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55 Cards in this Set
- Front
- Back
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primary active ingredient of compounds produced by hemp plant (cannabis sativa) -found in resinous material coating immature flowering tops and in leaves |
1-triangle9-tetrahydrocannabinol (THC) |
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resinous material of cannabis |
hashish -5-10 times more THC than marijuana |
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-how is THC absorbed and eliminated? |
-lipophillic absorbed rapidly through alveolar membranes and has a half life of two days |
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pharmacological effects of cannabis |
-increase in heart rate -sharpened sensory acuity, more alpha in EEG -impaired thinking and short term memory -relaxation -impairs motor performance, additive with alcohol -distortions in perception, hallucinations, acute psychotic episodes |
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receptors of THC that are found in high density in many brain areas -receptors found in periphery |
CB1 CB2 |
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how do cannabinoid receptors work? |
-G protein coupled receptors that decrease adenylyl cyclase activity, inhibiting N-type calcium channels and disinhibit potassium A channels |
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ligand for CB receptors that is endogenous |
anandamide |
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reinforcing effects of THC? |
CB1 receptor activation increases dopamine release in the nucleus accumbens |
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3 toxic effect of cannabis |
1. bronchitis and increased bronchopulmonary cancer rates in heavy smokers 2. amotivational syndrome 3. chromosomal damage, impaired immune response |
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therapeutic uses for cannabis |
1. nausea after chemo 2. glaucoma |
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strong CNS stimulants structurally related to NE |
amphetamines (only d form active centrally) |
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How do amphetamines work? -what is their effect? |
Act to release dopamine and NE from nerve terminals and also inhibit DA/NE transporters -increased alertness, speed of responses, reflexia |
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amphetamine OD effects? |
subject is flooded with thoughts, attention bounces around -sterotypy, paranoia, hallucinations (para schizo symptoms) |
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6 medical sues of amphetamines |
1. enhance performance 2. narcolepsy 3. parkinsons (dopamine releasing) 4. methylphenidate and adderall treat ADHD 5. raise mood 6. weight loss |
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toxic effects of amphetamines |
hypertension, severe tachycardia, convulsions, delerium, hyperpyrexia |
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nonlethal risks of amphetamines |
dependence and tolerance psychotic episodes |
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what is amphetamine syndrome? |
High doses lead to anxiety, hyperactivity, delusions, hallucinations, but no disorientation of loss of consciousness. -hallucinations due to misinterpretations rather than distorted percepton -reversible - could lead to schizo state in susceptible person
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isolated from cocoa leaves and has anesthetic and central stimulant properties |
cocaine |
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how does cocaine work? |
inhibitor of DA and NE reuptake from the synapse by presynaptic neuron very similar to amphetamine except amphets leave metallic taste in mouth |
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how is cocaine normally administered |
snorted or smoked, lead to rhinitis and a perforated nasal septum |
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low purity form of free base cocaine that volatiles when heated |
crack |
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-an extremely potent hallucinogen with only the d isomer showing activity |
lysergic acid diethyl amide (LSD) |
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symptoms of LSD in humans |
fluctuations in brightness, shape distortion, halos around objects, confused perception of distance and time, -synesthesia -mescaline - geometric shapes with eyes closed |
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psychic symptoms of LSD |
dreamlike feeling, difficulty expressing thoughts, fixation on specific stimuli, depersonalization |
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LSD mechanism |
binds to NE, DA and serotonin receptors |
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how does tolerance to LSD develop? |
rapidly due to down regulation of serotonin receptors -cross tolerance to mescaline only no withdrawal |
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hallucinogen persisting perception disorder |
seen in a minority of hallucinogen users, persistent visual disturbances that were also seen when drug was taken |
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common side effect of LSD |
bad trips that can trigger psychotic breakdowns in individuals with chronic emotional problems |
