Recommended
More Related Content
Similar to stimulants including khat.pptx
Similar to stimulants including khat.pptx (20)
Recently uploaded
Recently uploaded (20)
stimulants including khat.pptx
- 1. Stimulants including khat Cocaine , Amphetamine, khat 8/5/2022 Stimulants including khat, SPHMMC Prepared by : Tesfatsion Bisetegn Moderator: Dr. Girma
- 2. Objectives: To know what cocaine , amphetamine and khat are & their constituents To understand the pharmacology and the effect of cocaine , amphetamine and khat. To understand the diagnoses of Stimulant related disorders and management modalities. 8/5/2022 Stimulants including khat, SPHMMC 2
- 3. Outline: Cocaine ,amphetamine, khat Introduction Epidemiology Neuropharmacology Clinical effects Stimulant related disorders Management 8/5/2022 Stimulants including khat, SPHMMC 3
- 4. Famous addicted Doctors and … 8/5/2022 Stimulants including khat, SPHMMC 4
- 5. What is Cocaine? • Bitter, white, odorless, crystalline psychoactive drug. • Extracted and refined from the Coca plant. • A highly addictive stimulant that produces profound feelings of pleasure. 8/5/2022 Stimulants including khat, SPHMMC 6
- 6. 8/5/2022 Stimulants including khat, SPHMMC Brief Background 7
- 7. 8/5/2022 Stimulants including khat, SPHMMC Epidemiology Higher in age 18-27 Prevalence ~=2% Cocaine use disorder 0.6% The prevalence of lifetime substance use=35%( 7.2% cocaine) (Ataye TVET college, Ethiopia) 8
- 8. How is Cocaine Used? Onset Duration Snorted 1 minute 20-40 minutes Injected 1-5 seconds 15-20 minutes Smoked Immediate 5-15 minutes 8/5/2022 Stimulants including khat, SPHMMC 9
- 9. Forms ? Coca leaf <2%cocaine Cocaine HCL-powder Freebase paste Crack-rock cocaine 8/5/2022 Stimulants including khat, SPHMMC 10
- 10. 8/5/2022 Stimulants including khat, SPHMMC Neuropharmacology 11
- 11. Neuropharmacology 8/5/2022 Stimulants including khat, SPHMMC 12
- 12. Effects of the drug Euphoria Violent Behavior.. Increased self-esteem Dilated pupils Loss of inhibitions Increased libido sweating and increased body temperature ↑ blood pressure Tachycardia or bradycardia Nausea Loss of appetite Dry mouth Nasal damage Lung damage 8/5/2022 Stimulants including khat, SPHMMC 13
- 13. At higher dose • Increased Alertness • Decreased Fatigue • Insomnia • Increased Irritability • Hallucinations • Confused Behavior • Increased Fear • Extreme Paranoia • Severe Anxiety Attacks 8/5/2022 Stimulants including khat, SPHMMC 14
- 14. Withdrawal sxs • Severe Irritability • Chronic Depression • Paranoia • Insomnia /excessive sleep • Loss of Sex Drive • Eating Disorders • Diarrhea • Heart Attack 8/5/2022 Stimulants including khat, SPHMMC 15
- 15. Amphetamine is one of the commonly used synthetic CNS stimulant drug that possesses conditioning and addictive property due to it psych stimulating and performance enhancing effect. used to treat ADHD and narcolepsy. 8/5/2022 Stimulants including khat, SPHMMC 16
- 16. Back ground 8/5/2022 Stimulants including khat, SPHMMC 17
- 17. Epidemiology ~=0.75% in general US Life time use 5.4% AUD 0.3% of the population! 8/5/2022 Stimulants including khat, SPHMMC 18
- 18. Typical users students studying for exam. long-distance truck drivers on trips business people with pressing deadlines Athletes in competition soldiers during wartime 8/5/2022 Stimulants including khat, SPHMMC Typical use • To increase performance • To induce a euphoric feeling 19
- 19. Preparations Preparation: IV, inhale(snort), oral Pharmacokinetics : Orally taken have rapid onset of action (within 1hr) , IV–immediate effect. Duration -4 to 12 hours 8/5/2022 Stimulants including khat, SPHMMC 20
- 20. Neuropharmacology Is (CNS) stimulant by increasing the amounts of dopamine(commonly), norepinephrine, and serotonin (to a lesser extent) in the synaptic cleft through a variety of mechanisms. Inhibition of vesicular monoamine transporter 2 (VMAT2) Inhibition of monoamine oxidase (MAO) Transporter reversal of DAT 8/5/2022 Stimulants including khat, SPHMMC 21
- 21. Clinical effects of the amphetamine Increased BP Increased/ Decreased HR Myadrisasis Sweating Nuasea Loss of appetite Tremor At high dose and chronic use Hypertansion Arrythmia Cardiomyopathy Respiratory stimulation vomiting Anorexia Malnutrion Dykenesia 8/5/2022 Stimulants including khat, SPHMMC 22
