Psychiatry Flashcards
Define tolerance and withdrawal
Tolerance (needing higher amounts of the substance to achieve the desired
effect or experiencing diminished effects when repeating the same dose)
Withdrawal (a substance-specific syndrome occurring when a patient stops or reduces heavy/prolonged substance use)
(It is possible to have a substance use disorder without having phys- iological dependence (i.e., without having withdrawal or tolerance))
A 56 yo business executive is 1 day out from an uncomplicated cholecystectomy for symptomatic cholelithiasis. The nurse notices a significant variation in his VS compared to what was measured in the PACU. HR is 153 bpm, BP is 170/105. He has tremors and has been feeling nauseous. He is given a beta blocker for symptomatic relief. 24 hrs later he begins to describe a feeling of bugs crawling under his skin, appears delirious, and has a mild fever. He begins to have generalized tonic-clonic movements of his hands and legs. What is the next best step in the management of this patient?
a. IV Lorazepam therapy.
b. IV Phenobarbital therapy.
c. A 4-6 week course of Bupropion.
d. Referral for Alcoholics Anonymous counseling.
The best answer is A, Lorazepam therapy. This patient has gone into delirium tremens. He deserves a benzodiazepine.
(You should watch out for this specific scenario on the shelf/Step 2)
This is alcohol withdrawl - give short acting benzo like lorazepam iv; don’t give bupropion may make sxs worse; phenobarbital not first line - try benzo first
MOA for benzodiazepine in treating delirium tremens
increases frequency of chloride channel opening which hyperpolarizes neurons (via GABA receptor)
(Ie., work by potentiating the effects of gamma-aminobutyric acid (GABA))
(Facilitate GABA action by frequency of Cl– channel opening (“frenzodiazepines” increase frequency). )
Alcohol effects on GABA and glutamate receptors?
Alcohol activates GABA, dopamine, and serotonin receptors in the CNS. It inhibits glutamate receptor activity and voltage-gated calcium channels. GABA receptors are inhibitory, and glutamate receptors are excitatory; thus, alcohol is a potent CNS depressant.
Most adults will show some signs of intoxication with BAL ——— and obvious signs with BAL
———mg/dL.
> 100
> 150
Tx alcohol intoxication:
- Monitor: Airway, breathing, circulation, glucose, electrolytes, acid–base status.
-Give parenteral thiamine (to prevent or treat Wernicke’s encephalopathy) and folate. Remember thiamine must be given before glucose, as it’s a necessary cofactor for glucose metabolism.
Ethanol, along with methanol and ethylene glycol, can be a cause of ——— acidosis.
anion gap metabolic
Confabulation—inventing stories of events that never occurred—is often associated with
Korsakoff’s “psychosis,” or alcohol-induced neurocognitive disorder
(Patients are unaware that they are “making things up”)
What are the typical features of Wernicke’s encephalopathy?
The classic triad is confusion (altered mental status), ataxic gait, and oculomotor findings (typically nystagmus or gaze palsies).
A 42-year-old man has routine surgery for a knee injury. After 72 hours in the hospital he becomes anxious, flushed, diaphoretic, hypertensive, and tachycardic. What most likely accounts for this patient’s symptoms? Treatment? What are you most concerned about?
Dx: Alcohol withdrawal
Tx: Benzodiazepines (chlordiazepoxide [Librium] or lorazepam [Ativan] are considered the drugs of choice)
Concerns: Seizures, delirium tremens, autonomic instability, and cardiac arrhythmias. Remember that alcohol withdrawal can be fatal.
Signs and symptoms of alcohol withdrawal syndrome include
insomnia, anxiety, hand tremor, irritability, anorexia, nausea, vomiting, autonomic hyperactivity (diaphoresis, tachycardia, hypertension), psychomotor agitation, fever, seizures, hallucinations, and delirium tremens
Alcohol withdrawal induced seizures are treated with
benzodiazepines
Long-term treatment with anticonvulsants is not recommended for alcohol withdrawal seizures.
