2a:I[856015,["/_next/static/immutable/chunks/1xzisbplk9czp.js","/_next/static/immutable/chunks/3j2i1faptc_-9.js","/_next/static/immutable/chunks/3ne0dxjrpj6b3.js","/_next/static/immutable/chunks/08tq8rmv423j5.js","/_next/static/immutable/chunks/397rsnspirpiy.js","/_next/static/immutable/chunks/32zk736rs0hqw.js","/_next/static/immutable/chunks/0lbgs964whs_0.js","/_next/static/immutable/chunks/1a_hqhrsle_n_.js","/_next/static/immutable/chunks/0hcnvyarhzl7i.js"],"default"] 2b:T6118,

Summary Table

Category	Details
Risk Factors	Adolescents and young adults; male sex; psychiatric comorbidities (anxiety, depression, ADHD); peer use; early age of first use; low socioeconomic status; history of childhood adversity
Etiology	Delta-9-tetrahydrocannabinol (THC) binds to CB1 cannabinoid receptors in the central nervous system, producing psychoactive effects. Withdrawal results from downregulation and desensitization of CB1 receptors after chronic heavy use.
Patient Presentation	Intoxication: euphoria, relaxation, impaired coordination, slowed reaction time, increased appetite. Withdrawal: irritability, insomnia, decreased appetite, restlessness, anxiety within days of cessation in a chronic user.
Classic Physical Exam	Intoxication: conjunctival injection (red eyes), dry mouth, tachycardia, increased appetite, impaired short-term memory. Withdrawal: diaphoresis, tremor, abdominal discomfort (no autonomic instability like alcohol withdrawal).
Key Diagnostic Results	Urine drug screen positive for THC-COOH (metabolite); may remain positive for up to 30 days in chronic users. No confirmatory lab for withdrawal (it is a clinical diagnosis).
Management	Intoxication: supportive care; benzodiazepines for severe anxiety or agitation. Withdrawal: supportive and symptomatic care. Long-term: cognitive-behavioral therapy, motivational enhancement therapy. No FDA-approved pharmacotherapy exists for cannabis use disorder.
Keywords	"Red eyes," "munchies," "conjunctival injection," "euphoria then paranoia," "chronic daily smoker who quit and now can't sleep," "irritable after stopping marijuana"

1. Pathophysiology

Cannabis exerts its psychoactive effects primarily through delta-9-tetrahydrocannabinol (THC), which acts as a partial agonist at CB1 cannabinoid receptors. These receptors are densely distributed in the hippocampus, cerebral cortex, basal ganglia, and cerebellum, which directly explains the clinical profile of intoxication.

Activation of CB1 receptors in the hippocampus impairs short-term memory and learning. In the cerebellum and basal ganglia, CB1 stimulation leads to impaired motor coordination and slowed reaction time. Cortical CB1 activation produces the characteristic euphoria, altered time perception, and at higher doses, paranoia or frank psychosis. The hypothalamic effects drive increased appetite ("munchies") by stimulating orexigenic pathways. Tachycardia results from sympathetic activation and decreased parasympathetic tone, not from direct cardiac stimulation.

The conjunctival injection (red eyes), the single most recognizable physical exam finding, is caused by vasodilation of conjunctival blood vessels mediated through CB1 receptor activation.

With chronic, heavy use, the brain downregulates and desensitizes CB1 receptors as a compensatory adaptation. When cannabis is abruptly discontinued, the sudden loss of exogenous cannabinoid signaling in a system with reduced receptor sensitivity produces a withdrawal syndrome. This withdrawal is real and recognized in the DSM-5, though it is not life-threatening and does not produce seizures or delirium tremens, unlike alcohol or benzodiazepine withdrawal. The irritability, insomnia, and appetite loss of withdrawal are essentially the mirror image of the intoxication effects (euphoria becomes dysphoria, increased appetite becomes anorexia, sedation becomes insomnia).

A related and highly testable condition is cannabinoid hyperemesis syndrome (CHS), seen in long-term heavy users. CHS presents with cyclical nausea, vomiting, and abdominal pain paradoxically relieved by hot showers or baths. The pathophysiology is not fully understood but is thought to involve dysregulation of the endocannabinoid system in the gut and hypothalamus with chronic CB1 overstimulation.

