Depression & anxiety

Question 1

what defines an anxiety disorder ?

Answer 1

• an inappropriate or excessive anticipatory manifestation of the fear response to a stressor (to what should be considered a normal response)
• disturbance in the HPA (may be overactive) - presence of stressor isn’t required
• imbalance amongst limbic system circuitry
• impairment in synapse activity

Question 2

How do BZ drugs work?
(diazepam, nitrazepam)

(anti- anxiolytic drug)

Answer 2

• Bind to an allosteric site on inhibitory GABAa receptors
• act as PAMs
• increase receptor binding site affinity for GABA
• increased cl influx leading to increased hyper polarisation
• reduction in anxiety and aggression
• sleep inducing hypnotic

Question 3

identify some problems associated with BZ usage

Answer 3

• sedation
• acute overdose (profound sedation + alcohol) = serious respiratory depression
• long term usage
  tolerance/ drug dependence/ withdrawal effects
• tachycardia, tremor, insomnia, seizures
• used as a short term management

Question 4

What does Buspirone do?

Answer 4

• 5-HT1ar agonist
• present in limbic circuitry
• slow to act (2 weeks)- related to neuroplasticity
• change in circuitry
• better option than BZS
• no sedation or motor impairment
• non-addictive and no withdrawal effects

Question 5

why are a-adrenoR Antagonists given to treat anxiety?

Answer 5

• reduce somatic symptoms of anxiety and are used for situational phobias
• prevent tremor, palpitations, sweating, tachycardia
• doesn’t target cause but relieves symptoms

Question 6

why prescribe SSRIs to patients suffering with anxiety ?

Answer 6

• AD drugs effective strategy for tackling AD

- link neurobiologically between depression + anxiety

Question 7

what are the symptoms of MDD?

Answer 7

• misery, despair, loss of motivation, appetite loss, suicidal
• reactive vs endogenous

Question 8

What is the monoamine theory of depression?

Answer 8

depression is due to hypoactivity at monoaminergic (NA and 5-HT) synapses in the brain

evidence for

-AD drugs act by raising MA levels in brain

evidence against

• Ads take 1/3 weeks to work
• cocaine and amphetamine can both rapidly change levels of MA in the brain, but exhibit no AD action

Question 9

how do MAOIs work? and what are their unwanted s/e?

moclobemide

Answer 9

• euphoria immediate effect
• prevents metabolism and breakdown of MA via MAO
• make take 4 weeks to see action
• increase intra-terminal MA and intra-Synaptic levels

unwanted s/e

• cheese reaction
• mimics effects of Nad on periphery
• elevated levels of tyramine displace NA from vesicles and increases SNS mediated affects
• anti- must effects
• a1 r antagonism

Question 10

how TCAs work?

Answer 10

• amitriptyline , imipramine
• slow onset
• 5-HT/NA reuptake inhibition
• unwanted s/e include
• anti-musc/ sedative (H1 r antagonism)
• overdose = dangerous

Question 11

How do SSRIs work?

Answer 11

-fluoxetine/ paroxetine

• increase levels of synaptic 5-HT (intrasynaptic)
• via 5-HT reuptake inhibition
• less dangerous/ unwanted s/e than TCAs/ MAOs
• immediate increase in synaptic 5-HT
• still has a 2-4 weeks delay (inherent delay)
• age affects efficacy of drug (better in younger)