Delirium tremens is a dangerous form of alcohol withdrawal involv- ing ——— and treated with ———
Sxs: mental status and neurological changes; Symptoms include disorientation, agitation, visual and tactile hallucinations, and autonomic instability (increase in respiratory rate, heart rate, and blood pressure)
(It carries a 5% mortality rate but occurs in only 5% of patients that experience EtOH withdrawal. Patients often require ICU level of care)
treatment: supportive care and benzodiazepines
Timing of minor alcohol withdrawal sxs (ie Tremulousness, mild anxiety, headache, diaphoresis, palpitations, anorexia, gastrointestinal upset; normal mental status)
6-36 hours
Timing of seizures with alcohol withdrawal
6-48 hours
Definition and timing of alcoholic hallucinosis following alcohol withdrawl
Alcoholic hallucinosis=Visual, auditory, and/or tactile hallucinations with intact orientation and normal vital signs
12-48 hours (.5-2 days)
Definition and timing of delirium tremens following alcohol withdrawl
Definition: Delirium, agitation, tachycardia, hypertension, fever, diaphoresis
Timing: 48-96 hours (2-4 days)
Tx delirium tremens
Benzodiazepines (lorazepam, diazepam, or chlordiazepoxide)
Parenteral thiamine, folic acid, and a multivitamin to treat nutritional deficiencies (“banana bag”)
Alcoholic Ketoacidosis: Defintion
Hallmark is ketosis without hyperglycemia and a negative alcohol level
Frequently seen in the setting of alcohol cessation after an alcohol binge secondary to protracted vomiting and lack of oral intake
(Alcoholic ketoacidosis stems from the patient’s inability to ingest, absorb and utilize glucose from their diet. The vomiting and nausea prevent adequate solute intake from the gastrointestinal tract. The alcohol further depresses gluconeogenesis in the body and keeps blood sugar levels low. An anxiety state and alcohol withdrawal further exacerbate the patient’s ability to eat. The lack of nutrients other than alcohol causes the formation of ketones and elevated gap ketoacidosis in the absence of diabetes.)
Alcoholic Ketoacidosis: lab findings and treatment
Laboratory studies reveal a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus
Treatment consists of hydration with D5NS, and replacing electrolytes.
Lab findings suggestive of excessive long-term alcohol use
AST:ALT ratio ≥2:1 and elevated GGT
(they take a few weeks to return to normal during abstinence)
At-risk or heavy drinking for men is more than ——— drinks per day or more than ——— drinks per week. For women, it is more than ——— drinks per day or more than ——— drinks per week
4
14
3
7
Wernicke’s encephalopathy caused by
thiamine (vitamin B1) deficiency resulting from poor nutrition; Acute and can be reversed with thiamine therapy
Features of Wernicke’s encephalopathy
Ataxia (broad-based)
confusion
ocular abnormalities
(nystagmus, gaze palsies)
What is the treatment for Wer- nicke’s encephalopathy?
High dose parenteral (IV or IM) thiamine should be given for 2–7 days, followed by daily oral thiamine
Give all patients with altered mental status ——— before glucose, to avoid ———
thiamine
precipitating Wernicke–Korsakoff syndrome (Thiamine is
a coenzyme used in carbohydrate metabolism)
If left untreated, Wernicke’s encephalopathy may progress to Korsakoff syndrome, which is
Chronic amnestic syndrome (Reversible in only about 20% of patients)
Features: Impaired recent memory, anterograde amnesia, compensatory confabulation (unconsciously making up answers when memory has failed)
First line tx alcohol use disorder:
Naltrexone (Opioid receptor antagonist; reduces cravings and the “high” associated with alcohol intoxication)
Acamprosate (Likely modulates glutamate transmission.)
