Psychiatric Disorders: Anxiety Disorders

  1. What are the major categories (5) of anxiety disorder?
    GAD (generalized anxiety disorder), PTSD (Posttraumatic Stress Disorder), Obsessive-Compulsive Disorder (OCD), Panic Disorders, and severe phobias
  2. How many sx does someone need to experience to qualify as suffering a panic attack? Approx. how long should it take to reach its peak?
    4 or more. Within 10 minutes.
  3. What kind of emotions does a person suffering from a panic attack suffer from?
    Intense fear or discomfort.
  4. T/F. all the diagnostic criteria have to be fulfilled to diagnose an individual with GAD. What is GAD?
    True. Generalized Anxiety Disorder.
  5. Excessive anxiety and worry needs to occur more days than not for a period of at least how long?
    6 months.
  6. How many sx should a pt. be exp. To be diagnosed with GAD? What is GAD?
    3 or more. General anxiety disorder.
  7. How many sx should a child be experiencing to be diagnosed with GAD? What is GAD?
    1 sx. General anxiety disorder.
  8. What are the exclusion criteria for diagnosing GAD? What is GAD?
    That the anxiety and worry is not caused by other Axis I disorders or by a drug or general medical condition. It also should not occur exclusively during a mood disorder, psychotic disorder, or a pervasive developmental disorder. Generalized anxiety disorder.
  9. What is a cause of PTSD?
    Experiencing a traumatic event.
  10. What sx will a person suffering from PTSD experience?
    Nightmares of the event, flashbacks, increased physiological response to reminders of the event, sleep disturbances and blunted emotional responses or irritability.
  11. What are two components of OCD?
    Obsession and compulsion.
  12. What are the main differences b/w obsession and compulsion? What mental illness are they components of?
    Obsessions are thoughts and compulsions are actions/behaviors. Compulsions are repetitive rituals to relieve the obsessive thoughts. They are components of OCD.
  13. What are the sx of panic disorder?
    Sx. Of a panic attack w/o warning or in a situation where an attack previously occurred.
  14. What is the typical onset of panic disorder?
    Late 20’s.
  15. What is the definition of a severe phobia?
    Fears that are irrational.
  16. What is the major brain region involved in anxiety disorders? Why?
    Amygdala because it controls emotions.
  17. Imbalances in what neurotransmitter systems are believed to be involved in Anxiety Disorders?
    Mainly GABAergic, Noradrenergic, and Serotonergic. DAnergic and cholinergic are also believed to contribute.
  18. What types of drugs are used to treat Anxiety Disorders?
    Sedative-Hypnotics and Antidepressants.
  19. What are the two classes of Sedative-Hypnotics?
    Barbiturates and Benzodiazepines.
  20. T/F. Sedative-Hypnotics are CNS depressants.
  21. What is the general MOA of Sedative-Hypnotics?
    Increases the inhibitory effect of GABA on GABA receptors by causing hyperpolarization of parts/cells such as neurons depression of CNS.
  22. What does a sedative do?
    Decreases activity, moderates excitement and calms a person.
  23. What does a hypnotic do?
    Produces drowsiness, facilitates the onset and maintenance of sleep that resembles sleep.
  24. What kind of channel is GABAA receptor?
    Cl Ion Channel.
  25. T/F. GABA_A is a pentameric channel containing alpha, beta, and gamma subunits.
  26. Most sedative-hypnotics bind to which alpha sites on a GABA_A receptor?
    A1, a2, or a3 sites.
  27. Alpha subunit is involved in what?
    Sleep and amnesia.
  28. Sleep and amnesia are regulated by what subunit on the GABA_A receptor?
  29. What are a2 and a3 subunits of GABA_A receptor involved in?
    Reduction of anxiety and muscle relaxation.
  30. What GABA_A subunits are involved in muscle relaxation and anxiety reduction?
    A2 and a3.
  31. T/F. Sedative-Hypnotics are GABA agonists.
  32. What is the term that describes a sedative-hypnotics effect on the GABA_A receptor? Explain the effects of sedative-hypnotics on GABA_A receptors.
    They are positive allosteric modulators. They enhance the effect of GABA, by helping modify the receptor in such a way that increases the influx of Cl- ion causing hyperpolarization.
  33. What happens to the GABA_A ion channel in the presence of a sedative-hypnotic and the absence of GABA?
    Nothing; GABA must be present for the receptor to function (open).
  34. How do Barbiturates work?
    They enhance GABAergic neurotransmission by increasing the amount of time the GABA ion channel remains open. This allows more Cl- to flow in.
  35. How do Benzodiazepines work?
    They enhance GABAergic neurotransmission by increase the frequency of GABA ion ch. Opening allow more Cl- to flow in.
  36. Which has greater GABA enhancing effects- Barbiturates or Benzodiazepines? Why?
    Barbs, because they increase the amount of time GABA ch. Is open for.
  37. What are the dangerous side effects of barbiturates?
    Cognitive impairment, respiratory depression, high potential abuse, rapid metabolic tolerance, and low therapeutic index (w/ chronix usage).
  38. T/F. It is difficult to become tolerant to adverse effects? Explain.
    True. Because the dose needed to experience an adverse effect remains similar, but there is tolerance to the desired therapeutic effect (therefore you get a narrow therapeutic window when tolerance develops cause of chronic use).
  39. Why are barbiturates no longer commonly used to treat anxiety disorders?
    Rapid development of tolerance.
  40. For barbiturates, what one factor affects brain penetration, onset and duration of action?
    Lipid solubility.
  41. If a barbiturate has high lipid solubility, what will it’s onset and duration of action be like? Give examples of this kind of barbiturate and their use.
    Their onset of action is quick with a quick duration of action. Examples are: Thiopental (pentothal) and Methohexital (Brevital)- used for IV anesthesia.
  42. If a barbiturate has medium lipid solubility, what will it’s onset and duration of action be like? Give examples of this kind of barbiturate and their use.
    Onset is not too slow, not too fast. Duration of action longer than high lipid soluble drugs, but shorter than low lipid soluble drugs. Examples are: Amo (amytal), Seco (seconal), Pentobarbital (nembutal). All used for surgical anthestia and sleep induction.
  43. If a barbiturate has low lipid solubility, what will it’s onset and duration of action be like? Give examples of this kind of barbiturate and their use.
    It’s onset is slow and duration is long. Examples are: Pheno (luminal) and Mephobarbital(mebaral). Prolonged sedation and seizure control.
  44. T/F. In the continuum of sedative-hypnotic actions, the responses at different doses are independent of one another.
  45. What happens as you increase dose of sedative-hypnotic? (answer is not a specific physiological response)
    Decreasing consciousness.
  46. What are the advantages of benzodiazepines?
    Less cognitive impairment, lower abuse potential, lower chance of tolerance, higher therapeutic index.
  47. What is a disadvantage of benzodiazepines?
    A weaker allosteric modulator compared to barbiturates and other anesthetic agents, like EtOH)
  48. T/F. Benzodiazepines are good at treating emotional response of anxiety.
    False. They are better at treating physical changes.
  49. T/F. Chronic use of benzodiazepine can lead to physiological dependence.
  50. What sx will sudden d/c of benzodiazepine lead to?
    Rebound anxiety, insomnia, restlessness, muscle tension, irritability, some cases= seizures
Card Set
Psychiatric Disorders: Anxiety Disorders
5223 1/10/12