⁨⁨أسئلة الرابعة GIT الدلتا - Nausea, Vomiting

• Nausea is a subjective sensation of unease in the throat or epigastrium that often immediately precedes vomiting.
• Vomiting is the rapid and forceful oral expulsion of gastric contents, accompanied by contraction of abdominal musculature.
• Retching involves active and repetitive spasmodic contraction of abdominal musculature with the glottis closed, without expulsion of gastric contents.
• Regurgitation is the passive retrograde movement of esophageal or gastric contents back into the mouth without diaphragmatic or muscular activity.

Pathophysiology

• Afferent pathways to the vomiting center include the cerebral cortex, gastrointestinal tract, vestibular system, and chemoreceptor trigger zone (CTZ).
• Efferent pathways coordinate the contraction of abdominal and chest wall musculature, leading to vomiting.
• Vomiting events include cessation of antral contractions, relaxation of the stomach, increased pyloric tone, lower esophageal sphincter relaxation, contraction of the abdominal wall and diaphragm, and expulsion of gastric contents into the oropharynx.
• Neurotransmitters involved in vomiting sequence include serotonin, dopamine, histamine, acetylcholine, substance P, and endocannabinoids.

Differential Diagnosis

• The differential diagnosis of nausea and vomiting (N/V) is extensive and assessing symptom duration is important to determine if its acute or chronic.

Acute N/V

• Symptom duration is 7 or fewer days.
• Causes:
  • Short-lived medical condition (viral gastroenteritis).
  • Self-limited somatic disorder (musculoskeletal trauma, acute myocardial infarction).
  • Transient medication adverse effect.
• Treatment involves treating symptomatically without further investigations.

Chronic N/V

• Symptom duration is 4 weeks or more.
• Causes:
  • Medication adverse effects.
  • Neurologic causes.
  • Gastrointestinal diseases.
  • Metabolic and endocrine conditions.
  • Psychogenic disorders.
• Medications and toxins, such as NSAIDs, antiarrhythmic agents, antibiotics, antiepileptic drugs, opiates, and levodopa, can stimulate the CTZ.
• Excessive and long-term cannabis use may lead to cannabinoid hyperemesis syndrome (CHS).
• Neurologic disorders that may cause N/V, include increased ICP, CNS mass lesions, infection, hydrocephalus, and idiopathic intracranial hypertension and hemorrhage, potentially with or without nausea.
• Labyrinthine causes include Ménière disease, vestibular schwannoma, and benign paroxysmal positional vertigo.
• Both acute and chronic pain may be associated with N/V.
• Gastrointestinal irritants cause the release of serotonin (5-HT3) from enteroendocrine cells of intestinal epithelium, stimulating 5-HT3 receptors on afferent vagal fibers.
• Acute N/V infections (gastroenteritis), inflammatory diseases (pancreatitis or appendicitis), and intestinal obstruction (volvulus, intussusception, or strangulated hernia).
• Chronic N/V dyspepsia, gastroparesis, and chronic intestinal pseudo-obstruction.
• Pregnancy is the most common endocrine cause of N/V, affecting 50% to 75% of women, with hyperemesis gravidarum occurring in 1% to 5% of pregnancies, treated with pyridoxine (vitamin B6).
• Other endocrine causes, that stimulate the CTZ, include:
  • Diabetic ketoacidosis
  • Uremia
  • Adrenal insufficiency
  • Hyperparathyroidism
  • Thyroid disorders
  • Electrolyte disorders (hyponatremia, hypokalemia, hypercalcemia)
  • Paraneoplastic syndromes
  • Hematologic disorders.
• Psyhcogenic causes include Anxiety, Depression, Anorexia nervosa, and Bulimia nervosa.

Nausea and Vomiting Syndromes

• Functional Vomiting: frequent episodes of recurrent vomiting without organic, psychiatric, systemic, or metabolic diseases explaining the symptoms.
• Cyclic Vomiting Syndrome (CVS): stereotypical and recurrent episodes of vomiting with symptom-free periods, similar in onset, symptoms, and duration.
• Cannabinoid Hyperemesis Syndrome (CHS): vomiting from prolonged cannabis exposure, resolving with cannabis cessation; may mimic CVS, and compulsive bathing to relieve symptoms is a characteristic feature.