- 22. Khat 8/5/2022 Stimulants including khat, SPHMMC 23
- 23. Khat is a leafy green plant indigenous to Eastern Africa and Southern Arabia. The leaves and buds are chewed and held between the cheek and gums after chewing. Khat contains two main stimulant drugs called cathinone and cathine. Their main effects are similar to, but less potent than, amphetamine . 8/5/2022 Stimulants including khat, SPHMMC 24
- 24. Epidemiology =~10 million people around the world chew Khat. Leadin in East Africa ,Saudi arabia prevalence of khat chewing among the hosanna Ethiopia residents reaches 58.0%.(Riyaz Rather et al, 2021) Higher school students Saudi Arabia( 18.85%) >Ethiopia(13.59% )( least in Amhara region , highest in Oromia region) > Yemen(13.04% ).(Getinet Ayano et al, 2019) among medical students in Gonder 21.5%(Tsegaye A et al, 2021) 8/5/2022 Stimulants including khat, SPHMMC 25
- 25. why do they use? social and a culture-based activity. Enhance social interaction Improve performance Minor ailments such as headaches, colds, body pains, fevers, arthritis and also depression. 8/5/2022 Stimulants including khat, SPHMMC 26
- 26. How can it be used? The fresh khat leaves and buds Substituted cathinone -Bath salts 8/5/2022 Stimulants including khat, SPHMMC 27
- 27. Why fresh is needed? It has to be used immediately as it is cultivated . As it loses its freshness: desired effect reduces as cathinone converted to cathine. Freshness kept : by moistening khat with water and wrapping with banana leaves during transportation. 8/5/2022 Stimulants including khat, SPHMMC 28
- 28. Why they held it in the check a long time ? 60% absorption takes place in the buccal mucosa 8/5/2022 Stimulants including khat, SPHMMC 29
- 29. Neuropharmacology Cathinone metabolised to cathine and norephedrine. analogous to the effects of amphetamine. differences in dosage and the mode of consumption. 7–10 times more potent than cathine The effect of cathinone is maximum after 15–30 minutes. serum half life =5 +/- 0.8 hours cathine slower onset of action, serum half-life =5.2 +/– 3.4 hrs unwanted side effects 8/5/2022 Stimulants including khat, SPHMMC 30
- 30. Neuropharmacology cathinone increases synaptic catecholamine levels by inhibiting the dopamine, serotonin, and norepinephrine reuptake transporters in a fashion similar to cocaine. Most also facilitate catecholamine release, similar to amphetamine 8/5/2022 Stimulants including khat, SPHMMC 31
- 31. Clinical effects of khat Acute effects Increased alertness insomnia Increased talkativeness irritability and agitation Increased HR blood pressure hypertension Euphoria psychotic reactions Pupil dilation Depression , sleepiness and lethargy on the next morning 8/5/2022 Stimulants including khat, SPHMMC 32
- 32. Long term effects Malnutrion Psychotic reactions manic and delusional behaviors Depressive reactions Iritative disorders of GI gastritis ,enteritis Cardiovascular disorders Hemorrhoids Sexual dysfunction Periodontal disease, mucosal pigmentation and lesion, teeth discoloration and loss 8/5/2022 Stimulants including khat, SPHMMC 33
- 33. Stimulant related disorders The essential feature of a stimulant related disorder is a cluster of Cognitive, Behavioral, and Physiological symptoms 8/5/2022 Stimulants including khat, SPHMMC 34
- 34. Stimulant-Related Disorders Stimulant Use Disorder Stimulant Intoxication Stimulant Withdrawal Stimulant Intoxication induced delirium Stimulant-Induced Mental Disorders 8/5/2022 Stimulants including khat, SPHMMC 35
- 35. Stimulant use disorder (criteria DSM-TR-5) A. => 2 of the following manifestations within a 12-month period (11 points) Impaired control Social impairment Risky use Pharmacological criteria 8/5/2022 Stimulants including khat, SPHMMC 36
- 36. Impaired control over substance … 1. Take the substance in larger amounts or over a longer period than was originally intended 2. Express a persistent desire to cut down - unsuccessful efforts 3.Spend a great deal of time obtaining the substance, using the substance, or recovering from its effects 4.Craving is manifested by an intense desire or urge for the drug 8/5/2022 Stimulants including khat, SPHMMC 37
