321: APPROACH TO THE PATIENT WITH o Secretes intrinsic factor (required for vitamin B12
GASTROINTESTINAL DISEASE absorption).
o Regulates acid production for digestion and
defense.
I. ANATOMIC CONSIDERATIONS 4. Small Intestine
• General Structure • Primary site of nutrient absorption.
o GI tract extends from mouth to anus. • Structural specialization:
o Composed of organs with distinct functional o Villus architecture maximizes surface area.
specializations. o Contains specialized enzymes and transporters.
o Sphincters separate regions and regulate flow • Duodenum:
between compartments. o Receives chyme, pancreatic juice, and bile.
• Gut Wall Organization o Pancreatic juice: enzymes + bicarbonate (optimizes
o Mucosa: pH for enzymatic activity).
▪ Acts as a barrier to luminal contents. o Bile: essential for lipid emulsification and
▪ Site of nutrient and fluid absorption. absorption.
o Smooth muscle (circular and longitudinal): • Regional specialization:
▪ Mediates propulsion and mixing of o Proximal intestine: rapid absorption of nutrients
luminal contents. and minerals.
▪ Controlled by the enteric nervous o Ileum: absorption of vitamin B12 and bile acids.
system (ENS). • Bile: also facilitates excretion of toxins, bilirubin, drugs, and
o Serosal layer: cholesterol.
▪ Provides structural support. 5. Colon (Large Intestine)
▪ Allows external input (nerves, vessels). • Primary function: dehydration and storage of stool.
• Associated Systems • Fluid absorption: reduces ileal effluent (1000–1500 mL) to
o Pancreaticobiliary conduits: deliver bile and 100–200 mL stool output.
digestive enzymes into the duodenum. • Microbiome:
o Vascular supply: dynamically modulated by GI o Dense bacterial population.
activity. o Ferments undigested carbohydrates to produce
o Lymphatics: participate in immune surveillance short-chain fatty acids.
and lipid transport. o Modulates immune and metabolic functions.
o Nervous control: • Motility:
▪ Intrinsic (ENS): local regulation of o Proximal colon: mixing and absorption.
propulsion and secretion. o Distal colon: peristaltic contractions and mass
▪ Extrinsic (autonomic): provides movements for stool evacuation.
voluntary and involuntary control. o Transit time: >1 day in most individuals.
• Anus:
II. FUNCTIONS OF THE GI TRACT o Dual control: volitional and involuntary sphincters
A. Major Functions for continence and defecation.
• Assimilation of nutrients. 6. Ileocecal Junction
• Elimination of waste products. • Functions as a sphincter.
B. Regional Functions • Prevents coloileal reflux and excessive bacterial
1. Mouth contamination of small intestine.
• Mechanical processing and lubrication of food.
• Mixing with salivary amylase for starch digestion. III. EXTRINSIC MODULATION OF GUT FUNCTION
• Formation and propulsion of bolus toward esophagus. • Environmental Interface
2. Esophagus o Gut is in direct continuity with the external
• Propels food to the stomach via coordinated peristalsis. environment.
• Upper and lower esophageal sphincters: prevent air entry o Constant exposure to food antigens, drugs, and
and reflux. pathogens.
• Squamous mucosa: protective, minimal absorption. • Protective Mechanisms
• Peristaltic coordination ensures efficient swallowing. o Mucosal immune system:
3. Stomach ▪ Epithelial and lamina propria
• Functions: lymphocytes.
o Triturates and mixes food with gastric acid and ▪ Plasma cells and organized lymph nodes.
pepsin. o Paneth cells: secrete antimicrobial peptides.
o Acid sterilizes food and initiates protein digestion. o Liver (via portal circulation): detoxifies absorbed
• Regional specialization: substances.
o Proximal stomach: storage; receptive relaxation • Neural Control
after meals. o Intrinsic nerves (ENS): coordinate local motility
o Distal stomach: mixing and grinding; phasic and secretion.
contractions propel contents to pylorus. o Extrinsic pathways (vagal and splanchnic):
• Secretory roles: ▪ Modulate reflexes and regional activity.
o Brain-gut axis:
, ▪ Links emotional and cognitive centers • Microbiome dysbiosis: linked to IBD, celiac disease, IBS,
with gut function. and cancer.
▪ Stress may alter motility, secretion, and E. Impaired Gut Blood Flow
visceral sensitivity. • Ischemic injury:
o Causes: embolism, thrombosis, venous occlusion,
IV. OVERVIEW AND CLASSIFICATION OF GI DISEASES hypoperfusion.
GI diseases arise from structural, functional, immune, vascular, or o Results: mucosal necrosis, bleeding, perforation.
neoplastic abnormalities. • Chronic ischemia: may form strictures.
A. Impaired Digestion and Absorption • Radiation enterocolitis: reduced mucosal perfusion.
• Common causes: F. Neoplastic Degeneration
o Lactase deficiency (most common; benign gas and • Common malignancies:
diarrhea). o Colorectal cancer (most common in U.S.).
o Celiac disease. o Gastric cancer (prevalent in Asia).
o Bacterial overgrowth. o Esophageal carcinoma (linked to reflux, alcohol,
o Infectious enteritis. tobacco).
o Crohn’s ileitis. o Pancreatic, biliary, hepatic cancers (poor
o Radiation enteritis. prognosis).
• Consequences: malnutrition, anemia, dehydration, • Associated features:
electrolyte imbalances. o Weight loss, pain, jaundice, bleeding.