Cannabinoid Hyperemesis Syndrome (Rome IV Criteria)

• Requires all criteria:
  • Stereotypical episodic vomiting similar to cyclic vomiting syndrome in onset, duration, and frequency.
  • Presentation after prolonged excessive cannabis use.
  • Relief of vomiting episodes by sustained cessation of cannabis use.
• These criteria must be fulfilled for the last 3 months, with symptom onset at least 6 months before diagnosis.
• A supportive remark is association with pathologic bathing behavior (prolonged hot baths or showers).

Potential Mimickers

• Elevated intracranial pressure
• Acute intoxication
• Pancreatitis
• Ovarian and testicular torsion
• Gastroesophageal dysmotility
• Mitochondrial disorders
• Acute intermittent porphyria
• Opioid-Induced N/V: occurs shortly after medication intake, thought to be mediated by reduced gastrointestinal motility, CTZ activation, and vestibular system activation.
• Conditioned N/V anticipatory or learned, triggered by specific environmental sensory stimuli.

Differences Between Cannabinoid Hyperemesis Syndrome (CHS) & Cyclical Vomiting Syndrome (CVS)

• CHS involves a prolonged cannabis use of more than 6 months and resolves by cannabis cessation.
• CVS isnt linked to cannabis use and is a brain-gut disorder that does not improve with cannabis cessation.
• CHS should stop marijuana for one to two weeks as vomiting will lessen while for CVS, its vomitting will persist
• Testing compulsvie behavior will reveal that both CHS and CSV patients are equally present to compuslive bathing behavior to relieve symptoms.
• Treatments for CVS:
• Prophylactic first line thrapy with tricyclic antidepressants are inter-episodic phase
• Abortive therapy using antiemetics, Sumatriptans, and sedatives

Complications of Vomiting

• Trauma to the distal esophagus: recurrent vomiting may result in laceration of esophageal mucosa at gastro-esophageal junction, causing bleeding (hematemesis), typically following repeated vomiting.

Trauma Forms

• Mallory-Weiss tear, where laceration of mucosa into submucosa causes bleeding.
• Boerhaave's syndrome, where laceration extends through submucosa and serosa to result in esophageal perforation, typically entering the left chest cavity and producing intense pain.
• Aspiration of the vomitus into the lungs, particularly in patients with neurologic defects or impaired consciousness from alcohol intoxication.
• Severe Fluid and Electrolyte disturbances: recurrent vomiting causes loss of secretions of the stomach and upper small intestine, resulting in metabolic alkalosis, hypokalaemia, and dehydration (hypochloraemic hypokalaemic metabolic alkalosis). For chronic, its impact is impaired quality of life.

Initial Evaluation of Vomiting

• Important Factors To Consider:
  • The onset of symptoms (abrupt vs gradual).
  • Timing (in relation to food, frequency).
  • Nature of emesis (undigested or partially digested food, presence of bile, volume).
  • Associated symptoms (abdominal pain, weight loss, early satiety, bloating, change in bowel habits, and neurologic deficits).
• History of the patient's comorbid diseases, medication list, and substance use history (eg, alcohol, tobacco, marijuana).

Possible causes based on features:

• Partially digested food several hours after meal: gastroparesis or gastric outlet obstruction.
• Bilious emesis: small bowel obstruction or intestinal pseudo-obstruction.
• Morning emesis before breakfast: pregnancy, uremia, alcohol ingestion, or increased intracranial pressure
• Episodes of severe unrelenting vomiting: cyclic vomiting syndrome and cannabinoid hyperemesis syndrome.
• Headache, vertigo, focal neurologic signs: central nervous system process or vestibular process.
• Intermittent abdominal pain that improves after vomiting: small bowel obstruction.
• Weight loss: malignant disease.

Physical Examination.

• Assessment & observations should include:

1. Signs of dehydration (skin turgor and mucous membranes).
2. Assessment of orthostatic vital signs, especially in inpatient setting.
3. Presence of lymphadenopathy, jaundice, abdominal masses.
4. Signs of depression and anxiety should be noted.
5. Systemic Features: increased skin and mucosal hyperpigmentation in Addison disease, tremor or lid lag in thyrotoxicosis
6. Abdominal Examination: succussion splash, suggesting gastric outlet obstruction.
7. Carnial Nerve and Neurologic Examination in those presentuing with neurologic and vestibular symptoms.