- 37. …Social impairment 5. Failure to fulfill major role obligations at work, school, or home 6. Continue substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance. 7. Important social, occupational, or recreational activities may be given up or reduced because of substance use. 8/5/2022 Stimulants including khat, SPHMMC 38
- 38. …Risky use of the substance 8.Recurrent substance use in situations in which it is physically hazardous. 9. continue substance use despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance 8/5/2022 Stimulants including khat, SPHMMC 39
- 39. …Pharmacological criteria 10. Tolerance is signaled by requiring a markedly increased dose of the substance to achieve the desired effect or a markedly reduced effect when the usual dose is consumed. 11. Withdrawal – syndrome manifested as The characteristic withdrawal syndrome for the stimulant (refer to Criteria A and B of the criteria set for stimulant withdrawal) or taking other substance to relieve from the withdrawal symptoms. 8/5/2022 Stimulants including khat, SPHMMC 40
- 40. Specify if: In early remission In sustained remission In controlled environment 8/5/2022 Stimulants including khat, SPHMMC Severity: • Mild : 2-3 sxs • Moderate: 4-5 sxs • Sever : =>6 sxs 41
- 41. Prevalence: High prevalence in youth(18-25 year old) Stimulant use disorder ;)- amphetamine-type substances: 0.3% (US) cocaine: 0.6%(US) 8/5/2022 Stimulants including khat, SPHMMC 42
- 42. Risk factors Temperamental :other substance use disorders, mental disorders, being male. Environmental : Early childhood violence, Intimate partner violence, Associating with dealers and users , Economic instability, Criminal behaviors Cultural: Genetic: 8/5/2022 Stimulants including khat, SPHMMC 43
- 43. Ddx Stimulant intoxication Stimulant withdrawal Stimulant-induced mental disorders Independent mental disorders 8/5/2022 Stimulants including khat, SPHMMC 44
- 44. Stimulant Intoxication Common changes in intoxication Disturbances of perception Wakefulness Attention Thinking Judgment Psychomotor behavior Interpersonal behavior 8/5/2022 Stimulants including khat, SPHMMC 45
- 45. Stimulant Intoxication A. recent use B. significant problematic behavioral or psychological changes that developed during, or shortly after, use of a stimulant. Euphoria or affective blunting Changes in sociability Hypervigilance interpersonal sensitivity Anxiety Tension, or anger Stereotyped behaviors impaired judgment 8/5/2022 Stimulants including khat, SPHMMC 46
- 46. C. => 2 of the following sns/sxs, developing during, or shortly after, stimulant use. 1.Tachycardia or bradycardia. 2. Pupillary dilation. 3. Elevated or lowered blood pressure. 4. Perspiration or chills. 5. Nausea or vomiting. 6. Evidence of weight loss. 7. Psychomotor agitation or retardation. 8. Muscular weakness, respiratory depression, chest pain, or cardiac arrhythmias. 9. Confusion, seizures, dyskinesias, dystonias, or coma D. Not explained by other medical condition or mental disorder including intoxication with an other substance. 8/5/2022 Stimulants including khat, SPHMMC 47
- 47. Specify if perceptual disturbance: hallucinations(auditory, visual, tactile), illusion in the absence of delirium. Specify The specific stimulant 8/5/2022 Stimulants including khat, SPHMMC 48
- 48. Ddx Stimulant-induced mental disorders Independent mental disorders 8/5/2022 Stimulants including khat, SPHMMC 49
- 49. Stimulant Withdrawal A. Cessation of (or reduction in) prolonged stimulant use. B. Dysphoric mood and =>2 of the following physiological changes within a few hours to several days after Criterion A. 1. Fatigue. 2. Vivid, unpleasant dreams. 3. Insomnia or hypersomnia. 4. Increased appetite. 5. Psychomotor retardation or agitation. C. sns/sxs in Criterion B cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. D. Not explained by other medical condition or mental disorder including intoxication or withdrawal from another substance 8/5/2022 Stimulants including khat, SPHMMC 50
- 50. Ddx Stimulant-induced mental disorders Stimulant withdrawal is distinguished from stimulant-induced mental disorders (e.g., stimulant-induced depressive disorder, with onset during withdrawal) because the symptoms (e.g., depressed mood) in these latter disorders are in excess of those usually associated with stimulant withdrawal, predominate in the clinical presentation. 8/5/2022 Stimulants including khat, SPHMMC 51
