Matthew Adetifa Nurse Practitioner (Mental Health & AOD) … · Same efficacy (except Clozapine)...
Transcript of Matthew Adetifa Nurse Practitioner (Mental Health & AOD) … · Same efficacy (except Clozapine)...
Matthew AdetifaNurse Practitioner (Mental Health & AOD)
Latrobe Regional HospitalTraralgon ,Victoria, Australia
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
World health Organisation(WHO) 1999 - 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.
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.
Role of Health Professionals (Mental Health Nurses)
Provide psycho-education
Choice of treatments.
Provide most appropriate treatment
Collaboration with consumers and other health professionals
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.
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)
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.
Actions= Blockade of receptors Example
• Dopamine 2
• Muscarinic / Cholinergic • Movement disorder
• Alpha Adrenergic• Causes dizziness, reduced BP
• Histaminergic receptors• Causes Weight gain, drowsiness
• Haloperidol (Haldol)
• Thioridazine ( Melleril)
• Loxapine (Loxitane)
• Fluphenazine (prolixin)
• Trifluoperazine (stelazine)
• Chlorpromazine (Largactil)
• Depots such as Flupenthixol, zuclopenthixol etc
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
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
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.
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
Examples in Australia
• Olanzepine
• Risperidone
• Quatiapine
• Amisulpride
• Ziprasidone
• Clozapine
• Risperdal consta injection• Aripiprazole oral & depot• Paliperidone oral & Depot
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
Hyper-prolactinaemia –Leads to galactorrhoea,
amenorrhoea &
low libido
Osteoporosis
QTc prolongation– causing cardiac arrhythmias
Sexual dysfunction
EPSE Acute dystonia
Laryngeal spasm, oculogyric crisis
Akathesia
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
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.
Inducer inhibitors
Anticonvulsants: Carbamazepine, Phenytoin reduces the concentration of oral contraceptives and quetiapine—Inducing CYP3A4.
• Smoking induces olanzapine and clozapine metabolism
SSRI: Fluvoxamine, fluoxetine & Paroxetine inhibit CYP2D6 thereby preventing the metablism of codeine to morphine.
• Fluvoxamine inhibits olanzapine and clozapine metabolism.
Matthew AdetifaNurse Practitioner (Mental Health & AOD)
Latrobe Regional HospitalTraralgon ,Victoria, Australia
https://www.youtube.com/watch?v=-I_Lche2otU
Def.
Epidemiology
Pharmacology
Clinical Manifestations
Course
Screening Assessment
Diagnosis
management
A Chronic, relapsing illness that involves the misuse
of prescribed opioid medications, use of diverted
opioid medications or illicitly obtained opioid.
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
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
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.
Prior history of substance use disorder
Demographic features including age (Peer pressure, adventure
Severe or chronic pain
Co-morbid mental disorders
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
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
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
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
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
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 superviseddosing.
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
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
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) & 24-72 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 )
Thanks You.
Martin, J & Fay, Michael 2001. Cytochrome P450 drug interactions: are they clinically relevant? Australian Prescriber. DOI: 10.18773/austprescr.2001.007
RACGP guidelines on management of pain. Retrieved on 1/5/18 from www.racgp.org.au/your-practice/guidelines/silverbook/common-clinical-conditions/pain-management/#1
Gowing, L, Ali, R, Dunlop, A, Farrell, M & Lintzeris, N, (2014). National Guidelines for Medicated-Assisted Treatment of opioid Dependence. Commonwealth of Australia
Johnson, R. E., Strain, E. C., & Amass, L. (2003). Buprenorphine: how to use it right. Drug and Alcohol Dependence, 70 (Suppl.2). S59-S77.
www.opioiddruginteractions.com