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BY: AROOJ KHALID ALVI Mphill.Pharmacology 1 For more presentations and information visit

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1 BY: AROOJ KHALID ALVI Mphill.Pharmacology 1 For more presentations and information visit

2 Pain and the Pain management Endogenous Opioid Peptides Opioid receptors and effects Chemical Structure and Binding Features of Opioid Analgesics Types of Opioid Analgesics 2 For more presentations and information visit

3  Pain is a crucial aspect of the body’s defense mechanisms  Pain “is a part of a rapid warning relay instruction of the motor neurons of the central nervous system to minimize detected physical harm.”  Pain can be defined as a somatic sensation of acute discomfort, a symptom of some physical hurt or disorder, or even emotional distress.  Pain can be classified into two types:  Acute pain  Chronic pain 3 For more presentations and information visit

4 Acute pain is short-term pain or pain with an easily identifiable cause Acute pain “is the body's warning of present damage to tissue or disease. It is often fast and sharp followed by aching pain. Acute pain is centralized in one area before becoming somewhat spread out. This type of pain responds well to medications.” Chronic pain is pain that last much longer than pain normally would with a particular injury. Chronic pain can be constant or intermittent and is generally harder to treat than acute pain. Pain can also be grouped by its source and related pain detecting neurons such as cutaneous pain, somatic pain, visceral pain, and neuropathic pain Opioid Analgesics can be used to treat many types of pain 4 For more presentations and information visit

5 There are certain nociceptive receptors present on on the skin and various organs of the body. When any traume or stimuli for pain approaches, certain substances are released at the site, causing the signalling from sensory neurons. These neurons release excitatory neurotransmitters which relay signals from one neuron to another. “The signals are sent to the thalamus, in which pain perception occurs. From the thalamus, the signal travels to the somatosensory cortex in the cerebrum, at which point the individual becomes fully aware of the pain.” Pain Signaling 5 For more presentations and information visit

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7 Analgesia simply means the absence of pain without loosing consciousness. “The analgesia system is mediated by 3 major components : the periaquaductal grey matter (in the midbrain), the nucleus raphe magnus (in the medulla), and the pain inhibitory neurons within the dorsal horns of the spinal cord, which act to inhibit pain-transmitting neurons also located in the spinal dorsal horn.” These areas are the areas in which the chemical mechanisms of opioid analgesics will take place 7 For more presentations and information visit

8 8 For more presentations and information visit

9 Opioids are drugs derived from or related to the Opium Opium is derived from the juice of the opium poppy, Papaver somniferum Opium contains over twenty distinct alkaloids (morphine was the first alkaloid of opium to be isolated in 1806) By the late 19 th century use of these “pure” opium derivatives spread throughout the medical world, however, the method by which these drugs works was unknown. 9 For more presentations and information visit

10 In 1973 researchers determined the existence of opiate binding sites in the brain through the use of radioligand-binding assays In 1975, an endogenous opiate-like factor called enkephalin was found and shortly after this two more classes of endogenous opiate peptides were isolated, the dynophorins and the endorphins. “Endogenous opioid peptides are the naturally occurring ligands for opioid receptors.” These peptides are produced by the pituitary gland and by the hypothalamus Opioid peptides are found in the central nervous system mainly in limbic and brainstem areas associated with pain reception, and the certain areas of the spinal cord. Their distribution corresponds to “areas of the human brain where electrical stimulation can relieve pain.” 10 For more presentations and information visit

11 These natural peptides work as ligands that interact with their specific receptors causing structural changes that result in other changes in the effected neuron such as the opening or closing of ion gated channels or the activation or deactivation of certain enzymes. Opioid peptides work by modulating the release and uptake of specific neurotrasmitters in the neurons they are found. This alteration of neurochemical balance creates a vast amount of possible physiological effects, one of which is analgesia. All of the endogenous opioid peptides are derived from a corresponding precursor proteins and all share a common amino- terminal sequence which is called the “opioid motif.” 11 For more presentations and information visit

12 Shortly after the discovery and observance of endogenous opioid peptides, multiple classes of unique opioid receptors were found Types: the mu receptor, the delta receptor, the kappa receptor, and the ORL-1 receptor. The receptors are found on cell membranes of cells in the nervous system (neurons) and are found in unique distributions and have different effects. 12 For more presentations and information visit

