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Drug Action III > Mood Disorders (Pathology) - Block 3 > Flashcards

Mood Disorders (Pathology) - Block 3 Flashcards

1
Q

What is the 2nd leading cause of diability worldwide?

A

Depression

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2
Q

Who is more affected by depression?

A

Females

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3
Q

What is depression?

A

Depressed mood and not being able to enjow normal activities that is maintained for at least 2 weeks

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4
Q

What is the chief complaint in depressed patients?

A

Physical sx

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5
Q

What are the clinical subtypes of depression?

A

MDD
Persistent Depressive Disorder
Depressive episode (most common)
Atypical
SAD
Bipolar

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6
Q

What is persistent depressive disorder?

A

Dysthymia: sx of depressed mood that occurs on most days, and persist for at least one year

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7
Q

How does dysthymia differ from MDD?

A

Less severe and moreschronic, symptoms are greater in:
1. Number
2. Severity
3. Duration
4. Interference with functioning

  • Reflected in the DSM diagnostic criteria for depression and dysthymia
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8
Q

What is bipolar I?

A

Suffering from alternating depressive episodes that alternate with manic episodes

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9
Q

What are the characteristics of manic episodes?

A
  1. High moods
  2. Hyperactivity
  3. Restlessness
  4. Irritability
  5. Talkativeness
  6. Reduced need for sleep
  7. Delusions
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10
Q

How can mania have adverse outcomes?

A
  1. Traffic accidents
  2. Arrests
  3. Spending money
  4. Hypersexuality
  5. Psychiatric hospitalizations
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11
Q

What is hypomania?

A

Persistent mood disinhibition, increased creativity, and euphoria
* Less severe than full mania
* Associated with Bipolar II

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12
Q

How do patients switch from depressive to mania?

A

Using antidepressants

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13
Q

Describe the course of depression?

A

Self-limiting: episodes will resolve in 3-6 months

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14
Q

What is the underlying cause of depression?

A

We don’t really know
* Environmental: trauma
* Neurobiological: genetics

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15
Q

What are the risk factors of depression?

A

Genetics:
* monozygotic twins (50%)
* dizygotic twins (10-25%)

Vulnerabiltiy to developing depression and anxiety from stressors

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16
Q

What are the neurobiological influences that contribute to depression?

A

Emotional function:
* Abnormalities in the amygdala, hippocampus, cingulate cortex, and prefrontal cortex
* HPA axis dysregulation, variants in BDNF, altered neurotransmitter function

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17
Q

What areas of the brain are affected by depression?

A
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18
Q

What are the neurochemical theories of MDD?

A
  1. Biogenic (Monoamine) Amine theory
  2. Receptor Sensitivity theory
  3. Dysregulation hypothesis
  4. Neuroendocrine theories
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19
Q

What is the amine hypothesis?

A

Depression is often characterized by changes in monoamine neurotransmitters (NE, D, Serotonin)

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20
Q

How do medications support the amine hypothesis?

A

Antidepressants and amphetamines increase NT -> decrease depression
Reserpine: decrease NE and DA -> Increases depression

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21
Q

What metabolite in CSF/urine support the amine hypotheis?

A

NE -> major metabolite is 3-Methoxy-4-hydroxyphenylglycol (MHPG)

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22
Q
A
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23
Q

According to monoamine theory what drugs revealed to have an effects on mood?

A

Imipramine, iproniazid, reserpine

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24
Q

Imipramine/Deipramine

MOA

A

Blocks 5HT transporters and its active metabolite desipramine blocks NE transported -> Increases NTs in the synapse

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25
Q

Iproniazid

MOA?

A

Inhibits MAO prevetning the degradation of 4HT, NE, and DA in the neuron after reuptake

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26
Q

How does reserpine induce depression?

A

Depletes 5HT, NE, and DA by inhibitng the transport by irrevirsibly binding to VMAT

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27
Q

Depressed patients have shown to have decreased ____?

A

CSF levels of 5-Hydroxyindoleacetic acid (5-HIAA), which is the major metabolite of serotonin (5-HT)

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28
Q

What is the problem with amine hypothesis?

A

Antidepressant medications block transmitter reuptake immediately, but there is a significantly delayed effect on the patient’s symptom improvement of about 4 weeks

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29
Q

What is the receptor sensitivity theory?

A

The reuptake blockade alters the sensitivity of pre and postsynaptic NE and 5HT receptors over time

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30
Q

What is the dysregulation hypothesis?

A

Depression is the failure to maintain homeostatic regulation of various neurotransmitter systems (not dependent on changeing levels of NT)

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31
Q

What are the the hypothalmic endocrine changes that occur with depression?

A
  1. Hypersecretion of cortisol
  2. Hyposecretion of TSH/TRH
  3. Reduced BDNF levels
32
Q

What is the major target for depression therapies?

A

Dopamine

33
Q

Overall, depression is a caused by an insuffiency in what NTs?

A

NE and 5-HT

34
Q

What are the types of anxiety disorders?

A
  1. GAD
  2. Phobias
  3. PTSD
  4. Panic disorders
  5. OCD
35
Q

Women are about 2x as likely as men to have anxiety disorders except for ___?

A

OCD

36
Q

What is anxiety?

A

Diffuse Response About Impending Real or Imagined Threat or Danger
* excessive or the perceived threat is out of proportion with the actual threat
* Difficulty controlling the worry or anxiety process, so that it interferes with daily activities

37
Q

What is the cause of anxiety disorders?

A

we really don’t know

38
Q

If most mental illness causes are unknow, how would be define the neuropathophysiology of a disorder?

