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64 Cards in this Set
- Front
- Back
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behavioral continuum of sedation |
normal-> relief from anxiety->disinhibtion->sedation->hypnosis->general anesthesia->coma-> death |
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effects of all depressants |
ease anxiety, tension diminish environmental awareness reduce response to sensory stimulation depress cognitive functioning decrease spontaneity reduce physical energy |
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properties of all depressants |
-potentiation -physiological dependence -psychological dependence -cross-tolerance -cross-dependence |
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drugs in the depressant class |
ethyl alcohol inhalants barbiturates general anesthetics anti-epileptics benzodiazepines some anti insomnia drugs |
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three classes of alcoholic beverages |
beer, wine and hard liquor produced through fermentation and distillation alcohol content of a beverage: expressed by volume or weight proof of alcoholic beverage =percent of alcohol in it |
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pharmacology of alcohol |
-alcohol depresses the CNS -dissolves in lipid membrane, one of the reasons why it is so toxic -GABA, serotonin, glutamate, dopamine are significant |
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sites of action of alcohol |
-primarily absorbed in the small intestine and then distributed to all tissues on the body -blood receives a large amount of the alcohol -rate of alcohol absorption is dependent on person, not consistent, based on psychological and situational factors |
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pharmacokinetics of alcohol |
primarily affects the CNS BAC(blood alcohol concentration)-including alcohol dose and time, also considers gender, body fat percentage, rate of alcohol metabolism -breath analysis-practical method of measuring BAC |
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alcohol metabolism |
-body metabolizes more than 90% of the alcohol it absorbs -occurs primarily in the liver - the liver: ---metabolizes alcohol at a constant rate of about 0.35 ounce of alcohol per hour ----cannot quicken the pace |
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tolerance and dependence on alcohol |
-leads to dispositional tolerance, acute tolerance and functional tolerance -heavy use can lead to physical dependence -alcohol withdrawal syndrome can lead to death |
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acute tolerance |
same level of alcohol but when coming down, less impaired |
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functional tolerance |
? |
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acute effects of alcohol |
-physiological, sensorimotor, behavioral effects -as the BAC increases these effects increase in number and intensity -individual experiences differ based on person and psychological |
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physiological acute effects |
inhibits anti-diuretic hormones reduces fat oxidation peripheral dilator-makes you feel warm increases gastric secretion, stimulates appetite increases corticosteroids disruption of REM memory impairment- black outs, grey outs hangovers vision decreases in acuity taste, smell, pain insensitivity body sway/gait impairs psychomotor skills |
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psychological acute effects |
impacts emotion and mood situational and cognitive factors significant mood effects may differ depending on rising and falling BAC impairs short term memory over estimate the passage of time attention and concentration impairment |
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psychological-behavioral effects |
alcohol and aggression -co-occurence especially prevalent in 18-30 year old men -early theories-reduced impulse control, impaired cognitive function, alcohol myopia -disinhibition theory questioned -alcohol and sex-must incorporate social and psychological factors |
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effects of chronic heavy drinking |
-damages the bodys organ systems -damage to the brain:impaired memory, other cognitive factors -korsakoff's syndrome:irreversible structural damage to the brain, memory impairment -fatty liver(if stop drinking will go away), alcohol hepatisis, cirrhosis(scar tissue, not reversible) |
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definition of chronic use |
varies 7 per week for women, 14 for men |
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korsakoffs |
memory impairment, brain damage |
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wernickes |
nutritional deficienes, lose ability to focus visually |
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fetal alcohol syndrome |
results from mother drinking during pregnancy(not necessarily happens) consists of physical deformities that are identifiable at birth associated with continued physical problems below average intellectual functioning |
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moderate drinking and health |
moderate alcohol consumption is associated with lowered risk of cardiovascular disease and mortality research conclusions: still remain controversial |
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alcohol non-specific actions |
-alcohol readily crosses cell membranes including the blood brain barrier -non specific actions result from changes in membrane lipids, alcohol interacts with the polar heads, alters lipid composition and disturbs the relationships of proteins in the membrane |
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alcohol specific actions |
it interacts with particular proteins influences several ligand gated channels and alters second messenger systems |
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effects of glutamate |
-excitatory -has effect on NMDA receptors -ligand gated channels that allow Ca2+ and Na+ to enter and cause localized depolarization |
