromazine (Thorazine)
  • Non-phenothiazine - Haloperidol (Haldol)
  • D2 antagonist to decrease positive symptoms of SCZ
43
Q

FGA Side Effects

A
  1. Extrapyramidal Symptoms - block of striatal D2 receptors which leads to acute dystoria (involuntary movement), pseudoparkinsons, Tardive dyskinesia (involuntary movements long term)
  2. Prolactin Increase - lactation and breast swelling
  3. Other - antihistamine, anticholinergic (dry mouth, constipation, tachycardia), sedation, weight gain
44
Q

Second Generation Antipsychotics

A
  • Olanzapine
  • Quetiapine
  • Risperidone
  • Aripiprazole (Abilify)

-Atypical Antipsychotics and have D2 antagonism to decrease positive symptoms AND 5HT antagonism to decrease negative and cognitive symptoms by increase DA release in cortex

45
Q

Are Antipsychotics only used for SCZ?

A

No, they have many uses. SCZ, bipolar disorder, plus others.

46
Q

SGA Beneficial Therapeutic Effects (3)

A
  1. Treats negative and positive symptoms (increased efficacy)
  2. Decrease in extrapyramidal side effects and tardive dyskinesia
  3. Less prolactin elevation
47
Q

SGA Side Effects (3)

A
  1. Weight gain - longer treatments lead to more weight gain
  2. Diabetes Mellitus - increased with long term treatment and may be related to weight gain
  3. Increased cholesterol levels up to 10% in a short amount of time with some drugs
48
Q

SGA + Cholesterol Levels

A
  • Olanzapine - high likelihood of side effect
  • Quetiapine & Risperidone - Moderate likelihood
  • Abilify - low to no side effect
49
Q

How to choose between SGA & FGA?

A

Depends on which symptoms one is trying to prevent and which side effects one is trying to avoid.

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