16210198
| Pregunta | Respuesta |
| what is tolerance? | the capacity of the body to endure or become less responsive to a substance especially with repeated use or exposure |
| what is physical dependence? | caused by chronic use of a tolerance-forming drug of which abrupt cessation results in unpleasant symptoms |
| dependence syndrome means | when you need the drug to be present to maintain normal function |
| what are the 2 types of withdrawal syndrome? | acute withdrawal that lasts for days protracted withdrawal syndrome which means the person experiences cravings for years after detox |
| what is withdrawal brought about by (4) | abrupt cessation rapid dose reduction decreasing blood level of drug administration of an antagonist |
| what is addiction? | the intense desire to obtain increasing amounts of a substance(s) over all other activities it is a chronic, neurobiological disease with genetic, psychosocial, and environmental factors |
| addiction behaviour is characterised by (4) | compulsive use of substance drug seeking behaviour continued use despite physical, social, and economic harm high tendency to relapse |
| what reward pathway do all drugs of abuse activate? outline the structures involved in this pathway | mesolimbic dopamine pathway comprises ventral tegmental area (VTA) which is connected to the ventral striatum by dopamine neurons. the nucleus accumbens (NAc) and the olfactory tubercle make up the ventral striatum. |
| what is the effect alcohol has on the CNS and how does it achieve this effect? | alcohol is a CNS depressant it acts on GABAaRs to increase inhibitory transmission (it also enhances the CNS depressant effects of other drugs) |
| acute alcohol effects include | increase in GABAaR activity --> cellular hyperpolarisation decrease Ca conductance via NMDA recetpors --> decrease depolarisation |
| outline how neuroadaptation in chronic alcoholism occurs | overtime, the body internalises normal alpha 1 GABAaRs and increases the expression of 'low alcohol sensitivity' alpha 4 GABAaRs NMDA receptors are phosphorylated and so there will be less on the cell surface |
| name some of the effects/symptoms of chronic alcoholism (6) | fatty liver disease impaired testicular steroid synthesis --> feminisation and impotence pseudo-cushing's syndrome chronic gastritis because alcohol destroys the gastric mucosa peripheral neuropathy dementia, motor impairment because of cerebral cortex thinning and degeneration of cerebellum |
| outline what happens, on a cellular level, in alcohol withdrawal syndrome | decreased inhibitory GABA transmission and increased excitatory glutamate transmission ---> CNS hyperactivity |
| outline symptoms of alcohol withdrawal syndrome | in the first 24 hours you get sweating, tremor, fever, sometimes hallucinations then you get seizures, agitation, aggresesion, severe hallucinations delrium tremens (onset on the 3rd day) is a medical emergency: delirium, hallucinations, course tremor, disorientation, hyperthermia, seizures |
| treatment for acute alcohol withdrawal | long-acting benzodiazepines (chloradiazepoxid) + haloperidol (adjuvant) prenteral thiamine if suspected/confirmed wernicke's korsakoff syndrome |
| treatment options to aid abstinence from alochol | disulfiram = acetylaldehyde dehydrogenase inhibitor --> accumulation of acetylaldehyde when alcohol is consume giving unpleasant effects: flushing, headache, nausea, vomiting acamprosate = NMDA receptor antagonsist and GABA agonist (helps with CNS hyperactivity and decreases craving) naltrexone = opiate antagonist that reduces the reinforcing effects of alcohol also pancreatic enzyme supplementation, high dose oral thiamine |
| name 3 opioids | heroin morphine codeine |
| outline cellular effects of acute opioid use | activation of mu receptors --> increase K conductance + inhibit adenylyl cyclase --> cellular hyperpolarisation |
| outline how neuroadaption occurs with prolonged opioid use | tolerance to eurphoria is due to: increase of mu receptor phosphorylation leading to internalisation and degration decreased efficacy of mu opioid signal transduction hyperactivation of adenylyl cyclase signaling --> enhanced GABA action |
| what happens on a cellular level when you go through opioid withdrawal? | enhanced GABA action inhibits VTA dopamine neurons leading to dysphora and anhedonia |
| what is the meaning of anhedonia? | unable to feel pleasure in normally pleasurable activities |
| treatment of opioid overdose | naloxone (a synthetic opioid receptor antagonist) |
| 3 drugs used in opioid detoxification | methadone - decreases withdrawal symptoms without producing a high buprenorphine - partial mu receptor agonist that prevents withdrawal symptoms by blocking the actions of other opioids clonidine - alpha 2 noradrenergic agonist that decreases autonomic overactivity and thereby decreases withdrawal |
| benzodiazepine MOA | increase frequency of Cl channels opening in response to GABA and GABAaRs leading to increased neuronal inhibition |
| dependence on benzodiazepines can develop during long-term clinical use, so... | only short courses (2-3 weeks) recommended discontinue with tapered dose |
| withdrawal of benzodiazepines is associated with (3) | rebound anxiety insomnia seizures |
| nicotine targets which receptor? | nicotinic AChRs located centrally and peripherally and at NMJs |
| how does nicotine activate the dopamine reward pathway? | activating AChRs on dopaminergic neurons in VTA to increase dopamine release |
| activation of central nicotinic receptors produces | anxiolytic effects increased arousal appetite suppression |
| activation of peripheral nicotinic receptors produces | increased BP increased smooth muscle contraction |
| smoking cessation treatment: buproprion | an antidepressant that increases dopamine and NA pathways in CNS |
| smoking cessation treatment: varenicline | partial agonist at alpha 4 beta 2 AChR - decreases craving and pleasurable effects of cigarettes |
| what is the primary mechanism of action for psychostimulants | augment the effects of dopamine |
| examples of psychostimulants (4) | cocaine amphetamine methamphetamine cannabinoids |
| active compound in cannabinoid | delta 9 tetrahydrocannabinol (THC) |
| what receptors do cannabinoids act on | G-couple proteins: CB1 (brain) CB2 (immune cells) |
| name 2 hallocinogens | LSD MDMA |
| where does LSD come from | mushrooms (ergot) |
| how does MDMA work? | increase serotonin release and blocks erotonin reuptake |
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