2. Classification and Clinical Manifestation

Cannabis Intoxication

Feature	Clinical Manifestation
Behavioral/Psychological	Euphoria, relaxation, impaired judgment, social withdrawal, anxiety or paranoia (especially at high doses), slowed sense of time
Physical Signs (at least 2 required)	Conjunctival injection, increased appetite, dry mouth (xerostomia), tachycardia
Cognitive	Impaired short-term memory, difficulty concentrating, slowed reaction time
Severe/High-Dose Effects	Acute psychosis (hallucinations, delusions), panic attacks, depersonalization, severe paranoia
Duration	Onset within minutes if smoked (30 to 60 minutes if ingested); effects last 2 to 6 hours (longer with edibles)

Cannabis Withdrawal

Feature	Clinical Manifestation
Eligibility	Cessation after prolonged and heavy use (typically daily or near-daily use for at least several months)
Psychological Symptoms	Irritability, anger, aggression; anxiety or nervousness; depressed mood; restlessness
Sleep	Insomnia, disturbing or vivid dreams
Appetite	Decreased appetite, weight loss
Physical Symptoms	Abdominal pain, tremor, diaphoresis, fever, chills, headache
Onset	Within 1 to 3 days of cessation
Peak	Days 2 to 6
Duration	Resolves within 1 to 2 weeks (sleep disturbances may persist longer)
Key Distinction	No seizures, no autonomic instability, no risk of death (unlike alcohol/benzodiazepine withdrawal)

Cannabinoid Hyperemesis Syndrome (CHS)

Phase	Clinical Manifestation
Prodromal	Morning nausea, abdominal discomfort, fear of vomiting; may last months to years
Hyperemetic	Severe, intractable cyclical vomiting; diffuse abdominal pain; compulsive hot bathing for symptom relief; dehydration
Recovery	Resolution after cessation of cannabis; symptoms return with re-use

3. Diagnostic Workup

Test	Role	Key Details
Urine Drug Screen (UDS)	Best initial test	Detects THC-COOH (inactive metabolite); positive for 3 to 5 days in occasional users, up to 30 days or more in chronic heavy users
Serum/Blood THC Level	Confirmatory (rarely needed clinically)	Confirms recent use; more useful in forensic or emergency settings
Clinical Assessment (DSM-5 criteria)	Gold standard for diagnosing withdrawal	Withdrawal is a clinical diagnosis; no lab test confirms or rules it out
Comprehensive Metabolic Panel	Supportive	Evaluate for dehydration and electrolyte abnormalities, especially in CHS
ECG	If indicated	Tachycardia is expected; rule out arrhythmia in patients with cardiac history or synthetic cannabinoid use
CT Abdomen	If CHS suspected	Rule out other causes of cyclical vomiting (obstruction, pancreatitis); imaging is typically normal in CHS

The diagnostic approach to cannabis intoxication begins with clinical recognition. The combination of euphoria, conjunctival injection, increased appetite, and tachycardia in a young patient should immediately raise suspicion. A urine drug screen is the best initial confirmatory step and is widely available.

However, a critical testing pearl is the prolonged detection window of THC-COOH in urine. Because THC is highly lipophilic, it accumulates in fat tissue and is slowly released. A positive urine screen in a chronic user does not confirm acute intoxication; it only confirms use within a broad time window. If timing of use matters (e.g., emergency department presentation, altered mental status workup), a serum THC level is more informative because it reflects recent exposure.

Cannabis withdrawal requires no laboratory testing for diagnosis. It is diagnosed clinically using DSM-5 criteria: cessation after heavy prolonged use, followed by at least three characteristic symptoms (irritability, insomnia, decreased appetite, restlessness, depressed mood, or physical symptoms like tremor and diaphoresis) within approximately one week. The key diagnostic task on the exam is recognizing the clinical pattern and distinguishing it from other withdrawal syndromes.

For cannabinoid hyperemesis syndrome, diagnosis is clinical and requires the triad of chronic heavy cannabis use, cyclical vomiting, and relief with hot bathing. Workup is primarily aimed at excluding other diagnoses (e.g., cyclic vomiting syndrome, gastroparesis, small bowel obstruction). Imaging and labs are typically unremarkable aside from signs of dehydration.

