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Medications and Behavior > Exam 1 (CHAPTERS 1-4) 4 > Flashcards

Exam 1 (CHAPTERS 1-4) 4 Flashcards

1
Q

Fear is what?

A

Adaptive and necessary to avoid harm

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2
Q

What receives sensory info regarding threat and initiates fear response?

A

Amygdala

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3
Q

What tells the hypothalamus to trigger hormones?

A

Amygdala

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4
Q

What tells pons and medulla to control movement, facial expression, and heart/respiration rate?

A

Amygdala

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5
Q

What integrates emotional content from stimuli to guide response to fear?

A

Prefrontal cortex

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6
Q

What is used for planning and hurts planning if damaged?

A

Prefrontal cortex

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7
Q

What is anxiety?

A

The perception of threat - typically vague
- NOT danger, necessarily, but perceived danger
- Body reacts same way to fear and anxiety
- Anxiety effects can be long lasting because not a specific fear stimulus

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8
Q

Types of Anxiety disorders

A

1) Panic Disorder with/without Agoraphobia
2) Generalized Anxiety Disorder
3) Post-traumatic Stress Disorder (PTSD) - separate category in DSM 5

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9
Q

Panic Disorder

A

1) Repeated and unexpected panic symptoms characterized by discrete periods of intense fear
2) At least one month of persistent worry about having panic episode
3) Symptoms may be expected (cued) or unexpected (uncued)
4) with or without agoraphobia

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10
Q

What is agoraphobia?

A

Fear of panic attack in inescapable situation

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11
Q

Generalized Anxiety Disorder lifetime prevalence?

A

5%

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12
Q

What is GAD

A

Excessive worry and difficulty controlling the worry

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13
Q

Pathology of GAD

A
  • Low heritability and NO identified genes
  • Strong associations with major depression
  • Neurotransmitter of interest: GABA
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14
Q

With GAD, what does it have a deficiency of in its neurotransmitter of interest?

A

Deficiency in receptor expression and in messenger RBA (transcribes receptor)

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15
Q

What is the lifetime prevalence of PTSD?

A

8%

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16
Q

What are the 3 primary symptom clusters of PTSD?

A
  • re-experiencing
  • avoidance
  • hyperarousal
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17
Q

What is the Pathology of PTSD?

A
  • Decreases in hippocampal and pre-frontal cortex volumes
    • This is due to increased glucocorticoid and
      catecholamine release in response to stress and
      underactive prefrontal cortex
  • Enhanced amygdala response
    • Not suppressed from cortical inhibition
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18
Q

Who discovered barbiturates?

A

Bayer laboratories in 1903

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19
Q

What do Barbiturates depress?

A

CNS

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20
Q

What is a GABA agonist and has effects similar to alcohol?

A

Barbiturates

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21
Q

What is the problem with Barbiturates?

A

You can’t separate anxiolytic effects from sedative effects

22
Q

What kind of therapeutic index do Barbiturates have?

A

Narrow, especially when combined with alcohol

23
Q

What has Barbiturates been used for?

A

Seizures, anxiety, insomnia, and anesthesia

24
Q

Sodium amytal

A

Barbiturate used for hypnosis and truth serum (not supported by research due to false memories)

25
Q

Mechanisms of Barbiturates

A
  • Bind to barbiturate site on ionotropic GABA-A receptor and open a Chloride channel
  • Produces hyperpolarization of postsynaptic membrane
  • Postsynaptic cells cannot easily produce an action potential which reduces the firing rate in receiving neurons
  • Barbiturates can work in absence of NT GABA on barbiturates site in GABA receptor complex
  • Net effect: inhibition
26
Q

Side effects of Barbiturates

A
  • Confusion, impaired judgment, loss of muscle coordination, impaired speech
  • Disruption of sleep cycles &REM deprivation
27
Q

What happens if Barbiturates disrupts sleep and REM a few nights? A week?

A

few nights: irritability, poor concentration
1 week: psychotic symptoms

28
Q

Barbiturate tolerance

A

Increased liver metabolism and GABA receptor downregulation (but NOT with respiratory suppression)

29
Q

When were Benzodiazepines discoverd?

A

the 50s ( Librium then Valium)

30
Q

Benzos Mechansims

A

Bind to GABA receptor like barbiturates
- Causes hyperpolarization
- Can’t open chlorine channels on their own, need GABA present

31
Q

Benzos side effects

A
  • Sedation, cognitive impairments, motor movement impairment, slurred speech
  • Disrupts sleep cycles when used long term
  • Less risk of respiratory depression but still interacts with alcohol
32
Q

What Benzo produces euphoria, sedation, and amnesia when combined with alcohol?

A

Rohypnol

33
Q

Tolerance with Benzos

A

Benzo receptor downregulation

34
Q

Third- Generation Anxiolytics two kinds

A

Partial GABA agonists and Serotonin agonists

35
Q

Partial GABA agonists

A
  • minimize sedative side effects
  • less binding efficacy than full agonists
  • not used in US
36
Q

Serotonin agonists

A
  • 5HT receptors located in anxiety brain areas
  • Not immediate effect like benzos but less side effects
  • Buspirone is one
37
Q

Buspirone

A

Downregulation/desensitization of autoreceptors leading to increased 5HT production

38
Q

Alternatives for Anxiety

A

Valerian
- herb (dating back to Hippocrates)
- not well researched
- one study suggested efficacy in mice

39
Q

Obsessive part of OCD

A

Recurrent unwanted thoughts

40
Q

Compulsions part of OCD

A

Repetitive behavior

41
Q

Relationship between obsessive and compulsive

A

Typically compulsions are to prevent or reduce obsessions
- there is a recognition of unreasonable/excessive nature

42
Q

When is the onset of OCD?

A

Early adolescence/adulthood but can occur in kids

43
Q

What is the rate between men and women in OCD

A

Equal rates (except for kids, greater in boys than girls)

44
Q

What is the lifetime prevalence of OCD?

A

2.5%

45
Q

OCD Pathology

A
  • Neural dysfunction between orbitofrontal cortex, cingulate gyrus, caudate nucleus, globus pallidus, and thalamus
46
Q

What is Normal vs OCD pathology?

A

Normal: DA in caudate nucleus inhibits globus pallidus which inhibits thalamus
OCD: DA inhibition in globus palidus leads to lack of thalamus suppression which leads to increased activity in orbitofrontal cortex

47
Q

Cingulotomy

A

Surgically disrupting excitatory input from cingulate gyrus to frontal cortex

48
Q

Can SSRIs and SNRIs be used for Anxiety?

A

Yes, but mechanism is unclear

49
Q

What is the initial efficacy of Serotonin on Anxiety disorders?

A

50-60%

50
Q

What happens to blood flow for those with an Anxiety disorder who respond to SSRIs or SNRIs?

A

Decreases blood flow to thalamus

51
Q

What happens to DA receptors in caudate nucleus when SSRIs or SNRIs are used for anxiety disorders?

A

It increases

52
Q

Write out Fight/ Flight and Rest/Digest increases and decreases

A

Fight/Flight (synaptic NS)
- HR/BP - both increase
- Digestion - Decreases
- Breathing - Rate increases, depth decreases
- Sweating - Increases
- Immune functioning - Decreases

Medications and Behavior (40 decks)

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