Second line tx alcohol use disorder:
Disulfiram (Blocks aldehyde dehydrogenase, causing buildup of acetaldehyde and aversive symptoms (flushing, headache, nausea/vomiting, palpitations, shortness of breath))
Topiramate (Anticonvulsant; potentiates GABA and inhibits glutamate receptors)
Naltrexone for alcohol use disorder: pros vs cons
Pros: First-line treatment. Available as an oral tablet (can be taken daily, or as-needed on drinking days), or monthly injection. Can allow some patients to engage in moderate alcohol use without escalating to binge drinking.
Cons: Will precipitate withdrawal in patients with physical opioid dependence. Can interfere with anesthesia (e.g., for acute injury or planned surgeries). Risk of LFT elevation.
Acamprosate for alcohol use disorder: pros vs cons
Pros: First-line treatment. Can be used for patients with liver disease. Typically used for relapse prevention in patients who have already stopped drinking.
Cons: Contraindicated in severe renal disease
Alcoholism may be associated with the development of what syndrome:
reversible confusion, ophthalmoplegia, and ataxia (Wernicke’s, give thiamine)
OR
Making stuff up (confabulations)/amnesia + Wernicke sxs which are largely not reversible (Korsakoff’s psychosis)
In alcohol withdrawal, differentiate the ——— sxs associated with Delirium Tremens from the ——— sxs associated with alcoholic hallucinosis
seizures and autonomic instability
visual hallucinations and relative autonomic stability
A 50 y/o known alcoholic presents to the ER with tonic clonic seizures. BP 180/110, HR 118, T 100.1. How long since his last drink?
~12-24hrs. (bimodal peak at 8 and 48hrs)
A 50 y/o known alcoholic presents to the ER with tonic clonic seizures. BP 180/110, HR 118, T 100.1. How long till he develops confusion, fluctuations in consciousness and feeling of ants crawling on him (formication)?
~48-72 hrs (2-3 days) since last drink is the when delirium tremens usually
start
(When admit someone for alcohol detox at least got to watch them for 72 hrs; preferably a day longer than that at 96 hrs (4 days))
A 50 y/o known alcoholic presents to the ER with tonic clonic seizures. BP 180/110, HR 118, T 100.1. His blood alcohol level is 225mg/mL. How long till its out of his system?
~9hrs, Alcohol is metabolized by zero order kinetics (same amt/unit time = 25mg/hr)
(Alcohol metabolized by zero order kinetics so if you have a “buttload” of alcohol in your system, it will take longer than if you have less; zero order kinetics is a certain amount of drug metabolized per unit time, not a certain percentage)
What is the average rate of alcohol metabolism?
Between 15 and 35 mg/dL per hour
Zero-order elimination of drug: definition and example drugs
Rate of elimination is constant regardless of Cp (ie, constant amount of drug eliminated per unit time). Cp decreases linearly with time. (Capacity-limited elimination)
Examples of drugs—Phenytoin, Ethanol, and Aspirin (at high or toxic concentrations) (PEA (a pea is round, shaped like the “0” in zero-order))
Zero-order elimination of drug: impact on half-life over time
Time of t1/2 decreases as concentration decreases
First-order elimination of drug: definition and example drugs
Rate of first-order elimination is directly proportional to the drug concentration (ie, constant fraction of drug eliminated per unit time). Cp decreases exponentially with time. (First-order=Fraction=Flow-dependent elimination)
Applies to most drugs
First-order elimination of drug: impact on half-life over time
Time of t1/2 is constant as concentration decreases
A 50 y/o known alcoholic presents to the ER with tonic clonic seizures. BP 180/110, HR 118, T 100.1. If his medications included propranolol, lactulose, and allopurinol, what would be the best sign to monitor for his withdrawals?
Beta-blockers mask the signs of autonomic hyperactivity, but you can follow hyperreflexia to dose the benzos during w/drawal
(Propranolol will blunt tachycardia; one of signs autonomic instability is hyperactive reflexes- this will still be there with beta blocker)
A 50 y/o known alcoholic presents to the ER with tonic clonic seizures. BP 180/110, HR 118, T 100.1. Best initial treatment of our patient?
