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Gastroenterology
Gastroesophageal Reflux Disease (GERD)
I. Definition
Gastroesophageal Reflux Disease (GERD) is a chronic condition where gastric
contents reflux into the esophagus, causing symptoms or complications due to
lower esophageal sphincter (LES) dysfunction.

II. Etiology & Risk Factors

1. Pathophysiology
LES Dysfunction → Weak sphincter allows acid reflux.

Hiatal Hernia → Stomach herniates into thorax, weakening LES.

Delayed Gastric Emptying → Prolongs acid exposure in the stomach.

Decreased Esophageal Clearance → Impaired acid neutralization.

2. Risk Factors
Category Examples

Dietary Fatty foods, caffeine, alcohol, spicy foods, chocolate

Lifestyle Obesity, smoking, supine position after meals

Medications NSAIDs, Calcium Channel Blockers, Nitrates

Anatomical Hiatal Hernia

Pregnancy Increased intra-abdominal pressure

III. Clinical Features

Gastroenterology 1
 Symptom Description

Burning sensation in retrosternal area, worse after meals &

Heartburn (Pyrosis)
lying down

Regurgitation Sour/bitter taste in mouth due to gastric content reflux

Dysphagia Due to chronic inflammation or stricture formation

Extraesophageal
Chronic cough, hoarseness (laryngopharyngeal reflux)
Symptoms

Alarm Symptoms (Suggest Complications or Cancer)

Dysphagia, Odynophagia (painful swallowing).

Unintentional weight loss.

Recurrent vomiting.

GI bleeding (melena, hematemesis).

IV. Diagnosis
1. Clinical Diagnosis
If classic symptoms (heartburn, regurgitation) → Empirical trial of PPIs for
4-8 weeks.

2. Confirmatory Tests (If Symptoms Persist or Alarm Features

Present)

Test Findings Indications

Upper Endoscopy (EGD) (Best Esophagitis, Barrett’s Alarm symptoms, high-

Test for Alarm Symptoms) esophagus, Strictures risk patients

24-hour pH Monitoring (Gold If EGD is normal but

Confirms acid reflux
Standard) symptoms persist

If motility disorder
Esophageal Manometry Measures LES pressure
suspected

Barium Swallow Hiatal hernia, strictures Used in dysphagia cases

Gastroenterology 2
 V. Management
1. Lifestyle & Dietary Modifications (First-Line for Mild Cases)
Weight Loss (Most effective lifestyle change).

Avoid trigger foods (caffeine, alcohol, spicy food, fatty meals).

Elevate head of bed (for nighttime symptoms).

Avoid lying down within 3 hours of eating.

Smoking & alcohol cessation.

2. Pharmacologic Therapy (Step-Up Approach)

Drug Class Examples Mechanism Indications

Proton Pump Omeprazole, Moderate-severe

Block H⁺/K⁺ ATPase,
Inhibitors (PPIs) Esomeprazole, GERD, erosive
reducing acid
(Most Effective) Pantoprazole esophagitis

H2 Receptor Ranitidine, Block histamine at Mild GERD, adjunct

Blockers (H2RAs) Famotidine H2 receptors to PPIs

Aluminum
Hydroxide, Neutralize stomach Short-term symptom
Antacids
Magnesium acid relief
Hydroxide

Increase LES tone, Refractory GERD

Metoclopramide,
Prokinetics promote gastric (rarely used due to
Domperidone
emptying side effects)

3. Surgical Management (For Severe or Refractory GERD)

Procedure Indications

Failed medical therapy, hiatal hernia,

Nissen Fundoplication
complications

Linx Device (Magnetic Sphincter Alternative to fundoplication, maintains LES

Augmentation) integrity

VI. Complications

Gastroenterology 3
 Complication Description

Esophagitis Chronic inflammation due to acid reflux

Esophageal Stricture Fibrosis → Narrowing of esophagus, leading to dysphagia

Metaplasia (Squamous → Columnar epithelium),

Barrett’s Esophagus
premalignant

Esophageal Progression from Barrett’s esophagus (increased risk in

Adenocarcinoma chronic GERD)

Barrett’s Esophagus Monitoring

No dysplasia → EGD every 3-5 years.

Low-grade dysplasia → EGD every 6-12 months, consider ablation.

High-grade dysplasia → Endoscopic mucosal resection or ablation.

Peptic Ulcer Disease (PUD)

I. Definition
Peptic Ulcer Disease (PUD) refers to chronic ulcers in the gastric or duodenal
mucosa due to an imbalance between mucosal defense and acid-peptic injury.

II. Etiology & Risk Factors

1. Common Causes
Cause Mechanism

Helicobacter pylori (H. pylori) (Most

Produces urease, weakens mucosal barrier
Common, 70-90%)

Inhibit prostaglandins, ↓ mucus &

NSAIDs (Aspirin, Ibuprofen, Naproxen)
bicarbonate

Zollinger-Ellison Syndrome (ZES) Gastrinoma → Excess acid secretion

Smoking & Alcohol Delayed healing, increased acid production

Gastroenterology 4
 ↑ Acid secretion (Stress Ulcers: Cushing’s &
Stress (ICU patients, burns, head trauma)
Curling’s Ulcers)

2. Risk Factors
H. pylori infection (most common).

Frequent NSAID use (elderly, chronic pain patients).

Smoking, alcohol abuse, corticosteroids.

Severe physiological stress (burns, sepsis, trauma).

III. Clinical Features

Feature Gastric Ulcer Duodenal Ulcer

Worse with meals (30-60 min after Better with meals, worse 2-5 hrs
Pain Timing
eating) later

Epigastric pain, right upper

Pain Location Epigastric pain, left upper quadrant
quadrant

Night Pain Uncommon Common (Nocturnal pain)

Food Effect Worsens symptoms Relieves symptoms

Weight Weight loss (due to pain with Weight gain (due to relief with
Changes eating) food)

Alarm Symptoms (Indicate Possible Malignancy or Perforation)

Unintentional weight loss.

Persistent vomiting or dysphagia.

GI bleeding (melena, hematemesis).

Severe pain with guarding (perforation).

IV. Diagnosis
1. Endoscopy (EGD) (Best Test for Suspected PUD with Alarm
Symptoms)

Gastroenterology 5
 Indications:

Age >45-50 with new symptoms.

Alarm symptoms (bleeding, weight loss, persistent vomiting).

Refractory ulcers despite treatment.

Findings:

Gastric Ulcer: Biopsy to rule out gastric cancer.

Duodenal Ulcer: No biopsy needed (rarely malignant).