13 Morphine and its analogues bind most strongly to this receptor and in fact most used opioid analgesic drugs are selective for this specific receptor type. Location: They are seen in significant amounts in all areas of the central nervous system associated with pain control Types: There are two subtypes of the mu-receptor. 1. μ1-receptors: analgesic activities and the 2. μ2-receptors: effects of respiratory depression and constipation. 13 For more presentations and information visit

14 Mechanism: When an opioid binds to the mu-receptor it induces a change in shape which in turn induces a change in the ion channels of the associated cell membrane The mu-receptor opens up the ion channel allowing potassium ions to flow out of the cell causing hyperpolarization of the membrane potential. This hyperpolarization causes it to become extremely difficult for an action potential to be reached and therefore the firing of the neuron become far less frequent and the neurons excitability decreases. The release of potassium ions also causes less calcium ions to enter the terminal end of the neuron. This is where neurotransmitters are stored and as a result this significantly reduces neurotransmitter release. These effects of a ligand binding to a mu-receptor essentially turn off the neuron and in doing so block the relaying of pain signals from pain receptors. 14 For more presentations and information visit

15 Effects produced by the stimulation of mu-rec.: When and opioid binds to the mu-receptor it produces the effects of analgesia. The mu-receptor is also associated with other effects such as “sedation, reduced blood pressure, itching, nausea, euphoria, decreased respiration, miosis (constricted pupils) and decreased bowel motility often leading to constipation. Respiratory depression is considered the deadly side effect of opioid analgesic drugs. It is the cause of death in all overdose cases. 15 For more presentations and information visit

16 Synapses between afferent nociceptive neurons and secondary ascending neurons relay pain signals to the brain. The entry of Ca 2+ into the pre-synaptic primary neuron and the release of K + from the post-synaptic secondary neuron are processes involved in signal transmission across the synapse. 16 For more presentations and information visit

17 Opioids binding to ion channel associated  receptors inhibit the influx of calcium ions into the pre-synaptic terminal and increase the outflow of potassium ions from the post-synaptic membrane. This has the effect of reducing the release of the neurotransmitter glutamate and hyperpolarising the post-synaptic membrane. Synaptic transmission is inhibited. 17 For more presentations and information visit

18 The kappa receptor is very different from the mu-receptor in the fact that there are not many significant agonist of the kappa receptor known Types: There are three subtypes of the kappa receptor however the difference between these subtypes is not clearly known. Effects : The kappa receptor is associated directly with analgesia and sedation but with none of the undesired side effects associated with the mu receptor. Because of this, it is an area of focus in current research and shows promise in the development of a safer analgesic. 18 For more presentations and information visit

19 Mechanisn: When and agonist or ligand binds to the kappa receptor it induces a conformational change that results directly in the closing of the calcium ion channels in the terminal of the neuron and the neuron can not relay pain messages. Diff. from mu-rec: Another difference between the kappa and mu receptors is that the kappa receptors only effect nerves that relay “pain produced by non-thermal stimuli,” and mu receptors inhibit all pain signals. 19 For more presentations and information visit

20 The delta receptor is the strongest binding site of the body’s natural pain killer, the class of opioid peptides called the enkephalins. Morphine and other commonly used opioid analgesics also bind to this receptor strongly and act as an agonist much like they do with the mu receptor. Location: The delta receptor is found in larger cells than the other receptors and seems to be important in spinal analgesia. Present in spinal and limbic areas,so responsible for reinforcement and dependence actions.. 20 For more presentations and information visit

21 Mechanism: The delta receptor is a G-protein linked receptor. When an agonist binds to the delta receptor is induces a conformational change that causes the activation of a specific G-protein. This G-protein “inhibits the membrane bound enzyme adenylate cyclase and prevents the synthesis of cAMP. The transmission of the pain signal requires cAMP to act as a secondary messenger, and so inhibition of this enzyme blocks the signal.” Also causes hyperpolarization by increase k+-efflux. Effects: Most effects are similar to mu-rec, however kappa appears to have some opposite effects in certain areas. 21 For more presentations and information visit

22 The ORL-1 receptor or the “orphan” receptor was very recently discovered. The natural opioid peptide that is a ligand for this receptor is nociceptin which is also called orphaninFQ. Whole system is called N/OFQ system. Effects: The ORL-1 receptor is associated with many different biological effects such as memory processes, cardiovascular function, and renal function. Capable of opposing mu-rec mediated analgesia as well as modulating memory and learning processes. It is thought to have effects on dopamine levels and is associated with neurotransmitter release during anxiety. 22 For more presentations and information visit

