A few words first...
- Review, review, review
- I'll focus on key points
- Special attention to red text
- Special attention to "most common cause of..."
- Special attention to triads, quadrads
- Always consider deadly causes first
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Dysphagia
- Difficulty swallowing, sensation of impaired food passage
- Solids: mechanical (obstructive)
- Solids and liquids: motility disorder
- Oropharyngeal dysphagia: neuromuscular disorder (CVA)
- Progressive (CA) vs. non-progressive (web)
- Strictures 2° to reflux
- Workup
- Esophagram, endoscopy, motility studies
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- Treat underlying disease process
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Dysphagia
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- Infectious
- Botulism, diptheria, poliomyelitis, rabies, Sydenham's chorea (rheumatic fever), tetanus
- Immunologic
- Scleroderma, multiple sclerosis, myasthenia gravis, polymyositis
- Motor/nerve dysfunction
- Achalasia
- Aperistalsis of esophagus (loss of Auerbach's plexus in the esophagus)
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- Cranial nerve palsies
- Achalasia
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Dysphagia Mechanical
- CA (usually squamous)
- Risk factors: smoking, achalasia, caustic ingestion
- Extraluminal obstruction (tumor)
- Thyroid goiter
- Zenker's diverticulum
- Rare, elderly patients
- Pharyngoesophageal outpouching (above the upper esophageal sphincter)
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Dysphagia Obstructive Mechanical
- Proximal obstruction
- Café coronary: Sudden cyanosis and collapse caused by food obstruction
- Distal obstruction
- Steakhouse syndrome: Most common cause of distal obstruction (improperly chewed meat)
- Schatzki ring: ring-like constriction of lower esophagus
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- Webs (Congenital or acquired)
- Circumferential mucosal outpouchings
- Plummer-Vinson syndrome: anterior esophageal webs+ iron deficiency anemia + spooning of the nails
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Singultus
Hiccups/Hiccoughs/Singultus
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- Involuntary stimulation of the respiratory reflex with spastic contraction of inspiratory muscles on closed glottis
- Benign: gastric distention, smoking, EtOH
- Persistent: damage to vagus or phrenic nerves, CNS lesions
- Treatment: Chlorpromazine (Thorazine) if persistent
- Organic
- CNS: neoplasm, MS, ? ICP
- PUD, goiter, pericarditis, pacemaker, STEMI?
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Esophageal Rupture
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- Majority are iatrogenic
- Endoscopy, dilatation, biopsy, sclerotherapy
- Most at pharyngoespohageal junction
- Mallory-Weiss tear (partial thickness tear)
- Location: GE junction
- Common cause of upper GI bleeding
- Vomiting, retching
- Risk factors: EtOH, hiatal hernia
- Spontaneous resolution is common
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Esophageal Rupture
- Boerhaave's syndrome (full-thickness tear)
- Usually males, ages 40-60
- Typically associated with vomiting
- Left posterior distal rupture
- Mediastinitis (first chemical, then infectious)
- Severe chest pain, shock, sepsis (antibiotics)
- Air in mediastinum (Hamman's crunch)
- Pyopneumothorax
- Gastrografin (water-soluble) UGI, CT
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- X-ray: mediastinal air, left pleural effusion, pneumothorax, widened mediastinum
Pneumomediastinum / Subcutaneous Emphysema
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Esophageal Foreign Bodies
- Levels of narrowing
- Cricopharyngeus muscle (C6)
- Aortic arch (T4)
- Tracheal bifurcation (T6)
- Gastroesophageal junction (T11)
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- Coin X-rays
- AP orientation: coin in trachea (same plane as vocal cord orientation- sagittal)
- Transverse orientation: coin in esophagus
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Foreign Body
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Esophageal Foreign Body
Esophageal Foreign Bodies
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- Disk batteries characteristic double density radiographic appearance.