2. H. pylori Testing
Test Use Comments

Urea Breath Test (UBT) (Best Stop PPIs & antibiotics 2 weeks
Active infection
Noninvasive Test) prior

Good for initial diagnosis & post-

Stool Antigen Test Active infection
treatment confirmation

Past or current
Serology (IgG Antibodies) Not used for active infection
infection

Endoscopic Biopsy (CLO Test, Used if endoscopy is already

Gold standard
Histology, Culture) indicated

V. Management
1. General Measures
Stop NSAIDs (Switch to acetaminophen or COX-2 inhibitors if needed).

Avoid smoking, alcohol, and spicy foods.

Stress reduction & dietary modifications.

2. Pharmacologic Therapy

Drug Class Examples Mechanism Indications

PPIs (Most Omeprazole, Block H⁺/K⁺ ATPase, First-line for ulcer

Effective) Pantoprazole, reduce acid secretion healing & H. pylori

Gastroenterology 6
 Esomeprazole eradication

Ranitidine, Block histamine at H2 Alternative if PPIs not

H2 Blockers
Famotidine receptors tolerated

Sucralfate, Forms protective Adjunct for ulcer

Bismuth barrier healing

3. H. pylori Eradication Therapy

Triple Therapy (First-Line, 14 Days)

PPI + Clarithromycin + Amoxicillin (or Metronidazole if allergic).

Quadruple Therapy (If Clarithromycin Resistance or Failure of

Triple Therapy)
PPI + Bismuth + Tetracycline + Metronidazole.

Confirm Eradication: UBT or stool antigen test 4 weeks after treatment.

VI. Complications
Complication Description Management

Bleeding (Most Hematemesis (Coffee-ground Endoscopic hemostasis,

Common) vomiting), Melena IV PPI

Perforation (Surgical Sudden severe epigastric pain, rigid Emergency surgery, IV

Emergency) abdomen, free air on CXR fluids, antibiotics

Gastric Outlet Endoscopy, NG tube, PPI

Nausea, vomiting, early satiety
Obstruction therapy

Chronic ulcers (especially in the

Gastric Cancer Biopsy all gastric ulcers
stomach) may lead to malignancy

Inflammatory Bowel Disease (IBD) –

Crohn’s Disease & Ulcerative Colitis

Gastroenterology 7
 I. Definition
Inflammatory Bowel Disease (IBD) is a chronic immune-mediated disorder of the
gastrointestinal (GI) tract, primarily including:

1. Ulcerative Colitis (UC) – Affects the colon and rectum, with continuous
mucosal inflammation.

2. Crohn’s Disease (CD) – Affects any part of the GI tract (mouth to anus) with
skip lesions and transmural inflammation.

II. Etiology & Risk Factors

Risk Factor Ulcerative Colitis (UC) Crohn’s Disease (CD)

Yes (HLA-B27 Stronger genetic predisposition (NOD2

Genetic
association) mutation)

Smoking Protective Increases risk

NSAIDs Use Worsens disease Worsens disease

Microbiome
Yes Yes
Alterations

III. Clinical Features

Feature Ulcerative Colitis (UC) Crohn’s Disease (CD)

Rectum → Colon Mouth → Anus (skip lesions, terminal

Location
(continuous) ileum common)

Depth of Mucosal & Submucosal

Transmural (full thickness)
Involvement Only

Bloody diarrhea
Diarrhea Non-bloody diarrhea (common)
(frequent)

Abdominal Pain LLQ pain (left-sided) RLQ pain (terminal ileum involvement)

Fistulas,
No Yes (common in CD)
Abscesses

Perianal Disease No Yes (fistulas, fissures, abscesses)

Malabsorption No Yes (B12, fat-soluble vitamins)

Gastroenterology 8
 Risk of Colon
High Moderate
Cancer

IV. Extraintestinal Manifestations

System Manifestations

Joints Arthritis (Seronegative Spondyloarthritis, Ankylosing Spondylitis)

Skin Erythema nodosum, Pyoderma gangrenosum

Eyes Uveitis, Episcleritis

Hepatobiliary Primary Sclerosing Cholangitis (PSC) (More common in UC)

V. Diagnosis
1. Lab Tests
Test Findings Comments

Anemia (iron deficiency, B12 deficiency in

CBC Chronic inflammation
CD)

CRP, ESR Elevated Disease activity marker

Fecal Differentiates IBD from

Elevated
Calprotectin IBS

2. Imaging & Endoscopy

Investigation Ulcerative Colitis (UC) Crohn’s Disease (CD)

Continuous colonic inflammation,

Colonoscopy (Gold Skip lesions, Cobblestone
loss of haustra ("Lead Pipe
Standard) mucosa, aphthous ulcers
Appearance")

Crypt abscesses, mucosal Transmural inflammation,

Biopsy
inflammation granulomas (non-caseating)

String sign (terminal ileum

Barium Study "Lead pipe" colon
narrowing)

CT/MR Thickened bowel loops,

Not necessary
Enterography strictures

Gastroenterology 9
 Avoid Colonoscopy in Acute Severe UC → Risk of perforation.

VI. Management
1. Acute Flare Treatment

Severity Ulcerative Colitis (UC) Crohn’s Disease (CD)

Budesonide (for ileal

Mild-Moderate 5-ASA (Mesalamine, Sulfasalazine)
disease)

IV Corticosteroids IV Corticosteroids, Biologics

Moderate-Severe
(Methylprednisolone, Prednisone) (Infliximab, Adalimumab)

Anti-TNF (Infliximab, Adalimumab) Anti-TNF, IL-12/IL-23

Severe/Refractory
or JAK inhibitors (Tofacitinib) inhibitors (Ustekinumab)

2. Maintenance Therapy (To prevent relapse)

Drug Class Examples Indications

UC only (not effective for

5-ASA (Mesalamine, Sulfasalazine) First-line for UC
CD)

Thiopurines (Azathioprine, 6-MP) Immunosuppressants Both UC & CD

Methotrexate Used in CD Not used in UC

Biologics (Anti-TNF: Infliximab, Moderate-severe

Both UC & CD
Adalimumab) cases

3. Surgery
Procedure Indications

Total Colectomy (Curative for UC) Severe UC, toxic megacolon, dysplasia

Segmental Resection (For CD) Fistulas, strictures, refractory disease

VII. Complications
Complication Ulcerative Colitis (UC) Crohn’s Disease (CD)

Gastroenterology 10
 Yes (life-threatening dilation >6
Toxic Megacolon Rare
cm)

Yes (can cause bowel

Strictures No
obstruction)

Fistulas & Yes (common in perianal

No
Abscesses disease)

Colon Cancer Risk High Moderate

Colon Cancer Screening:

UC: Colonoscopy every 1-2 years starting 8 years after diagnosis.

CD: Screening based on extent of colonic involvement.

Cirrhosis & Portal Hypertension

I. Definition
Cirrhosis is a chronic, progressive liver disease characterized by fibrosis and
nodular regeneration, leading to hepatic dysfunction and portal hypertension.

