ESOPHAGEAL DISORDERS
Gastroesophageal Reflux Disease (GERD)
Symptoms: Chronic heartburn, acid reflux, odynophagia Diagnosis: Clinical; EGD if alarm features (dysphagia, weight loss, hematemesis) Treatment: Lifestyle (elevate head, avoid triggers), PPI (first line)
Esophagitis
Types:
- Erosive: GERD, severe reflux
- Infectious: Candida, HSV, CMV (immunocompromised)
- Eosinophilic (EoE): Immune response to food antigens; dysphagia, food impaction
- Pill-induced: Tetracyclines, bisphosphonates, NSAIDs, K+ supplements
- Mechanism: Direct caustic injury to mucosa
- Prevention: Take upright with full glass of water, wait 30 min before lying down
Barrett’s Esophagus
Definition: Columnar metaplasia of squamous epithelium (result of chronic GERD) Appearance: “Tongue of salmon-colored mucosa at the GEJ” Risk Factors: Chronic GERD, obesity, male, White Diagnosis: EGD with biopsy Surveillance: EGD per dysplasia grade; monitor for malignant transformation
Esophageal Cancer
Types:
- Adenocarcinoma: Classically lower 1/3; arises from Barrett’s
- Squamous Cell: Classically upper 2/3; RF—tobacco, EtOH, achalasia
Symptoms: Progressive dysphagia (solids → liquids if severe), weight loss, melena Diagnosis: EGD with biopsy; staging = CT chest/abdomen/pelvis + PET + EUS Treatment: Localized → esophagectomy; Advanced → chemo/radiation
Dysphagia Classification
Oropharyngeal (difficulty initiating swallow):
- Localized to oropharynx
- Causes: CNS (stroke), H&N cancer, external compression (osteophytes), radiation
- Evaluation: bedside swallow assessment, modified barium swallow, ENT referral
Esophageal (difficulty during swallow):
- Episodic (liquids + solids) → MOTILITY PROBLEM
- Esophageal spasm, achalasia, ineffective peristalsis
- Obtain manometry (functional assessment)
- Constant, progressive (solids then liquids if severe) → STRUCTURAL PROBLEM
- Schatzki’s ring, stricture, cancer
- Obtain EGD FIRST (structural assessment before manometry)
Esophageal Motility Disorders
Achalasia:
- Pathophysiology: Incomplete LES relaxation + loss of peristalsis; autoimmune destruction of myenteric plexus
- Symptoms: Progressive dysphagia to solids/liquids, regurgitation of undigested food, odynophagia
- Diagnosis: Manometry (gold standard); “bird beak” on esophagram classic
- Treatment: Pneumatic dilation (EGD), surgical/endoscopic myotomy (POEM), botox (temporary)
Distal Esophageal Spasm:
- Pathophysiology: High-amplitude tertiary contractions → ineffective peristalsis
- Symptoms: Dysphagia + chest pain (can mimic angina)
- Diagnosis: Manometry (gold standard); “corkscrew esophagus” or “rosary bead” on esophagram
- Treatment: Calcium channel blockers, nitrates, PPI
Zenker Diverticulum
Definition: Outpouching of mucosa/submucosa through Killian’s triangle (weakness between cricopharyngeus and inferior pharyngeal constrictor) Symptoms: Dysphagia, regurgitation of undigested food, halitosis, weight loss Diagnosis: Barium esophagram, transnasal endoscopy by ENT Treatment: Surgical or endoscopic closure (ENT)
Esophageal Varices
Pathophysiology: Portal HTN → dilated veins at gastroesophageal junction Prophylaxis: NSBB or endoscopic variceal ligation (EVL) Active hemorrhage: IV octreotide + band ligation Refractory bleeding: TIPS (transjugular intrahepatic portosystemic shunt) Surveillance EGDs: Per variceal grade
Mallory-Weiss Tear
Definition: Superficial tear in esophageal mucosa (not full thickness like Boerhaave) Cause: Forceful/repeated vomiting; associated with alcohol, bulimia Presentation: Hematemesis after retching/vomiting episodes Treatment: Usually self-limited; severe → endoscopic hemostasis
Boerhaave Syndrome
Definition: Full-thickness esophageal rupture Classic presentation: Severe chest pain + vomiting + subcutaneous emphysema (crepitus on chest wall) Diagnosis: CT with contrast (confirm perforation); Gastrografin swallow Treatment: Emergent surgical intervention Prognosis: High mortality if delayed >24h
GASTRIC DISORDERS
H. pylori & Peptic Ulcer Disease
H. pylori Epidemiology:
- Colonizes ~50% of world’s population
- Causes PUD, gastric cancer (adenocarcinoma, MALT lymphoma)
H. pylori Diagnosis:
- Off PPIs 2+ weeks, H2-blockers 24h: Stool antigen or UBT (urea breath test)
- On PPIs: EGD with biopsies
- Eradication confirmation: Stool antigen or breath testing (4 weeks off abx, 2 weeks off PPI)
H. pylori Treatment:
- Quadruple therapy (FIRST LINE): PPI + bismuth + metronidazole + tetracycline
- Vonoprazan dual therapy (ALSO first line): Vonoprazan + amoxicillin
Peptic Ulcer Disease:
Etiologies: H. pylori (most common), NSAIDs (second), ZES (rare)
