What are the key concepts and diagnoses in gastroenterology, including peptic ulcer disease, achalasia, gastrointestinal bleeding, gut obstruction, inflammatory bowel disease, irritable bowel syndrome, liver disease, pancreatitis, and their respective causes, diagnoses, and management?

Gastroenterology Key Concepts

Peptic Ulcer Disease (PUD)

Four Most Common Complications of PUD

The four major complications of peptic ulcer disease are bleeding (most common at 73%), perforation (9%), gastric outlet obstruction (3%), and penetration. 1, 2, 3

• Hemorrhage is by far the most frequent complication, with an annual incidence of 0.02-0.06% in the general population and a 30-day mortality of 8.6% 1
• Perforation occurs less commonly (annual incidence 0.004-0.014%) but carries the highest mortality at 23.5% and accounts for approximately 40% of all ulcer-related deaths 1
• Gastric outlet obstruction has become rare (3% of complications) due to improvements in medical management 3
• Penetration into adjacent organs represents the fourth major complication 2

The perforation-to-bleeding ratio is approximately 1:6, though perforation remains the most common indication for emergency surgery 1

Most Common Causes of PUD

Helicobacter pylori infection (42% of cases) and NSAID/aspirin use (36% of cases) are the two principal causes of peptic ulcer disease. 3, 4

• H. pylori infection affects approximately 42% of patients with PUD and increases the lifetime risk of peptic ulcer to approximately 1 in 6 (17%) among infected individuals 1, 3
• NSAID and aspirin use accounts for 36% of PUD cases, with risk particularly elevated in elderly patients 3, 4
• Other contributing factors include alcohol abuse, smoking, and stress, though these are less significant primary causes 1
• Chronic NSAID use in patients with H. pylori infection synergistically increases PUD risk 4

H. pylori Treatment Regimens

Triple therapy consists of a proton pump inhibitor (PPI) plus two antibiotics (typically clarithromycin and amoxicillin or metronidazole), while quadruple therapy adds bismuth to a PPI with tetracycline and metronidazole. 1, 4

Standard Triple Therapy:

• PPI (e.g., omeprazole or lansoprazole) + clarithromycin + amoxicillin (or metronidazole) 4
• Only recommended when local clarithromycin resistance is low 4
• Duration typically 10-14 days 4

Quadruple Therapy:

• Bismuth + PPI + tetracycline + metronidazole 1, 3
• Preferred when clarithromycin resistance is high 4
• Can achieve eradication rates reducing ulcer recurrence from 50-60% to 0-2% 3

Alternative Regimens:

• Sequential therapy: PPI + amoxicillin for 5 days, followed by PPI + clarithromycin + metronidazole for 5 days 4
• Levofloxacin-based triple therapy: PPI + levofloxacin + amoxicillin 4

H. pylori Diagnosis

Urea breath tests and stool antigen tests are the most accurate non-invasive methods for detecting H. pylori infection and can confirm eradication; serologic tests are less accurate and cannot confirm cure. 4

• Urea breath tests have the highest accuracy for active infection and can be used to confirm cure after treatment 4
• Stool antigen tests are equally accurate and can also confirm eradication 4
• Serologic antibody tests are convenient but less accurate and remain positive after successful eradication, making them unsuitable for confirming cure 4
• Endoscopic biopsy with histology or rapid urease testing provides definitive diagnosis when endoscopy is performed for other indications 4

Important caveat: The test-and-treat strategy is only appropriate for patients younger than 55 years without alarm symptoms (weight loss, bleeding, dysphagia, anemia); older patients require upper endoscopy to rule out malignancy 4

Achalasia

Diagnosis of Achalasia

Achalasia is diagnosed by esophageal manometry showing incomplete lower esophageal sphincter (LES) relaxation and absent peristalsis, typically after barium esophagram shows a dilated esophagus with bird-beak narrowing at the gastroesophageal junction.