II. Etiology & Risk Factors

Cause Examples

Chronic Alcohol Use (Most

Alcoholic liver disease
Common in Western Countries)

Chronic Viral Hepatitis Hepatitis B, Hepatitis C

Non-Alcoholic Fatty Liver Disease

Obesity, Diabetes, Metabolic Syndrome
(NAFLD)

Autoimmune Hepatitis, Primary Biliary Cholangitis

Autoimmune Diseases
(PBC), Primary Sclerosing Cholangitis (PSC)

Metabolic Disorders Wilson’s Disease (Copper), Hemochromatosis (Iron)

Drugs & Toxins Methotrexate, Amiodarone

Gastroenterology 11
 III. Pathophysiology
1. Chronic Liver Injury → Activation of hepatic stellate cells → Excess collagen
deposition → Fibrosis.

2. Loss of Hepatic Architecture → Disrupted blood flow → Portal Hypertension.

3. Liver Dysfunction → Decreased albumin, clotting factors, and detoxification

→ Ascites, Coagulopathy, Hepatic Encephalopathy.

IV. Clinical Features

1. Symptoms
Fatigue, weakness (due to malnutrition).

Jaundice (hyperbilirubinemia).

Abdominal distension (ascites).

Easy bruising/bleeding (coagulopathy).

Pruritus (due to bile salt accumulation).

2. Signs of Chronic Liver Disease

Feature Description

Spider Angiomas Dilated blood vessels (upper chest, face)

Palmar Erythema Red palms due to vasodilation

Gynecomastia & Testicular Atrophy Due to increased estrogen

Caput Medusae Dilated abdominal veins (portal hypertension)

Asterixis Flapping tremor (Hepatic Encephalopathy)

V. Diagnosis
1. Laboratory Tests
Test Findings in Cirrhosis

Gastroenterology 12
 Liver Enzymes (AST/ALT) ↑ Mildly (AST > ALT in Alcoholic Cirrhosis)

Alkaline Phosphatase (ALP) ↑ If biliary obstruction (PBC, PSC)

Bilirubin ↑ If jaundice present

Albumin ↓ (Hypoalbuminemia → Edema, Ascites)

PT/INR ↑ (Coagulopathy due to ↓ clotting factors)

2. Imaging & Special Tests

Test Findings Indications

Abdominal Ultrasound (First- Nodular liver, Screening for cirrhosis &

Line Imaging) Splenomegaly, Ascites portal hypertension

FibroScan (Transient Measures liver stiffness Non-invasive alternative to

Elastography) (fibrosis) biopsy

Liver Biopsy (Gold Standard) Confirms cirrhosis If diagnosis is unclear

Cirrhosis patients should

Endoscopy (EGD) Esophageal Varices
undergo screening

VI. Complications & Management

1. Portal Hypertension & Variceal Bleeding
Definition: ↑ Portal venous pressure (>10 mmHg) → Varices (Esophageal,
Gastric).

Diagnosis: Endoscopy (screen for varices in all cirrhotics).

Management:

Primary Prevention: Non-selective beta-blockers (Propranolol, Nadolol).

Acute Bleeding:

IV Octreotide (reduces portal pressure).

Endoscopic Band Ligation.

TIPS (Transjugular Intrahepatic Portosystemic Shunt) if refractory.

Gastroenterology 13
 2. Ascites & Spontaneous Bacterial Peritonitis (SBP)
Complication Features Management

Na+ restriction, Diuretics

Abdominal distension,
Ascites (Spironolactone + Furosemide),
shifting dullness
Paracentesis

SBP (Bacterial Infection Fever, abdominal pain, Empiric IV Cefotaxime, Albumin

in Ascites Fluid) altered mental status infusion

Diagnosis of SBP:

Ascitic Fluid Polymorphonuclear Cells (PMNs) >250/mm³.

3. Hepatic Encephalopathy (HE)

Stage Symptoms Treatment

I Asterixis, Confusion Lactulose (First-Line)

II-III Lethargy, Disorientation Rifaximin (Add-on to Lactulose)

IV (Coma) Unresponsive ICU care

Pathophysiology: ↑ Ammonia (NH3) due to impaired detoxification.

Treatment : lactulose ( to reduce NH3)

Diagnostic: EEG, serum NH3 , head CT

4. Hepatorenal Syndrome (HRS)

Type Features Management

Type 1 (Rapid-onset, Acute kidney failure (Cr >2.5 Albumin + Terlipressin

Severe) mg/dL), Oliguria (Vasopressors)

Type 2 (Chronic, Slowly Moderate kidney failure, Na+ Liver transplant (definitive
Progressive) retention cure)

5. Hepatocellular Carcinoma (HCC)

Risk Factors Diagnosis Management

Gastroenterology 14
 Cirrhosis (Main Risk Factor), Alpha-fetoprotein (AFP) + Liver Resection,
Chronic Hepatitis B/C, Liver Imaging (US, CT/MRI Transplant, Ablative
Aflatoxin exposure with contrast) therapy (RFA, TACE)

Cirrhosis Patients Need HCC Screening Every 6 Months with Ultrasound ±

AFP.

Treatment: surgical ( transarterial chemoembolisation) TACE

VII. Prognosis & Liver Transplant Criteria

1. MELD Score (Model for End-Stage Liver Disease)
Used to predict 3-month mortality & transplant priority.

Formula:
MELD = 9.6 × log(Cr) + 3.8 × log(Bilirubin) + 11.2 × log(INR) + 6.4

MELD Score 3-Month Mortality

<10 <5%

10-19 6-20%

20-29 20-50%

30-40 50-90%

2. Liver Transplant Indications

Decompensated Cirrhosis (Refractory Ascites, HE, HRS).

Variceal Bleeding Unresponsive to Treatment.

HCC (Milan Criteria: Single tumor ≤5 cm OR ≤3 tumors ≤3 cm each).

VIII. Summary of Management

Complication First-Line Treatment

Portal Hypertension Beta-blockers (Propranolol)

Variceal Bleeding Octreotide + Endoscopic Banding

Gastroenterology 15
 Ascites Spironolactone + Furosemide, Paracentesis

SBP IV Cefotaxime

Hepatic Encephalopathy Lactulose + Rifaximin

Hepatorenal Syndrome Albumin + Vasopressors (Terlipressin)

HCC Screening US ± AFP every 6 months

Acute & Chronic Pancreatitis

I. Acute Pancreatitis
1. Definition
Acute pancreatitis is a sudden inflammatory process of the pancreas, leading to
pancreatic enzyme activation, autodigestion, and local/systemic complications.

