Physiological Disorders Flashcards
Antagonist vs agonist
Antagonist – drug that blocks neurotransmitter
Agonist - drug that mimics or increases effect
Affinity v efficacy
Affinity – tendency to bind to a receptor
Efficacy – tendency to activate the receptor
Genetic influence Alcoholism:
associated with variation in ADH1B and ALDH2. Involved in metabolism of ethanol into acetaldehyde
Generic Influence dopamine
Variation of DRD2 gene reduces activity in dopaminergic system
Nucleus accumbens:
increased dopamine release in the nucleus accumbens reinforces experiences
Type 1 v type 2 alcoholism
• Type 1 alcoholism: late onset
• Type 2: early onset
• Family history, stress and cortisol
Dopamine receptors
Dopamine: D3 Receptors involved in addiction
o Distributed throughout reward systems
o High affinity to endogenous dopamine
o Upregulation in those with addiction
o D3 antagonists may help prevent relapse
Cravings:
insistent search for activity, abstinence increases sensitivity to addictive substances and visual cues can trigger a craving
Tolerance –
decrease in effect as an addiction develops. Tolerance is learned, can be weakened
Treatments
• Cognitive-behaviour therapy
• Contingency management (rewards for being drug free)
• Deep brain stimulation
• Medication (e.g. antabuse results in nausea after drinking, may be a deterrent)
Monoamine hypothesis:
decreased concentration of monoamines (serotonin, dopamine and norepinephrine in the synapse causes depression)
Example of Genetic influence varying within environment
short form of the serotonin transporter gene influences reaction to stressful events
Hemispheric dominance:
brain activity associated with depression:
Hemispheric dominance cortex involved
Left prefrontal cortex: decreased activity (processes positive emotions, decision making and anticipation of joy and pleasure)
• Right prefrontal cortex: increased activity. (processes negative emotions, response to fear-based stimuli and promotes self-reflective cognition)
Tricyclics
block transporter proteins that reabsorb serotonin, dopamine and norepinephrine into presynaptic neuron. Blocks histamine , acetylcholine receptors and certain sodium channels (side effects including drowsiness, dry mouth, heart irregularities
SSRI/SNRI/NRI
SSRIs (selective serotonin reuptake inhibitors, block reuptake of serotonin and based on serotonergic deficit hypothesis), SNRIs (Block reuptake of serotonin and norepinephrine) and NRIs (block reuptake of norepinephrine).
Monoamine oxidase inhibitors (MAOIs)
block the enzyme oxidase. Results in more transmitters in the presynaptic terminal available for release. Side effects: dry mouth, nausea, insomnia and dizziness.
Atypical antidepressant drugs
include a misc group of drugs with antidepressant effects and milder side effects. EG bupropion (inhibits reuptake of dopamine and norepinephrine, but not serotonin) and Trazodone (serotonin antagonist and reuptake inhibitor)
New substances
include Ketamine – antagonises NMDA type glutamate receptors, produces rapid antidepressant effects, not suitable (produces delusions and hallucinations) but may lead to something similar. Research suggests increases BDNF
Why are antidepressants effective?
• People with depression have lower than average brainderived neurotrophic factor (BDNF). As a result, people with depression show smaller hippocampus, impaired learning and reduced production of hippocampal neurons.
• Antidepressants may act by increasing BDNF.
CBT and exercise
Appears to influence abnormal activity in the ACC, VLPFC, DLPFC, amygdala an hippocampus
Electroconvulsive therapy (ECT)
o Electrically induced seizure for treatment o For patience who have not responded to medication
o Side effects include memory impairment
o High risk of relapse without continued treatment
o Mechanisms: May increase BDNF and promote neural development in hippocampus Recent research suggests no change to BDNF
Categories of antidepressants
- tricyclics
- SSRI/SNRI/NRI
- MOAI
- atypical
- new substance