Symptoms:
- Gastric ulcer: Gnawing epigastric pain immediately after eating
- Duodenal ulcer: Pain 2-3 hours after meals or at night (wakes from sleep)
Complications: UGIB, perforation, peptic stricture (DU only)
Diagnosis: EGD, H. pylori testing; check fasting gastrin if recurrent/unexplained
Treatment:
- If UGIB: Volume resuscitation (fluids, RBCs; goal Hgb >7, or >8 if CAD)
- IV PPI then oral PPI BID × 8 weeks
- Eradicate H. pylori if present
- Avoid NSAIDs (or use COX-2 inhibitor + PPI if necessary)
- IV octreotide/BB if portal hypertension
Pyloric Stenosis
Definition: Pyloric muscle hypertrophy causing gastric outlet obstruction Age: <6 months at diagnosis; peak 3-5 weeks Classic presentation: Non-bilious projectile vomiting after feeds (hypochloremic hypokalemic metabolic alkalosis) Physical exam: Palpable “olive-shaped” mass in RUQ Diagnosis: Ultrasound (gold standard) Treatment: Surgical pyloromyotomy
Gastroparesis
Etiology: DM (autonomic neuropathy), idiopathic, meds (GLP-1 RA, opioids), post-surgical Symptoms: Early satiety, nausea, vomiting of undigested food Diagnosis: EGD first to exclude obstruction; gastric emptying scintigraphy (gold standard) Treatment: Anti-emetics, prokinetics (metoclopramide max 12 weeks), dietary modification (small frequent meals, low fat/fiber), pyloromyotomy if refractory
Gastric Cancer
Epidemiology: >90% adenocarcinoma; MC in men, Hispanic, Asian/Pacific Islander, Black populations Risk Factors: Untreated H. pylori (always confirm eradication!), EBV, Lynch, FAP, tobacco, sedentary, poor diet Symptoms: Asymptomatic early; later → dyspepsia, UGIB, weight loss Red flag: New onset dyspepsia in person >60 → EGD Exam finding: Virchow node (left supraclavicular lymphadenopathy) Other types: MALT lymphoma, GIST, NET
Upper GI Bleed (UGIB)
Differential Diagnosis:
- Chronic heartburn/reflux + odynophagia → Esophagitis
- Epigastric pain + NSAID use → PUD
- Cirrhosis + hemodynamic instability → Esophageal varices
- Repeated nausea/vomiting + EtOH/bulimia → Mallory-Weiss tear
- Severe chest pain + crepitus → Boerhaave syndrome
Evaluation & Treatment:
- Resuscitate: IV access, fluids, PRBCs; goal Hgb >7 (>8 if CAD)
- IV PPI (high-dose, BID if varices)
- Octreotide/NSBB if portal hypertension
- Labs: H. pylori stool antigen, CBC, PT/INR, lactate
- Diagnostic EGD (therapeutic intervention)
- CT Angiography if too unstable for EGD (diagnostic, NOT therapeutic; guides IR embolization)
INTESTINAL DISORDERS
Celiac Disease
Pathophysiology: Immune response to gliadin (gluten protein) Genetics: HLA-DQ2 or DQ8 required Risk Factors: FHx, T1DM, Down syndrome, Turner syndrome
Clinical Presentation:
- GI: Diarrhea, steatorrhea, bloating, nausea; sometimes asymptomatic
- Extraintestinal: IDA, osteoporosis, elevated ALT/AST, infertility
- Pathognomonic: Dermatitis herpetiformis (pruritic rash on elbows, knees, buttocks)
Diagnosis:
- Screening serology ON GLUTEN-CONTAINING DIET: Anti-tTG IgA + total IgA (check total IgA to avoid false negatives)
- Gold standard: EGD with duodenal biopsies (on gluten diet)
Treatment: Strict gluten-free diet
Irritable Bowel Syndrome (IBS)
Definition: Functional GI disorder; no structural abnormality Diagnosis: Rome IV criteria (abdominal pain ≥1 day/week × 3 months + bowel habit changes) Subtypes: IBS-D (diarrhea), IBS-C (constipation), IBS-M (mixed), IBS-U (unclassified) Treatment: Dietary modifications, stress management, medications PRN (antispasmodics, loperamide, laxatives)
Inflammatory Bowel Disease (IBD)
Crohn’s Disease:
- Location: Transmural inflammation anywhere in GI tract (MC: ileum + colon, but can be anywhere)
- Complications: Strictures, fistulae, abscess
- Colonoscopy findings: Cobblestone appearance, skip lesions (non-continuous)
- Imaging: CT/MRE shows transmural inflammation
Ulcerative Colitis:
- Location: Continuous inflammation in ascending pattern FROM RECTUM (always involves rectum)
- Extent: Rectum only to entire colon
- Complications: Toxic megacolon (if severe)
- Colonoscopy findings: Confluent erythema, edema, loss of vascularity, erosions/ulcerations
- No skip lesions
General IBD: Risk Factors: FHx, personal hx of autoimmune disease Symptoms: Abdominal pain, diarrhea, ±hematochezia Labs: ESR, CRP, fecal calprotectin; colonoscopy with biopsies
Treatment - Induction of Remission:
- Mild: 5-ASA (mesalamine)
- Moderate-Severe: Corticosteroids (prednisone PO, budesonide PO, methylprednisolone IV) OR biologics
- Goal: Symptomatic AND endoscopic remission
Treatment - Maintenance:
- Mild: 5-ASA
- Moderate-Severe: Biologics (“-mab” drugs: infliximab, adalimumab, etc.)