23 ReceptorSubtypesLocationFunction delta (δ) delta (δ) OP 1 (I) δ 1, δ 2  brain brain  pontine nuclei(learning motor-skills) pontine  Amygdala(emotional rxns) Amygdala  olfactory bulbs(smell) olfactory bulbs  deep cortex(sens.,motor, perception)cortex  analgesia analgesia  antidepressant effects antidepressant  physical dependence physical dependence  Increase hormone release(growth hormone) kappa (κ) kappa (κ) OP 2 (I) κ 1, κ 2, κ 3  brain brain  Hypothalamus(endo +regulatory functions) Hypothalamus  periaqueductal gray(analgesia) periaqueductal gray  Claustrum(functional timing) Claustrum  spinal cord spinal cord  substantia gelatinosa(conduct pain sens.) substantia gelatinosa  Spinal and supra-spinal analgesia  sedation sedation  miosis miosis  inhibition of ADH release(diuresis)ADH  dysphoria dysphoria 23 For more presentations and information visit

24 mu (μ) mu (μ) OP 3 (I) μ 1, μ 2, μ 3  brain brain  cortex (laminae III and IV) cortex  thalamus thalamus  Striosomes(moods) Striosomes  periaqueductal gray periaqueductal gray  spinal cord spinal cord  substantia gelatinosa substantia gelatinosa  intestinal tract(myentric & submucosal plexus) intestinal tract μ 1 :  supraspinal analgesia supraspinalanalgesia  physical dependence physical dependence μ 2 :  respiratory depression respiratory depression  miosis miosis  euphoria euphoria  reduced GI motilityGI  physical dependence physical dependence μ 3 :  ? Nociceptin receptor Nociceptin receptor OP 4 ORL 1  brain brain  cortex cortex  amygdala amygdala  Hippocampus(memory) Hippocampus  septal nuclei(reward & reenforcement=euphoria) septal nuclei  Habenula(pain,nutrition,slee p,stress,reward) Habenula  hypothalamus hypothalamus  spinal cord spinal cord  anxiety  depression  appetite  development of tolerance to μ agonists 24 For more presentations and information visit

25 In order to examine important structural features of Opioid analgesics, which are all derived from the opiate structure, we will refer to the structure of morphine, the first identified alkaloid. 25 For more presentations and information visit

26 The structure of morphine consists of five rings forming a T-shaped molecule The important binding groups on morphine are the phenol, the aromatic ring, and the ionized amine. These groups are found in all Opioid analgesics.. “A free phenol group is crucial for analgesic activity.” The aromatic ring of the opiate also seems to be integral to its function as compounds that lack the aromatic ring show no analgesic activity. The ionized amine also plays an important role in its activity and is common in opioid structure. In experiments where the Nitrogen was replaced by a Carbon no analgesic activity was found. It interacts with certain analgesic receptors in its ionized form. 26 For more presentations and information visit

27 A. Opoid-agonists. 1.Natural opium alkaloids: i.Phenanthrene group: morphine codeine thebaine ii.Benzyl-isoquinoline group: noscapine papaverine 2.Semisynthetic opium derivatives: i.Morphine derivatives heroin hydromorphine oxymorphine ii.Codeine derivatives. hydrocodone oxycodone iii.Thebaine derivatives. buprenorphine 3.Synthetic opium substitutes: i.Piperidine derivatives. 27 For more presentations and information visit

28 pethidine fentanyl sulfentanil,alfentanil ii.Phenyl-heptylamine derivatives. methadone propoxyphene. iii.Morphinans levorphanol dextromethorphans B. Opoids with mixed receptor actions: 1.Phenanthrenes. nalbuphine buprenorphine 2.Morphinans. butorphanols 3.Benzomorphans pentazocine. C.Pure antagonists. naloxone naltraxone nalmefene 28 For more presentations and information visit

29 :Morphine: Morphine is the golden standard among opioid analgesics to which the structure and strengths of all other drugs are compared It is the primary ingredient in opium and was isolated in 1806 Morphine has strong binding affinity for the mu and delta opioid receptors and some weak affinity for the kappa receptor 29 For more presentations and information visit