- 51. Stimulant Intoxication induced delirium Delirium (DSM-5-TR criteria) A. Disturbance in attention (i.e., reduced ability to direct, focus, sustain, and shift attention) accompanied by reduced awareness of the environment. B. Disturbance develops over a short period of time (usually hours to a few days), represents a change from baseline attention and awareness, and tends to fluctuate in severity during the course of a day. C. Disturbance in cognition (e.g., memory deficit, disorientation, language, visuospatial ability, or perception). D. Criteria A and C are not better explained by another preexisting, established, or evolving neurocognitive disorder and do not occur in the context of a severely reduced level of arousal, such as coma. E. There is evidence that the disturbance is a direct physiological consequence of another medical condition, substance intoxication or withdrawal (i.e., due to a drug of abuse or to a medication), or exposure to a toxin, or is due to multiple etiologies. 8/5/2022 Stimulants including khat, SPHMMC 52
- 52. Stimulant induced mental disorder Stimulant-Induced -Psychotic Disorder -Mood Disorder -Anxiety Disorder -Obsessive-Compulsive Disorder -Sexual Dysfunction -Sleep Disorder 8/5/2022 Stimulants including khat, SPHMMC 53
- 53. TREATMENT AND REHABILITATION Detoxification and Early Treatment Psychosocial Therapies Pharmacologic Adjuncts 8/5/2022 Stimulants including khat, SPHMMC 54
- 54. Detoxification and Early Treatment Stabilization Supportive therapy Specific measures 8/5/2022 Stimulants including khat, SPHMMC 55
- 55. Psychosocial Therapies In individual therapy MET CBT Group therapy Family therapy Network Therapy 8/5/2022 Stimulants including khat, SPHMMC 56
- 56. Pharmacologic Adjuncts no pharmacologic treatments produce decreases in stimulant use. However, investigators have explored several agents, and those are summarized below Amphetamine :)- Opioid receptor antagonist, naltrexone and the dopamine antidepressant, bupropion have both shown promise in those with less severe amphetamine use disorders, 8/5/2022 Stimulants including khat, SPHMMC 57
- 57. Cocaine: Disulfiram has demonstrated potential benefits in the pharmacotherapy of cocaine use disorder Tricyclic antidepressant drugs yielded some positive results when used early in treatment with minimally drug-dependent patients; 8/5/2022 Stimulants including khat, SPHMMC 58
- 58. References: KAPLAN & SADOCK’S SYNOPSIS OF PSYCHIATRY 20th edition DSM-5-TR Uptodate Lecturio article, stimulant disorders, 2022 Prevalence of Khat ( Catha edulis) Chewing and Its Determinants: A Respondent-Driven Survey from Hossana, Ethiopia(Riyaz A Rather et al 2021) Prevalence, withdrawal symptoms and associated factors of khat chewing among students at Jimma University in Ethiopia(Tilahun A et al, 2017) Epidemiology of khat (Catha edulis) consumption among university students:(Getinet A et al, 2019) Khat Chewing Practice and Associated Factors among Medical Students in Gondar Town, Ethiopia, 2019(Tsegaye A et al, 2021) 8/5/2022 Stimulants including khat, SPHMMC 59
- 59. 8/5/2022 Stimulants including khat, SPHMMC 60
Editor's Notes
- When to use pharmacological intervention in ?
- Throughout his professional life, he was addicted to cocaine and later also to morphine,[4][5] which were not illegal during his time. As revealed by Osler's diary, Halsted developed a high level of drug tolerance for morphine. He was "never able to reduce the amount to less than three grains daily" (approximately 200 mg).[6] Halsted's addictions resulted from experiments on the use of cocaine as an anesthetic agent that he performed on himself
- Erythroxylum coca Used in its raw form for more than 1500 years indigenous to South America, where the leaves of the shrub are chewed by local inhabitants to obtain the stimulating effects among mostly abused psychostimulant substance
- Regular local anesthetics for eye surgery Was added in coca cola beverage 1976 –freebase developed 1980-crack popularized
- Methods Cocaine can be snorted, injected, smoked or eaten. The level and length of the effects depend on how the drug was induced.
