Psychiatry

Question 1

Define tolerance and withdrawal

Answer 1

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))

Question 2

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.

Answer 2

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

Question 3

MOA for benzodiazepine in treating delirium tremens

Answer 3

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). )

Question 4

Alcohol effects on GABA and glutamate receptors?

Answer 4

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.

Question 5

Most adults will show some signs of intoxication with BAL ——— and obvious signs with BAL
———mg/dL.

Answer 5

> 100

> 150

Question 6

Tx alcohol intoxication:

Answer 6

• 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.

Question 7

Ethanol, along with methanol and ethylene glycol, can be a cause of ——— acidosis.

Answer 7

anion gap metabolic

Question 8

Confabulation—inventing stories of events that never occurred—is often associated with

Answer 8

Korsakoff’s “psychosis,” or alcohol-induced neurocognitive disorder
(Patients are unaware that they are “making things up”)

Question 9

What are the typical features of Wernicke’s encephalopathy?

Answer 9

The classic triad is confusion (altered mental status), ataxic gait, and oculomotor findings (typically nystagmus or gaze palsies).

Question 10

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?

Answer 10

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.

Question 11

Signs and symptoms of alcohol withdrawal syndrome include

Answer 11

insomnia, anxiety, hand tremor, irritability, anorexia, nausea, vomiting, autonomic hyperactivity (diaphoresis, tachycardia, hypertension), psychomotor agitation, fever, seizures, hallucinations, and delirium tremens

Question 12

Alcohol withdrawal induced seizures are treated with

Answer 12

benzodiazepines
Long-term treatment with anticonvulsants is not recommended for alcohol withdrawal seizures.

Question 13

Delirium tremens is a dangerous form of alcohol withdrawal involv- ing ——— and treated with ———

Answer 13

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

Question 14

Timing of minor alcohol withdrawal sxs (ie Tremulousness, mild anxiety, headache, diaphoresis, palpitations, anorexia, gastrointestinal upset; normal mental status)

Answer 14

6-36 hours

Question 15

Timing of seizures with alcohol withdrawal

Answer 15

6-48 hours

Question 16

Definition and timing of alcoholic hallucinosis following alcohol withdrawl

Answer 16

Alcoholic hallucinosis=Visual, auditory, and/or tactile hallucinations with intact orientation and normal vital signs

12-48 hours (.5-2 days)

Question 17

Definition and timing of delirium tremens following alcohol withdrawl

Answer 17

Definition: Delirium, agitation, tachycardia, hypertension, fever, diaphoresis

Timing: 48-96 hours (2-4 days)

Question 18

Tx delirium tremens

Answer 18

Benzodiazepines (lorazepam, diazepam, or chlordiazepoxide)

Parenteral thiamine, folic acid, and a multivitamin to treat nutritional deficiencies (“banana bag”)

Question 19

Alcoholic Ketoacidosis: Defintion

Answer 19

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.)

Question 20

Alcoholic Ketoacidosis: lab findings and treatment

Answer 20

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.

Question 21

Lab findings suggestive of excessive long-term alcohol use

Answer 21

AST:ALT ratio ≥2:1 and elevated GGT

(they take a few weeks to return to normal during abstinence)

Question 22

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

Answer 22

4

14

3

7

Question 23

Wernicke’s encephalopathy caused by

Answer 23

thiamine (vitamin B1) deficiency resulting from poor nutrition; Acute and can be reversed with thiamine therapy

Question 24

Features of Wernicke’s encephalopathy

Answer 24

Ataxia (broad-based)

confusion

ocular abnormalities
(nystagmus, gaze palsies)

Question 25

What is the treatment for Wer- nicke’s encephalopathy?

Answer 25

High dose parenteral (IV or IM) thiamine should be given for 2–7 days, followed by daily oral thiamine

Question 26

Give all patients with altered mental status ——— before glucose, to avoid ———

Answer 26

thiamine precipitating Wernicke–Korsakoff syndrome (Thiamine is a coenzyme used in carbohydrate metabolism)

Question 27

If left untreated, Wernicke’s encephalopathy may progress to Korsakoff syndrome, which is

Answer 27

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)

Question 28

First line tx alcohol use disorder:

Answer 28

Naltrexone (Opioid receptor antagonist; reduces cravings and the “high” associated with alcohol intoxication) Acamprosate (Likely modulates glutamate transmission.)

Question 29

Second line tx alcohol use disorder:

Answer 29

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)

Question 30

Naltrexone for alcohol use disorder: pros vs cons

Answer 30

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.