Surgery:
- Crohn’s: Stricturing disease, fistulizing disease, failure to medical therapy (NOT curative)
- UC: Failure to medical therapy; colectomy generally curative
Toxic Megacolon
Definition: Severe complication of colonic inflammation (dilated colon with systemic toxicity) Causes: IBD (especially UC), C. difficile
Pathophysiology: Severe inflammation → colonic dilation (>6cm) → systemic toxicity
Symptoms: Fever, tachycardia, hypotension, abdominal pain/distension, altered mental status
Diagnosis: Clinical + imaging (colonic dilation >6cm WITHOUT mechanical obstruction)
- 3-6-9 rule: Colonic dilation >6cm is classic
- Imaging: Abdominal X-ray or CT
Treatment:
- Medical (first line, 48-72h trial): IVF, high-dose corticosteroids, vancomycin PO + enema if C. difficile
- Surgical (if no improvement in 48-72h or perforation): Subtotal colectomy with ileostomy
Ileus
Definition: Functional (not mechanical) impairment of GI tract; usually post-operative Symptoms: Abdominal distension, pain, decreased bowel sounds, N/V, absence of flatus/BM Diagnosis: Clinical; imaging shows dilated bowel WITHOUT transition zone (no mechanical obstruction) Imaging findings: Dilated loops, air in rectum/colon, NO transition point Treatment: Bowel rest, NG decompression if necessary
Intestinal Obstruction
Small Bowel Obstruction:
- Etiology: Adhesions (most common post-op), hernias, volvulus, strictures, malignancy
- Imaging: CT abdomen/pelvis (first line; shows dilated small bowel with transition point)
- Treatment: NPO, NG tube decompression; surgery if mechanical cause confirmed
Large Bowel Obstruction:
- MC cause: Colorectal carcinoma
- Other: Sigmoid volvulus (MC volvulus), cecal volvulus, strictures
- Imaging: CT abdomen/pelvis
- Volvulus: Sigmoid (MC) > cecal; can be managed with colonoscopic decompression if uncomplicated
Ischemic Bowel Disease
Acute Mesenteric Ischemia:
- Etiology: Arterial thrombosis/embolism (AF), venous thrombosis
- Symptom: Severe abdominal pain OUT OF PROPORTION to exam findings
- Labs: May have elevated lactate (late finding)
- Diagnosis: CT angiography (gold standard)
- Treatment: Anticoagulation; interventional embolectomy, stenting, or bypass; resect nonviable bowel
Chronic Mesenteric Ischemia (Intestinal Angina):
- Etiology: Atherosclerotic disease
- Symptom: Postprandial (post-eating) abdominal pain within 1 hour of eating; leads to weight loss (“food fear”)
- Diagnosis: CT angiography
- Treatment: Stenting, surgery if refractory
Ischemic Colitis:
- Pathophysiology: Usually non-occlusive; affects watershed areas (SMA/IMA junction at splenic flexure, IMA/internal iliac junction at rectosigmoid)
- Risk Factors: Atherosclerosis, HTN, DM, cocaine use, marathon running, aortic surgery
- Symptoms: Sudden crampy abdominal pain → hematochezia within 24 hours
- Diagnosis: CT with contrast (submucosal edema, wall thickening), colonoscopy
- Treatment: Supportive care (fluids, antibiotics if severe); surgery if fulminant/perforation
BILIARY DISORDERS
Cholelithiasis (Gallstones)
Risk Factors: 4 F’s—Female, Forty, Fat, Fertile (also: Native American, rapid weight loss, ileal disease) Diagnosis: RUQ ultrasound (gold standard) Treatment: Asymptomatic → observation; symptomatic → cholecystectomy
Acute Cholecystitis
Definition: Inflammation of gallbladder, usually from stone impaction in cystic duct Symptoms: RUQ pain, fever, N/V (Murphy sign positive) Diagnosis: RUQ ultrasound; HIDA scan if ultrasound equivocal Treatment: Cholecystectomy (laparoscopic preferred); antibiotics if complicated
Chronic Cholecystitis
Definition: Repeated episodes of inflammation from recurrent stone impaction Diagnosis: Thickened gallbladder wall on ultrasound Treatment: Elective cholecystectomy to prevent acute episodes
Cholangitis
Definition: Infection/inflammation of common bile duct; usually from obstruction (stone, stricture, malignancy) Classic triad: Fever + RUQ pain + jaundice (Charcot triad); adds hypotension + altered mental status = Reynolds pentad Diagnosis: ERCP (diagnostic + therapeutic) Treatment: IV antibiotics, ERCP with sphincterotomy ± stone extraction