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effects of alcohol on glutamate |
-inhibits glutamate release from hippocampus -glutamate antagonist -associated with impairing learning and memory -repeated use results in up regulation of NMDA receptors -during withdrawal, glutamate release increases after 10 hours resulting in hyperexcitation which leads to seizures, typical of alcohol abstinence syndrome -elevated glutamate during withdrawal causes increased Ca2+ influx, leading to cell death -frequent withdrawals may be responsible for the brain damage seen |
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GABA and alcohol |
-inhibitory -binds to GABA a receptors and opens the channels, allowing Cl- to enter the cell to hyperpolarize the membrane - alcohol increases Cl- flux and stimulates GABA release - repeated exposure to ethanol reduces Gaba a mediated Cl-flux -may contribute to the appearance of tolerance and withdrawal |
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Dopamine and alcohol |
-dopaminergic mesolimbic system plays a significant role in reinforcement and motivational mechanisms -the nucleus accumbens is part of the extended amygdala, which is involved in integrating emotion with hormonal responses and sympathetic nervous system activity -NAcc plays role in reinforcing qualities that lead to repeated drug use and motivation for the drug -increased dopaminergic transmission occurs in most drugs of abuse |
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sleep and anxiety relationship |
treat them based on the same category of drugs |
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what is anxiety |
-activation of the sympathetic autonomic nervous system produces sweating, increased heart rate, and other signs of fight or flight -it warns of danger and allows us to cope with emergencies -anxiety is not helpful for tests |
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the cycle of anxiety |
-if high anxiety damages a performance, this leads to more anxiety -depression may develop |
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DSM 5 anxiety disorders |
seperation anxiety disorder selective mutism specific phobia social anxiety disorder panic disorder agoraphobia generalized anxiety disorder OCD |
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three component model of anxiety |
potential stressors-> if stressor perceived as a threat then creates bodily effects, upsetting thoughts, ineffective behavior |
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history of drugs used to treat anxiety |
originally used propanediol carbamates ---meprobamate(miltown, equanil), nonbarbiturate sedative hypnotic(for marketing purposes), targets acetycholine tranquilizers, sedatives, benzodiazepines ---valium(most prescribed), ativan, xanax, targets GABA, ED and LD close together buspirone (buspar) ---serotonin-also rationale for SSRIs |
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the fifties |
were the age of anxiety propanediol carbamates ---factors contributing to rapid rise -----selective anti-anxiety effects -----large advertising campaign -----safety ------no formal diagnostic guidelines |
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propanediol carbamates |
-relieves tension through muscle relaxation, decreases action of ACH -only slight depression of respiratory center -side effects: drowsiness, intoxication, disrupt motor coordination, suppresses REM, physical dependence-tolerance and withdrawal - clinical factors ---more selective in treating anxiety ---anterograde amnesia ---safety margin higher, negligible depression of respiratory center ---not used for chronic anxiety ----good for panic attacks and phobias |
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neuroanatomy of anxiety |
-the amygdala is a major component of several emotion processing circuits -it receives highly processed sensory and cognitive info from the sensory thalamus, sensory and association cortices and hippocampus -these brain areas project to the lateral nucelus of the amygdala |
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neurobiology of anxiety-NE and GABA |
1. norepinephrine 2. GABA-inhibitory neurotransmitter ***GABA a most significant ---benzodiazepines (BDZ) and barbiturates cause sedation and reduced anxiety by binding to modulatory sites on the receptor complex 3. serotonin plays a large role in anxiety modulation ---enhancing 5-HT function by blocking the reuptake transporter or stimulating 5-HT 1a receptors reduces anxiety SSRIs enhance 5-HT function, are used to treat a variety of anxiety disorders 4. Dopamine- has a modulatory role which is supported b the DA projections from the VTA to the mPFC and limbic regions including the amygdala ---stress increases firing of mesocortical dopaminergic neurons and increases DA turnover in the prefrontal cortex |
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current drugs for treating anxiety |
-anxiolytics produce a calm and relaxed state, with drowsiness, mental clouding and incoordination -induce sleep at higher doses and called hypnotics -at highest doses, depress CNS and cause coma and death |
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benzodiazepines |
the first to be produced was chlordiazepoxide(librium) --first true anxiolytic that targeted anxiety without producing excessive sedation, had low incidence of tolerance, less severe withdrawal than barbiturates and a safe therapeutic index |
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current drug treatment for anxiety |
-primary mechanism of action involves enhancing GABA transmission -GABA is the major inhibitory NT; the GABA a receptor is a Cl- channel -GABA and GABA agonists allow Cl- to move into the cell and result in hyperpolarization |
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drugs for treating anxiety -benzodiazepines |
-benzodiazepines enhance the effect of GABA but in the absence of GABA, they have no effect on channel opening -all BZDs have similar molecular structure and mechanism of action but onset of action is determined by lipid solubility, the most soluble are quickest to be absorbed and moved through the blood brain barrier |
