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161 Cards in this Set
- Front
- Back
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Name 3 legal and 3 medically controlled drugs whose consuption can lead to dependance: |
Nicotine, Alcohol and caffeine Barbiturates, opiates and amphetamines |
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What is dependence? |
The craving or need to take the drug which is experienced during drug absitence. |
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What widely abused drugs don't give rise to dependence? |
Cannabinoids, phenycyclidine (angel dust) Lysergic acid diethylamide (LSD) and mescaline
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What adaptive changes occur in the brain from dependence producing drugs = psychoactive drug? |
Prolonged exposure results in adaptive neural mechanisms to overcome the prolonged stimulation or inhibition produced by the drug- generally counteracting the effects of the drugs themselves such that the presence of the drug and the adaptive changes are necessary for normal function of systems affected. |
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What is drug withdrawal? |
The cessation of administration of the drug to the point at which the plasma and brain levels are neglible. |
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What are the 2 types of drug dependence? |
1. Psychological 2. Physical |
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Decribe psychological dependence: |
Long lasting, craving/compulsion type of dependence produced by cocaine, amphetamine and caffeine. |
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What are the 4 components of the limbic system: |
The amygdala, the nucleus accumbens, the striatum and cingulate gyrus. |
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What are 4 withdrawal symptoms: |
Mood changes Anxiety Agitation Feeling unable to cope |
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What type of dependence plays the most important role in maintaing drug taking behaviour? |
Psychological as it is the most distressing. |
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Describe the characteristics of physical dependence: |
It is a clear cut syndrome of physical symptoms of illness, only seen with some drugs of dependence relatively short lived, duration of 2 weeks. |
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What drugs give a physical depedence syndrome? |
Opiates: diarrhoea, nausea, abdo cramps, sweating, hypertension, convulsions
Barbiturates: epileptic fits, sweating, tremors, delirium tremens (delirium), anxiety
Benzodiazapeines: convulsions, panic attacks, anxiety
Alcohol: convulsions, sweating tremors, delirium tremens. |
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What are the most important reasons for maintainging drug seeking behaviour: |
Satisfying cravings Avoiding withdrawal effects |
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What is tolerance? |
The phenomen by which the effect of the drug diminishes with repeated and excessive usage.
Some types of toelrance can be overcome by taking larger and larger doses of the drug. |
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What are the 2 main types of tolerance? |
1. Acute 2. Chronic - a: cellular tolerance, b. pharmacokinetic tolerance |
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Name 3 drugs that develop tolerance but not dependence? |
LSD Anticholinesterases Glyceryl trinitrate |
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What is acute tolerance/tachpylaxis? |
Short lasting toelrance, occurs when a receptor becomes desensitised by the first dose.
Occurs with nicotine in tobacco. Causes a depolarising block on nicotinic recepors at which it acts. Over the smoking day the nicotine induced increase in HR diminishes. (so HR increase becomes progressively less with each cigarette smoked throughout the day. HR response recovers after overnight abstinence. |
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What does tachyphlaxis or desensitisation cause? |
Acute tolerance |
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Chronic tolerance: what is another name for cellular tolerance? |
Pharmacodynamic tolerance |
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Chronic tolerance: what is another name for pharmacokinetic tolerance? |
Metabolic tolerance |
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What is the major contributor of drug tolerance? |
Cellular tolerance |
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What happens in cellular tolerance? |
Neuroadaptive changes occur mainly in the brain and these produce a diminshed response to the drugs. |
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When does cellular tolerance occur? |
Following chronic expousre to almost all drugs of dependence and can be measured as reduced response for a given dose giving submaximal effect. |
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What happens to the dose response curve following chronic drug exposure? |
It shifts to the right. |
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What is pharamcokinetic tolerance? |
Where a drug is metabolised faster due to an induction of liver enzymes responsible for its degradation - resutls in a diminished response per dose of drug - can be overcome by taking larger and larger doses. |
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What enzyme is reposnbile for pharamkokineitc tolerane in barbiturates? |
Induction of the ctytochrome ezyme P450 in the liver- faster metabolism occurs. |
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What would be seen on a plasma conc vs time graph showing normal vs. pharmakokinetic tolerance? |
Reduced area under graph- at each time the plasma drug conc is lower compared to normal. |