Many patients become physically dependent on benzodiazepines and require
increasing amounts for the same clinical effect (i.e., tolerance)
(potential for abuse)
How is benzodiazepine overdose treated?
Flumazenil; however, be careful not to induce withdrawal too quickly—this can be life threatening.
Which substances of abuse have potentially fatal withdrawal syndromes?
Alcohol, benzodiazepines, and barbiturates
Flumazenil’s MOA is ——— used for treating ———
very short-acting BZD antagonist
BZD overdose (Use with caution when treating overdose, as it may precipitate seizures)
Flumazenil is used for ——— BUT its use can cause ———
benzodiazepine overdose reversal
seizures especially in those patients with a low seizure threshold (Use with caution, and have an airway cart ready in case airway control becomes necessary)
(Remember that benzodiazepine withdrawal can be life threatening)
What is a potential consequence of using benzodiazepines with alcohol?
BDZs can be lethal when mixed with alcohol. Respiratory depres- sion may cause death.
Half life and examples of long acting vs intermediate acting vs short acting benzos:
Long acting (half-life: >20 hours)
• Diazepam (Valium)
• Clonazepam (Klonopin)
Intermediate acting (half-life: 6–20 hours)
• Alprazolam (Xanax)
• Lorazepam (Ativan)
• Oxazepam (Serax)
• Temazepam (Restoril)
Short acting (half-life: <6 hours)
• Midazolam (Versed)
In chronic alcoholics or those with liver disease, use benzodiazepines that are
not metabolized by the liver
There are a LOT of them: Lorazepam
Oxazepam
Temazepam
Benzos should not be given for long periods of time to prevent
“dependence” (if ever see answer of recurrent prescription for benzo- almost always wrong- because addictive)
Benzos used for:
They are used in the short term to calm down actively seizing individuals (or individuals with acute episodes of anxiety)
Essentially all Benzos end in
“pam” with the exception of Chlordiazepoxide
(Lorazepam is one of the poster child benzos)
Most benzos are eliminated by the ——— and metabolized by ——— (exceptions: ———)
liver
3A4
Lorazepam, it is cleared by the liver and metabolized by glucuronidation (phase 2 metabolism), the same holds true for Oxazepam and Temazepam, give these 3 in liver dysfunction (even if severe liver dysfunction, glucuronidation still works fairly well)
Give ——— in the setting of BZD overdose
flumazenil (GABA receptor antagonist)
Barbiturates also work like BZDs but have the mechanism of
increasing the duration of chloride channel opening
(“Ben likes it more frequently, Barb likes it to last longer”- benzos increase frequency of opening of Cl channels, causing neuronal hyperpolarization so stop firing; vs barbiturates that increase duration of opening of cl channels)
Barbiturate overdose sxs and rescue medication:
Barbiturates cause significant respiratory depression and are more lethal than BZDs in overdose. There is no rescue agent. (“Just intubate pt and hope for the best”)
(For barbiturate overdose, first aid also says: Alkalinize urine with sodium bicarbonate to promote renal excretion.)
Z drugs for insomnia (e.g., —(3)—) can be reversed with ———
Zolpidem, Zaleplon, and Eszopiclone
flumazenil
(Note: also have addictive potential)
ETOH moa includes —— ; This is why ——— are first line in the tx of delirium tremens
GABA receptor agonism
Benzos
A 50 y/o known alcoholic presents to the ER with tonic clonic seizures. BP 180/110, HR 118, T 100.1. Best initial treatment of our patient?
Diazepam or chlordiazepoxide b/c they have 80 & 120hr 1⁄2-lives respectively.