- Cocaine hydrochloride salt: 80% less potent Water-soluble formulation Can be ingested orally, intranasally, or intravenously Freebase cocaine – potent –free of the drug’s hydrochloride additive.converted to cocaine sulphate. Extremely potent Heat-stable formulation that can be smoked Very rapid onset of action Extremely addictive Crack rock- produced by dissolving powdered cocaine in a mixture of water and sodium bicarbonate (baking soda) and boiled till it becomes solid -slid pieces -lethal
- Most brain dopamine produced where? What aout ne and sero action? 1/MC) Projetcs VTA to pfc Regulates cognition ,emotions, affect and functioning. Associated with –sxs and depressive sxs of schizophrenia 2/ML Projects VTA to Nucleus accumbens in the limbic system Regulates rewards ,pleasure ,reinforcement, learning and conditioning and addiction systems. Substances enhance the reward system , Associated with +sxs of schizophrenia …. 3/NG Substantia nigra to stratium Regulate movement 4/tuberiinfundibular Hyphothalamus to pitotary Reguale prolactin prodaction As it is sympathomimtic nuerotransmittor….can act in adrenergic receptor (a and b)….so other effects (not related to z topic)Can also be converted to norepinephrine by catalase reaction by enzyme dopamine-beta hydrooxalase Cocaine targets the dopamine (DAT), norepinephrine (NET) and serotonin (SERT) transporters blocking reuptake thereby increasing neurotransmitter levels within mesocorticolimbic circuits. These circuits include dopaminergic cells in the ventral tegmental area (VTA) that project to the nucleus accumbens (NAc) and prefrontal/orbitofrontal cortex (PFC). Both the VTA and NAc receive glutamaterigc inputs from the PFC. Neurons from the noradrenergic cell body region, locus coeruleus (LC), also project to the PFC and VTA significantly influencing cellular activity. The reinforcing effects of cocaine are generally attributed to increases in dopamine (DA) within limbic circuits. However, recent evidence indicates norepinephrine (NE) also plays an important role in the reinforcing effects of stimulants providing another possible therapeutic targe
- binding in dopamine-rich brain regions, including the caudate-putamen and the VTA. Moderate levels of cocaine binding also occur in the substantia nigra, amygdala, hypothalamus, and locus coeruleus. In humans, cocaine rapidly permeates the striatum, then quickly redistributes out of it with a half-life of about 20 minutes. The time course of self-reported “high” closely follows this pattern of rapid uptake and clearance. Drug-related reinforcement is most strongly related to the dopaminergic projections from the VTA to the nucleus accumbens. Cocaine administration causes transient increases in extracellular dopamine levels in these regions by binding to the presynaptic dopamine transporter (DAT), thereby inhibiting dopamine reuptake
- cocaine causes a hypermetabolic state with increased heat production. However, because cocaine-induced hyperthermia occurs primarily in hot weather, it is hypothesized that cocaine also impairs thermoregulatory adjustments that mediate heat dissipation. Cns effects Cardiac Gi Generale
- Aggressiveness, psychosis.
- Cocaine is one of the most addictive drugs known to man. Those who use cocaine heavily or regularly find it extremely difficult to stop and often suffer through serious withdrawal symptoms such as:
- It is a cns stimulant but used for ADHD! Amphetamines-like substances called in different names Dextroamphetamine(ice) Methamphetamine(crystal) mixed dextroamphetamine-amphetamine salt(crystal meth) amphetamine-like compound methylphenidate(speed) Types of amphetamines Classical amphetamines : Dextroamphetamine , methylphenidate , and methamphetamine Detected in routine urine drug screening (false positive results may occur with the use of pseudoephedrine, bupropion , or beta-blockers ) Nonclassical amphetamines : chemically categorized as amphetamines , but clinically considered to be hallucinogens Substituted amphetamines or “designer” drugs: Includes MDMA (“ecstasy ” or “party drug”) Not detected by urine drug screening Bath salts: Synthetic cathinones (large family of amphetamine analogs) Mechanism of action is similar to that of amphetamines . Prolonged duration of effect (days to weeks) Not detected in urine drug screening
- Amphetamine is one of the commonly used stimulants. Sinthesized from Chinese ephedra plant 1887- 1st synthesized 1930- for congestion, narcolepsy, post encephalitic parkinsonism, depression, 1914 -Used in WW II to fight fatigue and enhance performance and lethargy. 1970s-US FDA–approved indications for amphetamine Narcolepsy Obesity Depression and dysthymia Chronic fatigue syndrome Acquired immunodeficiency syndrome (AIDS) Cancer-related fatigue End-of-life care (depressive symptoms) Dementia Multiple sclerosis Fibromyalgia
- Drug Alcohol Depend . 2021 Oct 1;227:108921. doi: 10.1016/j.drugalcdep.2021.108921. Epub 2021 Jul 28. Methamphetamine use among American Indians and Alaska Natives in the United States Lara N Coughlin 1, Lewei Allison Lin 2, Mary Jannausch 2, Mark A Ilgen 2, Erin E Bonar 3
- Although not as addictive as cocaine, amphetamines are nonetheless addictive drugs. Other amphetamine-like substances are ephedrine, pseudoephedrine, and phenylpropanolamine (PPA)