HEPATIC DISORDERS
Acute Hepatitis
Alcoholic Hepatitis:
- Transaminitis pattern: AST:ALT >2:1 (very characteristic)
- Diagnosis: Clinical, biopsy if needed
- Treatment: Abstinence, corticosteroids if severe (discriminant score >32), nutritional support
MASLD (Metabolic Dysfunction-Associated Steatotic Liver Disease):
- Definition: Hepatic steatosis + cardiometabolic risk factors (obesity, HTN, HLD, T2DM)
- Diagnosis: FIB-4 score, transient elastography, fibroscan
- Treatment: Avoid alcohol, weight loss >10%, GLP-1 RA, resmetirom (GLP-1/GCG agonist), vitamin E (non-diabetic MASH only)
Viral Hepatitis:
- Hep A & E: Fecal-oral transmission
- Hep B & C: Blood-borne transmission
- Hep B serology:
- Surface Ab ONLY = vaccinated
- Surface Ab + Core Ab = previous infection (±immunity)
- Surface Ag = ACTIVE INFECTION
- Treatment: Supportive for A/E; antivirals for B/C
Drug-Induced Liver Injury (DILI):
- Common drugs: NSAIDs, statins, acetaminophen, antibiotics
- Pattern varies by agent
- Management: Discontinue offending drug, supportive care
Autoimmune Hepatitis:
- Diagnosis: Elevated transaminases + elevated immunoglobulins + positive autoantibodies
- Treatment: Corticosteroids, azathioprine
Cirrhosis
Compensated Cirrhosis:
- No complications (no ascites, encephalopathy, variceal bleed, jaundice)
- Supportive care, address underlying cause
Decompensated Cirrhosis (must have ≥1 of):
1. Jaundice
- Mechanism: Hepatic synthetic dysfunction
- Management: Supportive, monitor for hepatic encephalopathy
2. Hepatic Encephalopathy:
- Pathophysiology: Ammonia accumulation + neuroinflammation
- Precipitants: Dehydration, infection, over-diuresis, GI bleed, high protein diet, constipation, opioids, sedatives
- Symptoms: Forgetfulness → sleep-wake reversal → confusion/disorientation → lethargy/coma
- Sign: Asterixis (flapping tremor)
- Diagnosis: Clinical (ammonia levels NOT useful)
- Treatment:
- Lactulose (first line): Titrate to 2-3 soft BMs daily (goal 3-4/day); divides into 2-3 doses
- Rifaximin: Add-on/second-line if inadequate lactulose response
- Identify/treat precipitants
- Thiamine before glucose in altered patients
3. Ascites:
- Pathophysiology: Portal HTN → ↑ hydrostatic pressure → plasma leakage into peritoneal space
- Diagnosis: Ultrasound; diagnostic paracentesis → calculate SAAG (serum-ascites albumin gradient)
- Treatment:
- Sodium restriction: <2 g/day
- Diuretics (ratio 100:40):
- Spironolactone 100 mg daily (potassium-sparing)
- Furosemide 40 mg daily
- Therapeutic paracentesis: Remove fluid; give IV albumin if >5L removed (or >4.5L per some sources)
- Refractory ascites: TIPS
4. Spontaneous Bacterial Peritonitis (SBP):
- Definition: Infection of peritoneal fluid (no perforation)
- Typical organisms: E. coli, Klebsiella pneumoniae
- Diagnosis: Paracentesis—PMN >250 cells/μL is diagnostic (don’t need positive culture)
- Symptoms: Fever, abdominal pain, altered mental status
- Treatment: IV cefotaxime + IV albumin (improves renal function/survival)
5. Variceal Hemorrhage:
- Pathophysiology: Portal HTN → dilated veins at gastroesophageal junction
- Prophylaxis: NSBB (reduces portal pressures) OR endoscopic variceal ligation (EVL)
- Acute bleeding: Endoscopic control, blood/volume resuscitation, IV octreotide
- Secondary prevention: NSBB + EVL
- Refractory: TIPS
6. HCC (Hepatocellular Carcinoma) Surveillance:
- RUQ ultrasound every 6 months in cirrhotic patients
- Diagnosis: Imaging (CT/MRI) or biopsy if imaging equivocal
- Treatment: Depends on stage (resection, transplant, locoregional therapy, systemic therapy)
Transaminitis Patterns (AST/ALT)
<200: Chronic liver disease, mild acute hepatitis 200-1000: Moderate acute hepatitis >1000: Acute viral hepatitis, “shock liver” (hypoxic/hypotensive), severe DILI (especially acetaminophen)
GI BLEEDING
Upper GI Bleeding