A 50 y/o known alcoholic presents to the ER with tonic clonic seizures. BP 180/110, HR 118, T 100.1. Best initial treatment of our patient if he’s a Child’s class C cirrhotic?
Lorazepam, oxazepam or temazepam b/c they are glucuronidated prior to elim
(“Preferrred in elderly pt and pt w/ liver failure”)
A 50 y/o known alcoholic presents to the ER with tonic clonic seizures. BP 180/110, HR 118, T 100.1. Most specific test for ETOH consumption in the past 10 days?
Carbohydrate-deficient transferrin. Less specific-elevated GGT and AST more than twice ALT.
Our next patient comes in w/ confusion, ataxia, and you find pic below on physical exam: Dx? Best first step?
Wernicke Encephalopathy. Caused by thiamine deficiency Give thiamine 1st, then glucose containing fluids.
(Pic is showing ophthalmoplegia) (so w/ wernicke expect confusion, ataxia, and either jiggly or paralyzed eyes)
(Remember give thiamine first before glucose b/c can’t utilize glucose unless have thiamine as co-factor; glucose before thiamine worsens encephalopathy)
Our next patient comes in w/ confusion, ataxia, and you find pic below on physical exam: Could progress to?
Can progress to Korsakoff’s syndrome (irreversible damage to mamillary bodies, etc)- apathy, anter/retrograde amnesia and confabulation. Can see MB atrophy on MRI
(Wernicke reversible with administration of thiamine)
25 yo college senior is combative and disoriented. Complains that bugs are crawling under his skin. BP is 210/140, HR is 180 bpm, RR is 40. His is sweating profusely, and his pupils are dilated. He is brought to the ED by friends b/c he has been complaining of chest pain. Dx? Moa?
This is cocaine intoxication. Cocaine blocks the reuptake of catecholamines at the adrenergic synapse. Remember that the SNS causes mydriasis and a “sympathetic response”. On the psych shelf, look for “eye findings” as the “kind giveaways” to the OD scenarios.
25 yo college senior is combative and disoriented. Complains that bugs are crawling under his skin. BP is 210/140, HR is 180 bpm, RR is 40. His is sweating profusely, and his pupils are dilated. He is brought to the ED by friends b/c he has been complaining of chest pain. Tx?
This patient deserves a BZD, not a beta-blocker. Cocaine withdrawal is the opposite of all these sxs. If a BZD is not an answer choice, consider answer choices like phenoxybenzamine/phentolamine (alpha blockers) or Carvedilol/Labetalol (alpha/beta blockers).
(Don’t give beta blocker b/c don’t want unopposed alpha activation; same business as with pheochromocytoma- if someone has a pheo and u want to pretreat them before surgery, u block alpha receptors first (so u don’t get unopposed alpha) before then blocking beta receptors)
Why should beta-blockers be avoided for patients who regularly use cocaine?
Cocaine has both alpha-
and beta-adrenergic effects.
If a beta-blocker is given simultaneously, unopposed alpha-adrenergic activity can cause coronary vasoconstriction and induce myocardial infarction.
——— and ——— can both cause formication, a tactile hallucination of something crawling on or under the skin.
Cocaine and amphetamines
Cocaine moa?
blocks the reuptake of dopamine, epinephrine, and norepinephrine from the synaptic cleft, causing a stimulant effect
Cocaine intoxication signs and sxs?
General: Euphoria, heightened self-esteem, increase or decrease in blood pressure, tachycardia or bradycardia, nausea, dilated pupils, weight loss, psychomotor agitation or depression, chills, and sweating.
Dangerous: Seizures, cardiac arrhythmias, hyperthermia, paranoia, and hallucinations (especially tactile). Since cocaine is an indirect sympathomimetic, intoxication mimics the fight-or-flight response.
Deadly: Cocaine’s vasoconstrictive effect may result in myocardial infarction (MI), intracranial hemorrhage, or stroke.
Tx cocaine overdose:
For mild-to-moderate agitation and anxiety: Reassurance of the patient and benzodiazepines.