- Classic and designer amphetamines are less addictive than cocaine. Amphetamine is a central nervous (CNS) system stimulant that functions by increasing the amounts of dopamine, norepinephrine, and serotonin (to a lesser extent) in the synaptic cleft through a variety of mechanisms. Amphetamine enters the presynaptic axon terminal through diffusion or uptake by the monoamine transporters DAT, NET, and SERT. Once inside the presynaptic terminal, amphetamine increases the amounts of monoamine neurotransmitters in the cytosol through the inhibition of vesicular monoamine transporter 2 (VMAT2) as well as through disruption of the electrochemical gradients necessary for vesicular transporter function. Amphetamine also inhibits the metabolism of monoamine neurotransmitters by inhibiting monoamine oxidase (MAO). At the same time, amphetamine stimulates the intracellular receptor TAAR1, which induces internalization or transporter reversal of DAT. The effects of TAAR1 on DAT may also extend to NET and SERT, although co-localization of TAAR1 with these two transporters has only been indirectly evidenced in studies thus far. The net result of this activity is increased efflux of dopamine into the synaptic cleft and reuptake inhibition in the synaptic cleft through DAT internalization and direct competition
- Amphetamine is a central nervous (CNS) system stimulant that functions by increasing the amounts of dopamine, norepinephrine, and serotonin (to a lesser extent) in the synaptic cleft through a variety of mechanisms. In addition to dopamine …..norepinephrine…. Norepinephrine is z 1 neurotransmitter used by z sypmathethic nurve system….in cns is linked to aruasal, alertness and attenction. Anlike epinephrine nor epinephrine more act on alpha receptors/vasoconstriction/inc BP. But may be converted to epi and act equally at a and b…(noreepi act on a1=vasocon. b1 =heart-tachy+arythmia.---inc.bp….due to inc.systolic and diastolic blood pressure they will be bradycardia(by Musca(m2).is nonselective a and b1 agonist! By different proposed mechanisms it acts on the affect aruasal ,cognition and attention of the brain
- Why khat on cheeks? More than 40 alkaloids, terpenoids, flavonoids, sterols, glycosides, tannins, amino acids, vitamins and minerals. The khat phenylalkylamines comprise cathinone, cathine and norephedrine Cathinone is more potent than cathine Cathine converted to Cathinone will metabolized to norephedrine
- Subst Abuse Rehabil . 2021 Aug 15;12:41-48. doi: 10.2147/SAR.S324711. eCollection 2021. Prevalence of Khat ( Catha edulis) Chewing and Its Determinants: A Respondent-Driven Survey from Hossana, Ethiopia Riyaz Ahmad Rather 1, Solomon Berhanu 1, Lemma Abaynah 1, Mohammed Sultan 2 BMC Psychiatry . 2017 Apr 17;17(1):142. doi: 10.1186/s12888-017-1284-4. Prevalence, withdrawal symptoms and associated factors of khat chewing among students at Jimma University in Ethiopia Tilahun Abdeta 1, Daniel Tolessa 2, Kristina Adorjan 3 4 5, Mubarek Abera Meta-Analysis BMC Public Health . 2019 Feb 4;19(1):150. doi: 10.1186/s12889-019-6495-9. Epidemiology of khat (Catha edulis) consumption among university students: a meta-analysis Getinet Ayano 1, Kalkidan Yohannis 2, Mebratu Abraha 3 Affiliations collapse Affiliations 1Research and Training Department, Amanuel Mental Specialized Hospital, POBOX: 1971, Addis Ababa, Ethiopia. babiget2015@gmail.com. 2Department of Psychiatry, Dilla University, Dilla, Ethiopia. 3Department of Psychiatry, Paulo's millennium medical college, Addis Ababa, Ethiopia Review PLoS One . 2018 Apr 12;13(4):e0195718. doi: 10.1371/journal.pone.0195718. eCollection 2018. Prevalence and predictors of khat chewing among Ethiopian university students: A systematic review and meta-analysis Alemu Gebrie 1, Animut Alebel 2, Abriham Zegeye 1, Bekele Tesfaye 2 Subst Abuse . 2021 Mar 2;15:1178221821999079. doi: 10.1177/1178221821999079. eCollection 2021. Khat Chewing Practice and Associated Factors among Medical Students in Gondar Town, Ethiopia, 2019 Tsegaye Adane 1, Walelegn Worku 1, Jember Azanaw 1, Lamrot Yohannes 1
- Bath salts(synthethic cathinone)-very strong white powder eople typically swallow, snort, smoke, or inject synthetic cathinones.
- Cathonine acts by increasing the realease of DAS and inhibition of norepi and sero. Cathonine is unstable
- Schizophreniform psychosis paranoid delusions auditory hallucinations (frequently of a persecutory or threatening type) Consumption is ceased, resolution occurs 3–11 days but there is a tendency for the psychosis to recur if chewing is restarted. Manic psychosis grandiose delusions with flight of ideas and tangential thought processes, and a labile mood varying from euphoria to anger. subsides spontaneously within about 8 hours of chewing 3. Depression Arises on cessation of use. This has, on occasions, been associated with self-harm and suicide. Self-harm, suicide and violence Rare,documented during both chewing and the subsequent intoxication phase.
- StUD is one the 10 class of drug disorder , as any SUD, indicating that the individual continues using the substance despite significant substance-related problems.
