Drugs and Behavior Study Guide Midterm I
Drugs and Behavior Study Guide Midterm I 333
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This 8 page Study Guide was uploaded by Sarah Kincaid on Friday October 14, 2016. The Study Guide belongs to 333 at 1 MDSS-SGSLM-Langley AFB Advanced Education in General Dentistry 12 Months taught by Caine in Fall 2016. Since its upload, it has received 47 views. For similar materials see Drugs and Behavior in Psychology at 1 MDSS-SGSLM-Langley AFB Advanced Education in General Dentistry 12 Months.
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Date Created: 10/14/16
Drugs and Behavior Study Guide for Exam I Basics drug – substance that you ingest that is not a food/drink; it doesn’t change your thinking/behavior but alters your physiology Pharmacist – package/dispense drug Pharmacology/Pharmacologist – study drugs in lab Behavioral/Clinical Classification – how drug alters behavior Pharmacodynamic Classification – how drug alters brain’s physiology (brain system) Chemical Classification & Name: abbreviated C; chemical functional/structural properties Trade/proprietary Name: abbreviated as T; patent holds for 17 years Generic/nonproprietary Name: abbreviated as G; after 17 years -anti – “opposite of" -ergic – increase of neurotransmitter activity in brain system Rx – prescription Tx – therapeutic effects Sx – side effects Formulation: 1. Combination of two drugs (hydrocodone = acetaminophen + codeine-like drug) 2. Combination of active ingredients and inert stuff (time-release pills) The Neuron - Golgi & Cajal coined the concept - Dendrites: receive information as neurotransmitter binds to receptors - Axons: transport materials and conduct impulse to nerve terminal - Presynaptic neuron aka nerve terminal: sends neurotransmitter - Synaptic vesicles: store neurotransmitter - Postsynaptic neuron: receives neurotransmitter signal - Reuptake channels: recycle neurotransmitter back into presynaptic cell - Neurotransmitter depletion: occurs when reuptake is blocked and cell cannot produce enough neurotransmitter to keep up with signals *Neurons are named for the primary neurotransmitter released from the nerve terminal* Resting potential is -65 mV or -70 mV. Depolarization K+ floods in making membrane potential (mV) more positive. If threshold, -55 mV, is reached, then an action potential happens as Na+ floods in until +40 mV, at which repolarization, K+ exiting, makes -90 mV, the refractory period, mV is below the resting potential. After letting in a few more + ions, the mV returns to resting potential. Drugs and Behavior Study Guide for Exam I Postsynaptic IPSPs: inhibitory postsynaptic potential (make mV more -) Potentials EPSPs: excitatory postsynaptic potential (make mV more +) GABA Most common neurotransmitter in brain; IPSPs Alcohol (bud lite) < ANXIOLYTICS (XANAX) < SEDATIVES (Ambien, “good morning”) < General Anesthetics (remain unconscious under the knife) *Better as anxiolytics than SSRIs, but also more abuse potential Glutamate 2ndmost common neurotransmitter; EPSPs o cannot be enhanced like GABA – seizures (excitotoxicity) antagonist ketamine (dissociative anesthetics): block S R o veterinary surgeries not human (eyes open, drooling) Dopamine direct agonists/dopamine precursors – PD o l. dopa, direct dopamine D2 agonist dopamine releasers/reuptake inhibitors are psychostimulants – ADHD, narcolepsy o Adderall: 1) wakefulness 2) attention to new stuff 3) reward recall o Cocaine, crystal meth, bath salts are also releasers/RIs/psychostimulants dopamine antagonists – antipsychotics (schizophrenia) brain dopamine systems in addiction theory The Triad = where cortex, midbrain, & basal ganglia meet Serotonin Impulse control (mood disorders, depression, obesity, anxiety) SSRI antidepressants (control impulse to stay in bed and suicide impulse) Part of “reticular core” Norepinephrine (synonym of noradrenaline) Fight or flight (stress) – under direct threat adrenal gland adrenaline & noradrenaline dumped into blood Attention (signal: noise) Beta-blockers singular events (e.g. anxious for presentation) NSRI antidepressants: norepinephrine Acetylcholine Memory & cognition (puzzles: where is your car?) o AChE inhibitors enzyme inhibitors, AD treatment Alzheimer’s Disease (AD) Degeneration of acetylcholine neurons First in hippocampus (GPS), then in cortex (complex thinking) Pharmacodynamic Behavioral/Clinical Examples (C, G, T) Classification Classification Opioid Rx analgesics (pain killers) hydrocodone (G) - Vicodin (T) oxycodone (G) - Percocet (T) & Oxycontin (T) hydromorphone (G) Drugs and Behavior Study Guide for Exam I oxymorphone (G) SSRI Antidepressants PROzac (T) – fluoxetine (G) Antidopaminergic Major Tranquilizers aka haloperidol (G) – Haldol (T) antipsychotics (Tx), antischizophrenics (Tx), neuroleptics (Sx) GABAergie Minor Tranquilizers 1. diazepam (G) – Valium (T) 1. anxiolytic 2. Ambien (T), Lunestra (T) 2. sedative-hypnotic Serotonergic “psychedelic” aka LSD (C) – Delsyd (T) hallucinogen Dopaminergic Stimulants aka amphetamine (G) – Adderall psychostimulants, anti- (T) attention deficit Table 1. Drug Classifications Pharmacokinetics, pK – how drug is distributed through system (onset, duration, time course); time curve Absorption – drug bloodstream stomach, intestines, BBB*, pK Distribution – drug from one part of body to another therapeutic window st Metabolism – drug broken down by enzymes 1 pass** Excretion – metabolized drug exits body local enzymes *Blood Brain Barrier (BBB) – lipophilic epithelial cells that allow molecules into brain; traps molecules that are big, strongly polar, or lipophobic st **first pass metabolism (1 pass) - through GI tract (mouth-throat-esophagus-stomach); don’t get all of drug in bloodstream bc metabolizing some in digestive system Pharmacodynamics, pD –how action mechanism, often synaptic, functions for behavioral effect; dose effect curves 1. direct agonists – exogenous neurotransmitter fits into receptor for endogenous neurotransmitter and binds (thus mimic effect) e.g. hydrocodone 2. reuptake inhibitors – binds to reuptake channel/transporter e.g. SSRI 3. releasers –dump neurotransmitter from vesicles into presynaptic membrane and out via reverse transport e.g. Adderall 4. enzyme inhibitors – prevent enzymes from breaking down errant neurotransmitter in synapse e.g. MAOI NeuSropapaicaceohgay:sms– increase endogenous neurotransmitter in synapse 6. antagonists – receptor blockers 1-5 are agonists (stimulate neurotransmitter system) Pharmacotherapeutics – Tx of drug (MED, ED ) 50 binding to receptor)nists (do not work by directly 6 is an antagonist (blocks neurotransmitter system) Toxicology – harmful/toxic drug effects (LD ,50D , 50) Threshold Dose – when only one subject has been effected by the dose (used for min dosage) ED 50 – effective dose; ½ subjects have Tx Drugs and Behavior Study Guide for Exam I MED – minimum effective dose (100%); save $, reduce potential Sx, beat current drugs TD 50toxic dose; ½ subjects have toxic effects LD – lethal dose; ½ subjects die 50 ????????50 ???????????????????? ???????????????? ???????????????????????? TI – therapeutic index; higher #s are safer TI = ????????50= margin of safety = ????ℎ???????????????????????????????????? ???????????????????????? Dose Measurements – mg (humans), mg/kg bw (rats/mice) Graphs 1-3. Dose Effect Functions (potency, effectiveness), pD ~ Potency and effect are independent of each other (potent and not effective and vice versa) ~ Vehicles (V): transport drug via IV into body for absorption (e.g. saline solution, electrolytes) Graph 4. Co-admin aka “pretreatment, pD Graph 5. Therapeutic window, pK Competitive antagonism: agonist and antagonist compete, whichever has more wins G4 Surmountable antagonism: antagonist is surmounted by higher doses of agonist Rightward shift: moves dose effect curve to the right [drug] = drug concentration G5 Repeated doses are necessary when you need pain relief for longer than the duration period Graph 6. Time curve showing the onset, duration, time course. pK >time zero (t = 0) is the time of drug admin/ingestion >onset – how long for drug to work (full relief) >duration – how long drug continues to work >half-life – time for [drug] in blood to halve (numerical value used to estimate duration) Drugs and Behavior Study Guide for Exam I parental drug admin – injection; 2 most common after oral (po); more potent than pill intravenous, iv – life/death only (going into shock, immed treatment); almost instaneous (few seconds, each heartbeat propels it); risk of sepsis (bacteria in blood, deadly) intramuscular, im – most common parental route; almost instant (few minutes) subcutaneous, sc – most common in veterinary medicine nonparental drug admin oral (po) – most common drug adminstoute; pill/liquid; safe (no infection) & effective (long duration); 1 pass (downside) inhalation – mouth bronchioles bloodstream; similar to iv if vaporizes insufflation – snorting, similar to sc and im Cocaine hydrochloride does not vaporize. Thus you can’t snort it. However, crack vaporizes. You can smoke it but not snort it. Suppositories – anal (longest duration) Eye drops – ocular canal blood vessels bloodstream Transdermal – skin patch Drug Admin Onset + Duration = Time Course Half-life iv, inhalation* 3” 15’ Fastest onset, 5’ briefest duration sc, im, 3’ 40’ Medium, 30’ insufflation medium po 15’ 2 h Slowest onset, 2.5 h longest duration Key: ‘ = minute, “ = second, h = hour *only inhalation if drug vaporizes Opioids Exogenous = from outside the body Endogenous = produced inside body Opioid system 1. Endorphin mu receptor