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Signs & Symptoms + Treatment Intoxications and Withdrawal. Babatunde Idowu Ogundipe M.D. M.P.H. September 2 2011. Substance Abuse/Dependence. Lifetime prevalence substance abuse 20%. Approximately 10-16% people seen in outpatient general medicine suffer from problems of addiction.
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Signs & Symptoms + Treatment Intoxications and Withdrawal BabatundeIdowuOgundipe M.D. M.P.H. September 2 2011
Substance Abuse/Dependence • Lifetime prevalence substance abuse 20%. Approximately 10-16% people seen in outpatient general medicine suffer from problems of addiction. • Brain imaging studies of drug-addicted individuals show changes in areas of the brain that are critical to judgment, decision making, learning and memory, and behavior control. Together, these changes can drive an abuser to seek out and take drugs compulsively despite adverse consequences—in other words, to become addicted to drugs. • Comorbid psychiatric disorders common. drugabuse.gov
Substance Abuse/Dependence • Substance abuse: • Maladaptive pattern of usesignificant impairment • Failure to meet obligations(work/personal). • Substance use during hazardous activities (physically dangerous). • Substance-related legal problems. • Continued use despite social(interpersonal) problems. • Substance dependence when tolerance & withdrawal symptoms develop. Tolerance = user requires increasing amounts of the substance in order to become intoxicated. • Substance dependence: Taking larger amounts of the substance than intended, desire to decrease use yet persistent failed efforts to cut down, spending significant amount of time obtaining the substance, & withdrawal from activities.
Substance Abuse/Dependence • Diagnosis: • Important to screen every one for addiction as most patients will divulge that information only when specifically asked. • Best evidence long term drug use obtained by history and toxicology screen which is also beneficial in revealing exactly which drugs are currently being used by patient. This helps to weigh your treatment options. • i.e.approach to Alcoholism: • (1)Inquire current +past alcohol use + about family history alcohol problems. • (2)Obtain information on type, quantity, & frequency alcohol use. Useful to differentiate moderate from heavy drinkers. • (3)Use standard screening questionaire. i.e. CAGE (Ever need to Cut down? Ever felt Annoyed by criticism drinking? Ever felt Guilty about your drinking?Ever had a morning Eye opener? >1 yes + • (4)Ask more specific questions based on steps 1-3.
Substance Abuse/Dependence • Indications for toxicology screen: • (1)History of alcohol or drug use/abuse • (2)Evidence of drug use on physical exam (i.e. septal perforation) • (3)Signs of intoxication or withdrawal • (4)Altered mental status • Quantitative Tests useful in management patients with certain intoxications i.e. acetaminophen, TCA’s, antiepileptic drugs. • Qualitative tests. i.e. Urine immunoassay screens. Inexpensive & rapid, providing results within an hour. They can detect TCA’s, tetrahydrocannabinol, opiates, benzodiazepines, cocaine metabolites, barbiturates, phencyclidine, salicylates, & acetaminophen. • Offer HIV testing; check LFT’s & consider Hepatitis panel. • Treatment: • Drug addiction physical/psychological dependence associated with feelings ambivalence & denial.
Substance Abuse/Dependence • Effective drug treatment motivates users to change behaviors & modes of thinking. • Overall goal is achievement long term abstinence. • Short Term goals: • Decrease drug use. • Improve patients functionality. • Minimize social & medical consequences drug abuse. • Also treatment should make use of: • Drug Rehab programs = highly structured, drug free environment in conjunction with intensive individual & group therapy. • Group therapy (i.e. alcoholics/Narcotics anonymous) preferred means maintaining drug + alcohol abstinence. • Hospitalization may be necessary for acute withdrawal. • Methadone maintenance for opiate dependence.
Your Brain & Drugs-Pathophysiology • Drugs, chemicals that tap into the brain’s communication system, disrupt the way nerve cells normally send, receive, and process information. • 2 methods drugs do this: • (1) By imitating the brain’s natural chemical messengers (neurotransmitters). i.e. fooling the brains’s receptors & activating nerve cells to send abnormal messages. i.e. marijuana, heroin. • (2) By overstimulating the “reward circuit” of the brain. Nerve cells release abnormally large amounts of natural neurotransmitters, or prevent normal recycling these brain chemicals-needed to shut off signal between neurons. Such disruption produces an amplified message that disrupts normal communication patterns. i.e.cocaine, methamphetamine. • Nearly all drugs, directly or indirectly, target the brain’s reward system by flooding the circuit with dopamine.