• High-resolution manometry is the gold standard diagnostic test
• Barium swallow shows characteristic findings: dilated esophagus, air-fluid level, bird-beak appearance at the GE junction
• Upper endoscopy is performed to rule out pseudoachalasia from malignancy

Types of Achalasia (Chicago Classification)

Type I: Classic achalasia with absent contractility and minimal pressurization Type II: Achalasia with esophageal compression (panesophageal pressurization) - best prognosis Type III: Spastic achalasia with premature/spastic distal esophageal contractions - worst prognosis

Eckardt Score Calculation

The Eckardt score assesses achalasia severity based on four symptoms, each scored 0-3:

• Dysphagia: 0=none, 1=occasional, 2=daily, 3=each meal
• Regurgitation: 0=none, 1=occasional, 2=daily, 3=each meal
• Chest pain: 0=none, 1=occasional, 2=daily, 3=each meal
• Weight loss: 0=none, 1=<5kg, 2=5-10kg, 3=>10kg

Total score 0-12: Score ≤3 indicates treatment success; score >3 indicates treatment failure

Gastrointestinal Bleeding

Upper GI Bleeding Causes

Common causes of upper GI bleeding include peptic ulcer disease (most common), esophageal varices, Mallory-Weiss tears, erosive gastritis/esophagitis, and vascular malformations. 1

• Peptic ulcers account for the majority of UGIB cases
• Esophageal varices in cirrhotic patients carry high mortality
• Mallory-Weiss tears from forceful vomiting
• Erosive disease from NSAIDs, alcohol, or stress
• Dieulafoy lesions and vascular ectasias

Lower GI Bleeding Causes

Common causes of lower GI bleeding include diverticulosis, angiodysplasia, ischemic colitis, inflammatory bowel disease, hemorrhoids, and colorectal neoplasia.

• Diverticulosis is the most common cause in elderly patients
• Angiodysplasia particularly in patients with chronic kidney disease or aortic stenosis
• Ischemic colitis in elderly with vascular disease
• IBD (ulcerative colitis and Crohn's disease) 1
• Hemorrhoids and anal fissures for minor bleeding
• Colorectal polyps and cancer must be excluded

Clinical Differentiation: UGIB vs LGIB

Upper GI bleeding typically presents with hematemesis (coffee-ground or bright red) and/or melena, while lower GI bleeding presents with hematochezia (bright red blood per rectum). 1

• Hematemesis (vomiting blood) definitively indicates UGIB
• Melena (black, tarry stools) indicates UGIB in >90% of cases
• Hematochezia (bright red blood per rectum) usually indicates LGIB, but massive UGIB can present with hematochezia if transit time is rapid
• Nasogastric aspirate: bloody or coffee-ground aspirate confirms UGIB; clear aspirate does not exclude UGIB (particularly duodenal sources)

Key clinical point: Hemodynamic instability with hematochezia should prompt consideration of massive UGIB rather than assuming LGIB 1

Gut Obstruction

Partial vs Complete Obstruction: Clinical Differentiation

Complete bowel obstruction presents with absolute constipation (no passage of stool or flatus), while partial obstruction allows intermittent passage of stool and flatus with less severe symptoms.

Complete Obstruction:

• Absolute constipation: no flatus or stool passage
• Severe, constant abdominal pain
• Progressive abdominal distension
• Frequent vomiting (earlier with proximal obstruction)
• High-pitched or absent bowel sounds

Partial Obstruction:

• Intermittent passage of small amounts of stool or flatus
• Cramping, colicky abdominal pain
• Less severe distension
• Intermittent vomiting
• Hyperactive, high-pitched bowel sounds

Radiographic Evaluation of Gut Obstruction

Upright chest X-ray detects free air under the diaphragm indicating perforation; supine abdominal X-ray shows dilated bowel loops and their distribution; upright abdominal X-ray demonstrates air-fluid levels confirming obstruction.