analgesia, respiratory suppression, abuse potential 2. Enkephalin delta receptor nothing useful 3. Dynorphin kappa receptor no Tx, Salvia (hallucinogen) *Opioids work on endorphin system & mu receptor Addiction 1. Tolerance 2. Dependence 3. Withdrawal (physiological - worst symptom, treat that, Suboxone, and ppl can quit) Tolerance: rightward shift, increased ED50, decrease in potency Spontaneous withdrawal: body naturally gets rid of drug, takes time Precipitated withdrawal: inject antagonist (no more agonist), quick, withdrawal Rapid Detoxification: in humans, precipitated withdrawal + general anesthesia (GABAergic, not fentanyl bc its an opioid) Drugs and Behavior Study Guide for Exam I Withdrawal symptoms: sweating, muscle spasms, changes in body temp, vomiting, diarrhea Opioid agonists: pain relief (analgesics: pain relief w/o total loss of feeling, anesthetics: block all feeling including pain), cough suppressants, anti-diarrhoeals, addiction treatments Most common drugs prescribed: 95% hydrocodone (Vicodin) oxycodone (Oxycontin + Percocet) – 12 hr time release pill Better orally hydromorphone ~5% oxymorphone Morphine sulfate: parental injection (wars) Fentanyl: China White; analgesic during surgery & post-op; more potent than morphine (DEA disaster) loperamide (Immodium): 1 pass, lipophilic, contrasts intestines (anti-diarrhea) methadone: controversial addiction treatment; drug to “get you there,” behavioral/clinical therapy helps with addiction itself; less potent than fentanyl more potent than heroin Opioid antagonists: rescue from overdose (respiratory depression); fertility enhancers (stimulates pituitary glands), rapid detox, prevent abuse (Suboxone) naloxone (Narcan, also in Suboxone): inject for OD naltrexone (Vivitrol): pill Partial agonists: potency does not matter due to limited maximum effect; reduces withdrawal, respiratory depression, abuse potential, high; still can become dependent Suboxone: naloxone (antagonist, 1 pass unless crushed) + buprenorphine (partial agonist, to brain); targets withdrawal; limited effect, pD & time, pK fentanyl > buprenorphine > morphine (in potency) heroin > morphine (in potency, bc heroin crosses BBB better than morphine) fentanyl = morphine = hydrocodone (in effectiveness) Side effects: respiratory depression, nausea, sedation, constipation, abuse liability Most important: respiratory depression 2nd most important: addiction (doesn’t kill you directly, its RD) Most deterrent: nausea, sedation Alternative meds: NSAIDs, aspirin, acetaminophen, ibuprofen, Tylenol, Advil Parkinson’s Disease Major symptom: akinesia, difficulty in initiation of and movement Note: no seizures in PD! Other symptoms: resting tremors, poor posture, rigidity Most common med: Sinemet (l. dopa, precursor, + carbidopa, enzyme inhibitor) - L. dopa converted by AAD to dopamine, but carbidopa prevents l. dopa from converting before the BBB (dopamine is metabolized quickly) - L. dopa can cross BBB while carbidopa and dopamine cannot Major Tx: voluntary movement Major Sx: involuntary movement Drugs and Behavior Study Guide for Exam I Disorder of: basal ganglia nd 2 most common med: direct dopamine D2 agonist Tolerance: Tx (decreased potency, rightward shift, higher ED50) Sensitization: Sx (increased potency, leftward shift, lower ED50) Therapeutic window: collapses and Sx occur before Tx If you could put dopamine directly into brain, where would you put it? - Dorsal striatum In PD, the SN dorsal striatum pathway (voluntary movement) degenerates. PD symptoms do not develop until there is only 20% of striatum dopamine left (80% gone). Where are the nuclei of dopamine neurons? - SN (in midbrain) Where are the dopamine in dopamine neurons? - dorsal striatum (in forebrain) The VTA ventral striatum pathway is the one upon which Adderall acts. meperidine (Demerol): opioid analgesic Hollywood stars abused in 1980s MPPP: analog of Demerol; mu opioid agonist, like Vicodin, with a heroin high MPTP: toxic by-product when MPPP synthesis is messed up; induced PD MPP+: MPTP is converted into MPP+ by MAO; MPP+ destroyed SN MAO: converts MPTP to dorsal striatum destroying MPP+ MAOI: prevents MAO from converting MPTP MPP+ Idiopathic PD: 99.9% cases (something environmental, pesticides/herbicides/manganese, etc + old age); environmental factors interact with genes (which increase/decrease risk) Drugs and Behavior Study Guide for Exam I Two highly at risk populations - Agricultural (1/6 chance vs 1/40 over lifetime) - Chemists synthesizing pyridines (14x more likely) Encephalitis caused PD - 0.01% cases - Infected brain regions: dorsal striatum & SN Familial/Genetic PD - 2 cases, very rare - Parkin gene (and possibly lark2) 1/40 chance to get PD in life There is currently nothing we can do to prevent PD.
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