4. Management and Treatment

Setting	Intervention	Details
Acute Intoxication (Mild)	Supportive care	Calm environment, reassurance, monitor vital signs
Acute Intoxication (Severe anxiety/psychosis)	Benzodiazepines	Lorazepam 1 to 2 mg IV/IM or diazepam 5 to 10 mg PO/IV; repeat as needed
Acute Psychosis	Antipsychotics (if needed)	Haloperidol 5 mg IM or olanzapine 5 to 10 mg IM if psychotic features are prominent and not responding to benzodiazepines
Cannabis Withdrawal	Supportive and symptomatic	No FDA-approved pharmacotherapy. Symptomatic relief: sleep aids for insomnia, antiemetics for nausea, NSAIDs for headache
Cannabinoid Hyperemesis (Acute)	Capsaicin cream + IV fluids	Topical capsaicin (0.075%) applied to the abdomen is first-line for acute symptom relief; IV fluid rehydration; antiemetics (ondansetron) are often ineffective
Cannabinoid Hyperemesis (Definitive)	Cannabis cessation	Only definitive treatment; symptoms invariably recur with re-use
Long-Term Cannabis Use Disorder	Psychotherapy	Cognitive-behavioral therapy (CBT), motivational enhancement therapy (MET), contingency management
Pharmacotherapy for Cannabis Use Disorder	None approved	No FDA-approved medication. Investigational agents include gabapentin, N-acetylcysteine (especially in adolescents), and dronabinol, but none are standard of care

Acute intoxication is nearly always self-limited and requires only supportive care. Place the patient in a calm, quiet environment and provide verbal reassurance. Monitor heart rate (expect tachycardia) and observe for resolution. For patients with severe anxiety, panic attacks, or agitation, benzodiazepines are the treatment of choice: lorazepam 1 to 2 mg IV or IM, repeated every 15 to 20 minutes as needed.

If the patient presents with acute psychosis (hallucinations, severe paranoia, disorganized behavior), particularly after high-dose ingestion or use of edibles, benzodiazepines should be tried first. If psychotic symptoms persist, a low-dose antipsychotic such as haloperidol 5 mg IM may be added. It is important to note that there is no antidote for cannabis intoxication (unlike naloxone for opioids or flumazenil for benzodiazepines).

Cannabis withdrawal management is entirely supportive. There is no validated pharmacological protocol. Insomnia can be addressed with short courses of sleep aids (e.g., trazodone 50 to 100 mg at bedtime). Headache and myalgias respond to NSAIDs. Anxiety and irritability can be managed with brief reassurance and, if necessary, short-term anxiolytics. The patient should be counseled that symptoms are self-limited and will resolve within 1 to 2 weeks.

For cannabinoid hyperemesis syndrome, a high-yield exam pearl is that standard antiemetics (ondansetron, metoclopramide) are often ineffective. The best acute intervention is topical capsaicin cream (0.075%) applied to the periumbilical abdomen, which activates TRPV1 receptors and provides symptom relief. Intravenous fluids for rehydration and electrolyte correction are essential. The only definitive cure is complete cessation of cannabis use.

Long-term treatment of cannabis use disorder relies on behavioral therapies. CBT helps patients identify triggers and develop coping strategies. Motivational enhancement therapy addresses ambivalence about quitting. Contingency management uses incentive-based reinforcement for negative drug screens. There is currently no FDA-approved medication for cannabis use disorder, which is itself a testable fact.

