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43 Cards in this Set
- Front
- Back
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30. Wernicke’s encephalopathy?
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a. Caused by thiamine deficiency resulting form poor nutrition.
b. Acute and can be reversed by thiamine therapy. c. Features: Ataxia (broad-based), confusion, ocular abnormalities (nystagmus, gaze palsies). |
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31. If left untreated, Wernicke’s encephalopathy may progress to?
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a. Korsakoff syndrome.
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32. Korsakoff syndrome?
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a. Chronic amnestic syndrome
b. Reversible in only ~20% of pts. c. Features: 1. Impaired recent memory 2. Anterograde amnesia 3. Compensatory confabulation (unconsciously making up answers when memory has failed). |
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33. When should all pts w/altered mental status be given thiamine w/respect to giving glucose?!?
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a. BEFORE giving glucose!!! Otherwise, Wernicke-Korsakoff syndrome may be precipitated.
b. Thiamine is a coenzyme used for carbohydrate metabolism. |
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34. MOA of Cocaine?
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a. Cocaine blocks dopamine reuptake from the synaptic cleft, causing stimulant effect.
b. Dopamine plays a role in behavioural reinforcement (“reward” system of the brain). |
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35. General effects of Cocaine intoxication?
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a. Euphoria
b. Heightened self-esteem c. ↑ or ↓ Blood pressure d. Tachycardia or bradycardia e. Nausea f. Dilated pupils g. Weight loss h. Psychomotor agitation or depression i. Chills j. Sweating |
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36. Dangerous effects of Cocaine intoxication?
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a. Respiratory depression
b. Seizures c. Arrhythmias d. Paranoia e. Hallucinations (especially tactile). f. Since cocaine is an indirect sympathomimetic, intoxication mimics the fight or flight response. |
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37. Deadly effects of Cocaine?
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a. Cocaine’s vasoconstrictive effect may result in MI or stroke.
b. Cocaine overdose can cause death secondary to cardiac arrhythmia, MI, seizure, or respiratory depression. |
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38. Management of Cocaine intoxication?
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a. For mild-to-moderate agitation and anxiety: reassurance of the pt and BZDs.
b. For severe agitation or psychosis: antipsychotic (haloperidol) c. Symptomatic support (ie, control HTN, arrhythmias). d. Temp of >102 F is a medical emergency and should be treated aggressively. |
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39. Tx of cocaine dependence?
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a. There is no FDA-approved Rx for cocaine dependence.
b. Off-label meds are sometimes used (disulfiram, aripiprazole [Abilify]) |
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40. Cocaine withdrawal?
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a. Abrupt abstinence is NOT life threatening.
b. Produces post-intoxication depression (“crash”): Malaise, fatigue, hypersomnolence, depression, hunger, constricted pupils, vivid dreams, psychomotor agitation or retardation. i. Occasionally, these pts can become suicidal. |
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41. MOA of classic amphetamines/
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a. Block reuptake an facilitate release of dopamine and NE from nerve endings, causing a stimulant effect.
b. Examples: Dextroamphetamine (Dexedrine), methylphenidate (Ritalin), Methamphetamine (Desoxyn, “ice”, “speed”, “crystal meth”, “crank”. |
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42. How are methamphetamines manufactured?
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a. ‘easily” in home labs using over-the-counter meds (ie, pseudoephedrine).
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43. Use of amphetamines?
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a. They are used medically in the tx of narcolepsy, ADHD, and depression disorders.
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44. Substituted (“designed”, “club drugs”) amphetamines?
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a. Release dopamine, NE, and 5-HT from nerve endings.
b. I.e. MDMA (Ectasy), MDEA (eve) c. These substances are associated w/dance clubs and raves. d. Have both stimulant and hallucinogenic properties. e. 5-HT syndrome is possible if designed amphetamines are combined w/SSRIs. |
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45. Amphetamines and psychosis?
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a. Heavy use may cause amphetamine psychosis, a psychotic state that may mimic schizophrenia.
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46. Symptoms of amphetamine abuse!?!
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a. Dilated pupils
b. ↑ Libido c. Perspiration d. Respiratory depression e. Chest pain. |
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47. Effects of chronic amphetamine use?
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a. Acne and accelerated tooth decay “meth mouth”.
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48. Clinical presentation of Amphetamine intoxication?
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a. Similar to cocaine.
b. MDMA and MDEA may induce sense of closeness to others |
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49. Amphetamine Overdose?
