Matthew Adetifa Nurse Practitioner (Mental Health & AOD) Latrobe Regional Hospital Traralgon,Victoria, Australia

Transcription

1 Matthew Adetifa Nurse Practitioner (Mental Health & AOD) Latrobe Regional Hospital Traralgon,Victoria, Australia

2 Knowledge of the Country (National) Medicines Policy The doctrine of Quality use of Medicines Classes of medications use in psychiatry Antipsychotics Antidepressants Mood stabilisers Anti-cholinergic Anxiolytics Antipsychotics (conventional & Atypical ) Side effects Drug Interactions

3 World health Organisation(WHO) National Medicines Policy recommendation. To ensure timely access to medicines at a cost both individual and community can afford. Medicines meet appropriate standards of quality, safety and efficacy. Maintain a responsible and viable medicines industry Improve positive health outcomes.

4 Quality use of medicines: is a risk management approach to ensure safe and effective use of medicines for better healthcare outcomes. Judiciously used: only when non medication alternatives have been considered. Appropriately used: being the most appropriate therapy after considering clinical condition, risks and benefits, dose, length of treatment and cost. Safely used: under or over use is minimised. Efficaciously used: Achieve the goals of therapy, treatment delivers actual health outcomes.

5 Role of Health Professionals (Mental Health Nurses) Provide psycho-education Choice of treatments. Provide most appropriate treatment Collaboration with consumers and other health professionals

6 Action- Treatment of psychotic disorders (Schizophrenia, mania, psychotic depression). Reduces positive symptoms: Delusions, hallucinations, thought disorder. Some relief on negative symptoms: Amotivation, Blunted affect, cognitive impairment. Relapse prevention for psychotic illnesses.

7 Mode of action: Antagonise dopamine D2 receptors Dopamine Theory The dopamine hypothesis of psychosis Overactivity of dopamine neurons in the mesolimbic pathway of the brain may mediate the positive symptoms of psychosis. Mesolimbic pathway responsible for pleasure, effects of drugs and alcohol and hallucinations and delusions. Mesocortical Pathway: Enhance negative and cognitive psychotic symptoms Nigrostriatal Pathway: EPSE & Tardive Dyskinesia Tuberoinfundibular pathway: hyper-prolactinemia (Lactation, sexual dysfunction)

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10 Blockade of dopamine receptors increases the activity of Acetylcholine Over activity of acetylcholine causes EPSE Blockade of dopamine causes movement disorder in the Nigrostriatal pathway. Long term blockade causes upregulation and leads to Tardive Dyskinesia.

11 Actions= Blockade of receptors Dopamine 2 Muscarinic / Cholinergic Movement disorder Alpha Adrenergic Causes dizziness, reduced BP Histaminergic receptors Causes Weight gain, drowsiness Example Haloperidol (Haldol) Thioridazine ( Melleril) Loxapine (Loxitane) Fluphenazine (prolixin) Trifluoperazine (stelazine) Chlorpromazine (Largactil) Depots such as Flupenthixol, zuclopenthixol etc

12 The Ability of a drug to bind to a receptor Tightly bound drugs lead to increased sensitivity to dopamine blockade and likely to cause EPSE Low Affinity (loosely Bound) Example: Quetiapine, Olanzapine, Amisulpride, Clozapine High Affinity (tightly bound) Chlopromazine, Haloperidol, Flupenthixol, Fluphenazine

13 Mode of action Blockade of Dopamine (D2) and serotonin (5HT2A) receptors (as opposed to typical antipsychotics that blocks Dopamine and not serotonin receptors) Also acts on histamine, alpha adrenergic and cholinergic receptors

14 Atypical antipsychotic first binds to the D2 receptor then binds to the serotonin (5HT2A) receptor. The second action reverses the first by reverses the blockade of D2. The blocking of the serotonin receptor causes the dis-inhibition of the dopamine neuron causing dopamine release Serotonin opposes the release of dopamine in the Nigro-striatal and tuberofundibular pathways.