- type of psychoactive substance that increases activity in the brain and can temporarily elevate alertness, mood, and awareness.
- They generally follow the template for all substance use disorders
- ………………………………. Stimulant withdrawal syndromes ……………………………………………………. A. Cessation of (or reduction in) prolonged amphetamine-type substance, cocaine, or other stimulant use. B. Dysphoric mood and two (or more) of the following physiological changes, developing within a few hours to several days after Criterion A: 1. Fatigue. 2. Vivid, unpleasant dreams. 3. Insomnia or hypersomnia. 4. Increased appetite. 5. Psychomotor retardation or agitation
- In early remission: After full criteria for stimulant use disorder were previously met, none of the criteria for stimulant use disorder have been met for at least 3 months but for less than 12 months (with the exception that Criterion A4, In sustained remission: After full criteria for stimulant use disorder were previously met, none of the criteria for stimulant use disorder have been met at any time during a period of 12 months or longer (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the stimulant,” may be met). In a controlled environment: This additional specifier is used if the individual is in an environment where access to stimulants is restricted in early remission in a controlled environment or in sustained remission in a controlled environment). Examples of these environments are closely supervised and substance-free jails, therapeutic communities, and locked hospital units.
- to control weight to improve performance in school, work, or athletics. For the treatment of attention-deficit/hyperactivity
- While stimulant intoxication occurs in individuals with stimulant use disorders, intoxication is not a criterion for stimulant use disorder, which is confirmed by the presence of 2 of the 11 diagnostic criteria for use disorder
- While stimulant intoxication occurs in individuals with stimulant use disorders, intoxication is not a criterion for stimulant use disorder, which is confirmed by the presence of 2 of the 11 diagnostic criteria for use disorder
- What is it? Specify ….the specific stimulant! Bradycardia is often present and is a reliable measure of stimulant withdrawal. Anhedonia and drug craving can often be present but are not part of the diagnostic criteria
- Delirium associated with stimulant use generally results from high doses of a stimulant or sustained use, and so sleep deprivation affects the clinical presentation There is evidence either from history or physical or investigation findings
- The hallmark of SIPD is the presence of paranoid delusions and hallucinations(in 50%). Auditory hallucinations> visual and tactile. Rx for amphetamine-induced psychotic disorder is the short-term use of an antipsychotic medication such as haloperidol 2. SIMD includes the diagnoses of stimulant induced bipolar disorder and stimulant-induced depressive disorder, either of which can begin during either intoxication or withdrawal. In general, intoxication is associated with manic or mixed mood features, whereas withdrawal is associated with depressive mood features. 3. SIAD can occur during intoxication or withdrawal. Stimulants can induce symptoms similar to those seen in panic disorder and phobic disorders, in particular 4. SIOCD can occur during intoxication or withdrawal. After high doses of stimulants, some individuals develop time-limited stereotyped behaviors or rituals (i.e., picking at clothing, and arranging and rearranging items purposelessly) that share with OCD 5. People sometimes use amphetamines as an antidote to the sexual side effects of serotonergic agents such as fluoxetine, but stimulants are often misused by persons to enhance sexual experiences. High doses and long-term use are associated with erectile disorder and other sexual dysfunctions. 6. Stimulant-induced sleep disorder can begin during either intoxication or withdrawal, and sleep dysfunction can vary depending on the onset. Stimulant intoxication -insomnia and sleep deprivation, stimulant withdrawal -hypersomnolence and nightmares
- Cocaine and other substance abuse disorders are complex, involving biological systems as well as myriad social, familial, and environmental factors. Therefore, treatment of cocaine and stimulant abuse can be complex. As with any disorder, treatment strategies need to assess the biological, social, emotional, and pharmacological aspects of the individual's drug abuse. Behavioral therapies are often the only available effective treatment for many drug use problems, including cocaine use. Cognitive-behavioral treatment is a focused approach to helping cocaine abusers cut down or abstain, and remain abstinent, from abusing cocaine and other substances. The underlying assumption is that learning processes play an important role in the development and continuation of substance abuse. The same learning processes can be employed to help individuals reduce drug use and successfully cope with relapse. Cognitive-behavioral therapy aims to help patients recognize the situations in which they are most likely to use cocaine, avoid the situations when appropriate, and cope more effectively with a range of problems associated with drug abuse. CBT is also compatible with a range of other treatments, including pharmacotherapy. Another approach to treatment is harm reduction, whereby psychotherapeutic strategies are aimed at reducing the negative consequences associated with substance abuse without requiring the individual to commit to abstinence. Such an approach may eventually lead users to abstinence, and data shows that it often does, but its primary goal is to improve users' quality of life whether or not they are immediately