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mechanism of MDMA (ecstasy) how does it metabolize? |
promotes release and inhibits re-uptake of dopamine, norepinephrine and serotonin -inhibits its own metabolism via cyt P450 system - potential toxicity with repeated dosing |
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when taken, users feel openness, well being, self-awareness, empathy |
MDMA |
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How much alcohol is there in a standard drink? |
13.6 g 1 beer (4-5%) = 5 oz wine = 1.5 oz 40% alcohol |
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how is ethanol absorbed? |
through mucosal surfaces by diffusion, occurs most rapidly in small intestine, so delays in gastric emptying slows alcohol absorption -20-30% absorbed most quickly |
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What happens to ethanol after absorption? |
Quickly partitions into total body water, and its Vd can be used to estimate total body water |
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partition coefficient of alcohol between blood and air is ? |
2200:1 |
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how is ethanol metabolized? What is the rate-limiting step? |
ethanol metabolized to acetaldehyde by alcohol dehydrogenase. Acetaldehyde dehydrogenase then metabolizes into acetate. -step 1 with alcohol dehydrogenase in liver |
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why do alcoholics metabolize some other drugs more quickly? how much alcohol can be metabolized by a 70 kg person per hour? |
substantial amounts of alcohol can induce cyt. P450 enzymes (esp CYP2E1) -10 g |
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How can the rate of alcohol metabolism be increased? |
-reoxidation of NADH to NAD, which is used to oxidize ethanol to acetaldehyde. -sources of pyruvate such as glucose and fructose do this via Krebs Cycle |
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sinusoid |
-Hypoxia in the venous end can be produced by chronic heavy ingestion of alcohol which increases the rate of alcohol oxidation in the liver -why necrosis occurs in this part of the liver in heavy drinkers |
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4 mechanisms of ethanol actions |
1. inhibition of glutamate receptors 2. enhancement of GABA and glycine receptor function 3. inhibition of calcium channels 4. enhancement of adenylyl cyclase activity |
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6 effects of ethanol on nervous system |
1. skin vasodilation 2. effects on hypothalamus lead to increased HCl secretion in stomach and increased gastrointestinal motility 3. inhibit ADHormone secretion by pituitary 4. low doses = relaxation 5. higher doses =slow mental processes, slur speech, impair judgment 6. very high levels = anesthesia or possibly death by respiratory failure. |
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BAC at 0.05% |
mild signs of intoxication |
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BAC at 0.1% |
significant intoxication in most people
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BAC at 0.15% |
significant intoxication in almost everyone |
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BAC at 0.25% |
anesthesia or coma |
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BAC at 0.5% |
death |
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treatment of acute ethanol intoxication? |
1. supportive therapy - iv, artificial respiratory 2. haemodialysis |
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3 problems due to vitamin b1 deficiencies that occur in alcoholics |
peripheral neuropathy, wernicke's disease, korsakoff's psychosis |
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organ damage seen in alcholics |
alcoholic hepatitis, cirrhosis, cerebral cortical atrophy |
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what is fetal alcohol syndrome? |
irreversible damage characterized by small head, widely separated eyes, smooth philtrum, mental and physical retardation |
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what are contributors to the high rate of mortality in alcoholics? |
1. hypertensive heart disease 2. stoke 3. pharyngeal cancer 4. accidents |
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alcohol withdrawal syndrome after several days of drinking |
marked hyperirritability, exaggerated reflexes, tremor, sleeplessness, nausea |
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alcohol withdrawal syndrome after drinking for a week to months |
-two stage withdrawal reaction -symptoms as seen in short term withdrawal first, followed by severe hyperactivity, delirium, hallucinations, tachycardia -called delirium tremens, can be fatal |
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treatment of alcohol withdrawal? |
fluids, rest, benzodiazepines (severe cases), tapering doses of ethanol (severe) |
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metabolism of methanol why toxic? |
produces formaldehyde and formic acid, which are highly toxic to optic nerve and retina and may produce partial or complete permanent blindness formic acid can also produce acidosis |
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treatment for methanol intoxication |
1. iv of sodium bicarbonate 2. hemodialysis to remove methanol 3. repeated dosing of ethanol which competes with methanol for metabolism by alcohol dehydrogenase |