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What is the result of reduced drug response by liver enzyme induction? |
Reduced bioavailability. |
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What are the main drugs that are abused by western societies that cause dependence? |
Psychomotor stimulants: drugs that cause excitation and stimulation of brain activity plus increased locomotion. CNS depressants: sedative, depress brain activity. |
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Name 3 psychostimulants: |
Nicotine (weakest) Amphetamine Cocaine |
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Name 3 effects of nicotine and tobacco smoke: |
1. Increase alterness 2. Improve psychomotor performance esp. under conditions of boredom or fatigue 3. Reduce the disruption in performance caused by stress |
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What type of chronic dependence is caused by nicotine? |
Psychological. |
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Compare the tobacco in pipes and cigars to cigarette tobacco |
Greater proportion of the nictone is unionised and undergoes greater buccal absorption which is considerably slower at gaining access to the brain than by inhalation across the lungs. |
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What are the symptoms of acute tolerance to nicotine? |
Increase in HR and locomotor stimulation, acute to short lasting tolerace to drug due to desensitisation of the nicotinic receptors. |
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What are the symptoms of cellular tolerance to nicotine? |
Develop nausea, dizziness, sweating, |
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How much does pharmakokinetic tolerance contribute to nicotine tolerance? |
Only to a small degree. |
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Can acute tolerance be overcome by incresing the dose in the case of nicotine addiction? |
No, tolerance in this case is due to desensitisation of the receptors and increasing the dose deepens the receptor block - the greater the dose the longer the tolerance. |
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How does nicotine produce a rewarding effect? |
By stimulating nicotinic acetlycholine receptors in the brain. |
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What is the effect of mecamylamine? |
It is a nicotoin reeptor antagonist and can enter the brain, blocking the psychomoto stimualtn and pleasurable aspect of smoking. |
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What 4 areas of the brain does nicotine act on? |
1. Nucleus accumbens dopamine secretion here mediates dependence. 2. Hipocampus stimulating nicotonic receptors here increased attention and may be responsible for improved performance 3. Ventral tegmental area stimulates the nicotonic receptors on dopaminergic neurones this triggers the release of dopamine in the nucleus accumbens. Underlies dependence 4. Reticular formation nicotine induced sitmulation increased alterness (lesser extent than cocaine and amphetamine) |
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What are benzodiazepines useful for? |
Powerful anxiolytics- reduces anxiety, taming animals. Sedative effect Hypnotic effect- induces sleep quickly and increased duration of sleep Anticonvulsants- diazepam given IV is one of the main treamtnes of status epilepticus (repetivie seizures) |
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What 2 reaons make benzodiazepines useful in treating status epilepticus? |
They don't cause respiratory depression They dont cause dependence. |
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What is the half life of Diazepm? |
Long acting- 32 hr half life.
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What are the key metabolites of diazepam? |
N-desmethyldiazepam = half life of 60 hrs Oxazepam = half life of 8 hrs. |
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What is the main use of nitrazepam? |
Hynotic, half life of 28 hrs results in hangover sedative effects the following day |
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What is the main action of temazepam? |
Sedative prior to a minor operation due to its short half life of 8 hrs.
(can be abused and used to give a 'high) |
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What is Oxazepam? |
It is a metabolite of diazepamn, given alone as a short-acting and milder benzodiazepine treatment. |
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What is midazolam? |
It is the first water soluble benzodiazepine - IV introduction and sedative for minor operative procedures.
Rapid onset and short duration of action - and not being lipid soluble it avoids the problems of accumulation which can occur with otehr benzodiazepines. |
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Do benzodiazepines produce dependence? |
Yes, esp on thse who have been taking the drugs for a number of years. |
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What is the main origin of dependence on benzodiazepines? |
Iatrogenic: imposed by clinical prescription rather than willfull or self-imposed.
Abuse of temazepam by injecting IV drug rfom aspiriating the liqued contents of the prescription capsules into syringes and injecting them - gets rapidly to the brain and produces a high. |
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What are key symptoms of dependence? |
Anxiety, agiation, convulsions, panic attacks and epileptic fits (rarely) |
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What part of the benzodiazepine action induces tolerance the most? |
The anticonvulsant actions. |
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How do Benzodiazepines act? |
Bind to the GABA receptor- causing an allosteric change/modification of the receptor than results in an increase in GABA A receptor activity.