See “Upper GI Bleed (UGIB)” section under Gastric Disorders above
Lower GI Bleeding
Etiologies by age:
- Young: Hemorrhoids, anal fissures, IBD
- Middle-aged: Diverticular disease, angiodysplasia
- Elderly: Diverticulosis, angiodysplasia, ischemic colitis
Workup: Colonoscopy (gold standard for diagnosis and treatment) Massive bleeding: CT angiography if unstable or ongoing transfusion requirement
COLORECTAL DISORDERS
Hemorrhoids (Internal vs External)
Internal: Painless bright red blood per rectum, may prolapse External: Painful, especially with thrombosis Treatment: Dietary fiber, stool softeners, sitz baths; procedural (banding, sclerotherapy) if refractory
Anal Fissure
Symptoms: Severe pain with bowel movements, bright red bleeding Exam: Visible tear in anal canal (posterior midline most common) Treatment: Stool softeners, sitz baths, topical nitrates/calcium channel blockers; surgery if chronic/severe
Constipation
Causes: Low fiber, dehydration, medications, hypothyroidism, IBS-C, structural obstruction Workup: Rule out obstruction; colonoscopy if age >50 or red flags Treatment: Increase fiber, fluids, physical activity; osmotic/stimulant laxatives PRN; address underlying cause
Fecal Impaction / Incontinence
Impaction: Hard stool in rectum, often from chronic constipation; manual disimpaction, softeners Incontinence: Loss of sphincter control or stool leakage; assess for fecal impaction, sphincter injury, neurologic cause
Diverticular Disease
Diverticulosis (asymptomatic):
- Outpouching of colonic mucosa through muscular wall
- Increased risk with age, low-fiber diet
- No treatment if asymptomatic
Diverticulitis (symptomatic):
- Inflammation/infection of diverticulum
- Symptoms: LLQ pain, fever, N/V
- Diagnosis: CT abdomen/pelvis (gold standard)
- Treatment:
- Uncomplicated: Outpatient antibiotics + diet (or bowel rest)
- Complicated (abscess, fistula, perforation, obstruction): IV antibiotics ± percutaneous drainage ± surgery
Volvulus
MC types: Sigmoid (MC) > cecal Symptoms: Acute onset abdominal pain, distension, constipation Diagnosis: Abdominal X-ray (coffee bean appearance); CT confirms Treatment: Colonoscopic decompression if uncomplicated; surgery if complicated or recurrent
Toxic Megacolon
See under Inflammatory Bowel Disease section above
Rectal Prolapse
Definition: Protrusion of rectal mucosa or full-thickness rectum through anus Symptoms: Bloody stools, mucus discharge, sensation of mass Risk factors: Straining, chronic diarrhea, advanced age Treatment: Stool softeners, pelvic floor PT; surgery if refractory
Abscess / Fistula
Anorectal abscess: Collection of pus in tissue surrounding anus/rectum; presents with pain, fever, fluctuance
- Treatment: Incision and drainage
Fistula: Abnormal tract between anal canal and skin
- Often follows abscess drainage
- Treatment: Surgical fistulotomy or advancement flap
Polyps
Types: Hyperplastic, adenomatous (tubular, tubulovillous, villous), sessile serrated, traditional serrated Surveillance: Based on polyp size, histology, number Management: Polypectomy; colonoscopic resection preferred
PANCREATIC DISORDERS
Acute Pancreatitis
Etiologies: Gallstones (MC), alcohol (2nd MC), hypertriglyceridemia, medications, post-ERCP, trauma, idiopathic Symptoms: Severe epigastric pain radiating to back, N/V Diagnosis: Serum/urine lipase (>3x ULN); CT shows pancreatic inflammation Labs: Elevated lipase, amylase, may have elevated transaminases (suggests biliary obstruction) Treatment: NPO, IV hydration, pain control, address underlying cause Complications: Infected pancreatic necrosis, ARDS, multiorgan failure
Chronic Pancreatitis
Etiologies: Chronic alcohol use (MC), cystic fibrosis, hereditary, autoimmune, idiopathic Symptoms: Chronic epigastric pain (may be constant or episodic), malabsorption (steatorrhea), diabetes (from endocrine dysfunction) Diagnosis: CT/MRI shows chronic changes; pancreatic elastography; 72-hr fecal fat if malabsorption suspected Treatment: Pain management, pancreatic enzyme replacement, treat diabetes, alcohol cessation