A

Pharm therapies

39
Q

What are the NTs involved with anxiety?

A
  1. 5HT
  2. NE
  3. GABA
  4. CRH -> cortisol
40
Q

How does GABA play a role in anxiety?

A

When nerve signals fire too quickly, carrying anxiety-inducing signals, GABA would normally act to slow the response, reducing the overwhelming feelings of anxiety

  • Anxiety patients may have abnormalities in GABA
41
Q

Where is the major source of NE?

A

Locus coerulus

42
Q

What is the function of NE?

A
  1. NS activation
  2. Triggers fight or flight
43
Q

What are seratonin producing neurons located?

A

Raphe nuclei

44
Q

What med class has the strongest evidence of serotonergic system in the the tx for anxiety?

A

SSRI

45
Q

What areas of the brain produce response to anxiety provoking stimuli?

A
  1. Thalamus
  2. Amygdala
  3. Cortex
  4. Hypothalamus

Brain areas provuce ax provoking sx -> Activates HPA axis, stress hormones, and autonomic NS (fight or flight)

46
Q

What is the function of the amygdala?

A

Control of emotion: essential for the acquisition and expresison of fear

47
Q

How is the amygdala affected by those with phobias?

A

The amygdala is activated more rapidly and to a greater extent -> fight or flight

48
Q

What are examples of somatic sx?

A

Rx that are inappropriate to the situation:
1. Lock of concentration
2. Self-focused preoccupation
3. AUtonomic arousal
4. Easily startled, avoidance behaviors, restlessness

49
Q

How many of anxiety patient will eventually suffer from MDE?

A

1/3

50
Q

Common behavioral sx of ax?

A

Anything where the reaction is inappropriate to the situation.

51
Q

What is GAD?

A
  • Involves chronic, excessive, uncontrollable worry about everyday things
  • This constant worry affects daily functioning and can cause physical symptoms -> autonomic hyperactivity
  • Can occur with other axiety disorders
52
Q

What is the most common comorbid Axis I disorder?

A

DEPRESSION

53
Q

What are types of Axis 1 disorders?

A
  1. Dissociative disorders
  2. Eating disorders
  3. Mood disorders
  4. Psychotic disorders
  5. Substance use disorders
54
Q

What is the Benzodiazepine / GABA Receptor Model?

A

Benzodiazepines enhance GABA’s inhibitory effects by acting at the BZD binding site on the GABA-A receptor:
* Increased GABA = decreased anxiety

55
Q

What is the noradrenergic model?

A

Hypersensitive autonomic nervous system due to defects of the locus coeruleus and fight or flight response

56
Q

What is the serotonin model?

A

Buspirone, a selective serotonin anxiolytic, and the general effectiveness of SSRIs provides evidence for serotoninergic involvement

57
Q

What are the types of neurochemical theories for GAD?

A
  1. Benzodiazepine / GABA Receptor Model
  2. Noradrenergic model
  3. Serotonin model
58
Q

What is PTSD?

A

Reaction to intense fear, helplessness, or horror

59
Q

What are the sx classes of PTSD?

A
  1. Re-experiencing the traumatic event: nightmares, intrusive thoughts, flashbacks
  2. Avoidance of stimuli
  3. Increased arousal
60
Q

What are the causes of PTSD?

A
  1. Conditioned fear response
  2. Genetics
  3. Stress-induced neurotransmitter release of NE, CRF, cortisol
  4. The level of autonomic arousal immediately after the traumatic event predicts PTSD
61
Q

What is a panic disorder?

A

Unexpected, recurrent panic attacks

62
Q

What are panic attacks?

A

Sudden onset, peaks within 10 minutes:
* Abrupt Autonomic Surge
* Physical: SOB, DZ, Chills/heat
* Emotional: terror
* Cognitions: feelings of being out of control

63
Q

What are the sx of panic disorrders?

A

Feeling of imminent danger or doom

64
Q

Differentiate the types of panic attacks?

A

Unexpected: The attack “comes out of the blue” without warning and for no discernable reason.
Situational: Situations in which an individual will almost always have an attack. For example, entering a tunnel.
Situationally Predisposed: Situations in which an individual is likely to have a panic attack, but does not always have one.

65
Q

How do panic attacks cause issues with respiratory control?

A

Patients with panic disorder may have a hypersensitive respiratory control system, which operates at the level of brainstem chemoreceptors

66
Q

Describe the neurobiological aspects of panic attacks?

A
  1. Fear circuit overactivity (amygdala)
  2. Seratonin, GABA, NE
67
Q

What are the genetic aspects of panic attacks?

A

Heritability (50%)

*

68
Q

What is the NT hypothesis of panic disorders?

A

Dysregulation of norepinephrine, primarily with regard to function of the locus ceruleus

69
Q

What is agoraphobia?

A

fears or avoids situations because escape might be difficult or help might not be available

70
Q

What is a phobia?

A

where the anxiety is out of proportion to the actual threat posed by the situation

71
Q

What are specific phobias?

A

Unwarranted, excessive fear or anxiety evoked from specific objects or situations

72
Q

What are social phobia?

A

Marked and persistent fear of social situations which may involve “negative evaluation” by others (i.e. public speaking)

73
Q

What is OCD?

A

Uncontrollable obsessions and compulsions which the sufferer usually recognizes as being excessive or unreasonable

74
Q

How do you define obsessions?

A

Recurrent and persistent thoughts, impulses or images that are intrusive and unwanted that cause marked anxiety or distress

75
Q

How do you define compulsion?

A

Repetitive, purposeful behaviors that the person feels driven to perform in response to an obsession

Drug Action III (23 decks)

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