Upright Chest X-ray:

• Primary purpose: detect pneumoperitoneum (free air under diaphragm) indicating perforation
• More sensitive than upright abdominal films for detecting free air
• Should be obtained in all suspected perforations

Supine Abdominal X-ray:

• Shows distribution and caliber of dilated bowel loops
• Identifies small bowel vs large bowel obstruction pattern
• Detects bowel wall thickening or thumbprinting

Upright Abdominal X-ray:

• Demonstrates air-fluid levels characteristic of obstruction
• Multiple air-fluid levels at different heights confirm mechanical obstruction
• Step-ladder pattern in small bowel obstruction

Bowel Dilation Criteria:

• Small bowel: dilated if >3 cm in diameter
• Large bowel: dilated if >6 cm (colon), >9 cm (cecum)
• Cecum >12 cm: high risk of perforation, requires urgent intervention

Management of Gut Obstruction

Initial management includes nil per os (NPO), nasogastric decompression, IV fluid resuscitation, and correction of electrolyte abnormalities; surgery is indicated for complete obstruction, strangulation, or failure of conservative management.

Initial Conservative Management:

• NPO status immediately 5
• Nasogastric tube for decompression
• IV fluid resuscitation with crystalloids
• Electrolyte correction (particularly potassium and chloride)
• Foley catheter for urine output monitoring
• Serial abdominal examinations every 4-6 hours

Indications for Surgical Intervention:

• Complete obstruction not resolving within 24-48 hours
• Signs of strangulation: fever, tachycardia, peritonitis, leukocytosis, metabolic acidosis
• Closed-loop obstruction
• Free air on imaging indicating perforation
• Failure of conservative management after 3-5 days in partial obstruction

Antibiotic Therapy:

• Indicated if signs of strangulation, perforation, or peritonitis
• Broad-spectrum coverage for gram-negative and anaerobic organisms

Causes of Small Bowel Obstruction

Adhesions from prior surgery (60-75% of cases), hernias (15-20%), and malignancy (10-15%) are the three most common causes of small bowel obstruction in adults.

• Postoperative adhesions: most common cause overall (60-75%)
• Hernias: inguinal, femoral, ventral, internal hernias (15-20%)
• Malignancy: primary small bowel tumors or metastatic disease (10-15%)
• Crohn's disease: strictures from chronic inflammation
• Intussusception: rare in adults, usually has lead point
• Gallstone ileus: in elderly patients with cholecystoenteric fistula
• Foreign bodies or bezoars: less common

Inflammatory Bowel Disease (IBD)

Two Types of IBD and Differentiation

Crohn's disease and ulcerative colitis are the two inflammatory bowel diseases; Crohn's can affect any part of the GI tract with transmural inflammation and skip lesions, while ulcerative colitis is limited to the colon with continuous mucosal inflammation starting from the rectum. 1

Crohn's Disease:

• Location: mouth to anus, most commonly terminal ileum and colon
• Pattern: skip lesions (discontinuous inflammation)
• Depth: transmural inflammation (all layers of bowel wall)
• Complications: fistulas, abscesses, strictures
• Endoscopy: cobblestoning, linear ulcers, aphthous ulcers
• Histology: non-caseating granulomas (in 30-50%)
• Rectal involvement: often spared

Ulcerative Colitis:

• Location: limited to colon and rectum only
• Pattern: continuous inflammation (no skip lesions)
• Depth: mucosal and submucosal only (not transmural)
• Complications: toxic megacolon, perforation, colorectal cancer
• Endoscopy: continuous erythema, friability, loss of vascular pattern
• Histology: crypt abscesses, no granulomas
• Rectal involvement: always involved, extends proximally

Faecal Calprotectin in IBD

Faecal calprotectin >250 μg/g warrants urgent gastroenterology referral; levels 100-250 μg/g require repeat testing or routine referral; levels <100 μg/g suggest IBS rather than IBD. 1

• Calprotectin is a validated biomarker for endoscopic and histological disease activity in IBD 1
• Useful for distinguishing IBD from irritable bowel syndrome in primary care 1
• Can inform decisions on treatment escalation or de-escalation 1
• Not appropriate if NSAID use in past 6 weeks (causes false elevation) 1