SMALL INTESTINAL DISORDERS
Appendicitis
Symptoms: RLQ pain (McBurney point—1/3 distance from ASIS to umbilicus), fever, anorexia Diagnosis: CT abdomen/pelvis Treatment: Appendectomy; antibiotics perioperatively
Celiac Disease
See under Intestinal Disorders section above
Intussusception
MC age: 6 months–3 years (ileocolic most common) Symptoms: Colicky abdominal pain, palpable RUQ mass, bloody stools (“currant jelly”) Diagnosis: Abdominal ultrasound or CT Treatment: Air or hydrostatic reduction if uncomplicated; surgery if perforation/failed reduction
Small Bowel Obstruction
See under Intestinal Obstruction section above
INGESTION OF TOXIC SUBSTANCES, FOREIGN BODIES, FOOD IMPACTION
Food Bolus Impaction
Etiologies: EoE, Schatzki’s ring, peptic stricture, esophageal cancer Symptoms: Inability to swallow, regurgitation, chest pain/pressure, drooling Red flags for perforation: Fever, subcutaneous emphysema (crepitus on chest wall), severe chest/neck pain
- If perforation suspected → CT PRIOR to EGD Diagnosis: EGD Treatment: EGD for removal or advancement into stomach
- Timing: Within 24 hours typically; within 2 hours if unable to tolerate secretions
Foreign Body Ingestion
MC objects in children: Coins (most common in young kids); fish/chicken bones, button batteries, magnets MC objects in adults: Food bolus, fish/chicken bones, dentures High-risk populations: Children 6 months–3 years, psychiatric patients, elderly with dentures, prisoners
Spontaneous passage: 80-90% pass spontaneously Imaging: X-ray first (radiopaque objects, location); CT if negative X-ray or perforation suspected
Location & intervention:
- Above cricopharyngeus: ENT
- Below cricopharyngeus: GI
Timing of intervention:
- EMERGENT (<2 hours): Unable to tolerate secretions; high-risk objects in esophagus (button batteries, sharp objects)
- URGENT (2-24 hours): Esophageal FB; sharp objects in stomach/duodenum; magnets within endoscopic reach
- NON-URGENT (<72 hours): Smooth objects in stomach past endoscopic reach; objects likely to pass
Toxic Ingestion: Caustic Material
Examples: Bleach, drain cleaner, detergent, toilet cleaner Presentation: Oropharyngeal burns, drooling, dysphagia/odynophagia, chest pain, abdominal pain, stridor (suggests supraglottic injury)
Management:
- Assess airway: Intubate early if stridor or respiratory distress
- IV access, IV PPI
- DO NOT induce emesis (worsens injury)
- DO NOT give activated charcoal
- CXR, CT C/A/P if perforation suspected
- EGD within 12-24 hours (assess degree of ulceration)
- Prognosis: Deep ulceration → ↑ risk of stricture, esophageal SCC
Toxic Ingestion: Toxic Substances & Body Packing
Management:
- Contact Poison Control for all suspected toxic ingestions
- Activated charcoal: Most effective <1 hour; binds most drugs (NOT EtOH, metals, lithium, caustics)
- C/I: Unprotected airway, bowel obstruction/perforation
- Whole Bowel Irrigation (PEG 1-2 L/hr): For drug packets, iron, lithium, sustained-release meds not amenable to AC
Ingested drug packets:
- Imaging: CT (gold standard)
- Rupture risk: Life-threatening
- Management: Whole bowel irrigation if asymptomatic; surgery if ruptured or obstruction
Toxic Ingestion: Acetaminophen Overdose
Toxicity Mechanism: Toxic metabolite NAPQI accumulates → hepatocellular necrosis
Clinical Phases:
- Phase 1 (<24h): N/V, malaise, anorexia; labs often NORMAL (can falsely reassure)
- Phase 2 (24-72h): RUQ pain, AST/ALT rise, elevated PT/INR
- Phase 3 (72-96h): Peak hepatotoxicity—AST/ALT >1,000 (often 3k-10k), jaundice, coagulopathy, encephalopathy, AKI
- Phase 4 (4 days–2 weeks): Recovery OR progression to acute liver failure/death
Evaluation:
- Plot 4-hour serum APAP level on Rumack-Matthew nomogram
- Start NAC if at or above “possible toxicity” line (don’t wait for full results)
Treatment:
- IV N-acetylcysteine (NAC): Replenishes glutathione, helps metabolize toxic NAPQI
- Nearly 100% protective if given <8 hours of ingestion