2. Etiology & Risk Factors

Cause Mechanism

Gallstones (Most Common Cause,

Obstruct pancreatic duct → Enzyme activation
40-70%)

Alcohol (Second Most Common, 25-

Direct toxicity to pancreatic cells
35%)

Lipotoxicity → Free fatty acid-induced

Hypertriglyceridemia (>1000 mg/dL)
inflammation

Azathioprine, Valproate, Furosemide, Estrogens,

Drugs
Sulfonamides

Trauma Post-ERCP, Abdominal injury

Infections Mumps, Coxsackievirus, HIV, CMV

Autoimmune IgG4-Related Pancreatitis

3. Clinical Features

Gastroenterology 16
 Symptom Description

Severe Epigastric Radiates to the back, worsens with food, relieved by leaning
Pain forward

Nausea & Vomiting Common, often persistent

Fever, Tachycardia Systemic inflammation

Hypotension/Shock Severe cases (due to SIRS, third spacing)

Severe Signs (Necrotizing Hemorrhagic Pancreatitis)

Cullen’s Sign – Periumbilical bruising (Retroperitoneal hemorrhage).

Grey Turner’s Sign – Flank bruising (Hemorrhagic pancreatitis).

4. Diagnosis
Diagnostic Criteria (At Least 2 of 3 Required)

1. Typical Epigastric Pain.

2. Serum Lipase/Amylase ≥3x Upper Limit of Normal.

3. Imaging Evidence (CT, MRI, US).

Key Investigations
Test Findings in Acute Pancreatitis

Serum Lipase (Best Lab Test) ↑ ≥3x normal (More specific than amylase)

Serum Amylase ↑ ≥3x normal (Less specific)

LFTs (AST, ALT, ALP, Bilirubin) ALT >150 U/L → Gallstone Pancreatitis

Calcium ↓ (Hypocalcemia in severe cases due to fat necrosis)

CRP >150 mg/L Suggests severe pancreatitis

Imaging
Modality Findings Indications

Abdominal Ultrasound (First- Gallstones, bile duct If gallstone pancreatitis

Line for Gallstones) dilation suspected

Gastroenterology 17
 CT Abdomen with Contrast Pancreatic necrosis, If severe pancreatitis or no
(Best for Complications) fluid collections improvement in 48 hours

Detects bile duct

MRI/MRCP If unclear cause
obstruction

5. Severity Scoring (Predicting Mortality & ICU Need)

Ranson’s Criteria (At Admission & 48 Hours)

Variable (At Admission) Criteria

Age >55 years

WBC >16,000/mm³

Glucose >200 mg/dL

AST >250 IU/L

LDH >350 IU/L

≥3 Criteria → Severe pancreatitis risk ↑.

≥6 Criteria → 100% mortality.

Modified CT Severity Index (CTSI)

Score Mortality Risk

Mild (0-3) <5%

Moderate (4-6) 15%

Severe (7-10) >50%

6. Management

1. Supportive Care (Mainstay Treatment, No Specific Cure)

Treatment Details

IV Fluids (Aggressive Resuscitation) Lactated Ringer’s (Preferred)

Pain Control IV Opioids (Morphine, Fentanyl)

Bowel Rest (NPO Initially) Resume oral diet when pain improves

Gastroenterology 18
 Enteral Feeding (NG or NJ tube) If severe or prolonged NPO

2. Treat Underlying Cause

Cause Treatment

Gallstones ERCP (If cholangitis or bile duct obstruction present)

Hypertriglyceridemia Fibrates, Insulin, Plasmapheresis

Alcoholic Pancreatitis Alcohol cessation, Nutritional support

3. Management of Complications
Complication Management

Carbapenems + Surgical Debridement if

Pancreatic Necrosis (Sterile or Infected)
Infected

Pancreatic Pseudocyst (Fluid Collection >4

Observe if <6 cm, Drain if Symptomatic
Weeks)

Severe Hypocalcemia IV Calcium Gluconate

ARDS (Respiratory Failure) Oxygen, Mechanical Ventilation if needed

II. Chronic Pancreatitis

1. Definition
Chronic Pancreatitis is progressive inflammation and fibrosis of the pancreas,
leading to irreversible damage, exocrine & endocrine insufficiency.

2. Causes

Cause Mechanism

Chronic Alcohol Use (Most Common, >70%) Direct pancreatic injury

Genetic (CFTR Mutations, PRSS1 Gene – Hereditary

Early-onset pancreatitis
Pancreatitis)

Autoimmune Pancreatitis (IgG4-Related) Responds to steroids

Gastroenterology 19
 Leads to fibrosis &
Recurrent Acute Pancreatitis
calcifications

3. Clinical Features
Feature Description

Chronic Epigastric Pain Worsened by meals, radiates to back

Steatorrhea (Fatty Stools) Due to pancreatic enzyme deficiency

Weight Loss Malabsorption of fat-soluble vitamins

Diabetes Mellitus Due to pancreatic endocrine failure

4. Diagnosis
Test Findings

CT Abdomen (First-Line Test) Pancreatic calcifications (hallmark sign)

MRCP (Best for Detecting Strictures & Ductal

Dilated pancreatic ducts
Changes)

Fecal Elastase (<200 mcg/g) Exocrine insufficiency

Normal or mildly elevated (unlike acute

Serum Lipase/Amylase
pancreatitis)

5. Management
Treatment Indications

Alcohol & Smoking Cessation Prevents progression

Pancreatic Enzyme Supplementation If steatorrhea or malabsorption

Low-Fat Diet Reduces symptoms

Pain Management (NSAIDs, Tramadol, Pregabalin) Chronic pain control

Endoscopic or Surgical Drainage If strictures or pseudocysts present

Pancreatic Enzyme Therapy → Pancrelipase (Lipase, Protease, Amylase) +

PPI.

Gastroenterology 20
 6. Complications
Complication Management

Diabetes (Type 3c) Insulin therapy

Pancreatic Cancer Risk Annual imaging for high-risk cases

Biliary Obstruction Endoscopic stenting

Hepatitis (A, B, C, D, E)
I. Definition
Hepatitis is inflammation of the liver caused by viral infections, toxins, or
autoimmune conditions. The most common causes are hepatotropic viruses
(HAV, HBV, HCV, HDV, HEV).

II. Classification of Viral Hepatitis

Virus Transmission Acute or Chronic? Risk Factors

Hepatitis A Contaminated
Fecal-oral Only acute
(HAV) food/water, travel

IV drug use,
Hepatitis B Blood, sexual,
Acute & Chronic unprotected sex,
(HBV) perinatal
perinatal

Hepatitis C IV drug use,

Blood-borne Mostly chronic
(HCV) transfusions, tattoos

Hepatitis D Chronic (co-infection or HBV-infected

Requires HBV
(HDV) superinfection) individuals

Hepatitis E Acute (except in pregnancy Contaminated water,

Fecal-oral
(HEV) & immunosuppression) pregnancy (severe)

III. Clinical Features of Acute Viral Hepatitis

Gastroenterology 21
 Stage Symptoms

Prodromal (Pre-Icteric, 1-2

Fever, malaise, anorexia, nausea, RUQ pain
weeks)

Jaundice, dark urine (↑ bilirubin), pale stools,

Icteric Phase (2-6 weeks)
hepatomegaly

Recovery Phase Symptoms resolve, liver enzymes normalize over weeks

HAV & HEV → Self-limiting, no chronic infection.