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duration of action-benzodiazepines |
short acting ones such as restoril and lorazepam are metabolized in one step into metabolites, these also increase the duration of action |
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bdzs and improvement from past drugs and other effects |
-less cloudiness, more mild, less loss of motor coordination -longer acting BDZs are useful hypnotics and are useful muscle relaxants and others are anticonvulsants -can prevent alcohol withdrawal symptoms -have high therapeutic index -high doses induce disorientation, cognitive impairment and amnesia but with no respiratory depression -recreational use of BDZs is often paired with other alcohol, opioid or CNS depressants, which can be highly toxic -flumazenil (romazicon) is a competitive antagonist for the BDZ receptor and can be used to reverse the effects of BDZ |
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benzodiazepenes: benefits |
-do not induce liver enzymes, resulting in less tolerance -lower risk of dependence and abuse but can still occur -reinforcement is much lower than with barbiturates but those with rapid onset are likely to be self administered by animals |
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benzodiazepenes: second generation |
-developed to have fewer side effects -buspirone is less effective in reducing physical symptoms of anxiety and cognitive aspects of worry and poor concentration - weak agonist for serotonin |
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barbiturates: history |
-until 1970s, barbiturates were the sleep aid of choice - today, rapid onset ones with short duration are used as anesthetics, whereas slower ones are used for seizures |
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barbiturate effects |
-disinhibition -euphoria -sedation -loss of motor control -sleep -anesthesia -coma, death -respiratory depression |
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barbiturate: overdose risk |
-CNS neurons adapt to the drug and become less responsive with chronic drug use -respiratory depression does not show tolerance, so as dose needed to achieve a desired affect increases, the therpeutic index becomes smaller |
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effects of barbiturates |
-increase the affinity of GABAa receptor for GABA and can open Cl- channel without GABA -makes them potentially lethal, while benzodiazepines are not -have been replaced by BZDs for treatment of anxiety disorders |
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barbiturates: dependence and withdrawal |
-produce significant physical dependence and potential for abuse -terminating drug use after extended treatment produces fatal withdrawal syndrome simila rot alcohol |
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barbiturates side effects |
-alter sleep by reducing the amount of REM sleep -mental clouding, loss of judgement and slowed reflexes -high doses lead to gross intoxication -coma and death result from respiratory depression -very dangerous combined with alcohol |
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the psychostimulants |
-cocaine -amphetamine -4 methyl-methcathinone, mephedrone(bath salts, plant food) -nicotine -caffeine -drugs used for ADHD |
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shared physiological effects of psychostimulants |
sympathomimetic drugs -mimics activity of the sympathetic branch of autonomic nervous system- increased heart rate, blood pressure, sweating, blood flow decreases to internal organs but increases to large muscle groups, body temp elevated , pupls dilated |
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shared behavioral effects of psychostimulants |
elation, mood elevation, increased talking, alertness and arousal increased, insomnia, enhanced performance |
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shared psychological effects of psychostimulants |
euphoria, giddiness, self consciousness, boastfulness, anxiety, racing thoughts, enhanced cognitive performance |
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coca leaf |
-cocaine comes from the leaves of a coca bush, a shrub -the spanish introduced cocaine to europe |
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early use of cocaine |
-19th century: the process necessary to separate cocaine from the leaf was developed -major epidemic of cocaine abuse swept the world ; doctors prescribed it and it was available without prescriptions |
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cocaine and freud |
-in 1885, freud published monograph uber coca -in 1887, freud acknowledged its dangers when used to treat addiction - thought it could be used to treat anything but then figured out it was addictive |
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widespread cocaine use |
cocaine was a popular ingredient in many remedies and tonics in 1800s |
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the amphetamines |
-synthetic stimulant drugs discovered in the 1920s -became major drugs of abuse; widespread abuse in early 1960s on the west coast -amphetamines popularity waned in the 1970s and 1980s as cocaine returned to favor |
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cocaine epidemic 2 |
1980s and 1990s- cocaine became one of the most frequently abused drugs 1986: introduction of crack, an inexpensive smokeable form of cocaine today use has decreased but medical problems associated with cocaine use are still high |
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the return of meth |
1990s: methamphetamines regained popularity usage has dropped but associated health risks are still high |
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bath salts |
-synthetic cathinones became widely used stimulants in recent years, primarily marketed as plant food -two of these drugs mephedrone and MDPV were banned by the prevention of synthetic drugs act of 2012 -were used to treat narcolepsy and and asthma |