- Still beneficial up to 24 hours
- Continue even if acute liver failure develops (improves transplant survival)
- Continue until AST/ALT trending down, INR <2, clinical improvement
- Activated charcoal: If <4 hours and no C/I
- Liver transplant: Consider referral
NUTRITION & METABOLIC DISORDERS
Food Allergies & Intolerances
IgE-Mediated (Immediate, Anaphylactic):
- Top 9 allergens: Milk, eggs, fish, shellfish, tree nuts, peanuts, wheat, soybeans, sesame
- Treatment: Epinephrine 0.3 mg IM to anterolateral thigh (first-line); antihistamines/steroids are adjuncts
Food Protein-Induced Enterocolitis Syndrome (Non-IgE mediated):
- Presentation: Severe N/V/D within 1-4 hours
- Population: Typically infants; often outgrow by age 4
- Common triggers: Soy, milk, grains
- Treatment: Avoid trigger food
Lactose Intolerance:
- Mechanism: Lactase enzyme deficiency
- Symptoms: Bloating, gas, diarrhea after dairy
- Treatment: Dietary restriction OR lactase enzyme supplementation
- Pearl: Supplement calcium if avoiding dairy
Malnutrition & Refeeding Syndrome
Protein/Calorie Malnutrition:
- Assessment: By RD using ASPEN criteria
- Patterns:
- Calorie deficiency: Wasting (fat, muscle), preserved albumin initially, “skin and bones”
- Protein deficiency + adequate calories: Edema, ascites, low albumin, hepatic steatosis
- Supplemental feeding: Enteral (PO, NG, PEG, G-J) always preferred to TPN when possible
Refeeding Syndrome:
- Definition: Life-threatening complication when nutrition abruptly resumed in severely malnourished patient
- Mechanism: Insulin secretion → sudden intracellular shift in phosphate, K+, Mg → electrolyte abnormalities
- Risk factors: NPO >5-7 days, anorexia nervosa, chronic EtOH, cancer cachexia, starvation
- Complications: Cardiac dysrhythmias, respiratory failure, seizures, rhabdomyolysis, death
- Prevention (NICE Guidelines):
- Start at 10 kcal/kg/day, increase slowly over 4-7 days
- Supplement phosphate, K+, Mg BEFORE refeeding starts
- Thiamine 200-300 mg before and during refeeding
- Monitor electrolytes Q6H in high-risk patients
- Give thiamine BEFORE glucose in altered patients (prevent Wernicke encephalopathy)
Hypervitaminosis & Hypovitaminosis
General principles:
- Fat-soluble vitamins (A, D, E, K): Can accumulate → toxicity
- Water-soluble vitamins: Excess excreted in urine (rare toxicity)
Vitamin Deficiency Sites & Patterns:
- Duodenum: Iron absorption
- Jejunum: ADEK, water-soluble vitamins
- Ileum: B12, bile salts
- Post-bariatric: ADEK, iron, B12, thiamine (especially RYGB)
Specific Deficiencies:
| Vitamin | Symptoms | Associations |
|---|---|---|
| A | Night blindness, xerophthalmia | Fat malabsorption, RYGB |
| B1 (Thiamine) | Beriberi (wet: CHF/edema; dry: neuropathy/ataxia/weakness); Wernicke’s (encephalopathy, LR palsy, nystagmus, ataxia); Korsakoff’s (confabulation, anterograde amnesia) | Chronic EtOH, RYGB |
| B3 (Niacin) | Pellagra (4 D’s: dermatitis, diarrhea, dementia, death) | EtOH, RYGB |
| B6 (Folate) | Megaloblastic anemia, impaired cognition | EtOH, pregnancy, phenytoin, RYGB |
| B12 | Megaloblastic anemia, paresthesias, glossitis | Crohn’s ileitis, ileal resection, strict vegans, atrophic gastritis/pernicious anemia |
| C | Scurvy (fatigue, bleeding, poor wound healing, “corkscrew hairs”) | EtOH, poor intake, RYGB |
| D | Rickets (children; poor growth, delayed fontanelle, frontal bossing, rachitic rosary, bowing legs), osteomalacia (adults; bone pain, fractures), hypocalcemia, 2° hyperparathyroidism | Limited sunlight, CKD, fat malabsorption, obesity, RYGB, phenytoin |
| K | Prolonged PT/INR, easy bruising, newborn hemorrhagic disease | Warfarin, fat malabsorption, RYGB |
Vitamin Excess:
Vitamin A Excess:
- Sources: Excess supplementation, tretinoin
- At-risk: Infants, children (most susceptible); pregnant women (teratogenic)
- Acute symptoms: N/V, dizziness, blurry vision
- Chronic symptoms: Dry/cracked skin, hair loss, brittle nails, hepatic fibrosis/cirrhosis, idiopathic intracranial hypertension