For severe agitation or psychosis: Antipsychotics (e.g., haloperidol).
Symptomatic support (i.e., control hypertension, arrhythmias).
Cocaine withdrawal signs and sxs?
Produces post-intoxication depression (“crash”): Malaise, fatigue, hypersomnolence, depression, anhedonia, hunger, constricted pupils, vivid dreams, psychomotor agitation, or retardation. Occasionally, these patients can become suicidal.
(Treatment is supportive)
Pt presents with dilated pupils, seizure, tachycardia and HTN. Dx? Best first test?
Dx: Cocaine/Amphetamine intoxication
Best first test: EKG then urine tox screen.
Pt presents with dilated pupils, seizure, tachycardia and HTN. Tx for seizures? Tx for HTN and tachycardia?
If Dx, Cocaine/Amphetamine intoxication:
Then: Tx seizure w/ lorazepam.
Tx HTN and tachycardia with Calcium channel blocker.
Beta-blockers are CONTRAINDICATED!
Pt presents with SI, hypersomnia, depression and anergia. Dx?
Cocaine/Amphetamine withdrawal.
If you see a question detailing a teen from a party with seizures from hyponatremia, or a descriptor of an individual that has danced for hours on end, consider
MDMA (ecstasy) as the offending agent (also causes Serotonin Syndrome)
Classic amphetamines examples and moa?
Examples: Dextroamphetamine (Dexedrine), methylphenidate (Ritalin), methamphetamine (Desoxyn, “ice,” “speed,” “crystal meth,” “crank”).
(Methamphetamines are used in the treatment of narcolepsy, ADHD, binge eating, and occasionally depressive disorders)
Moa: Block reuptake and facilitate release of dopamine and norepinephrine from nerve endings, causing a stimulant effect.
Substituted (“designer,” “club drugs”) amphetamines: examples? Moa? Key complication?
Examples: MDMA (“ecstasy”), MDEA (“eve”); Often used in dance clubs and raves
Moa: Release dopamine, norepinephrine, and serotonin from nerve endings. Have both stimulant and hallucinogenic properties.
Key complication: Serotonin syndrome is possible if designer amphetamines are combined with SSRIs
Symptoms of amphetamine intoxication include
euphoria, dilated pupils, increased libido, tachycardia, perspiration, grinding teeth, and chest pain
(Similar sxs to cocaine intoxication)
Chronic amphetamine use leads to accelerated
tooth decay (“meth mouth”)
Both amphetamine and PCP use can cause:
rhabdomyolysis
Look for elevated creatine kinase (CK) and monitor closely for acute kidney injury. Treatment is mostly supportive and emphasizes hydration.
Overdose of amphetamines can cause
hyperthermia, dehydration (especially after a prolonged
period of dancing in a club), rhabdomyolysis, and renal failure
Extremely combative individual with vertical/horizontal nystagmus
PCP intoxication
PCP intoxication symptoms
RED DANES
Rage
Erythema (redness of skin)
Dilated pupils
Delusions
Amnesia
Nystagmus
Excitation
Skin dryness
——— is very common in PCP intoxication.
Nystagmus (especially rotary)
PCP intoxication is associated with ———, more so than other drugs.
violence
Ketamine (“special K”) can produce
tachycardia, tachypnea, hallucina- tions, and amnesia
(Ketamine is similar to PCP, but is less potent. Ketamine is sometimes used as a “date rape” drug, as it is odorless and tasteless.)
Pt presents s/p MVC with injected conjunctiva, sedation and is asking for Doritos (cool ranch plz).
Cannabis intoxication
——— is a pill form of THC that is FDA-approved for certain indications.
Dronabinol
(The main psychoactive component which produces the “high” in cannabis is THC (tetrahydrocannabinol).)
Pt presents with horizontal nystagmus, dilated pupils, ataxia and acute psychosis. Dx? Tx for acute psychosis?
