Anxiety

Question 1

Anxiety & The Amygdala

Answer 1

anxiety-provoking stimuli into the amygdala activates DA, NE, and ACh, leads to behavioral arousal and increased vigilance.

Question 2

Prefrontal cortex

Answer 2

responsible for amygdala activation & primitive behavioural responses.

Question 3

CRF

Answer 3

increases release of cortisol to induce physiological changes that allows us to adapt to environmental changes.

Question 4

How does NE affect sympathetic activation?

Answer 4

increased release of NE during sympathetic activation induces altering & fear responses (pupil dilation, increased heart rate).

Question 5

how do GABA-A agonists affect GABA?

Answer 5

Enhance function of GABA → sedation, reduced anxiety, anticonvulsant effects.

Question 6

Anxiolytics: Dose-Dependent Effects

Answer 6

Increasing dose of drug leads to decreasing consciousness; from alertness → relief of anxiety → sedation → general anesthesia → coma → death.

Question 7

Anxiolytics

Answer 7

drugs that are used to relieve signs of stress with minimal side effects like sedation.

Question 8

what is the main mechanism of sedative-hypnotics & what effects do this produce?

Answer 8

primary mechanism involves enhancing GABA transmission, induces sleep at high doses.

Question 9

Differences in lipid solubility in barbutates

Answer 9

• High lipid solubility → 10-20 second onset → 20-30 min duration.
• Moderate lipid solubility → 20-40 min onset → 5-8 hour duration.
• Low lipid solubility → 1+ hour onset → 10-12 hour duration.

Question 10

Where do barbiturates bind?

Answer 10

Barbituates bind on GABA-A receptor and enhance GABA effects.

Question 11

Barbiturate Side Effect

Answer 11

Reduce REM sleep.

Mental clouding.

Coma/death.

Impaired thinking.

Question 12

Barbiturate Abuse Potential

Answer 12

• Tolerance to mood changes & sedation.

- Significant physical dependence (withdrawal) & potential for abuse (reinforcement).

Question 13

Dose-response curve barbiturates

Answer 13

• early drug use –> mood effects without significant respiratory depression.
• with repeated use –> tolerance develops so larger amounts of drug are needed to experience sedation –> TI decreases.

Question 14

Biotransformation of BDZs

Answer 14

Long-lasting BDZs produce active metaboliteswith long half-lives.

Short-lasting BDZ termination depends on liver metabolism (direct metabolism & excretion).

Question 15

BDZs increase the _______ of GABA-A action.

Answer 15

BDZs incease the FREQUENCY of GABA-A action.

Question 16

BDZ Side Effects

Answer 16

Mild sedation.

Reduced stage 4 sleep.

Memory loss.

Question 17

Buspirone (Buspar)

Answer 17

• 2nd generation anxiolytic/anti-depressant.

- Less side effects.

Question 18

Onset/Duration of Buspar

Answer 18

Slow onset (several weeks of daily use).

Delayed action may be more useful for GAD than panic disorder.

Question 19

What receptors do 2nd gen anxiolytics act on (Buspar & Effexor)?

Answer 19

Buspar → partial agonist at 5-HT1A receptors.

Effexor → serotonin & NE receptors.

Question 20

SSRIs

Answer 20

block reuptake of 5-HT & enhance inhibition.

Question 21

Barbiturates increase _______ of __________ channels.

Answer 21

Increase DURATION of opening of GABA activated Cl channels.

Question 22

BDZ abuse potential

Answer 22

No metabolic tolerance.

High therapeutic index → lethal overdose is rare.

Lower probability of physical dependence & abuse.