402 Viva
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57 questions
| 🇬🇧 | 🇬🇧 |
| What is an agonist | A drug which binds to a receptor producing a physiological response within the cell. It has affinity and efficacy |
| What is an antagonist | A drug which binds to a receptor but does not produce a response. It blocks the receptors ability to be activated by an agonist. Competitive and non-competitive. |
| Competitive antagonist dose response curve | Parallel shift to the right, reaches max response |
| Non competitive agonist dose response curve | Downward non parallel shift |
| Name the 2 branches of the Autonomic Nervous System | Sympathetic and parasympathetic |
| Branch of ANS associated with rest and digest? | Parasympathetic |
| Neurotransmitter released by sympathetic NS? | Norepinephrine |
| Neurotransmitter released by parasympathetic NS? | Acetylcholine |
| Sympathetic NS effects | Increased HR, constricted blood vessels, dilated bronchioles, decreased digestion - FIGHT OR FLIGHT |
| Parasympathetic NS effects | Decreased HR, dilated blood vessels, constricted bronchioles, increased digestion - REST AND DIGEST |
| After sympathetic response, how is norepinephrine removed from synaptic cleft? | Reuptake into the presynaptic terminal via Norepinephrine transporter (NET) |
| After parasympathetic response how is acetylcholine removed? | Acetylcholine degraded by acetylcholinesterase into choline and acetic acid - choline transported back into presynaptic terminal and used in synthesis of new acetylcholine - acetic acid diffused into tissue |
| Types of acetylcholine receptors | Nicotinic and muscarinic |
| Types of noradrenaline receptors | Alpha adrenergic receptors (blood vessels), beta adrenergic receptors (heart) |
| Beta adrenergic agonist and antagonist | Agonist = salbutamol and noradrenaline, antagonist = propranolol |
| Muscarinic receptor agonist | Atropine |
| Hepatic portal system | Veins carrying blood from GI tract to liver. Hepatic portal vein delivers deoxygenated blood from small intestine to inferior vena cava. Hepatic artery delivers oxygenated blood. |
| Opioid receptors | Mu, delta, kappa, ORL-1. G protein coupled receptors. Metabotropic |
| What are endogenous agonists | Endorphins - modulate mood and response to pain |
| Effects of heroin | Euphoria, drowsiness, dry mouth, flushed skin - short term |
| Parenteral routes of administration | IV, transdermal |
| Enteral routes of administration | Oral, rectal |
| Which part of the brain do you associate with psychological addiction? | Mesocorticallimbic dopaminergic pathway |
| Naloxone effects | Immediate withdrawal symptoms |
| Misuse of Drugs Act 1971 (MDA 71) | Defines what it is legal to do with the drugs it controls |
| Misuse of Drugs Regulations 2001 (MDR 2001) | Lists restrictions and exemptions to MDA 71 - also explains what is not an offence (drs, chemists) |
| In MDA 71 what class of drugs are common opiates and why? | Class A - most harmful - morphine, morphine in low dose form, raw opium, medicinal opium Class B - codeine (unless injected) |
| In MDR 2001 what schedules do main opiates fall into and why? | Schedule 1 = raw opium; Schedule 2 morphine + medicinal opium + codeine; Schedule 5 = low dose morphine, low dose codeine (min risk of abuse) |
| Legitimate morphine sources contributing to a positive urine result | Prescription pain killers (codeine, fentanyl, morphine), cough syrup containing codeine, ingestion of products containing poppy seeds |
| Illegal sources of morphine contributing to a positive urine result | Abuse of prescription drugs, illicit drugs (heroin) |
| CASE STUDY Positive workplace drug testing result for morphine | If no solid state drugs recovered individual cannot be charged due to positive test alone. Positive test may be due to drug metabolites from legitimate use (prescription codeine/morphine). Ingestion of food products containing poppy seeds. Urine sample should be tested for other metabolites (6-MAM indicates heroin use). Codeine:Morphine ratio <6 indicates an additional source of morphine present. No previous drug use known, no drugs recovered, signed document - may be dismissed from job |
| Effects of opioids on mu receptor | Analgesia, euphoria, sedation, constipation, respiratory depression, withdrawal |