HBV, HCV, HDV → Can lead to chronic hepatitis, cirrhosis, liver cancer.

IV. Diagnosis of Hepatitis

1. Laboratory Tests
Test Findings in Acute Hepatitis

AST/ALT ↑ >1000 U/L (ALT > AST)

Bilirubin ↑ If jaundice present

Alkaline Phosphatase (ALP) Mildly ↑

2. Viral Serology

Hepatitis A (HAV) Serology

Marker Interpretation

Anti-HAV IgM Acute Hepatitis A

Anti-HAV IgG Past infection or vaccination

Hepatitis B (HBV) Serology

Marker Interpretation

HBsAg (Surface Antigen) Active Infection (Acute or Chronic)

Anti-HBs (Surface Antibody) Immunity (Recovery or Vaccination)

HBeAg (Envelope Antigen) Active Viral Replication (High Infectivity)

Anti-HBe Lower infectivity

Gastroenterology 22
 Anti-HBc IgM Acute HBV Infection

Anti-HBc IgG Past or Chronic HBV Infection

HBV Interpretation Table

HBsAg Anti-HBs Anti-HBc IgM Diagnosis

+ - + Acute Hepatitis B

+ - - Chronic Hepatitis B

- + - Recovered or Vaccinated

Hepatitis C (HCV) Serology

Test Interpretation

Anti-HCV (Antibody) Exposure (past or present)

HCV RNA (PCR) Confirms active infection

If Anti-HCV is positive → Check HCV RNA to confirm chronic infection.

Hepatitis D (HDV) Serology

Marker Interpretation

Anti-HDV IgM Acute HDV Infection

Anti-HDV IgG Chronic HDV Infection

HDV only infects individuals with HBV (HBsAg positive).

Hepatitis E (HEV) Serology

Marker Interpretation

Anti-HEV IgM Acute HEV Infection

Anti-HEV IgG Past Infection

Severe in pregnancy (Fulminant Hepatitis, high mortality in 3rd trimester).

V. Management of Hepatitis

Gastroenterology 23
 1. Hepatitis A & E (Self-Limiting, Supportive Care Only)
Supportive therapy (fluids, rest, avoid alcohol & hepatotoxic drugs).

No antiviral treatment needed.

2. Hepatitis B (HBV) Treatment

Indication for Treatment First-Line Drugs

Acute HBV Supportive (No antivirals needed)

Chronic HBV (High ALT, HBV DNA >2000 IU/mL) Entecavir, Tenofovir (First-Line)

Pregnant Women with High Viral Load Tenofovir to prevent transmission

Goal: Suppress viral replication (HBV is not curable).

3. Hepatitis C (HCV) Treatment

Regimen Duration

Direct-Acting Antivirals (DAAs) (Sofosbuvir + Velpatasvir, Ledipasvir) 8-12 weeks

HCV is curable in >95% of cases with DAAs.

No vaccine available.

4. Hepatitis D (HDV) Treatment

Pegylated Interferon-alpha (PEG-IFN-α) for 12-18 months (Limited
effectiveness).

Best Prevention = HBV Vaccination (Since HDV depends on HBV).

VI. Prevention & Vaccination

Hepatitis Vaccine Available? Who Should Get Vaccinated?

Yes (Inactivated Travelers, MSM, IV drug users, Chronic Liver

HAV
Vaccine) Disease

Yes (Recombinant All infants, Healthcare workers, IV drug users,

HBV
HBsAg) MSM

HCV No No vaccine available

Gastroenterology 24
 HDV No Prevented by HBV vaccine

HEV Yes (China only) Pregnant women in endemic areas

HBV Vaccine Schedule: 0, 1, and 6 months.

HAV Vaccine: Given to travelers, high-risk individuals.

VII. Complications of Chronic Hepatitis

Complication Hepatitis B (HBV) Hepatitis C (HCV)

Cirrhosis Yes (20-30%) Yes (50-60%)

Hepatocellular Carcinoma
Yes (Direct Carcinogenesis) Yes (Due to Cirrhosis)
(HCC)

Extrahepatic Polyarteritis Nodosa, Cryoglobulinemia,

Manifestations Glomerulonephritis Vasculitis

HCC Screening (for Cirrhotics & Chronic HBV patients) → Ultrasound ± AFP
every 6 months.

VIII. Summary of Hepatitis Management

Hepatitis Acute Management Chronic Management

HAV, HEV Supportive care No chronic disease

HBV Supportive Tenofovir, Entecavir (if criteria met)

HCV DAAs if chronic Sofosbuvir + Velpatasvir (8-12 weeks)

HDV Supportive, PEG-IFN-α HBV vaccine prevents HD

Liver Tumors (Benign & Malignant,

Including Hepatocellular Carcinoma – HCC)
I. Classification of Liver Tumors
Liver tumors can be benign or malignant and may arise primarily in the liver or as
metastases from other cancers.

Gastroenterology 25
 Type Examples

Hepatic Hemangioma, Focal Nodular Hyperplasia (FNH),

Benign Tumors
Hepatic Adenoma

Primary Malignant
Hepatocellular Carcinoma (HCC), Cholangiocarcinoma
Tumors

Secondary (Metastatic) Colorectal cancer, Breast cancer, Lung cancer metastases to

Tumors liver (Most Common Liver Malignancy)

II. Benign Liver Tumors

1. Hepatic Hemangioma (Most Common Benign Liver Tumor)
Feature Description

Epidemiology More common in women (hormonal influence)

Usually asymptomatic; may cause RUQ pain if

Symptoms
large

Imaging (Best Test: Contrast-Enhanced Peripheral nodular enhancement with

MRI/CT) centripetal filling

Treatment No treatment needed unless symptomatic

2. Focal Nodular Hyperplasia (FNH)

Feature Description

Pathology Hyperplastic hepatocytes with a central scar

Risk Factors Women (hormonal influence, but no OCP association)

Symptoms Asymptomatic

Imaging (CT/MRI) Central scar with arterial enhancement

Treatment No treatment unless symptomatic

3. Hepatic Adenoma
Feature Description

Risk Factors Oral contraceptive use, Anabolic steroids

Gastroenterology 26
 Complications Risk of rupture & hemorrhage, Malignant transformation (HCC risk)

Imaging Hypervascular lesion with no central scar

Management Stop OCPs, Surgical resection if >5 cm or symptomatic

III. Primary Malignant Liver Tumors

1. Hepatocellular Carcinoma (HCC) (Most Common Primary Liver
Cancer)

Risk Factors

Cause Mechanism

Cirrhosis (Most Common Risk Factor) Hepatitis B/C, Alcoholic Liver Disease, NAFLD