Your Brain & Drugs-Pathophysiology • Dopamine is a neurotransmitter present in regions of the brain that control movement, emotion, motivation, and feelings of pleasure. • The overstimulation of this system, which normally responds to natural behaviors linked to survival (eating, spending time with loved ones, etc.), produces euphoric effects in response to drugs of abuse. • Such a reaction sets in motion a pattern that “teaches” people to repeat the behavior of abusing drugs. blogs.plos.org
Your Brain & Drugs-Pathophysiology • As one continues to abuse drugs brain adapts to surges in dopamine by producing less dopamine or by reducing number of dopamine receptors in the reward circuit. • Thus dopamine’s impact on the reward circuit is lessened, reducing the abuser’s ability to enjoy the drugs and the things that previously brought pleasure. • Such a decrease compels those addicted to drugs to keep abusing drugs in order to attempt to bring their dopamine function back to normal. • Tolerance occurs now given that they require larger amounts of the drug than they first did to achieve the dopamine high. nida.nih.gov
Sedative-hypnotics • Alcohol, benzodiazepines, barbiturates • Signs/Sxs: CNS depression, respiratory depression, & coma • Withdrawal: anxiety, restlessness, confusion, disorientation, tremulousness, generalized seizure, psychosis, elev BP/HR/Temp. cc.utah.edu
Metabolic Acidosis If patient with combo acidemia (i.e.pH=7.05) & low bicarbonate (i.e.HCO3- = 8) then we have a metabolic acidosis. (1)Classify disorder. Is there an anion gap? Na – (HCO3- +Cl-). Normal is 12 + 4. if >16 then anion gap metabolic acidosis (AGMA). AGMA think “MUDPILES”: Methanol, Uremia(renal failure), Diabetic Ketoacidosis(DKA), Paraldehyde, Isoniazid, Lactic Acidosis, Ethylene glycol, Salicylates (ASA). Also for AGMA is alcohol, iron poisoning, starvation, seizures, sepsis, rhabdomyolysis. For Non-anion gap metabolic acidosis (NAGMA): uretosigmoidostomy, saline, early renal failure, diarrhea, carbonic anhydrase inhibitors, adrenal insuffiency, renal tubular acidosis (RTA), hyperparathyroidism, triamterene, & spironolactone. (2)If with AGMA use winters formula & delta anion gap to determine if any concomitant respiratory or metabolic acid-base disorders in addition to AGMA. Expected PCO2 =1.5 x bicarb +8. If actual PCO2 (ABG) > expected PCO2then there is pre-existing respiratory acidosis. If it is lower than the expected value then there is pre-existing respiratory alkalosis. (3)Delta anion gap. Is there additional metabolic acid-base problem? Delta anion gap = Calculated anion gap –normal anion gap. Delta anion gap + measured bicarb should = 25 (normal serum bicarb). If <25, then there is preexisting NAGMA. If > 25, then there is pre-existing metabolic alkalosis.
Osmolar Gap • If you have an anion gap metabolic acidosis with an unclear etiology, especially if there is a suspicion of toxic exposure it is important to measure an osmolar gap: • Osmolar Gap = Measured serum osmolarity – calculated/estimated serum osmolarity(2[Na]+Glucose/18 +BUN/2.8). • If OsmolarGap >10 there is exogenous source of an osmotically active substance: Ethylene Glycol (produces oxalate crystaluria) & Methanol (causes visual changes & blindness). Other causes osmolar gap: paraldehyde, ethanol, isopropyl alcohol (elevated osmolar gap without metabolic acidosis), mannitol ingestion, hyperlipidemia, hyperproteinemia.
References • Pictures: • nida.nih.gov • blogs.plos.org • drugabuse.gov • cc.utah.edu • Text: • http://drugabuse.gov/Infofacts/understand.html • FIRST AID for the USMLE 3, Tao Le, VikasBhushan, Robert W. Grow, Veronique Tache • Dr Conrad Fischer’s Internal Medicine Board Review 2008-2009 edition • Pocket Handbook of Primary Care Psychiatry. Harold I kaplan, M.D. Benjamin J. Sadock, M.D. • Psychiatry History Taking. Third Edition. A Current Clinical Strategies medical book. Alex Kolevzon, Craig L.Katz.