| Mu opioid receptor experiment | Transgenic mouse - 1 wild type (normal), 1 knockout (modified opioid gene OPMR-1) - after opioid administration normal mouse has all physiological effects, knockout has none due to no mu receptors. |
| Pharmacokinetics | What the body does to the drug (ADME) |
| Pharmacodynamics | What the drug does to the body (receptor binding, symptoms) |
| Opioid pharmacokinetics | ADME: Absorption, Distribution, Metabolism, Excretion A: IV - fast as no absorption phase, rapid increase in drug concentration in the brain. Oral - no euphoria, slow absorption, no sudden increase in drug concentration. D: CNS, crosses blood brain barrier (BBB) M: Liver - phase 1 (oxidation or hydrolysis), phase 2 (conjugation) - slow metabolism may cause overdose, may prolong drug effects E: kidneys - excreted as metabolites - depends on kidney function, reduced in elderly prolongs drug effects. Exception - methadone excreted via bile |
| Mu receptor effects | Analgesia, euphoria, sedation, respiratory depression, constipation, pupillary constriction |
| Delta receptor effects | Analgesia, proconvulsant |
| Kappa receptor effects | Analgesia, sedation, pupillary constriction, dysphoria |
| ORL-1 receptor effects | Analgesia, immobility, impairment of learning |
| Opioid use symptoms | Analgesia, euphoria, sedation, constipation, respiratory depression |
| Withdrawal symptoms (physiological) | Aggression, nausea, shaking, pain, hallucinations - Temporary |
| Addiction symptoms (psychological) | Changes in mesocorticallimbic dopaminergic pathway - craving - permanent |
| Opioid addiction treatment | Methadone - potent Mu agonist - orally = slow absorption, long lasting, slow release, no euphoria. Misused to achieve euphoria LAAM - potent Mu agonist - orally 3x per week Buprenorphine - partial agonist - reduces withdrawal - orally 3x per day. Misused Suboxone - combines buprenorphine and naloxone - sublingual or buccal (dissolved in mouth) - naloxone deterrent prevents misuse - if taken orally naloxone results in immediate withdrawal symptoms |
| Opioid toxicity symptoms | CNS depression, respiratory depression, constricted pupils, drowsiness |
| Relapse after abstinence | Decreased tolerance levels may lead to overdose if previously acquired tolerance dose administered |
| Metabolites of morphine | Morphine, hydromorphone, codeine |
| Heroin metabolite | Morphine, 6-MAM (only source is heroin)- Detection time 8hrs |
| UK maximum penalties under MDA 71 | Possession: Class A = 7 years & fine, class B = 5 years & fine, class C = 2 years & fine Supply: A = life & fine, B = 14 years & fine, C = 14 years & fine |
| Morphine levels | Oral - 10mg/5ml tablet; Fast reaction tablets 20 or 50mg; slow tablets 5-200mg; liquid, 10mg in 5mL; injection 10mg/1ml, iv 2.50-10mg/ml muscle 5-20mg |
| MDR 2001 Schedules | 1 = most stringently controlled (research) 2 & 3 = controlled drugs with a medical use - can be prescribed 4 = minor prescribed tranquilisers 5 = minimal risk of abuse - sold over the counter |
| Advantage of morphine administration into spinal cord | Lower risk of respiratory depression as further away from brain |
| Gamma-Amino-Butyric Acid (GABA) - ADDICTION | Inhibitory neurotransmitter blocks impulses between nerve cells and the brain (CNS) - Inhibits dopamine release Opioid (Mu) receptors on GABA neuron nerves - opioid may bind and inhibit GABA = increased dopamine production = euphoria Desensitisation in heroin addicts - need a higher dose for response |
| Morphine ADME | A – IV – rapid increase in drug concentration within the blood leading to the brain – faster route as no absorption phase – long lasting Oral – 40-50% of dose reaches CNS (30 mins for immediate release morphine, 90 mins extended release form) - Absorbed in the small intestine D – Liver, kidney, lungs or spleen, crosses BBB M – Metabolised in liver by demethylation and glucuronidation Metabolites = M6G, M3G, codeine, hydromorphone and normorphine Phase 1 and phase 2 by enzymes E – Metabolites eliminated via renal filtration - Elimination ½ life = 120 mins |
| Morphine daily dose | Different doses dependent on preparation type – maximum dose within a 24 hr period - max 120mg for morphine |