willing to aim for abstinence Pharmacological Approaches There are no medications currently available to treat cocaine abuse specifically. Consequently, the National Institute on Drug Abuse (NIDA) is aggressively pursuing the identification and testing of new cocaine treatment medications. Several emerging compounds are being investigated to assess their safety and efficacy. Two medicines currently marketed for other conditions, topiramate and modafinil, have shown promise. Additionally, baclofen, a GABA-B agonist, has shown promise in a subgroup of cocaine addicts with heavy use patterns. Antidepressant drugs are of some benefit with regard to mood changes experienced during the early stages of cocaine abuse. Medical treatments are also being developed to deal with acute emergencies resulting from excessive cocaine abuse. Medications are sometimes used in combination with behavioral therapy. Disulfiram (a medication that has been used to treat alcohol abuse) in combination with behavioral treatment, has been successful in reducing cocaine abus Amphetamine The most effective treatments for amphetamine addiction are cognitive-behavioral intervention and contingency-management models. The Matrix Model, for example, is a comprehensive behavioral treatment approach that combines behavioral therapy, family education, individual counseling, 12-step support, drug testing, and encouragement for non-drug-related activities; it has been shown to be effective in reducing amphetamine abuse. Contingency management interventions, which provide tangible incentives in exchange for engaging in treatment and maintaining abstinence, have also been shown to be effective. There are no specific medications that counteract the effects of amphetamines or that prolong abstinence from and reduce the abuse of amphetamines. However, there are a number of medications that are FDA-approved for other illnesses that might also be useful in treating amphetamine addiction. Recent findings indicate that bupropion, the anti-depressant marketed as Wellbutrin, may reduce a methamphetamine-induced high as well as drug cravings elicited by drug-related cues. This medication and others are currently in clinical trials, while new compounds are being developed and studied in preclinical models.
- reassurance; keep in safe and quiet environment. • Short-term use of sedatives to alleviate symptoms of anxiety and insomnia –benzodiazepines Stablization Iv line, cardiac monitoring ,O2 ,Measure core tempreture ,Head ct scan ,Evalue blood glucose, BUN, electrolye , ,Cbc ,urinalysis , coagulation profile Supportive measure Airway management ,Rapid rehaydreation ,Gastric decontamination if ingested , Assess psychological and neurological status Specific measures Agitation, anxiety ,hyperactivity , usualy controlled by enzadiazepines, diazepam is choice of drug Hyperthermia-should e talked with hypothermic blankets ,ice baths, dantrolene sodium infusion Tachycardia-amiodarone can be used Amphetamine indued chorea=diazepam and chloropromazine //// physiologic effects are not severe enough to require inpatient or residential drug withdrawal Most stimulant users do not come to treatment voluntarily. Their experience with the substance is too positive, and the adverse effects are perceived as duration is short as too minimal to warrant seeking treatment . …………. Supportive rx
- In individual therapy - therapists should focus on the dynamics leading to stimulant use, the perceived positive effects of the stimulant, and other ways to achieve these effects. Group therapy - often focus on discussions with other persons who use stimulants and on sharing experiences and effective coping methods. Family therapy- the way the patient’s past behavior has harmed the family and the responses of family members to these behaviors, on the future and on changes in the family’s activities that may help the patient stay off the drug and direct energies in different directions. All this is for outpatient! Network Therapy. a specialized type of combined individual and group therapy designed to ensure greater success in the office based treatment of addicted patients. Network therapy uses both psychodynamic and cognitive-behavioral approaches to individual therapy while engaging the patient in a group support network. The group, composed of the patient’s family and peers, is used as a therapeutic network joining the patient and therapist at intervals in therapy sessions. The approach promotes group cohesiveness as a vehicle for engaging patients in this treatment ///The patient, peers, family and the therapists are part of the group./// Psychological intervention usually involves individual, group, and family modalities. Individual therapy Motivational enhancement therapy (always) o Cognitive behavioral therapy o Interpersonal therapy (when indicated)
- Disulfiram Disulfiram (Antabuse®) is indicated for the treatment of alcohol use disorder however several randomized clinical trials have shown disulfiram decreases cocaine use [39]. Disulfiram and its metabolite diethyldithiocarbamate bind copper. Decreased copper levels inactivates copper-dependent enzymes such as dopamine-β hydroxylase (DβH) (Table 2), which converts DA to NE. DβH Inhibition increases DA and decreases the synthesis of NE [40]. Disulfiram also inhibits carboxylesterase and cholinesterase enzymes that metabolize cocaine thereby increasing plasma levels of cocaine [41]. Inhibition of DβH by disulfiram and subsequent decrease in central NE levels is likely responsible for its ability to decrease cocaine use [39]. Interestingly, a large clinical trial suggested that low doses of disulfiram (62.5mg and 124mg/day) increased whereas a higher dose decreased (250mg) cocaine use over time