- Soft drink aluminium pull tabs - radiolucent
- Contrast studies may be required
- CT scan- good for chicken and fish bones, small plastic pieces
- Most foreign bodies will pass if they traverse the pylorus (exceptions: pointed, sharp, large)
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Sharp Foreign Body
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Large-corrosive-impacted foreign Body
Esophageal Foreign Bodies
- Button batteries
- If seen in esophagus, must be removed immediately
- Rapid burns with perforation in 6 hours
- Lithium batteries have the worst outcomes
- Batteries that do not need to be removed
- Passed esophagus, asymptomatic
- Passed the pylorus within 48 hours
- Most will pass completely in 48-72 hours
- Asymptomatic batteries in the stomach are followed by serial X-rays
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- Treatment if in esophagus: Gl consult broad-spectrum antibiotics
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Esophageal Food Impaction
- Most patients with food impaction have underlying esophageal pathology
- Must evaluate for cause after dislodgement
- Treatment options
- Endoscopic retrieval
- Foley catheter removal
- Glucagon: relaxes lower esophageal sphincter
- Nifedipine: reduces lower esophageal tone
- Carbonated beverages: gaseous distention may push bolus into the stomach
- Avoid meat tenderizers (papain)
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Caustic Ingestions
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- Inconsistent relationship between oral and esophageal findings
- Gastric decontamination is contraindicated
- Dilution (water or milk) can cause vomiting
- Indicated only for solid alkali ingestions
- Neutralization can generate excess heat
- Indicated only for hydrofluoric acid ingestions (milk or magnesium citrate)
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Endoscopy is the best diagnostic tool
Caustic Ingestions
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- Complications
- Early: acute airway compromise due to edema, perforation
- Late: stricture, perforation
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Peptic Ulcer Disease
- Incidence decreasing in general population and increasing in the elderly (liberal use of NSAIDs)
- Duodenal > gastric (relief of pain with eating)
- Helicobacter pylori responsible for most cases
- Predisposing factors:
- Smoking, alcohol
- NSAIDs and steroids
- Zollinger-Ellison syndrome
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- Treatment:
- Antibiotics against H. pylori (amox, flagyl)
- H2 blockers
- Proton pump inhibitors (omeprazole)
- Surface protectants (sucralfate)
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- Complications:
- Bleeding
- Perforation (can cause pancreatitis)
- Gastric outlet obstruction
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GI Bleeding Definitions
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- Hematemesis
- UGI bleeding (proximal to ligament of Treitz)
- Hematochezia
- Anus, rectum, sigmoid: bright red
- Transverse and right colon: maroon
- Rapid UGI bleed (uncommon)
- Usually colon or small bowel
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- Melena (black, tarry stools)
- Usually UGI bleed
- Black color from effects of acid and digestion
- Gl breakdown of blood causes increased BUN
- Bismuth (Pepto-Bismol) black stool- heme-neg
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Upper GI Bleeding Adults
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- PUD most common (usually duodenal)
- Gastric erosions (alcohol, NSAIDs)
- Varices
- Mallory-Weiss tears
- Esophagitis (common in pregnancy)
- Duodenitis
- Patients with a previously documented GI lesion bleed from the same site in only 60% of cases
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Upper GI Bleed Therapies
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- No benefit to initiating PPI or H2 blocker in the ED for patients with UGIB
- Octreotide (Somatostatin) for esophageal varices / causes splanchnic blood flow reduction / sclerotherapy
- Vasopressin (vasconstrictor) – used in variceal hemorrhage to limit exsanguination when endoscopy unavailable or delayed
- Sengstaken-Blakemore tube – esophageal varices
- Linton tube – Gastric varices
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Upper GI Bleed Sengstaken Blakemore Tube
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Upper GI Bleed Linton Tube
Lower GI Bleeding Adults
- Upper GI Bleeding most common cause of LGIB
- Diverticulosis
- Angiodysplasia (AV malformations)
- Associated with hypertension and aortic stenosis
- Cancer/polyps
- Rectal disease
- Inflammatory bowel disease
- Aortoenteric fistula
- Erosion of synthetic vascular graft into gut (often preceded by premonitory bleed- prompt surgical consultation)
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GI Bleeding Low Risk Criteria –Discharge Home
- No comorbid diseases
- Normal vital signs
- Negative or trace positive stool guaiac
- Negative Gl aspirate (if done)
- Normal H/H (consider pt's baseline)
- Good home support
- Understanding of signs & symptoms of significant bleeding
- F/U arranged in 24hrs
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Osler-Weber-Rendu Syndrome
- Hereditary hemorrhagic telangiectasias
- Autosomal dominant
- Multiple small telangiectasias of the skin, mucous membranes, Gl tract
- Recurrent epistaxis, positive family history
- Recurrent episodes of GI bleeding, gross or occult
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Bilirubin
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- Increased unconjugated (indirect) bilirubin
- Hemolysis