BZDs do not substitue as an agonist for GABA but increase the frequency on channel opening events in the presence of GABA leading to increased cholride ion conductance and inhibiton of the action potential. |
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Where do Benzodiazepines act? |
They act on: 1. Raphe nuclei stimulating dorsal raphe nuclei increases serotonin activity producing anxiolytic effect. 2. Reticular formation inhibit neurones in the reticular formaiton to produce sedation |
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What was the first clincally useful barbiturate? |
Phenobarbitone |
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Why have barbiturates become less used? |
Previously usef majorly as sedatives, anxiolytics and anticonvulsants- hower the benzodizepine group has proved to have the same therapeutic benefits without the CVS and resp effects so their use has been phased ot. |
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What is the main action of phenobarbitone? |
Anticonvulsant at very low doses. |
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What is the main action of thiopentane? |
Induces general anaesthesia |
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What is onset and duration of action of phenobarbitone? |
Slow onset and long duration of action = so was used as a sedative.
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What is the onset and duration of action of pentobarbitone hexobarbitone and amylobarbitone? |
Medium rate of onset- duration of activity is 6hrs and so useful as sedative |
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What are the effects of barbiturates at high dosage? |
They depress the activity of all cells at high doses- depressing the CVS and resp system - cause death. |
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Where are barbiturates most selective for? |
Cells in the CNS |
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What is the range of effects that they produce? |
From anxiolytic to general anesthesia with increasing doses. |
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What are the main effect of barbiturates? |
1. Euophoria - feeling of well-being before sedation (taken orally) 2. Anxiolytics - sedated state, patient awake but less anxious 3. Sedation - all clinically effective doses cause sedation 4. Hynotic effects - at slightly higher doses, especially with the drugs that have a medium duration of action e.g. pentobarbitone, hexobarbitone - sleep and hynposis is induced. 5. Anticonvulsants - only some e.g. phenobarbitone- occurs at doses which cause minimal sedation. 6. General anaesthesia - all cause this, long and medium acting ones also cause resp depression. Only the highly lipid soluble, highly protein bound and therefore v. quick onset and short acting barbiturates e.g. thiopentone are used clinically as inducing agents |
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Why is thipentone not abused? |
it is highly lipid souble and highly protein bound- therefore very quick onset and short acting.
The onset of anaesthesia preceeed finishing the injection therefore no euphoria before sleeping. |
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Decribe the dependence to barbiturates: |
High dependence liability Physical and psychological dependence. |
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What is the result of abrupt cessation of treatment? |
Clear cut withdrawal symptoms: anxiety - 1st symptom, insomnia, sweating, delirium tremens - major withdrawl reaction very characterisitic of sedative hypnotic dependence (also in alcohol) confusion, epileptic fits (grand mal seizures or status epilepticus)
MANIFEST AS: tremors, delusions, agitation, disorientation, vivid auditory and visual hallucinations. |
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How quickly to the withdrawal symptoms develop and how long do they last? |
Within a few days and last 2 weeks. |
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What are the 2 types of tolerance? |
Cellular tolerance Pharmacokinetic tolerance = by inducing the liver enzyme P450 enxymes and causes a faster rate of metabolism. |
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For which effects does toelrance develop more readily? |
for euphoria and sleep inducing effects tolerance develops more readily than for the respiratroy depressant effect.
(so increasing dose to obtain euphoria in addicts runs the serious risk of respiratory depression) |
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P450 enzyme also acts on warfarin, digoxin, oral contraceptive and tricyclic antidepressants - so what effect on clinical efficacy would result from dependence to barbiturates? |
Decreased clinical efficacy |
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How do Barbiturates act? |
Potentiate the effects of GABA at GABA A receptors in the brain. So mediates CNS depressant effects
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What does GABA stand for and where does it act? |
It is the major inhibitory transmitter in the brain. Gamma amino bytyric acid. Acts on: GABA A: postsynaptic, ligand-gates ion channel. GABA B: presynaptic G protein coupled, liked to secondary messenger systems. |
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What produces insomnia on withdrawal? |
Occurs as a reboudn to the sedation produced by the drugs on GABA A receptors. |
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Where do barbiturates act? |
Dorsal raphe nuclei- produce anxiolytic effect via serotonin neurones
Reticular formation - inhibit neuornes to produce sedation. |
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What effect does alcohol have on the CNS? |
Depressant |
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What are the key signs of intoxication? |
1. Slurred speech 2. Staggering gait 3. Intellectual and motor impairement (+judgement) exception only in very anxious whose lack of confidence is improved- narrow therapeutic window for this 4. Sedation: as intoxication progressed beyond the point of euphoria. (when alcohol level reaches 400mg/100ml) 5. Euphoria- feeling of well-being. |
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What does the effect alcohol has on mood and behaviour depend on? |
Dose Rate of rise in blood ethanol concentration Personality |
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What is the commenest cause of alcohol-induced death? |
Inhalation of vomit. |
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What proportion of the population that drink in large quantities develop true alcohol dependence? |
10% |
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What is the dependence liability and how does this compare to the withdrawal syndrome? |
Low dependence liability but severity of withdrawal symptoms is high. |
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How severe is alcohol withdrawal syndrome? |
Extreme- can be life threatening. |
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What are the 3 phases of abstinece syndrome? |
Phase 1 (8-24 hrs after last drink) nervousness, anxiety, tremor, nausea, butterflies in stomach, apprehension.