30 Pharmacokinetics: i/v, S/C, I/M Oral bioavailability is low. T1/2 2-2.5 hrs, duration of analgesia is 4-5 hrs. Absorption: from GIT is usually slow and erratic so not given orally. Significant first-pass metabolism in liver Distributed in highly perfused aread as liver, kidney,brain, lungs and to lower conc in skeletal muscles (serving as a reservior) Only small amount cross BBB. Enters in the foetus,so shouldn’t be used in pregnancy. Metabolized in liver to 6 glucuronic acid(M6G),an active metabolite with more potent analgesic activity, and M3G,neuroexcitatory. Excreted via glucuronide conjugate into the urine. 30 For more presentations and information visit

31 1.Miosis: Due to excitation of autonomic segment of eye. 2.Respiration: Depressant effect. Due to direct effect on the brain-stem resp centres.Death is always due to resp.depression. 3.Cough: Depress the cough,in part dur to direct effect on the cough centre in medulla. 4.CVS: orthostatic hypotension and fainting. (due to the release of histamine and depression of vaso-motor centre) 5.Nausea and vomitting: By triggering CTZ(may involve vestibular component) Gastric stasis 31 For more presentations and information visit

32 6.GIT: Decrease HCl secretion.(indirectly due to the increased secretion of somatostatins from pancreas and reduces release of Ach). Diminish biliary, pancreatic and intestinal secretions. resting tone increased and spasms observed. Propulsive peristaltic movements in colon are abolished resulting in morphine-induced constipation. Along with this,inattention of the stimuli for defecation owing to central effects.resulting in tolerence to this dev. Biliary colics. Due to increased pressure due to the constriction of sphinctor of oddi 7.Ureter and urinary-bladder: inhibit the urinary voiding reflexes and tone of sphinctor and vol of bladder increase. 8.Uterus: may prolong labour,restoring tone, freq. and amplitude to normal.(if hyperactive by oxytocin) 32 For more presentations and information visit

33 9.Skin: Flushing of face,neck and upper thorax.(histamine release). 10.Immune-system: May modulate the actions of immune sys, by effects on lymphocyte proliferation,a.body prod, and chemotaxis.natural killer cell cytolytic activity and lymphocyte proliferative responses may be inhibited by these.(med by sympathetic sys. And a/f prolong use by hypothalmic- pituitaryadrenal sys.{corticosteroids}) 11.Neuroendocrine effects: Acts on hypothalamus to inhibit release of. GnRH,Corticotropic releasing factor.—low conc of circulating LH, FSH, a result of low conc. Of pituitary trophic hormones,the conc. Of testosterone and cortisol decrease. It may increase the release of prolactin,probably by inhibiting the dopaminergic inhibition of its secretion. Mu-agonists seems to have antidiuretic effects.(inc. release of ADH). 33 For more presentations and information visit

34 12..Analgesia. Opoid rec.on the terminal of pri afferent nerves mediate inhibition of n/t release.(substance-P) post-synaptic inhibition of interneuons that conveys nociceptive info to higher brain areas 13.Euphoria:(septal nuclei) Patnts in pain experience a pleasant feeling Ptnts not in pain feels dysphoria(malaise) 14.Sedation:(hebenula) drowsiness,clouding of mentation,impairment of reasoning ability and sleep. 15. Hypothermia:(hypothalamus) Alter the equilibrium point of hypothalamic heat-reg mech.such that body temp falls slightly. 16.Tolerence,physical dependence and potential for abuse:(locus cerelus) characteristic feature of all opoids. 34 For more presentations and information visit

35 1. Analgesia  headache  Post-operative pain  Terminal illness  Cancers  Obstetrical procedure 2.Cough( low dose) 3.Diarrhoea. 4.Anaesthesia: preanesthetic medication. 5.Acute pulmonary edema(reduced awareness of SOB,red.anxiety,red. Preload, red. afterload) 6.May have a.inflammatory effects(inh. Of subs. P) 35 For more presentations and information visit

36 Respiratory depression Nausea Vomitting Constipation Postural hypotension accenuated by hypovolemia Increased intracranial pressure(by retention of CO2) Urinary retention Itching and urticaria Apnoea Tolerence Physical and psychological dependence 36 For more presentations and information visit

37 Acute Action Analgesia Respiratory Depression Euphoria Relaxation and sleep Tranquilization Decreased blood pressure Constipation Pupillary constriction Hypothermia Drying of secretions Reduced sex drive Flushed and warm skin Withdrawl Sign Pain and irritability Hyperventilation Dysphoria and depression Restlessness and insomnia Fearfulness and hostility Increased blood pressure Diarrhea Pupillary dilation Hyperthermia Lacrimation, runny nose Spontaneous ejaculation Chilliness and “gooseflesh” 37 For more presentations and information visit