5. Differential Diagnosis and Distractors

Differential	Why It's Similar	Key Discriminator
Anticholinergic Toxidrome	Dry mouth, tachycardia, altered mental status	Anticholinergic toxicity causes mydriasis (dilated pupils), urinary retention, flushed hot dry skin, and absent bowel sounds. Cannabis causes conjunctival injection and increased appetite, not mydriasis or urinary retention. "Red as a beet, dry as a bone, mad as a hatter" points to anticholinergic.
Sympathomimetic Intoxication (Cocaine, Amphetamines)	Tachycardia, anxiety, altered behavior	Sympathomimetics cause hypertension, hyperthermia, mydriasis, diaphoresis, and psychomotor agitation. Cannabis produces tachycardia but typically with normal or low blood pressure, no hyperthermia, and relaxation rather than agitation.
Alcohol Intoxication	Impaired coordination, slurred speech, disinhibition	Alcohol causes nystagmus, ataxia, and respiratory depression at high doses. Cannabis does not cause nystagmus or respiratory depression. Conjunctival injection is absent in alcohol intoxication.
Synthetic Cannabinoid (K2/Spice) Intoxication	"Smoked something," altered mental status, positive cannabinoid history	Synthetic cannabinoids are full agonists at CB1 (versus THC, a partial agonist), producing far more severe effects: seizures, severe agitation, psychosis, rhabdomyolysis, acute kidney injury. Standard UDS may be negative because most synthetic cannabinoids are not detected on routine urine immunoassays.
Opioid Intoxication	Altered mental status, sedation	Opioids cause the classic triad of miosis (pinpoint pupils), respiratory depression, and CNS depression. Cannabis does not cause respiratory depression or miosis.
Cyclic Vomiting Syndrome	Recurrent episodes of nausea and vomiting (mimics CHS)	Cyclic vomiting syndrome is not associated with cannabis use and does not respond to hot bathing. CHS resolves completely with cannabis cessation and recurs with re-use. Always ask about cannabis use history in cyclical vomiting.
Alcohol Withdrawal	Irritability, insomnia, tremor, diaphoresis, anxiety after cessation	Alcohol withdrawal can cause seizures, delirium tremens, and autonomic instability (severe hypertension, tachycardia, hyperthermia), which are absent in cannabis withdrawal. Cannabis withdrawal is uncomfortable but never life-threatening.
Nicotine Withdrawal	Irritability, anxiety, difficulty concentrating, increased appetite	Nicotine withdrawal causes increased appetite (same as cannabis withdrawal). However, nicotine withdrawal does not cause abdominal pain, diaphoresis, or vivid disturbing dreams, which are more characteristic of cannabis withdrawal. Ask about the substance used.

6. Traps and High-Yield Pearls

The most common way students lose points on cannabis questions is by underestimating the clinical significance of withdrawal. Many students still believe cannabis withdrawal does not exist or is not clinically meaningful. It is a recognized DSM-5 diagnosis and can appear on the exam as a patient who is irritable, cannot sleep, has lost appetite, and recently stopped using marijuana after years of daily use. Recognizing this pattern is the core competency being tested.

A second frequent trap involves cannabinoid hyperemesis syndrome. The vignette will describe a young chronic cannabis user with recurrent vomiting and abdominal pain who has had multiple emergency visits and negative workups. The "hot shower relief" clue is pathognomonic, but some vignettes omit it and instead emphasize the cyclical nature and chronicity of cannabis use. Students who do not associate heavy marijuana use with vomiting will miss this diagnosis. The tested pearl here is that capsaicin cream, not ondansetron, is the best acute treatment.

Another trap is the urine drug screen detection window. A vignette may present a patient who last used cannabis three weeks ago and still tests positive. Students may incorrectly conclude this represents recent intoxication. The tested concept is that THC-COOH, being lipophilic, persists in urine for up to 30 days or more with chronic use, and a positive screen alone does not equate to acute intoxication.

Finally, students must differentiate cannabis intoxication from synthetic cannabinoid intoxication. The vignette will often describe a much more severe clinical picture (seizures, severe psychosis, renal failure) and may note that the routine urine drug screen is negative. The key teaching point is that synthetic cannabinoids are full CB1 agonists, are far more dangerous than plant-derived cannabis, and are not reliably detected on standard immunoassay panels.

1b:["$","$L2a",null,{"article":{"id":"8e3d9696-2660-4927-bed8-403ff4a9b231","title":"Ganja","content":"$2b","category":"Psikiatri","created_at":"2026-09-05T05:39:18.901584+00:00","status":"published","subcategory":null},"questionCount":0,"sections":[{"id":"section-pathophysiology","num":"01","title":"Pathophysiology"},{"id":"section-classification-and-clinical-manifestation","num":"02","title":"Classification and Clinical Manifestation"},{"id":"section-diagnostic-workup","num":"03","title":"Diagnostic Workup"},{"id":"section-management-and-treatment","num":"04","title":"Management and Treatment"},{"id":"section-differential-diagnosis-and-distractors","num":"05","title":"Differential Diagnosis and Distractors"},{"id":"section-traps-and-high-yield-pearls","num":"06","title":"Traps and High-Yield Pearls"}],"hasSummaryTable":true}]