Irritable Bowel Syndrome (IBS)

Diagnosis of IBS

IBS is diagnosed clinically using Rome criteria: at least 12 weeks of abdominal pain or discomfort in the past 12 months with two of three features: relief with defecation, change in stool frequency, or change in stool consistency. 1

Rome II Criteria (Current):

• 12 weeks or more in the last 12 months of abdominal discomfort or pain
• Two of the following three features:
  1. Relieved by defecation
  2. Associated with change in frequency of stool
  3. Associated with change in consistency of stool 1

Supportive Features:

• Altered stool frequency
• Altered stool form
• Altered stool passage (straining, urgency, incomplete evacuation)
• Passage of mucus
• Bloating or distension 1

Working Diagnosis in Primary Care:

• Can be safely made with typical symptoms, normal physical examination, and absence of alarm features 1
• Alarm features requiring investigation: weight loss, rectal bleeding, nocturnal symptoms, anemia, age >45 years 1
• Supportive of diagnosis: female sex, age <45, history >2 years, frequent past attendance with non-GI symptoms 1

When to Refer:

• Atypical symptoms
• Short history
• Age over 45 years
• Presence of alarm features 1

Investigations:

• Faecal calprotectin to exclude IBD (<100 μg/g supports IBS diagnosis) 1
• Full blood count, CRP, coeliac screen in primary care 1
• Sigmoidoscopy if referred to hospital with colonic symptoms 1
• Thyroid function, antiendomysial antibodies if indicated 1
• Lactose tolerance testing only if consuming >280 ml milk daily 1

Liver Disease

Diagnostic Tests for Liver Problems

Initial evaluation includes liver function tests (AST, ALT, ALP, GGT, bilirubin, albumin, PT/INR), hepatitis serology, and abdominal ultrasound to assess liver parenchyma and biliary tree.

Biochemical Tests:

• Aminotransferases (AST, ALT): hepatocellular injury
• Alkaline phosphatase and GGT: cholestatic injury
• Bilirubin: direct and indirect fractions
• Albumin and PT/INR: synthetic function
• Complete blood count: thrombocytopenia suggests portal hypertension

Serologic Tests:

• Hepatitis A, B, C serology
• Autoimmune markers: ANA, ASMA, anti-LKM, AMA
• Iron studies: ferritin, transferrin saturation (hemochromatosis)
• Ceruloplasmin: Wilson's disease
• Alpha-1 antitrypsin level

Imaging:

• Ultrasound: first-line imaging for liver parenchyma, biliary tree, portal vein
• CT or MRI: for mass lesions or detailed assessment
• MRCP: for biliary tree evaluation 1
• Transient elastography (FibroScan): non-invasive fibrosis assessment

Hepatitis Profile Interpretation

Hepatitis B surface antigen (HBsAg) indicates active infection; anti-HBs indicates immunity from vaccination or resolved infection; anti-HBc IgM indicates acute infection while IgG indicates past exposure.

Hepatitis B Markers:

• HBsAg positive: active infection (acute or chronic)
• Anti-HBs positive: immunity (vaccination or resolved infection)
• Anti-HBc IgM: acute infection
• Anti-HBc IgG: past or chronic infection
• HBeAg positive: high viral replication, high infectivity
• Anti-HBe positive: low viral replication (except in precore mutants)
• HBV DNA: quantifies viral load

Common Patterns:

• HBsAg+, anti-HBc IgM+: acute hepatitis B
• HBsAg+, anti-HBc IgG+: chronic hepatitis B
• Anti-HBs+, anti-HBc-: immunity from vaccination
• Anti-HBs+, anti-HBc IgG+: resolved infection with immunity
• Anti-HBc IgG+ alone: occult infection or false positive

Hepatitis C:

• Anti-HCV antibody: exposure to HCV (does not distinguish active from resolved)
• HCV RNA: confirms active infection
• Genotype: guides treatment selection

Significant Alcohol Intake Thresholds

Significant alcohol consumption is defined as >3 drinks per day (>42 g/day) for men or >2 drinks per day (>28 g/day) for women, sustained over years.