Question 31

Acamprosate for alcohol use disorder: pros vs cons

Answer 31

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

Question 32

Alcoholism may be associated with the development of what syndrome:

Answer 32

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)

Question 33

In alcohol withdrawal, differentiate the ——— sxs associated with Delirium Tremens from the ——— sxs associated with alcoholic hallucinosis

Answer 33

seizures and autonomic instability visual hallucinations and relative autonomic stability

Question 34

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?

Answer 34

~12-24hrs. (bimodal peak at 8 and 48hrs)

Question 35

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)?

Answer 35

~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))

Question 36

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?

Answer 36

~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)

Question 37

What is the average rate of alcohol metabolism?

Answer 37

Between 15 and 35 mg/dL per hour

Question 38

Zero-order elimination of drug: definition and example drugs

Answer 38

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))

Question 39

Zero-order elimination of drug: impact on half-life over time

Answer 39

Time of t1/2 decreases as concentration decreases

Question 40

First-order elimination of drug: definition and example drugs

Answer 40

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

Question 41

First-order elimination of drug: impact on half-life over time

Answer 41

Time of t1/2 is constant as concentration decreases

Question 42

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?

Answer 42

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)

Question 43

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?

Question 44

Many patients become physically dependent on benzodiazepines and require

Answer 44

increasing amounts for the same clinical effect (i.e., tolerance) (potential for abuse)

Question 45

How is benzodiazepine overdose treated?

Answer 45

Flumazenil; however, be careful not to induce withdrawal too quickly—this can be life threatening.

Question 46

Which substances of abuse have potentially fatal withdrawal syndromes?

Answer 46

Alcohol, benzodiazepines, and barbiturates

Question 47

Flumazenil’s MOA is ——— used for treating ———

Answer 47

very short-acting BZD antagonist BZD overdose (Use with caution when treating overdose, as it may precipitate seizures)

Question 48

Flumazenil is used for ——— BUT its use can cause ———

Answer 48

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)

Question 49

What is a potential consequence of using benzodiazepines with alcohol?

Answer 49

BDZs can be lethal when mixed with alcohol. Respiratory depres- sion may cause death.

Question 50

Half life and examples of long acting vs intermediate acting vs short acting benzos:

Answer 50

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)

Question 51

In chronic alcoholics or those with liver disease, use benzodiazepines that are

Answer 51

not metabolized by the liver There are a LOT of them: Lorazepam Oxazepam Temazepam

Question 52

Benzos should not be given for long periods of time to prevent

Answer 52

“dependence” (if ever see answer of recurrent prescription for benzo- almost always wrong- because addictive)

Question 53

Benzos used for:

Answer 53

They are used in the short term to calm down actively seizing individuals (or individuals with acute episodes of anxiety)

Question 54

Essentially all Benzos end in

Answer 54

“pam” with the exception of Chlordiazepoxide (Lorazepam is one of the poster child benzos)

Question 55

Most benzos are eliminated by the ——— and metabolized by ——— (exceptions: ———)

Answer 55

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)

Question 56

Give ——— in the setting of BZD overdose

Answer 56

flumazenil (GABA receptor antagonist)

Question 57

Barbiturates also work like BZDs but have the mechanism of

Answer 57

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)

Question 58

Barbiturate overdose sxs and rescue medication:

Answer 58

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.)

Question 59

Z drugs for insomnia (e.g., —(3)—) can be reversed with ———

Answer 59

Zolpidem, Zaleplon, and Eszopiclone flumazenil (Note: also have addictive potential)

Question 60

ETOH moa includes —— ; This is why ——— are first line in the tx of delirium tremens

Answer 60

GABA receptor agonism Benzos

Question 61

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?

Answer 61

Diazepam or chlordiazepoxide b/c they have 80 & 120hr 1⁄2-lives respectively.

Question 62

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?

Answer 62

Lorazepam, oxazepam or temazepam b/c they are glucuronidated prior to elim (“Preferrred in elderly pt and pt w/ liver failure”)

Question 63

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?

Answer 63

Carbohydrate-deficient transferrin. Less specific-elevated GGT and AST more than twice ALT.

Question 64

Our next patient comes in w/ confusion, ataxia, and you find pic below on physical exam: Dx? Best first step?

Answer 64

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)

Question 65

Our next patient comes in w/ confusion, ataxia, and you find pic below on physical exam: Could progress to?

Answer 65

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)

Question 66

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?

Answer 66

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.

Question 67

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?

Answer 67

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)

Question 68

Why should beta-blockers be avoided for patients who regularly use cocaine?

Answer 68

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.

Question 69

——— and ——— can both cause formication, a tactile hallucination of something crawling on or under the skin.