15 Typical Vs Atypical Antipsychotic Same efficacy (except Clozapine) Consider: Merits of high vs low affinity drugs ( the higher the affinity the more the EPSE) Adverse effect profile Physical health baseline Patient tolerability, preference and response

16 Examples in Australia Olanzepine Risperidone Quatiapine Amisulpride Ziprasidone Clozapine Risperdal consta injection Aripiprazole oral & depot Paliperidone oral & Depot

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18 Sedation Postural hypotension Anticholinergic effects Dry mouth Blurry vision Constipation Urinary hesitancy weight gain commonest in Olanzapine and clozapine Metabolic effects-- Increases serum lipids, impaired glucose tolerance

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20 Hyper-prolactinaemia Leads to galactorrhoea, amenorrhoea & low libido Osteoporosis QTc prolongation causing cardiac arrhythmias Sexual dysfunction EPSE Acute dystonia Laryngeal spasm, oculogyric crisis Akathesia

21 Parkinsonism (Neurological movement disorder) Tremor, rigidity, hyper-salivation Tardive Dyskinesia ( Irreversible Involuntary hyperkinetic movement) Involuntary movement of the mouth, lips, tongue, jaws with smacking Tic-like movements affecting the limbs and trunk Neuroleptic malignant Syndrome (Rare but potentially fatal) Characterised by hyperpyrexia, muscle rigidity, increased creatinine Kinase (CK), altered consciousness May occur at anytime during the antipsychotic treatment So Watch out Stop antipsychotics immediately if NMS occurs

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23 Cytochrome P450 system The cytochrome P450 system is an evolutionary system to deal with the breakdown of endogenous and exogenous chemicals in the body. It performs this function by oxidising, hydrolysing or reducing the chemicals thereby exercising regulatory mechanism to control the activity of the chemicals. Its significant in psychotropic drug interactions. The regulatory mechanism involve chemicals which induce or inhibit other cytochromes.

24 Inducer Anticonvulsants: Carbamazepine, Phenytoin reduces the concentration of oral contraceptives and quetiapine Inducing CYP3A4. Smoking induces olanzapine and clozapine metabolism inhibitors SSRI: Fluvoxamine, fluoxetine & Paroxetine inhibit CYP2D6 thereby preventing the metablism of codeine to morphine. Fluvoxamine inhibits olanzapine and clozapine metabolism.

25 Matthew Adetifa Nurse Practitioner (Mental Health & AOD) Latrobe Regional Hospital Traralgon,Victoria, Australia

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27 Def. Epidemiology Pharmacology Clinical Manifestations Course Screening Assessment Diagnosis management

28 A Chronic, relapsing illness that involves the misuse of prescribed opioid medications, use of diverted opioid medications or illicitly obtained opioid.

29 Refers to natural or synthetic substances that act at one of the three main opioid receptor systems: Mu Kappa Delta receptor Slang terms for opioid use Intranasal use Snorting or sniffing IV use Shooting up Subcutaneous Use--- Skin-popping Intramuscular use -- Muscling

30 Heroin Derivative of morphine commonly abused by injection Slang terms for heroin are Dope, horse, smack, china white, junk or tar Opium Extract of opium poppy containing morphine and codeine, mostly abused by smoking or eating. Prescribed Opioid Opiate: Morphine and codeine Synthetic opioid: Fentanyl, methadone, Oxycodone and Semi synthetic: hydrocodone

31 In the US 5.1million people (1.9% of persons age 12 or older) were estimated in 2015 to have used heroin in their lives. 3.8Million people aged 12 and older reported past misuse of a prescription pain medication in 2015 (National Survey on drug use and health, 2015). Heroin use is increasing for persons who begin by first having nonmedical use of opioid analgesics Prescription opioid is obtained mostly from friend or relative rather than clinician. Prescription opioid user at highest risk of Overdose obtain it from clinicians, relatives or friend.