- Decreased conjugation (Gilbert's syndrome, neonatal jaundice, sepsis)
- Increased conjugated (direct) bilirubin
- Hepatocellular disease (viral hepatitis, drug-induced hepatitis, cirrhosis, sepsis)
- Obstruction (stone, tumor, infection)
- CHF
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Hepatitis
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- Alcoholic hepatitis
- Causes: viral and toxic
- Malaise, jaundice, increased ALT (SGPT) and AST (SGOT), increased bilirubin
- Increased PT/INR: marker of significant liver dysfunction
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Hepatitis A
- Viral Type A (infectious)
- Fecal-oral transmission, contaminated water or food. Not associated with chronic carrier state
- Prophylaxis: Hep A vaccine
- Immune globulin within 2 weeks of exposure (travellers, household contacts)
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Hepatitis B
- Viral Type B (HBV)
- Percutaneous, parenteral or sexual exposure
- Incubation period is 1-6 months
- Complications: cirrhosis, liver cancer, carrier state (10%)
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- Markers
- HBsAg: positive early, active infection
- HBsAb: positive after clearance of HBsAg best marker for immunity to HBV
- HBeAg: implies high infectivity
- HBcAb: Appears after HBsAg, persists for life. Best indicator of history of HBV infection
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Hepatitis B
- Healthcare worker hepatitis B exposure (source known to be HBsAg-positive)
- Unvaccinated
- HB immune globulin
- Vaccination (0, 1 mo, 6 mos)
- Vaccinated
- Incomplete series: vaccine booster
- Test for HBsAb: if adequate antibodies, no treatment; otherwise: HBIG and vaccine booster
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Hepatitis C
- Formally referred to as non-A, non-B
- Linked to blood transfusions, injection drug use
- Higher incidence in HIV victims
- 50% develop chronic disease cirrhosis, CA
- Seroconversion after percutaneous exposure HCV-positive source is about 2%
- No effective vaccine for HCV
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Other Hepatitis Types
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- Hepatitis delta (HDV): Requires HBsAG for co-infection
- IV drug users, homosexual patient population, hemophiliacs / high likelihood for sequelae
- Hepatitis E Virus
- Oral-fecal transmission
- Encountered in Asia, Africa, Russia
- Hep G Virus: blood transfusions, sexual contact
- Indications for hospitalization (any hepatitis)
- Encephalopathy, PT/INR significantly increased, dehydration, hypoglycemia, bilirubin over 20, age over 45, immunosuppression
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Hepatic Encephalopathy
- Precipitants: “LIVER” (Librium [sedatives], Infection, Volume loss, Electrolytes disorders, Red blood cells in the gut)
- Others: dietary protein excess, worsening hepatocellular function
- Early sign is "sleep inversion” (sleeping during the day, awake at night)
- Asterixis ("liver flap")
- Ammonia levels: arterial is best
- Check for hypoglycemia
- Treatment: neomycin, lactulose, decrease dietary protein, avoid sedatives, avoid bicarbonate (alkalosis can worsen encephalopathy)
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Spontaneous Bacterial Peritonitis
- Occurs with chronic liver disease
- Portal hypertension ? bowel edema ? migration and leakage of enteric organisms (E. coli, Enterococcus)
- Abdominal tenderness, worsening ascites, encephalopathy, fever, sepsis, shock
- Diagnosis: paracentesis with increased WBCs
- Neutrophil count > 250 cells/µL
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Gallbladder (1)
- Stones: bilirubin or cholesterol (radiolucent)
- Biliary colic: pain and vomiting due to obstruction by stones (without inflammation)
- Cholecystitis
- Most common cause of surgical abdominal pain in the elderly
- Obstruction ? distention pain / vomiting / inflammation ? infection (usually E. coli, Klebsiella) ? increased WBCS
- Gallstone ileus: rupture of stone into small bowel with obstruction at ileocecal valve
- Pneumobilia: air in biliary tree (from bowel)
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Gallbladder (1)
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Gallbladder (2)
- Acalculous cholecystitis
- No stones
- Usually a complication of another process (trauma, burn, postpartum, post-op, narcotics)
- Patients often critically ill
- Can cause GB perforation
- Increased risk with diabetics and elderly
- Greater morbidity than calculous cholecystitis
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- Ascending cholangitis
- Infection spreading through biliary tree
- Charcot's triad: jaundice, fever, RUQ pain
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Gallbladder (3)
- Biliary ducts
- Common bile duct: from junction of cystic and hepatic ducts to duodenum
- Ultrasound is the diagnostic study of choice (shows stones, wall thickening, duct dilatation, sonographic Murphy's sign, but not inflammation)
- HIDA scan and U/S have similar sensitivities and specificities
- HIDA scan is positive if GB is not visualized (cystic duct obstruction; best test for GB function) Contrast excreted by hepatocytes into the biliary tree.
- ERCP: Indicated for choledocholithiasis (stone near ampula of vater)
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Gallbladder Ultrasound & HIDA Scan
Pancreatitis Causes
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Two leading causes: gallstones, ethanol abuse
- Obstructive: gallstones, tumors
- Toxic: ethanol, methanol
- Traumatic injury (pediatrics)
- Drugs: thiazides
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This download link is referred from the post: MBBS 2025 Lecture Notes for all subjects