Aflatoxin Exposure Aspergillus-contaminated food (Africa, Asia)

Hemochromatosis & Wilson’s Disease Iron & copper overload

Clinical Features
Feature Description

Unintentional Weight
Due to increased metabolism
Loss

RUQ Pain &

Tumor mass effect
Hepatomegaly

Jaundice & Ascites Late-stage disease

Paraneoplastic Erythrocytosis (EPO secretion), Hypercalcemia (PTHrP),

Syndromes Hypoglycemia

Diagnosis

Test Findings in HCC

↑ in 70% of cases (≥400 ng/mL highly suggestive of

Alpha-Fetoprotein (AFP)
HCC)

Liver Ultrasound (Screening

Hypoechoic mass
Test)

Gastroenterology 27
 Arterial enhancement, Washout in the venous phase
CT/MRI (Gold Standard)
(Hallmark of HCC)

Not always needed (risk of seeding), only if imaging is

Liver Biopsy
inconclusive

Surveillance in Cirrhosis: Ultrasound ± AFP every 6 months.

Management of HCC

Stage Treatment Comments

Early (Single Tumor ≤5 cm or

Liver Transplant (Best Cure), Milan Criteria for
≤3 tumors ≤3 cm each, No
Resection Liver Transplant
Metastases)

Intermediate (Multifocal HCC, Transarterial Used for local tumor

No Extrahepatic Spread) Chemoembolization (TACE) control

Advanced (Vascular Invasion or Systemic Therapy (Sorafenib,

Palliative treatment
Distant Metastases) Lenvatinib, Immunotherapy)

2. Cholangiocarcinoma (Bile Duct Cancer)

Feature Description

Primary Sclerosing Cholangitis (PSC), Liver Flukes (Clonorchis

Risk Factors
sinensis)

Symptoms Painless jaundice, Pruritus, Dark urine, Weight loss

Diagnosis CA 19-9 tumor marker, MRCP (biliary strictures), ERCP with biopsy

Surgical resection (if localized), Palliative chemo for unresectable

Treatment
cases

IV. Secondary (Metastatic) Liver Tumors

Most common malignant liver tumors (Liver is a frequent site of metastasis).

Primary sources: Colorectal cancer (Most Common), Breast, Lung,

Pancreas.

Diagnosis: CT/MRI shows multiple liver lesions with irregular enhancement.

Gastroenterology 28
 Treatment: Treat primary cancer, liver-directed therapy (TACE, Resection,
Radiofrequency Ablation for oligometastatic disease).

V. Summary of Liver Tumor Management

Tumor Type Key Features Management

Most common benign tumor, No treatment unless

Hepatic Hemangioma
Peripheral enhancement symptomatic

Focal Nodular
Central scar on imaging No treatment
Hyperplasia (FNH)

OCP use, Risk of rupture &

Hepatic Adenoma Resection if >5 cm
malignancy

Hepatocellular Arterial enhancement, Liver transplant, Resection,

Carcinoma (HCC) Cirrhosis-related TACE, Sorafenib

PSC association, Painless Surgical resection,

Cholangiocarcinoma
jaundice, CA 19-9 Palliative therapy

From colorectal, breast, lung Treat primary tumor +

Liver Metastases
cancer liver-directed therapy

Irritable Bowel Syndrome (IBS)

I. Definition
Irritable Bowel Syndrome (IBS) is a functional gastrointestinal disorder
characterized by recurrent abdominal pain and altered bowel habits (diarrhea,
constipation, or both) without any structural or biochemical abnormalities.

II. Epidemiology & Risk Factors

Factor Details

Prevalence Affects 10-15% of adults, more common in women

Age Group Typically presents in young adulthood (20-40 years)

Psychological Factors Anxiety, Depression, Stress, PTSD

Gastroenterology 29
 Dietary Triggers High-fat foods, caffeine, dairy, FODMAPs

Post-Infectious IBS Can develop after gastroenteritis (altered gut microbiota)

Gut-Brain Axis Dysfunction Increased visceral hypersensitivity & dysmotility

III. Pathophysiology
1. Altered Gut Motility → Hyperactive or hypoactive intestinal contractions.

2. Visceral Hypersensitivity → Increased pain perception from normal GI stimuli.

3. Gut Microbiota Changes → Dysbiosis may contribute to symptoms.

4. Increased Gut Permeability → Low-grade inflammation in some IBS patients.

5. Psychosocial Factors → Stress worsens symptoms via the gut-brain axis.

IV. Clinical Features

Feature Description

Recurrent Abdominal At least 1 day per week for the past 3 months, relieved by
Pain defecation

Altered Bowel Habits Diarrhea (IBS-D), Constipation (IBS-C), or Mixed (IBS-M)

Bloating & Gas Common in IBS patients

Mucus in Stool Present in some cases, without blood

Post-Prandial Symptoms Symptoms worsen after meals

Red Flag Symptoms (Not Typical for IBS, Requires Further

Workup)
Unintentional weight loss.

Anemia or GI bleeding (hematochezia, melena).

Nocturnal diarrhea (suggests organic disease).

Family history of colorectal cancer, IBD, or celiac disease.

Persistent vomiting or new-onset symptoms in age >50.

Gastroenterology 30
 V. Diagnosis (Rome IV Criteria for IBS)
IBS is a clinical diagnosis; no specific test confirms it.

Rome IV Criteria (IBS Diagnosis Requires All 3 Below)

1. Recurrent abdominal pain ≥1 day per week (for the last 3 months).

2. Associated with ≥2 of the following:

Pain relieved or related to defecation.

Change in stool frequency (diarrhea or constipation).

Change in stool form (appearance).