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a. Hyperthermia
b. Dehydration (especially after a prolonged period of dancing in a club) c. Rhabdomyolysis -> Renal failure. |
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50. Amphetamine withdrawal?
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a. Can cause prolonged depression.
b. Occasionally, complications of their long half-life can cause psychosis. |
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51. Tx of amphetamine intoxication?
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a. Rehydrate, correct electrolyte imbalance, treat hyperthermia.
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52. Note: Amphetamine us is associated w/↑ tolerance, but also can cause seizures.
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52. Note: Amphetamine us is associated w/↑ tolerance, but also can cause seizures.
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50. Amphetamine withdrawal?
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a. Can cause prolonged depression.
b. Occasionally, complications of their long half-life can cause psychosis. |
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53. Ketamine?
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a. Ketamine is similar to PCP, but is less potent.
b. Ketamine is sometimes used as a “date rape” drug, as it is odourless and tasteless. |
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54. Ketamine “special K” SE?
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a. Tachycardia, tachypnea, hallucinations, amnesia.
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55. PCP “angel dust”?
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a. PCP is a dissociative, hallucinogenic drug that antagonizes NMDA glutamate receptors and activates dopaminergic neurons.
b. It can have stimulant or CNS depressant effects, depending on the dose taken. |
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56. How is PCP used?
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a. PCP can be smoked as “wet” (sprinkled on cigarette) or as a “joint.
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51. Tx of amphetamine intoxication?
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a. Rehydrate, correct electrolyte imbalance, treat hyperthermia.
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57. Clinical presentation of PCP intoxication?
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a. Agitation, depersonalization, hallucinations, synesthesia, impaired judgement, memory impairment.
b. Nystagmus (rotary, horizontal, or vertical)! c. Ataxia d. Dysarthria e. HTN f. Tachycardia g. Muscle rigidity h. High tolerance to pain |
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52. Note: Amphetamine us is associated w/↑ tolerance, but also can cause seizures.
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52. Note: Amphetamine us is associated w/↑ tolerance, but also can cause seizures.
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58. Tx of PCP intoxication?
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a. Monitor vitals, temp, and electrolytes and minimize sensory stimulation.
b. Use BZDs (lorazepam) to treat agitation, anxiety, muscle spasms, and seizures. c. Use antipsychotics (haloperidol) to control severe agitation or psychotic sx. |
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53. Ketamine?
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a. Ketamine is similar to PCP, but is less potent.
b. Ketamine is sometimes used as a “date rape” drug, as it is odourless and tasteless. |
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59. Is there a PCP withdrawal?
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a. No withdrawal syndrome, but “flashbacks” (recurrence of intoxication sx due to release of the drug from body lipid stores) may occur.
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54. Ketamine “special K” SE?
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a. Tachycardia, tachypnea, hallucinations, amnesia.
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55. PCP “angel dust”?
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a. PCP is a dissociative, hallucinogenic drug that antagonizes NMDA glutamate receptors and activates dopaminergic neurons.
b. It can have stimulant or CNS depressant effects, depending on the dose taken. |
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56. How is PCP used?
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a. PCP can be smoked as “wet” (sprinkled on cigarette) or as a “joint.
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57. Clinical presentation of PCP intoxication?
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a. Agitation, depersonalization, hallucinations, synesthesia, impaired judgement, memory impairment.
b. Nystagmus (rotary, horizontal, or vertical)! c. Ataxia d. Dysarthria e. HTN f. Tachycardia g. Muscle rigidity h. High tolerance to pain |
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58. Tx of PCP intoxication?
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a. Monitor vitals, temp, and electrolytes and minimize sensory stimulation.
b. Use BZDs (lorazepam) to treat agitation, anxiety, muscle spasms, and seizures. c. Use antipsychotics (haloperidol) to control severe agitation or psychotic sx. |
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59. Is there a PCP withdrawal?
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a. No withdrawal syndrome, but “flashbacks” (recurrence of intoxication sx due to release of the drug from body lipid stores) may occur.
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60. Rotary nystagmus?
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a. Pathognomonic for PCP intoxication.
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61. What types of hallucinations are found in both PCP and cocaine abuse?
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a. Tactile and visual.
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62. Note: More than w/other drugs, intoxication w/PCP results in violence.
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62. Note: More than w/other drugs, intoxication w/PCP results in violence.
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