Vitamin D Excess:
- Source: Excess supplementation
- Mechanism: ↑ calcium absorption → hypercalcemia
- Symptoms: Kidney stones, muscle weakness, cardiac arrhythmias, GI symptoms (abdominal pain, N/V, constipation)
Metabolic Disorders
Phenylketonuria (PKU):
- Epidemiology: MC European ancestry; autosomal recessive
- Pathophysiology: Inability to metabolize phenylalanine → tyrosine (varies in severity)
- Presentation: Progressive developmental delay if undiagnosed; “musty urine” odor
- Diagnosis: Newborn metabolic screening
- Treatment: Low phenylalanine diet, blood monitoring
G6PD Deficiency:
- Epidemiology: African, Mediterranean, Asian descent; X-linked (MC in males)
- Pathophysiology: ↓ G6PD → ↓ resilience to oxidative stress → hemolysis
- Triggers: Fava beans, medications (sulfa, macrobid, antimalarials), infections
- Asymptomatic until oxidative stress → acute hemolysis (jaundice, dark urine, splenomegaly, back pain, renal insufficiency)
- Diagnosis: Newborn metabolic screening; labs show hemolytic anemia (↓Hgb, ↑LDH, ↓haptoglobin, ↑reticulocytes)
- Treatment: Eliminate triggers, hydration, transfusions for hemolytic episodes, folic acid (support RBC production)
Paget’s Disease:
- Epidemiology: MC males >60; unclear etiology (possibly paramyxovirus: measles/mumps)
- Pathophysiology: Disordered bone remodeling—lytic phase → mixed phase → sclerotic phase
- Location: 1+ bone (MC: pelvis, femur, lumbar spine, skull)
- Presentation: Bone pain, pathologic fractures
- Diagnosis: X-ray (lytic/sclerotic lesions, “cotton wool appearance”); biopsy (mosaic lamellar bone, large osteoclasts with many nuclei)
- Treatment: Bisphosphonates, surgery for fractures/malformations, PT
Rickets:
- Pathophysiology: Vitamin D deficiency → defective bone mineralization (osteomalacia in adults)
- Causes: Intestinal malabsorption, ↓ intake, ↓ sunlight, phenytoin, chronic liver/kidney disease
- Symptoms/Signs: Bone pain, fractures, hypocalcemic Sx (tetany, paresthesias); poor growth, delayed fontanelle closure, frontal bossing, craniotabes, rachitic rosary, enlarged epiphyses, bowing legs
- Labs: ↓ Vitamin D, ↓ calcium, ↑ ALP, ↑ PTH
- Treatment: Dietary supplementation (Vitamin D, calcium), address underlying cause
KEY PANCE GI EXAM PEARLS
Esophagus:
- Barrett’s = columnar metaplasia from chronic GERD; risk for adenocarcinoma
- Achalasia = bird beak + manometry; treat with dilation/myotomy/botox
- Zenker diverticulum = dysphagia/regurgitation/halitosis; requires surgery
- Always obtain EGD before manometry for constant/progressive dysphagia
- Boerhaave = emergency; high mortality if delayed >24h
Stomach:
- H. pylori MUST be confirmed eradicated after treatment
- PUD: GU pain immediately after eating; DU pain 2-3h after eating or at night
- New dyspepsia age >60 → EGD
- Pyloric stenosis = non-bilious projectile vomiting in infants <6 months
Intestines:
- Celiac = anti-tTG IgA + total IgA on gluten diet; gold standard = EGD biopsy
- IBD: Crohn’s = transmural + anywhere; UC = continuous from rectum only
- Toxic megacolon = >6cm dilation + systemic toxicity; medical 48-72h, then surgery
- Ischemic colitis = watershed areas; sudden pain → hematochezia
Liver:
- Ascites: sodium <2g/day + diuretics (100:40 ratio spiro:lasix) + therapeutic paracentesis
- SBP = PMN >250 (don’t need positive culture); treat with cefotaxime + albumin
- HE = lactulose 3-4 stools/day ± rifaximin; identify precipitants
- Variceal bleed = octreotide + band ligation; TIPS if refractory
Toxins:
- APAP: Plot 4-hour level; NAC within 8h (nearly 100% effective), still beneficial ≤24h
- Caustic ingestion: DO NOT induce emesis or give AC; EGD within 12-24h
- Foreign body: 80-90% pass spontaneously; emergency if button battery/sharp in esophagus
Nutrition:
- Refeeding syndrome: NPO >5-7 days; thiamine BEFORE glucose; supplement electrolytes BEFORE feeding
- RYGB: At risk for ADEK, iron, B12, thiamine deficiency
- Enteral nutrition always preferred to TPN