38 May be due to clinical overdose,accidental overdose or suicidal attempt.(40-60mg) Symptoms:  Respiratory depression  Stupor or comma  Cyanosis  Miosis  Fall in B.P.  Pulmonary edema at terminal stages  Death is due to resp depression The triad of coma, pinpoint pupil and depressed resp. strongly suggests opoid poisoning. :Treatment: Maintainance of ABC,lavage. Opoid antagonist as naloxone produce dramatic reversal of poisoning.(small i/v doses) 38 For more presentations and information visit

39  With mixed antagonist-agonist opioids  Patients with head injury  Patients with impaired pulmonary functions,asthma  Pregnancy  Liver disease  Patients with endocrine disease. Hydromorphones and Oxymorphones are strong opioid agonists with morphine-like effects. 39 For more presentations and information visit

40 Oxycodone and methadone are analogs of codeine Codeine itself has low binding affinity to all of the opioid receptors. Its analgesia producing effects come from its conversion to morphine. When codeine is administered about ten percent is converted to morphine by O-demethylation that occurs in the liver by an enzyme called cytochrome p450. Because of this Codeine is far less potent than morphine It differs structurally from morphine in that its phenol group is methylated. It is often referred to as methyl- morphine. 40 For more presentations and information visit

41 Codeine is usually administered orally and it is much more effective orally than morphine (about 60%) Slight sedation,NO euphoria and NO noticeable respiratory depression. Tolerence dev less rapidly and dependence occurs rarely. Uses: Cough Diarrhoea Somatic pain 41 For more presentations and information visit

42 It is administered through intravenous injections but can also be administered orally or vaporized. It binds most strongly to the mu receptor and is also active in the form of morphine as its acetyl groups are removed. It produces euphoric effects similar to morphine, however, it is thought that these effects are greater and more addicting because of its extremely rapid effect. Its fast action is a result of being extremely lipid- soluble because of its acetyl groups and therefore it immediately crosses the blood brain barrier. 42 For more presentations and information visit

43 The use of Heroin causes the body to produce far less of its natural opioid peptides, the endorphins. This creates a dependence on heroin. When a heroin user stops using the drug the withdrawal symptoms are severe. Withdrawal symptoms include anxiety, depression, cramps, vomiting, diarrhea, restless leg syndrome (hence kicking the habit), and a severe sense of pain caused by nothing. Many addicts in withdrawal experience “itchy blood” which can drive the addict to scratch cuts and bruises into his body. 43 For more presentations and information visit

44 1.Papaverine: No analgesic action Relaxes smooth muscles sp. Of blood vessels. Used in various spastic conditions of arteries of limbs 2.Noscapine: V effective cough suppressant. So used instead of codeine. Less addictive Causes constipation. 44 For more presentations and information visit

45 Pethidine: Most frequently prescribed opoid Strong agonist Posses most of the effects of morhpine but less histamine release. Also has anti-muscarinic effects of atropine No constipation and miosis Tachycardia(a.muscaranic action) Non-effective anti-tussive May cause bronchial dilation so may be given in asthma Less CNS depression For obstetrical analgesia as it doesn’t effect foetus. As an adjunct to anasthesia.(local) 45 For more presentations and information visit

46 Fentanyl: (100M) Strong agonist Chemically related to pethidine. Short duration and rapid onset Used in anesthesia 46 For more presentations and information visit

47 Strong agonist Pharmacologically v similar to morphine Methadone is often used to treat heroin addiction because it is a longer lasting opioid. Mild withdrawal effects. 47 For more presentations and information visit

48 An agonist of kappa-rec and weak agonist of mu and delta. Weaker analgesic than codeine but equally addictive Well absorbed orally Used in combination with aspirin or paracetamol for greater analgesia. No constipation and lesser incidence of N,V,drowsiness and dizziness. For the treatment of Myalgia Nauralgia Migraina Arthritis pain. 48 For more presentations and information visit

49 1.Phenanthrenes: Nalbuphine: Agonist activity at delta and kappa, and weak antagonist of mu-receptor. Given parenterally Analgesia equivalent to morphine with lower abuse potential At high dose,ceiling resp. depression. No reversal with naloxone Buprinorphine: Hign affinity for mu-rec act as partial agonist. Longer duration of action As effective in heroine-detoxification as methadone 49 For more presentations and information visit