3. Symptoms must have started ≥6 months before diagnosis.

VI. Subtypes of IBS

Type Stool Pattern

IBS-D (Diarrhea-Predominant) Loose stools ≥25% of the time

IBS-C (Constipation-Predominant) Hard stools ≥25% of the time

IBS-M (Mixed Type) Alternating diarrhea & constipation

IBS-U (Unclassified) Does not fit any specific pattern

VII. Investigations (To Rule Out Other Conditions)

Test Findings in IBS Indications

CBC (Hemoglobin, WBC) Normal Rule out anemia, IBD

CRP/ESR Normal Rule out inflammatory conditions

Fecal Calprotectin Normal Excludes IBD

Celiac Serology (Anti-TTG IgA) Negative Exclude Celiac Disease in IBS-D

Stool Studies (Ova & Parasites, C. Exclude infections in persistent

Negative
difficile) diarrhea

Colonoscopy Normal If alarm symptoms or age >50

Gastroenterology 31
 VIII. Management
1. General Lifestyle & Dietary Modifications
Recommendation Details

Low FODMAP Diet (Fermentable Oligo-, Di-, Avoid onions, garlic, legumes, dairy,
Monosaccharides, And Polyols) artificial sweeteners

Increase Soluble Fiber (For IBS-C) Psyllium (Metamucil)

Avoid Trigger Foods Spicy, fatty foods, caffeine, alcohol

Reduces stress and improves gut

Regular Exercise
motility

Yoga, Meditation, Cognitive Behavioral

Stress Management
Therapy (CBT)

2. Pharmacologic Therapy (Symptom-Specific)

Symptom First-Line Treatment Alternative

IBS-D (Diarrhea- Loperamide (Imodium) (Anti- Rifaximin (Antibiotic for

Predominant) motility) refractory cases), Eluxadoline

IBS-C (Constipation- Polyethylene glycol (PEG),

Psyllium (Soluble fiber)
Predominant) Linaclotide, Lubiprostone

TCAs (Amitriptyline,
Abdominal Antispasmodics (Dicyclomine,
Nortriptyline) for refractory
Pain/Bloating Hyoscine, Mebeverine)
pain

Peppermint Oil (Reduces

Global IBS Symptoms Probiotics (Mixed evidence)
spasms)

TCAs (e.g., Amitriptyline) → Used for pain & visceral hypersensitivity in IBS-
D.

SSRIs (e.g., Fluoxetine, Sertraline) → Used for IBS-C with

depression/anxiety.

IX. Complications & Prognosis

Gastroenterology 32
 Complication Details

Psychological Impact High association with anxiety & depression

Reduced Quality of Life Frequent doctor visits, dietary restrictions

No Increased Risk of Cancer Unlike IBD, IBS does not increase CRC risk

Prognosis: Chronic but non-life-threatening; symptoms can be well-

controlled with lifestyle changes and medication.

X. Summary of IBS Management

Approach IBS-D IBS-C Mixed IBS

Lifestyle Low FODMAP diet ↑ Fiber intake Identify triggers

Treat predominant
First-Line Therapy Loperamide Psyllium (Fiber)
symptom

Second-Line Rifaximin,
PEG, Linaclotide Titrate treatments
Therapy Eluxadoline

Antispasmodics, Antispasmodics,
Pain Management Antispasmodics, TCAs
TCAs TCAs

Psychological
CBT, SSRIs CBT, SSRIs CBT, SSRIs
Support

Celiac Disease (Gluten-Sensitive

Enteropathy)
I. Definition
Celiac disease is a chronic autoimmune disorder triggered by gluten ingestion in
genetically predisposed individuals, leading to intestinal inflammation,
malabsorption, and systemic complications.

II. Etiology & Risk Factors

Gastroenterology 33
 Factor Details

Genetic Predisposition HLA-DQ2 & HLA-DQ8 (Present in >95% of cases)

Environmental Triggers Gluten-containing foods (wheat, barley, rye)

Other Autoimmune Diseases Type 1 Diabetes, Hashimoto’s Thyroiditis, Addison’s Disease

Family History First-degree relatives have a 10% risk of celiac disease

Early Childhood Factors Infections, Gut microbiome changes, Antibiotic use

III. Pathophysiology
1. Gluten ingestion → Immune response in the small intestine.

2. T-cell activation & autoantibody production (Anti-TTG, Anti-EMA, Anti-

DGP).

3. Villous atrophy & crypt hyperplasia → Malabsorption of nutrients.

4. Systemic manifestations due to nutrient deficiencies & chronic

inflammation.

IV. Clinical Features

1. Classic Symptoms (Malabsorption Dominant)
Symptom Description

Chronic Diarrhea Fatty, foul-smelling stools (Steatorrhea)

Weight Loss & Failure to Thrive Nutrient malabsorption

Abdominal Bloating & Pain Due to gas & fermentation

Fatigue Iron & B12 deficiency

2. Atypical Symptoms (Extraintestinal)

System Manifestation

Skin Dermatitis Herpetiformis (Pruritic vesicular rash, Extensor surfaces)

Neurological Peripheral neuropathy, Ataxia, Depression, Anxiety

Hematological Iron-deficiency anemia (Most common), B12/Folate deficiency

Gastroenterology 34
 Endocrine Osteopenia, Osteoporosis (Vitamin D deficiency)

Gynecological Infertility, Recurrent miscarriages

3. Asymptomatic (Silent Celiac Disease)

No obvious symptoms but positive serology & villous atrophy.

V. Diagnosis
1. Serologic Tests (First-Line Screening)
Findings in Celiac
Test Comments
Disease

Anti-Tissue Transglutaminase
↑ Elevated First-line screening test
(Anti-TTG IgA) (Best Test)

Anti-Endomysial Antibodies (Anti- Highly specific but less

↑ Elevated
EMA IgA) sensitive than TTG

Anti-Deamidated Gliadin Peptide Used in IgA-deficient

↑ Elevated
(Anti-DGP IgA/IgG) patients

↓ Low in Selective IgA If IgA deficiency → Use

Total Serum IgA
Deficiency Anti-DGP IgG

False Negative Serology → If already on a gluten-free diet.

2. Confirmatory Test (Gold Standard) → Duodenal Biopsy via

Endoscopy
Findings in Celiac Disease

Villous Atrophy (Blunted Villi)

→ Decreased surface area for absorption

Crypt Hyperplasia
→ Compensatory increase in crypt cells

Intraepithelial Lymphocytosis

Gastroenterology 35
 Minimum 4-6 biopsies from the distal duodenum & jejunum.

3. Genetic Testing (HLA-DQ2 & HLA-DQ8)

Negative HLA-DQ2/DQ8 → Celiac disease is ruled out.

Used in equivocal cases or seronegative celiac disease.

VI. Differential Diagnosis

Condition Key Differentiating Features

Lactose Intolerance No autoantibodies, Normal biopsy

IBS (Irritable Bowel

No weight loss, No malabsorption
Syndrome)

Tropical Sprue History of travel to endemic areas (Caribbean, India)

Segmental involvement, Skip lesions, Transmural

Crohn’s Disease
inflammation

VII. Management
1. Gluten-Free Diet (Only Definitive Treatment)

Avoid (Gluten-Containing
Safe Foods
Foods)

Rice, Corn, Quinoa, Potatoes, Oats (Gluten-Free

Wheat, Barley, Rye, Malt, Beer
Certified)

Lifelong adherence required → Symptoms improve within weeks to months.