• Men: >210 g alcohol per week (approximately 15 standard drinks)
• Women: >140 g alcohol per week (approximately 10 standard drinks)
• One standard drink = 14 g of pure alcohol (12 oz beer, 5 oz wine, 1.5 oz spirits)
• Risk for cirrhosis increases significantly with >60-80 g/day for men, >40-60 g/day for women, over 10+ years

Stigmata of Chronic Liver Disease

Physical signs of chronic liver disease include spider angiomata, palmar erythema, gynecomastia, testicular atrophy, jaundice, ascites, caput medusae, and hepatic encephalopathy.

Cutaneous Signs:

• Spider angiomata (spider nevi): on upper body
• Palmar erythema: thenar and hypothenar eminences
• Jaundice: scleral icterus, skin yellowing
• Caput medusae: dilated periumbilical veins
• Bruising: from coagulopathy

Endocrine Signs:

• Gynecomastia: breast tissue enlargement in men
• Testicular atrophy
• Loss of body hair
• Female distribution of body fat

Abdominal Signs:

• Ascites: shifting dullness, fluid wave
• Hepatomegaly or small shrunken liver
• Splenomegaly: from portal hypertension

Neurological Signs:

• Asterixis (liver flap): see below
• Hepatic encephalopathy: confusion, altered mental status
• Fetor hepaticus: sweet, musty breath odor

Other Signs:

• Dupuytren's contracture: particularly with alcoholic liver disease
• Clubbing
• Leukonychia: white nails from hypoalbuminemia

Complications of Liver Cirrhosis

Major complications of cirrhosis include portal hypertension with variceal bleeding, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal syndrome, and hepatocellular carcinoma.

Portal Hypertension Complications:

• Variceal bleeding: esophageal, gastric, or anorectal varices
• Ascites: fluid accumulation in peritoneal cavity
• Spontaneous bacterial peritonitis (SBP): infection of ascitic fluid
• Hepatic hydrothorax: pleural effusion from ascites
• Splenomegaly and hypersplenism: thrombocytopenia, leukopenia

Hepatic Dysfunction Complications:

• Hepatic encephalopathy: altered mental status from ammonia accumulation
• Coagulopathy: prolonged PT/INR, bleeding risk
• Hypoalbuminemia: edema, ascites
• Jaundice: from impaired bilirubin metabolism

Renal Complications:

• Hepatorenal syndrome: functional renal failure
• Acute kidney injury: from various causes

Malignancy:

• Hepatocellular carcinoma (HCC): annual incidence 3-5% in cirrhosis

Testing for Asterixis

Asterixis is tested by having the patient extend both arms with wrists dorsiflexed and fingers spread; positive asterixis shows brief, irregular lapses in wrist extension producing a flapping motion.

• Patient position: arms outstretched, wrists hyperextended (dorsiflexed), fingers spread apart
• Observation period: 30-60 seconds
• Positive test: brief, irregular lapses in posture causing downward flapping movements
• Bilateral testing: typically bilateral in hepatic encephalopathy
• Also called: liver flap or flapping tremor
• Indicates: hepatic encephalopathy (grade 2 or higher), but also seen in uremia, hypercapnia, and other metabolic encephalopathies

Pancreatitis

Most Common Etiologies of Pancreatitis

Gallstones (40-50% of cases) and alcohol (30-40% of cases) account for approximately 80% of acute pancreatitis; other causes include hypertriglyceridemia, medications, ERCP, and trauma.

• Gallstones: most common cause overall (40-50%)
• Alcohol: second most common (30-40%), typically requires chronic heavy use
• Hypertriglyceridemia: when triglycerides >1000 mg/dL
• Post-ERCP: 3-5% risk after procedure 1
• Medications: azathioprine, valproic acid, thiazides, many others
• Trauma: blunt abdominal trauma
• Hypercalcemia: hyperparathyroidism
• Autoimmune pancreatitis
• Idiopathic: 10-20% of cases

Diagnostic Criteria for Pancreatitis

Acute pancreatitis requires two of three criteria: characteristic abdominal pain, serum lipase (or amylase) ≥3 times upper limit of normal, and/or characteristic imaging findings.