50 A kappa-agonist with weak mu-antagonist activity. Used orally or parenterally(no s/c) Generally effects are similar to morphine but some analgesic effects are due to kappa-rec. High dose cause increase in heart-rate and B.P. Vomitting is less common than with morphine. Patients receiving opoids may experience abstinence synd. when given pentazocine. Used as an analgesic in those with drug-abuse prob. 50 For more presentations and information visit

51 Opioid Antagonists are used to treat opioid overdose cases. Most are derived from Thebaine (an alkaloid of Opium) The have strong binding affinity for the mu receptors They work by competitive inhibition at the binding site (It binds but does not change the receptor while at the same time blocking the agonist). These involves naloxone,naltrexone, and nalmefene. 51 For more presentations and information visit

52 Naloxone is an example of a opioid antagonist. It is administered intravenously. Short duration of action Metabolized by glucuronidation and excreted in urine. It is a competitive antagonist at mu- delta and kappa rec. with 10 fold higher affinity for mu than kappa.this explains reversal of resp. depression with minimal reversal of analgesia due to kappa. It can rapidly produce the withdrawal symptoms associated with opioid addiction. Naltrexone is another example of an opioid antagonist. It is more potent than Naloxone and is used in the treatment of alcohol addiction but its mechanism in this treatment is unknown. 52 For more presentations and information visit

53 Pharmacodynamics: Almost inert in the absence of agonist but with agonist reverses the effects within 1-3 min. In opoid- addicts it’ll instantaneously precipitate abstinance syndrome. There is no tolerence to antagonist activity. Uses: To treat acute opoid-toxicity. NALTREXONE:is also a pure antagonist and due to long duration it is used as a maintainance drug for addicts in the treatment prog. It is also used for the treatment of chronic alcoholism to decrease craving. Nalmefene:newest agent, derivative of naltrexone,only i/v available.t1/2=8-10 hrs,for opioid overdose. 53 For more presentations and information visit

54 Sedative-hypnotics Anti-psychotic tranquilizers MAO-inhibitors Increased CNS depression particularly resp depression Inc. sedation,accentuation of CVS effects(a.muscarinic &alpha-blocking effects) High incidence of hyperpyrexic coma.(either retard its metabolism or interaction at central n/t.) 54 For more presentations and information visit

55 Opioid analgesics Drug Route of administration Onset of action (min) Time to peak effect (min) Duration of action (h) Strong agonists Fentanyl (Sublimaze) IM7-1520-301-2 IV1-23-50.5-1 Hydromorphone (Dilaudid) Oral3090-1204 IM15 IV10-1530-602-3 Sub-Q3015-30 Levorphanol (Levo- Dromoran) Oral10-6090-1204-5 IM IV—604-5 Sub-Q10-60within 20 55 For more presentations and information visit

56 Meperidine (Demerol) Oral1560-902-4 IM10-15 IV30-502-4 Sub-Q1 Methadone (Dolophine) Oral30-6090-1204-6 IM IV10-2060-1204-5 Morphine (many trade names) Oral—60-1204-5 IM10-30 IV30-604-5 Sub-Q— Epidural10-30204-5 Oxymorphone (Numorphan) IM10-1530-903-6 IV Sub-Q5-1015-303-4 Rectal 56 For more presentations and information visit

57 Mild-to-moderate agonists Codiene (many trade names) Oral30-4060-1204 IM10-3030-604 Sub-Q10-304 Hydrocodone (Hycodan) Oral10-3030-604-6 (Percodan) Oral—603-4 Propoxyphene (Darvon, Dolene) Oral15-601204-6 Butophanol (Stadol) IM10-3030-603-4 IV2-3302-4 Nalbuphine (Nubian) IMwithin 15603-6 IV2-3303-4 Sub-Qwithin 15—3-6 Pentazocine (Talwin) Oral15-3060-903 IM15-2030-602-3 IV2-315-302-3 Sub-Q15-2030-602-3 57 For more presentations and information visit

58 Opioid antitussives: Dextromethorphan, Levopropoxyphene, Noscapine, Codeine Anaesthetic: Pethidine, Fentanyl Detoxification of heroine: Buprenorphine, Methadone, Naltrexone. Cardiac tachycardia and hypertension: Pentazocine, Pethidine. 58 For more presentations and information visit

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