2. Nutritional Supplementation
Deficiency Supplement

Iron Deficiency Oral Iron (Ferrous Sulfate)

Vitamin D & Calcium Prevention of osteoporosis

Folic Acid & Vitamin B12 Neurological & hematologic recovery

Gastroenterology 36
 3. Monitor Disease Progression

Follow-Up Test Indication

Repeat Anti-TTG IgA (6-12 months) Assess compliance & recovery

DXA Scan (Bone Density Test) If osteoporosis risk present

VIII. Complications
Complication Description

Refractory Celiac Disease (Persistent Consider other diagnoses (Tropical Sprue,

Symptoms Despite Gluten-Free Diet) SIBO)

Enteropathy-Associated T-Cell
Malignancies (Rare but Serious) Lymphoma (EATL), Small Bowel
Adenocarcinoma

Nutritional Deficiencies Iron, Folate, B12, Calcium, Vitamin D

Due to chronic malabsorption of calcium &

Osteoporosis/Osteomalacia
vitamin D

IX. Summary of Celiac Disease Management

Step Management

1. Confirm Diagnosis Serology (Anti-TTG IgA), Duodenal Biopsy

2. Gluten-Free Diet (Lifelong) Avoid wheat, barley, rye, Educate patients

3. Treat Nutrient Deficiencies Iron, Calcium, Vitamin D, B12, Folate

Repeat Anti-TTG IgA (6-12 months), DXA scan

4. Monitor Response
if osteoporosis risk

5. Consider Refractory Celiac Disease

Rule out SIBO, Tropical Sprue, IBD, Lymphoma
if No Response

Colorectal Cancer (CRC)

Gastroenterology 37
 I. Definition
Colorectal cancer (CRC) is a malignant tumor of the colon or rectum, arising from
adenomatous polyps due to progressive genetic mutations. It is the third most
common cancer worldwide and a leading cause of cancer-related death.

II. Risk Factors

Category Risk Factors

Age >50 years (Most cases)

Genetic (Hereditary Syndromes, Familial Adenomatous Polyposis (FAP), Lynch

Strongest Risk Factor) Syndrome (HNPCC)

CRC, Adenomatous polyps, Inflammatory Bowel

Personal or Family History
Disease (IBD – UC > Crohn’s)

Low fiber, High red/processed meat, Smoking,

Dietary & Lifestyle
Alcohol, Obesity, Sedentary lifestyle

Diabetes & Metabolic Syndrome Increased risk due to insulin resistance

III. Pathogenesis & Molecular Pathways

Pathway Mutation Sequence Cancer Type

Adenoma-Carcinoma Sequence APC (Tumor suppressor) → Sporadic CRC

(Most Common, Sporadic CRC) KRAS → p53 (80%)

Microsatellite Instability (MSI) MLH1, MSH2 Mutations Lynch Syndrome

Pathway (Mismatch Repair Deficiency) (HNPCC)

CpG Island Methylation (CIMP) Serrated

Hypermethylation of MLH1
Pathway Adenomas

IV. Clinical Features

Location Signs & Symptoms

Right-Sided (Proximal) Iron Deficiency Anemia (Fatigue, Pallor), Occult GI Bleeding,

Colon Cancer Weight Loss

Gastroenterology 38
 Left-Sided (Distal) Colon Change in Bowel Habits (Constipation/Diarrhea), Pencil-Thin
Cancer Stools, Hematochezia (Fresh Blood in Stool)

Tenesmus (Feeling of Incomplete Evacuation), Rectal

Rectal Cancer
Bleeding, Pelvic Pain

Red Flag Symptoms (Suggest Malignancy)

Unexplained weight loss.

Iron deficiency anemia (especially in older adults).

Rectal bleeding or persistent change in bowel habits.

Abdominal mass or obstruction symptoms.

V. Diagnosis
1. Screening (Asymptomatic Patients)

Recommended
Population Frequency
Screening Test

Colonoscopy (Gold
Average Risk (>50 years) Every 10 years
Standard)

Alternative Screening (If FIT (Fecal

Every Year
Colonoscopy Not Possible) Immunochemical Test)

High-Risk (Family History, Starting at 40 years or 10 years

Colonoscopy
Lynch Syndrome, IBD, FAP) before earliest family case

2. Diagnostic Workup (Symptomatic Patients)

Test Findings in CRC

Colonoscopy with Biopsy (Gold

Exophytic mass, Ulcerated lesion
Standard)

CT Abdomen/Pelvis (Staging) Liver, Lung metastases

Carcinoembryonic Antigen Tumor marker (Used for prognosis & recurrence

(CEA) monitoring, NOT for screening)

Gastroenterology 39
 VI. Staging (TNM System)
Stage Tumor Spread 5-Year Survival

Stage I Confined to mucosa/submucosa 90%

Stage II Invades muscularis but no lymph node involvement 75%

Stage III Lymph node involvement 50-60%

Stage IV Distant metastases (Liver, Lungs) <15%

VII. Treatment
1. Surgical Resection (Definitive Treatment for Localized CRC)
Tumor
Surgery
Location

Right Colon Right Hemicolectomy

Left Colon Left Hemicolectomy

Sigmoid Colon Sigmoid Colectomy

Low Anterior Resection (LAR) or Abdominoperineal Resection (APR, If

Rectal Cancer
Below Dentate Line)

2. Adjuvant Chemotherapy (Stage II-III, Node-Positive or High-

Risk Stage II)
Regimen Indications

FOLFOX (5-FU + Leucovorin + Oxaliplatin) Stage III & High-Risk Stage II

Capecitabine (Oral 5-FU Prodrug) Alternative to 5-FU

3. Targeted Therapy (For Metastatic CRC, Stage IV)

Drug Target Indications

Bevacizumab VEGF Inhibitor Used in metastatic CRC

Cetuximab, Panitumumab EGFR Inhibitor KRAS Wild-Type CRC Only

4. Radiation Therapy

Gastroenterology 40
 Used only in Rectal Cancer (Neoadjuvant or Adjuvant Therapy).

Not routinely used for Colon Cancer.

VIII. Complications
Complication Description

Bowel Obstruction Due to tumor growth causing luminal narrowing

Perforation & Peritonitis Tumor invasion → Free air on imaging

Liver & Lung Metastases Most common metastatic sites

Recurrence Surveillance colonoscopy required

IX. Post-Treatment Surveillance

Test Frequency

Colonoscopy 1 year post-surgery, then every 3-5 years

CEA Levels Every 3-6 months for 5 years

CT Scan (For Stage II-III CRC) Every 6-12 months for 3 years

X. Summary of CRC Management

Stage Treatment Prognosis

Stage I (Early CRC) Surgery Alone (Curative) 90% survival

Stage II (Invasive, No Surgery ± Adjuvant Chemotherapy (High-

75% survival
Nodes) Risk Cases)

Stage III (Lymph Node Surgery + Adjuvant Chemotherapy 50-60%

Involvement) (FOLFOX) survival

Chemotherapy ± Targeted Therapy

Stage IV (Metastatic CRC) <15% survival
(Bevacizumab, Cetuximab)

Gastroenterology 41
Gastroenterology 42