Phase 2 (>24hrs after last drink) agitation, muscle cramps, nausea/vomiting/hypertension
Phase 3: Occurs 2-4 days after last drink: manifests as: confusion, disorientation, delirium tremens, epileptic fits. |
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What is the association between alcohol intoxicationa dn violent offenders? |
High incidence of crimes against people - rape/assault and murder after from violent offenders who are at the time intoxicated |
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What is acute alcohol tolerance? |
Seen after one drink, where the effects wear off when the blood alcohol level is maintained.
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What is cellular alcohol tolerance? |
Cellular tolerance- occurs with regular drinking- even moderate drinkers will find that they required 2-3 times the amount of alcohol it initally took them to become intoxicated - mechanisms involve at least partly changes in the lipid membrane- making them less susceptible to alcohol. |
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What effect does alcohol have of membranes? |
Increases membrane lipid fluidity. Effect is reduced following repeated exposure. Cross tolerance with anaestethic drugs - so alcoholics need larger anaestehtic doses. |
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What is the effect on anaesthetic dose that alcoholics need? |
Increased dose needed due to increased membrane lipid fluidity. |
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In whom does pharmacokinetic tolerance occur? |
Severe alcoholics only. With high levels of chronic exposure to alcohol. P450 enzymes are induced. May account for the cross tolerance to barbiturates that is seen in alcohols. |
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How does alcohol have its effect? |
Mechanism of action not fully understood - selectively reduces the activity of activated calcium channels, which reduces the transmitter release. (depressor) |
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Where does alcohol act? |
j |
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What is the active ingredient of cannabis? |
Delta-9-tetrahydrocannabinol (9-THC) it exerts its action by binding to cannabinoid CB1 receptors in the brain. |
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What is the effect of 9-THC binding to CB1 receptors? |
Activation of G-proteins - this ultimately changes signal transduction pathways. G protein directly inhibits N and P/Q type voltage ca2+ channels and Na+ channels. (plus indirectly on other calcium channels by inhibiting adenylate cyclase) 9-THC binding and G protein activation also can ultimately activate inwardly rectifying potassium channels and the MAP kinase signalling pathway. |
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What is the cumulative complex effect of these pathways? |
Euphoria feeling. |
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Name 5 key opiates: |
1. Morphine - extracted from the poppy. 2. Heroin - made synthetically from morphine by synthetic acetylation of diamorphine. More potent that morphine. 3. Codeine - the 2nd most active alkaloid extracted from opium. Less potent than morphine. 10% of codeine is metabolised to morphine. 4. Pethidine - no structual similarity to morphine but similar analgesia effect. 5. Methadone- more active orally and longer lasting than morphine, otherwise similar.