Laboratory Testing

• Perform:

1. Pregnancy test for women of childbearing age.
2. Complete blood count.
3. Electrolyte analysis.
4. Inflammatory Markers (C-reactive protein) for suspected inflammatory process and serum drug levels or urine drug screen
5. Pancreatic enzyme
6. Liver Function Test
7. Glycosylated Hemoglobin Level in patients wth diabetes.
8. Thyroid-stimulating hormone level
9. Morning cortisol level (adrenal insufficiency).
10. Serum calcium concetration (hypercalcemia)

Imaging

• For those with a likely gastrointestinal cause, abdominal radio graphy and ultrasound are the first diagnostic imagine test of choice. CT abodmen may be necessary.
• For those with concomitant esophagia, Esophagogastroduodenoscopy (EGD) or esophageal manometry is necessary
• For patients wth suspected gastroparesis,a gastric emptying study may be performed. In those with suspected central nervous system causes, a brain magnetic resonsnce imaging is performced.
• Psychogenic assement should be considered in thouse with chronic, unexplain N/V

Vomiting Treatments

• Discontinuation of suspected medications: done safely.
• Adequate oral intake.
• Nutritional support (replacement of fluids and electrolytes).
• 5-HT3 antagonists: act through: central antagonsim in CTZ and peripheral antagonism on intestinal vagal afferents.
• Phenothiazines, such as prochlorperazine & promethazine, & butyrophenones, such as droperidol & haloperidol, can block D2 dopaminergic receptors. They are helpful in patients with vomiting of entral origin such as in miraine hearaches, motion sickness and toxic agents
• Anticholinergic & antihistamines, such as diphenhydramine & meclizine, can have centrail anticholinergic effects, making it useful for vertigo and motion sickness
• Metroclpramide: Is useful due to the vagal actions and its 5-HT3 and D2 receptor antagonism, and potent antiemetic proprties, making it effective or gasroparesis.
• Surgical treatment: indicated for certain cuases of N/V (gastric outlet obstuction)
• Enteral Nurtrtion: With percutaneous endoscopic gastrostomy or jejjunostomy tubes can be considered in those with severe, refractoyr symptoms, or conditions non amenable to surgical resecting

Alternate treatments

• Acupuncture

• Hypnotherapy

• Herbal Supllements like ginger & pyridoxine

• Olazamapine and mirtazapine can be in functional N/V while mitrazapine augments appitite and improves sleep, while taking, monitor its weight gain & changes to mood.

• Tricyclic antidepressants/low-dose gabapentin can be effective for patients with refractory systems

• Opiois should be avoided as it can worsen nauesa and motility.

Anti-emetics Side Effects

• Serotonin 5-hydroxytryptamine antagonists (ondansetron, granisetron): mild headache, constipation, QT prolongation
• Phenothiazines (prochlorperazine, promethazine): extrapyramidal symptoms (dystonia, tardive dyskinesia), QT interval prolongation
• Anticholinergic (scopolamine): dry mouth, vision changes, urinary retention, constipation
• Antihistamines (meclizine, diphenhydramine, cyproheptadine, hydroxyzine): drowsiness, xerostomia
• Corticosteroids (dexamethasone, methylprednisolone): hypertension, diabetes, metabolic bone disease, weight gain, insomnia, and mood changes
• Benzodiazepines (lorazepam, alprazolam): sedation, unsteadiness (older patients), dizziness, and dependence
• Neurokinin I receptor antagonists (aprepitant, fosaprepitant): asthenia, diarrhea, headache Extrapyramidal symptoms (dystonia, tardive dyskinesia), hyperprolactinemia
• Benzamides (metoclopramide, trimethobenzamide): extrapyramidal symptoms (dystonia, tardive dyskinesia), hyperprolactinemia

Case Study

• A 21-year old has episodic N/V every 2 months that gives mild abdominal pain. It is treatable without other neurological symptoms with screening showing nothing wrong. He feels the compulsion to take hot baths that help, and smoked marijuana. Treat by encouraging the cessation of use.
• His physical exams are unremarkable and gets good results is marijiuana is discontinued