Answer 69

Cocaine and amphetamines

Question 70

Cocaine moa?

Answer 70

blocks the reuptake of dopamine, epinephrine, and norepinephrine from the synaptic cleft, causing a stimulant effect

Question 71

Cocaine intoxication signs and sxs?

Answer 71

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.

Question 72

Tx cocaine overdose:

Answer 72

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).

Question 73

Cocaine withdrawal signs and sxs?

Answer 73

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)

Question 74

Pt presents with dilated pupils, seizure, tachycardia and HTN. Dx? Best first test?

Answer 74

Dx: Cocaine/Amphetamine intoxication Best first test: EKG then urine tox screen.

Question 75

Pt presents with dilated pupils, seizure, tachycardia and HTN. Tx for seizures? Tx for HTN and tachycardia?

Answer 75

If Dx, Cocaine/Amphetamine intoxication: Then: Tx seizure w/ lorazepam. Tx HTN and tachycardia with Calcium channel blocker. Beta-blockers are CONTRAINDICATED!

Question 76

Pt presents with SI, hypersomnia, depression and anergia. Dx?

Answer 76

Cocaine/Amphetamine withdrawal.

Question 77

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

Answer 77

MDMA (ecstasy) as the offending agent (also causes Serotonin Syndrome)

Question 78

Classic amphetamines examples and moa?

Answer 78

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.

Question 79

Substituted (“designer,” “club drugs”) amphetamines: examples? Moa? Key complication?

Answer 79

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

Question 80

Symptoms of amphetamine intoxication include

Answer 80

euphoria, dilated pupils, increased libido, tachycardia, perspiration, grinding teeth, and chest pain (Similar sxs to cocaine intoxication)

Question 81

Chronic amphetamine use leads to accelerated

Answer 81

tooth decay (“meth mouth”)

Question 82

Both amphetamine and PCP use can cause:

Answer 82

rhabdomyolysis Look for elevated creatine kinase (CK) and monitor closely for acute kidney injury. Treatment is mostly supportive and emphasizes hydration.

Question 83

Overdose of amphetamines can cause

Answer 83

hyperthermia, dehydration (especially after a prolonged period of dancing in a club), rhabdomyolysis, and renal failure

Question 84

Extremely combative individual with vertical/horizontal nystagmus

Answer 84

PCP intoxication

Question 85

PCP intoxication symptoms

Answer 85

RED DANES Rage Erythema (redness of skin) Dilated pupils Delusions Amnesia Nystagmus Excitation Skin dryness

Question 86

——— is very common in PCP intoxication.

Answer 86

Nystagmus (especially rotary)

Question 87

PCP intoxication is associated with ———, more so than other drugs.

Answer 87

violence

Question 88

Ketamine (“special K”) can produce

Answer 88

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.)

Question 89

Pt presents s/p MVC with injected conjunctiva, sedation and is asking for Doritos (cool ranch plz).

Answer 89

Cannabis intoxication

Question 90

——— is a pill form of THC that is FDA-approved for certain indications.

Answer 90

Dronabinol (The main psychoactive component which produces the “high” in cannabis is THC (tetrahydrocannabinol).)

Question 91

Pt presents with horizontal nystagmus, dilated pupils, ataxia and acute psychosis. Dx? Tx for acute psychosis?

Answer 91

Hallucinogen (PCP) intoxication. Can use haloperidol for acute psychosis.

Question 92

If an individual has conjunctival injection and an insatiable appetite for food on the shelf, consider

Answer 92

Marijuana intoxication

Question 93

——— flashback is a spontaneous recurrence of symptoms mimick- ing a prior ——— that may last for minutes to hours.

Answer 93

LSD LSD “trip”

Question 94

Associate LSD with

Answer 94

flashbacks

Question 95

Trigger words for drug intoxications: pupil constriction, decreased RR

Answer 95

Opioids

Question 96

Trigger words for drug intoxications: pupil dilated, delusion, increased HR and BP

Answer 96

Amphetamines

Question 97

Trigger words for drug intoxications: Hyperthermia, bruxism

Answer 97

MDMA (ecstasy)

Question 98

Trigger words for drug intoxications: nystagmus, ataxia, increased BP, clenching/grinding teeth (bruxism), random acts of violence and belligerence, hyperthermia

Answer 98

PCP

Question 99

Trigger words for drug intoxications: flashbacks, pupillary dilation, depression, hallucinations

Answer 99

LSD

Question 100

Trigger words for drug intoxications: increased appetite, conjunctival irritation, paranoia, hallucinations