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What is the action of opaites on the CNS? |
They cause CNS depression |
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What are their key pharmacological actions? |
1. Analgesia 2. Cough suppression codeine is more potent than morphine at inhibiting cough at doses that are sub-analgesic. codeine commonly used in cough medications. 3. Respiratory depression this is the main cause of opiate-induced death. 4. Sedation 5. Constipation by increasing tone and decreasing motility of the gut and by depressing CNS. 6. Pupillary constriction important diagnostic marker = 'pin point' pupil. 7. Nausea and vomiting emetic effect of opiates is due to action on the CNS. 8. Euphoria |
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How frequently does opiate dependence develop? |
Develops very readily. |
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What are the key characteristics of withdrawal syndrome? |
Diarrhoea, nausea and vomiting, abdo cramps, sweating, hypertension, convulsions, anxiety, goosebumps. |
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What are dilated pupils associated with (in opiate taking)? |
Respiratory depression and coma. |
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Rank these opiates in terms of potency: codeine, heroin and morphine: |
1. Heroin MOST POTENT 2. Morphine 3. Codeine. LEAST POTENT |
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What is the typical onset and duration of psycholigcal vs physical withdrawal symptoms? |
Physical- within 2 days and last for up to14 days. Psychological = several months to years after giving up drug. |
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How quickly does cellular tolerance develop? |
Within 24hrs of morphine treatment. |
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What symptoms show tolerance? |
Vomitting and Nasuea PLUS the euphoirc, analgesic and respiratory depression effect
RESP DEP- addict could take 50 times normal dose and show little resp depression whilst this dose would kill normal individual. |
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What effects of morphine show less tolerance? |
Pupillary constriction and constipation. |
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What are the 3 main types of opiate receptors? |
Mu Kappa Delta |
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What are the endogenerous ligands for these receptors? |
1. Beta-endorphin = 31 aa peptide, equal activity on 3 receptors. 2. Leucine-enkephalin or leu-enkephalin = pentapeptide (Try-Gly_Gly-Phe-Leu) active on delta type receptors. 3. Methionine-enkepalin or met-enkephalin = pentapetide (Try-Gly-Gly-Phe-Met) most active on mu and delta receptors. 4. Dynoprin = 17 aa peptide, most active on kappa receptors. |
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Which receptor binding mediates the dependence producing properties of opiates? |
The binding to mu receptors. They cause hyperpolarisation of these receptors by increasing K+ conductance. |
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What is the MOA of opiates? |
Act on MU receptors => cause hyperpolarisation of the receptors by increasing K+ conductance and inhibit nerve cell firing plus inhibits NT release. |
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Where do Opiates act? |
d |
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What are the key consequences of taking cocaine? |
Causes euphoria, increases energy levels, enhanced physical performance, suppression of appetite, local anaesthetic. |
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How strong a local anaesthetic is cocaine? |
It is a relatively potent local anaesthetic. Used as an opthalmic anaestetic. Apply locally to the cornea rendering it insensible. Causes dilatation of the pupils, mydriasis and reduces intra-ocular pressure due to its catecholamine activity. |
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What is thedepeendnce liability of cocaine? |
Great dependence liability.
Smoked or IV- reaches the brain within seconds to produce a 'high' or 'hit'.
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What are the main symptoms of withdrawal from cocaine? |
Craving for the drug, acute depression, anxiety and agitation, intense fatigue. |
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How are amphetamine and cocaine withdrawal syndromes similar? |
They both lead to psychological but not physical withdrawal effects. |
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What is dependence liability? |
The potnetial of the drug to induce dependence in those that self-administer the drugs chronically.
Great dependence liabilty is seen in drugs that induce dependence in the majority of uses after relatively short periods of chronic treatment. |
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What is the dependence liability of cocaine? |
It has a great dependence liability since virtually all partient who experiment with cocaine daily for a few weeks will become dependent. |
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Graphs |
j |
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Graphs |
d |
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Graphs |
d |
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What causes cocaine induced psychosis? |
Binging on cocaine in those that have developed toerlance in attempt to receive a high. |
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What types of behaviours are exhibited by those who have cocaine-induved psychosis? |
They act violently as if threatened or being persecuted by innocent bystanders. |
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What 2 CVS risk are cocaine users suseptible to suffering? |
Stroke and heart attacks. |
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What are the symptoms of cocaine induced psychosis? |
Paranoid delusions Auditory and visual hallucinations Tactile hallucinations (believe that they have insects crawling underneath their skin) |
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What is the key effect of cocaine on the brain? |
It stimulates catecholamine effect by inhibiting the dopamine uptake transporter. inhibits the uptake of DA, but unlike amphetamine is not a substrate of the DA uptake transporter. |
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Where does cocaine act? |
s |
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What is the most widely self-administered psycho-active drug in the world? |
Caffeine. |
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What are some of the psychostimulant effects of caffeine? |
Restlessness, anxiety, cardiovascular stimulant, insomnia.
However at the normal doses- like those consumed in coffee and tea the effects are: reduced fatigue, increased arousal. |
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How common are withdrawal symptoms? |
Only seen in a small proportion of heavy consumers.