Hallucinogen (PCP) intoxication.
Can use haloperidol for acute psychosis.
If an individual has conjunctival injection and an insatiable appetite for food on the shelf, consider
Marijuana intoxication
——— flashback is a spontaneous recurrence of symptoms mimick- ing a prior ——— that may last for minutes to hours.
LSD
LSD “trip”
Associate LSD with
flashbacks
Trigger words for drug intoxications: pupil constriction, decreased RR
Opioids
Trigger words for drug intoxications: pupil dilated, delusion, increased HR and BP
Amphetamines
Trigger words for drug intoxications: Hyperthermia, bruxism
MDMA (ecstasy)
Trigger words for drug intoxications: nystagmus, ataxia, increased BP, clenching/grinding teeth (bruxism), random acts of violence and belligerence, hyperthermia
PCP
Trigger words for drug intoxications: flashbacks, pupillary dilation, depression, hallucinations
LSD
Trigger words for drug intoxications: increased appetite, conjunctival irritation, paranoia, hallucinations
Marijuana
Trigger words for drug intoxications: dry skin, flushing, fever, urinary retention, dilated pupils, delirium, cardiac conduction delays, thirst, increased HR
Anticholinergics: TCAs, pesticides
Trigger words for drug intoxications: Salivation, decreased HR, vomiting, urination, defecation, constricted pupils
Cholinergic poisoning: organophosphates, anticholinesterases
Trigger words for drug intoxications: Anxiety, ataxia, life threatening respiratory depression, somnolence
Benzodiazepines, barbiturates
Trigger words for drug withdrawal: “flu-like” symptoms, rhinorrhea, piloerection, anxiety
Opioids
Trigger words for drug withdrawal: hunger, hypersolmnolence
Amphetamines
Trigger words for drug withdrawal: depression
PCP
Trigger words for drug withdrawal: depression, irritability, decreased appetite, nausea
Marijuana
Trigger words for drug withdrawal: anxiety, insomnia, seizures
Benzodiazepines, barbiturates
What is the dx that best matches the following information cluster?
-pH 6.9, pCO2 is 80.
-Constipation.
-Pupillary constriction.
-Patient is unresponsive.
Opioid overdose. This patient has a respiratory acidosis with miosis and constipation.
What is the reversal agent that best matches the Dx for the following information cluster?
-pH 6.9, pCO2 is 80.
-Constipation.
-Pupillary constriction.
-Patient is unresponsive.
Opioid overdose.
The reversal agent that will be the right answer on a test is Naloxone (an opioid receptor antagonist). Do not be deceived by the NBME putting Naltrexone as an answer choice in the same Q. It does the same thing but is longer acting (ie, naloxone shorter acting, acts very quickly). One weird use of Naltrexone is as a means of treating alcohol dependence.
Mnemonic for use of naloxone vs naltrexone vs methadone:
NalOxone reverses Overdose
NaltRExone prevents RElapse
And Methadone for Maintenance is what I use but could also be prevents Withdrawal (upside down M)
Opioid dependence can be treated with
Buprenorphine (partial mu receptor agonist) in combination with naloxone (combo is called Suboxone). Methadone (long acting opioid agonist, but less risk of addiction) can also be used for this purpose
(If person actively going through withdrawl and are buprenorphine naive, probably don’t want to dump buprenorphine on them,
b/c can make withdrawal symptoms worse)
Key side effect methadone
prolongs the QT interval
——— can be used in the treatment of dependence on tobacco.
A partial nicotine receptor agonist (Varenicline)
You are called to evaluate a 25 yo M prior to discharge after spending 3 days in central booking for driving under the influence. He feels completely dissatisfied with life, is restless, and has not slept for the past 2 days. You wonder how boring you must be as he constantly yawns during the interview. He has a bad runny nose and there’s copious amounts of saliva dripping from the lateral side of his mouth. His PE is notable for marked pupil dilation. He runs to use the restroom 3x during the interview. What is the next best step in the management of this patient?
a. Dextroamphetamine therapy.
b. Supportive care
c. Referral to alcoholics anonymous.
d. Naltrexone therapy.
e. Flumazenil therapy.
b. Supportive care (opioid withdrawal, not life threatening!)