32 Prior history of substance use disorder Demographic features including age (Peer pressure, adventure Severe or chronic pain Co-morbid mental disorders

33 Mechanism of action Opioid activates specific transmembrane neurotransmitter Opioid receptors of Mu, Kappa, Delta Some opioids also activate other CNS neurotransmitters like Dopamine, GABA and glutamate. Effects of activation will depend on location, type of neural tissue, frequency and duration of use. CNS = Respiratory depression, Analgesia and euphoria PNS = stimulation of smooth muscle of the bronchi leading to suppression of cough And smooth muscle of the intestine leading to opioid-induced constipation

34 Acute Intoxication Opioid Withdrawal Opioid Overdose Itching and Scratching Dilation of pupils Hypotension Slurred Speech Anxiety Bradycardia Drowsiness Muscle and bone ache Pulmonary Oedema Pinpoint pupils (meiosis)+ Sleep disturbance Respiratory Depression Fresh injection sites Sweating, Hot and cold flushes Pinpoint Pupils Lowered BP Dilation of pupils Loss of Consciousness Slowed Pulse Nausea & Vomiting Increased Pulse and BP

35 Infection HIV, Hep C, Localised or systemic infections Opioid-induced Hyperalgesia Opioid-induced Bowel Syndrome Increased risk of accidents Risk of Overdose and High Mortality

36 Substance use history Age of first use Frequency of consumption, Route (IV, Intranasal (snorting) ) Amount, past history of problematic use Sign of tolerance Treatment history Physical examination ( to detect common complication of OUD) Laboratory evaluation UDS, Hepatitis serology, LFT, FBE

37 Problematic pattern of Opioid use that causes significant impairment manifested by 2 or more of the under-listed within a 12 month period: Taking large amount over a longer period than intended Persistent desire or unsuccessful effort to control use Increased Time spent in obtaining, using and recovering from the effect of use. Craving Evidence of aberrant behaviours Use resulting in a failure to fulfil role obligations like work, school or home Persistent use despite knowledge of having a persistent physical or psychological problem. Tolerance and withdrawal

38 Type of Treatment Advantages Disadvantages Substitution Therapy Reduce opioid use Expenses to patient Decrease mortality Stigma Improve quality of life Prevent withdrawal symptoms in physically ill or unstable patients Restriction due to supervised dosing. Detoxification Short-term commitment Poor long term outcome Easy access point to treatment Increased risk of overdose if patient return to using Re-emergent of chronic pain conditions Antagonist Treatment (Naltrexone) Effective in patient keen to end opioid abuse with using opioid Requires detox first: All detox disadv. applies

39 Type of treatment Advantages Disadvantages Residential (rehab) Effective for those with complex social problems Mostly medication free Entry is ONLY post detox. Long waiting list Expensive to provide service Outcome is mostly dependent on aftercare available. Outpatient counselling (No Medication) Effective during the early stage of OUD with less severity Poor outcome in patients with severe dependence Dependent on the quality of counselling services

40 Methadone Introduced in 1969 Synthetic opioid agonist with long half-life (20-36 Hrs) Buprenorphine / Buprenorphine-naloxone Introduced in 1980 Mixed agonist/antagonist (partial opioid agonist with high receptor affinity) 8-12 hrs half life at low doses (2mg) & hrs at high dose (>16mg) Natrexone Introduced in 1999 Opioid Antagonist with less effect on opioid with high affinity for opioid receptors (e.g Buprenorphine )

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42 Thanks You.

43 Martin, J & Fay, Michael Cytochrome P450 drug interactions: are they clinically relevant? Australian Prescriber. DOI: /austprescr RACGP guidelines on management of pain. Retrieved on 1/5/18 from Gowing, L, Ali, R, Dunlop, A, Farrell, M & Lintzeris, N, (2014). National Guidelines for Medicated-Assisted Treatment of opioid Dependence. Commonwealth of Australia

44 Johnson, R. E., Strain, E. C., & Amass, L. (2003). Buprenorphine: how to use it right. Drug and Alcohol Dependence, 70 (Suppl.2). S59-S77.