Answer 100

Marijuana

Question 101

Trigger words for drug intoxications: dry skin, flushing, fever, urinary retention, dilated pupils, delirium, cardiac conduction delays, thirst, increased HR

Answer 101

Anticholinergics: TCAs, pesticides

Question 102

Trigger words for drug intoxications: Salivation, decreased HR, vomiting, urination, defecation, constricted pupils

Answer 102

Cholinergic poisoning: organophosphates, anticholinesterases

Question 103

Trigger words for drug intoxications: Anxiety, ataxia, life threatening respiratory depression, somnolence

Answer 103

Benzodiazepines, barbiturates

Question 104

Trigger words for drug withdrawal: “flu-like” symptoms, rhinorrhea, piloerection, anxiety

Answer 104

Opioids

Question 105

Trigger words for drug withdrawal: hunger, hypersolmnolence

Answer 105

Amphetamines

Question 106

Trigger words for drug withdrawal: depression

Answer 106

PCP

Question 107

Trigger words for drug withdrawal: depression, irritability, decreased appetite, nausea

Answer 107

Marijuana

Question 108

Trigger words for drug withdrawal: anxiety, insomnia, seizures

Answer 108

Benzodiazepines, barbiturates

Question 109

What is the dx that best matches the following information cluster? -pH 6.9, pCO2 is 80. -Constipation. -Pupillary constriction. -Patient is unresponsive.

Answer 109

Opioid overdose. This patient has a respiratory acidosis with miosis and constipation.

Question 110

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.

Answer 110

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.

Question 111

Mnemonic for use of naloxone vs naltrexone vs methadone:

Answer 111

NalOxone reverses Overdose NaltRExone prevents RElapse And Methadone for Maintenance is what I use but could also be prevents Withdrawal (upside down M)

Question 112

Opioid dependence can be treated with

Answer 112

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)

Question 113

Key side effect methadone

Answer 113

prolongs the QT interval

Question 114

——— can be used in the treatment of dependence on tobacco.

Answer 114

A partial nicotine receptor agonist (Varenicline)

Question 115

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.

Answer 115

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)

Question 116

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?

Answer 116

Dx: opioid overdose First step: Intubate the patient. Then give IV or IM naloxone (full mu-opiate antagonist)

Question 117

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?

Answer 117

Dx: opioid overdose Dilated pupils from the hypoxia secondary to respiratory depression

Question 118

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?

Answer 118

Dx: opioid overdose Withdrawal: Joint and muscle pain, photophobia, goosebumps, diarrhea, tachycardia, HTN, GI cramps, dilated pupils, anxiety/depression

Question 119

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?

Answer 119

Clonidine for autonomic sxs, ibuprofen for muscle cramps, loperimide for diarrhea. Methadone, buprenorphrine or Naltrexone can be used for long-term dependence.

Question 120

——— is a common ingredient in cough syrup.

Answer 120

The opioid dextromethorphan

Question 121

——— is the exception to opioids producing miosis.

Answer 121

Meperidine (Demerol) (Demerol Dilates pupils)

Question 122

———is the treatment of choice for opiate overdose.

Answer 122

Naloxone

Question 123

Classic triad of opioid overdose:

Answer 123

Rebels Admire Morphine Respiratory depression Altered mental status Miosis

Question 124

Opioid intoxication sxs

Answer 124

Nausea, vomiting, sedation, decrease in pain perception, decrease in gastrointestinal motility, pupil constriction, and respiratory depression (which can be fatal)

Question 125

Eating large amounts of ——— can result in a urine drug screen that is positive for opioids.

Answer 125

poppy seed bagels or muffins

Question 126

——— following the administration of IV naloxone (a potent opioid antagonist) is consistent with opioid overdose.

Answer 126

Rapid recovery of consciousness

Question 127

Withdrawal symptoms of opiates:

Answer 127

flu-like symptoms (body aches, anorexia, rhinorrhea, fever), diarrhea, anxiety, insomnia, and piloerection. These are not life threatening.

Question 128

——— opioid and monoamine oxidase inhibitors taken in combination may cause serotonin syndrome, with sxs of ———

Answer 128

Meperidine hyperthermia, confusion, hypertension or hypotension, and hyperreflexia

Question 129

Txt opioid withdrawal:

Answer 129

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

Question 130

Cocaine toxicity is a clinical diagnosis, supported by ——— features such as ———

Answer 130

sympathomimetic agitation, mydriasis, tachycardia, hypertension, and diaphoresis

Question 131

First-line treatment for agitation and hemodynamic changes in cocaine intox:

Answer 131

Benzodiazepines