Revised Atlanta Criteria (2012):

Two of the following three features:

1. Abdominal pain: acute onset, severe, persistent epigastric pain often radiating to back
2. Serum lipase or amylase: ≥3 times the upper limit of normal
3. Imaging findings: characteristic findings on CT, MRI, or ultrasound

Key points:

• Lipase is preferred over amylase (more sensitive and specific)
• Imaging not required if first two criteria met
• CT should be delayed 48-72 hours unless diagnosis uncertain or complications suspected

Management of Pancreatitis

Initial management includes aggressive IV fluid resuscitation with crystalloids (250-500 mL/hour), early oral feeding when tolerated, pain control, and treatment of underlying cause; antibiotics are NOT indicated for uncomplicated acute pancreatitis.

Initial Resuscitation:

• Aggressive IV fluid resuscitation: 250-500 mL/hour of lactated Ringer's or normal saline
• Goal urine output >0.5 mL/kg/hour
• Avoid overhydration: monitor for fluid overload

Nutrition:

• Early oral feeding (within 24 hours) when tolerated, even with mild nausea
• Start with low-fat solid diet (no need for clear liquids first)
• Enteral nutrition (nasogastric or nasojejunal) if unable to tolerate oral intake
• Parenteral nutrition only if enteral route not feasible

Pain Management:

• Opioid analgesia as needed (no evidence that morphine worsens pancreatitis)
• Patient-controlled analgesia for severe pain

Treatment of Underlying Cause:

• ERCP with sphincterotomy for gallstone pancreatitis with cholangitis or persistent obstruction
• Cholecystectomy during same admission for gallstone pancreatitis (after inflammation subsides)
• Alcohol cessation counseling
• Triglyceride lowering if hypertriglyceridemia

Antibiotic Indications in Pancreatitis

Antibiotics are indicated ONLY for documented infected pancreatic necrosis or extrapancreatic infections (cholangitis, bacteremia, pneumonia, UTI); prophylactic antibiotics are NOT recommended for sterile necrosis or uncomplicated acute pancreatitis.

Indications for Antibiotics:

• Infected pancreatic necrosis: confirmed by FNA with positive culture or gas in necrosis on CT
• Cholangitis: with gallstone pancreatitis
• Extrapancreatic infections: pneumonia, UTI, bacteremia, catheter-related infections

NOT Indicated:

• Sterile pancreatic necrosis: no benefit, increases fungal infections
• Prophylaxis in severe pancreatitis: multiple trials show no benefit
• Uncomplicated acute pancreatitis

Antibiotic Selection (when indicated):

• Carbapenems (imipenem, meropenem): best pancreatic penetration
• Fluoroquinolones + metronidazole: alternative
• Duration: 7-14 days depending on clinical response

Charcot's Triad and Reynolds Pentad

Charcot's Triad

Charcot's triad consists of fever, right upper quadrant pain, and jaundice, indicating acute cholangitis from biliary obstruction.

The three components:

1. Fever (with or without rigors)
2. Right upper quadrant abdominal pain
3. Jaundice

• Present in only 50-70% of cholangitis cases
• Indicates ascending biliary infection from obstruction (gallstones, stricture, malignancy)

Reynolds Pentad

Reynolds pentad adds altered mental status and hypotension to Charcot's triad, indicating severe suppurative cholangitis with sepsis requiring urgent biliary decompression.

The five components:

1. Fever
2. Right upper quadrant pain
3. Jaundice
4. Altered mental status (confusion, disorientation)
5. Hypotension (septic shock)

• Present in only 5-10% of cholangitis cases
• Indicates life-threatening suppurative cholangitis
• Requires urgent biliary drainage (ERCP or percutaneous transhepatic cholangiography)
• Mortality approaches 50% without prompt intervention