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What are typical withdrawal symptoms? |
Craving, fatigue, irritability and headaches. |
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Do the psychomstimulant effects of caffeine show tolerance? |
Little tolerance is shown and therefore people do not tend to binge of caffeine as they might with cocaine or amphetamines. |
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What class of compounds is caffeine a member of? |
Methylxanthines |
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What are the actions of methylaxnthines? |
1. They inhibit phosphodiesterase (the enzyme that hydrolyses cAMP to inactive 5' AMP
2. They inhibit adenosine type receptors A1 (stimulation of these would inhibit cAMP production)
= NET ACTION = increase in cAMP. |
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Why does increasing cAMP have a psychostimulant effect? |
It is a second messenger for G protein coupled receptors including catecholamine receptors e.g beta-adrenergic receptors and Dopamine D1-type receptors.
This potentiates the psychostimulant effects by potentiating catecholamines in the brain to act on their receptors. |
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Where does caffeine act? |
s |
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Name 3 amphetamine-like drugs: |
Amphetamine Dexamphetamine Methylamphetamine |
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What is the psychostimulant effect of amphetamines? |
Powerful psychostimulants:
They causes: euphoria, increase energy levels enhance physical performance appetite suppressants. |
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Compare amphetamine to dextamphetamine and methylampehetamine: |
Methlamphetamine = methyl group replaces one of the hydrogens on the terminal amine group. similar potency to amphetamine.
Dexamphetamine= is a more active isomer than amphetamine. |
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What is the dependence liabilty of amphetamines? |
They have powerful dependence liability- such that chronic exposure very rapidly produces dependence.
Occurs when drug is administered IV or orally. |
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What type of dependence does amphetamine produce? |
It produces a psychological not a pysiological dependence. |
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What are tsome of the withdrawal symptoms seen in amphetamine addicts? |
Craving for the drug Anxiety/aggitation Sleep disturbances Acute depression. |
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How quickly does cellular tolerance develop to amphetamine? |
It develops very rapidly - e.g. the hydpertension from hyper-stimulation of the CVS is subject to toerance - the severe hypertension that would be seen in a non-addict would have little effect on the CVS of an addict. |
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How and why is amphetamine injected? |
Injected intravenously (amphetamine commonly known as speed) in order to induce a rapid high.
Tolerance can develop to the euphoric effects. |
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What is amphetamine-induces psychosis? |
Symptoms similar to Schizophrenia - paranoid delusions, auditory hallucinations, compulsive and repetitive behaviour e.g. hand washing and jaw grinding.
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How long can an addict maintain the escalating tpye of administration? |
For days - at most a couple of weeks before crashing into a deep sleep and exhaustion/depression. Probably exhaustion is the result of the exhaustion of the stores of NTs. |
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What is the structure of amphetamine similar to? |
It is similar to the structure of catecholamines such as dopamine, NA and adrenaline.
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How doe amphetamines act, what can they be described as? |
They are indirectly acting sympathomimetics. They potnetiate the effects of catecholamine in 3 ways:
1. Stimulate catecholamine release 2. Inhibit the recapture of catecholamines by the uptake system. 3. Inhibit monoamine oxidase activity (MAO) |
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How does amphetamine affect uptake? |
It competes with dopamine for the DA uptake transporter and so the uptake of dopamine is competively inhibited. |
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How does amphetamine effect release of catecholamines? |
Increases the release of catecholamines by being taken up into the DA transporter system and thus displacing catecholamines into the synaptic clef. |
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How does amphetamine affect MAO? |
It blocks the enzyme at high doses.
MAO usually metabolises MAO to DOPAC. (dihydrophenylacetic acid) |
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Where does amphetamine act? |
s |
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Generally what is the major contributor to overall tolerance? |
Cellular tolerance. |
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What 5 drugs produce physical dependence signs? |
Alcohol Benzodiazepines Opiates Barbiturates Caffeine
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Classify barbiturates according to their CNS effect |
CNS depressant. |
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Classify benzodiazepines according to their general effects: |
CNS depressants |
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Classifiy opiates according to their general effects? |
CNS depressants |
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What are the general effects of Amphetamines? |
Psychomotor stimulant |
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What effect does Nictoine have on the CNS? |
Psychomotor stimulant. |
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Classify barbiturates according to general CNS effect? |
CNS depressants |
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Classifty cocaine according to its general effects: |
Psychomotor stimulant. |
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Do psychomotor stimulant drugs tend to produce physical as well as psychological dependence? |
Yes |