(Remember life threatening withdrawals: alcohol, benzos, barbiturates)
(If had really bad opioid withdrawal sxs- could give clonidine; opioid action: if bind for example mu receptor prevent release of catecholamines at adrenergic synapse (one potential moa), so if withdrawing from opioids have hyeradtenergic sxs, so may want to dump down sympathetic ns; so can give clonidine b/c clonidine is an alpha 2 agonist so decrease norepinephrine release; think of clonidine as a non opioid, opioid- why sort of becoming controlled b/c has street value)
A patient is brought into the ER in a non-responsive state. His BP is 100/60, HR is 50, RR is 6. He has multiple track marks on his arms. Dx? Best first step?
Dx: opioid overdose
First step: Intubate the patient. Then give IV or IM naloxone (full mu-opiate antagonist)
A patient is brought into the ER in a non-responsive state. His BP is 100/60, HR is 50, RR is 6. He has multiple track marks on his arms. Dx? You realize his pupils are dilated. Significance?
Dx: opioid overdose
Dilated pupils from the hypoxia secondary to respiratory depression
A patient is brought into the ER in a non-responsive state. His BP is 100/60, HR is 50, RR is 6. He has multiple track marks on his arms. Dx? What sxs to you expect as he starts to withdraw?
Dx: opioid overdose
Withdrawal: Joint and muscle pain, photophobia, goosebumps, diarrhea, tachycardia, HTN, GI cramps, dilated pupils, anxiety/depression
A patient is brought into the ER in a non-responsive state. His BP is 100/60, HR is 50, RR is 6. He has multiple track marks on his arms. Dx? How to treat his withdrawl?
Clonidine for autonomic sxs, ibuprofen for muscle cramps, loperimide for diarrhea.
Methadone, buprenorphrine or Naltrexone can be used for long-term dependence.
——— is a common ingredient in cough syrup.
The opioid dextromethorphan
——— is the exception to opioids producing miosis.
Meperidine (Demerol)
(Demerol Dilates pupils)
———is the treatment of choice for opiate overdose.
Naloxone
Classic triad of opioid overdose:
Rebels Admire Morphine
Respiratory depression
Altered mental status
Miosis
Opioid intoxication sxs
Nausea, vomiting, sedation, decrease in pain perception, decrease in gastrointestinal motility, pupil constriction, and respiratory depression (which can be fatal)
Eating large amounts of ——— can result in a urine drug screen that is positive for opioids.
poppy seed bagels or muffins
——— following the administration of IV naloxone (a potent opioid antagonist) is consistent with opioid overdose.
Rapid recovery of consciousness
Withdrawal symptoms of opiates:
flu-like symptoms (body aches, anorexia, rhinorrhea, fever), diarrhea, anxiety, insomnia, and piloerection. These are not life threatening.
——— opioid and monoamine oxidase inhibitors taken in combination may cause serotonin syndrome, with sxs of ———
Meperidine
hyperthermia, confusion, hypertension or hypotension, and hyperreflexia
Txt opioid withdrawal:
Moderate symptoms: Symptomatic treatment with clonidine (for autonomic sxs), NSAIDs for pain, loperamide for diarrhea, dicyclomine for abdominal cramps, promethazine for nausea, etc.
Severe symptoms: Detox with buprenorphine or methadone
Cocaine toxicity is a clinical diagnosis, supported by ——— features such as ———
sympathomimetic
agitation, mydriasis, tachycardia, hypertension, and diaphoresis
First-line treatment for agitation and hemodynamic changes in cocaine intox:
Benzodiazepines