• Pancreatic disorders: o May present as adenocarcinoma, lymphoma, or
o Chronic pancreatitis or cancer → enzyme other histologic types.
deficiency and maldigestion. G. Functional (Nonorganic) Disorders
• Biliary obstruction: impaired fat digestion. • Examples: IBS, functional dyspepsia, functional heartburn.
• Gastrinoma: excess acid damages mucosa, inactivates • Features:
pancreatic enzymes, accelerates transit. o No detectable structural or biochemical
B. Altered Secretion abnormalities.
• Hypersecretion: o Possible disordered motility or visceral
o Gastrinoma, G-cell hyperplasia, retained antrum. hypersensitivity.
o Results in duodenal ulcers, diarrhea. o Brain-gut dysregulation; may co-occur with
• Hyposecretion: psychological stress.
o Atrophic gastritis, pernicious anemia. H. Genetic Influences
• Secretory diarrhea causes: • Familial clustering in IBD, colorectal, esophageal, pancreatic
o Infectious (bacterial, viral, parasitic). cancers.
o SIBO, bile salt diarrhea, microscopic colitis. • Inherited dysmotility syndromes (rare).
o Endocrine tumors (VIPoma). • Functional disorders may show familial behavior patterns
C. Altered Gut Transit rather than true heredity.
• Mechanical obstruction:
o Esophagus: stricture, tumor, eosinophilic V. SYMPTOMS OF GI DISEASE
esophagitis. A. Abdominal Pain
o Stomach: peptic ulcer, carcinoma. • Visceral pain: midline, dull, poorly localized.
o Small intestine: adhesions, Crohn’s, radiation, • Parietal pain: sharp, localized.
drugs. • Inflammatory causes: peptic ulcer, appendicitis,
o Colon: carcinoma, IBD stricture, diverticulitis. diverticulitis, IBD, pancreatitis.
• Motor dysfunctions: • Noninflammatory: biliary colic, ischemia, neoplasia.
o Achalasia: impaired LES relaxation and peristalsis. • Common functional causes: IBS, functional dyspepsia.
o Gastroparesis: delayed gastric emptying (often B. Heartburn
diabetic). • Burning substernal discomfort; intermittent in 40% of adults.
o Intestinal pseudoobstruction: enteric
• Classic cause: acid reflux.
nerve/smooth muscle damage.
• Other causes: nonacid reflux, esophageal hypersensitivity.
o Slow-transit constipation: reduced colonic
C. Nausea and Vomiting
propulsion.
o Dyssynergic defecation: failure of anal relaxation. • Causes:
o GI obstruction, toxins, medications, infection, CNS
• Rapid transit disorders:
or endocrine disease.
o Dumping syndrome, hyperthyroidism, IBS,
o Chronic causes: gastroparesis,
functional dyspepsia.
pseudoobstruction, IBS.
D. Immune Dysregulation
o Functional syndromes: chronic nausea vomiting
• Celiac disease: gluten-triggered mucosal inflammation.
syndrome, cyclic vomiting, cannabinoid
• Eosinophilic GI diseases: eosinophilic hyperemesis.
esophagitis/gastroenteritis. D. Altered Bowel Habits
• IBD: ulcerative colitis and Crohn’s disease. • Constipation:
• Microscopic colitis: lymphocytic or collagenous infiltration. o Causes: obstruction, motility disorder, medications,
• Infectious enterocolitis: bacterial, viral, or protozoal. hypothyroidism.
, o Symptoms: infrequent stool, straining, incomplete • Pain timing:
evacuation. o Ulcer pain: intermittent, weeks–months.
• Diarrhea: o Biliary colic: sudden onset, lasts hours.
o Causes: infection, inflammation, malabsorption, o Pancreatitis: severe, lasts days–weeks.
medications. • Defecation and meals:
o IBS: alternating constipation/diarrhea, mucus in o Diarrhea after meals or pain relief after defecation
stool. → IBD or IBS.
o IBD: blood and pus in stool. • Stress: exacerbates functional bowel disorders.
o Steatorrhea: fat malabsorption. • Nocturnal pain (awakens from sleep): suggests organic
E. GI Bleeding disease.
• Upper GI bleeding: • Effect of fasting:
o Manifestations: melena, hematemesis. o Improves malabsorptive diarrhea,
o Causes: ulcers, esophagitis, varices, malignancy. o No effect on secretory diarrhea.
• Lower GI bleeding: 3. Association with Other Factors
o Manifestations: hematochezia (bright red blood). • Post-surgical adhesions: suggest obstruction.
o Causes: hemorrhoids, diverticulosis, IBD, ischemic • Post-gastrectomy/cholecystectomy: dumping or
or infectious colitis, neoplasm. postcholecystectomy diarrhea.
• Occult bleeding: may present as iron deficiency anemia. • After travel: infectious cause.
F. Jaundice • Medications: may cause pain, altered bowel habits, or
• Posthepatic causes: bleeding.
o Biliary obstruction (stones, tumors, cholangitis, • Ethnicity:
PSC). o Celiac disease → northern European descent.
o Pancreatic disease (pancreatitis, stricture, cancer). o IBD → Jewish populations.
G. Other Symptoms • Sexual history: infection or immunodeficiency risk.
• Dysphagia, odynophagia → esophageal disease. 4. Functional Bowel Disorders
• Globus sensation → functional or pharyngoesophageal • Diagnosed using symptom-based criteria (e.g., Rome
causes. criteria).
• Weight loss, anorexia, fatigue → malignancy, • Sensitivity/specificity ~55–75% vs. structural findings.
inflammation, dysmotility. • Caution needed in high-risk patients to avoid missing
• Systemic manifestations: organic disease.
o IBD → arthritis, eye/skin/hepatobiliary disease.
o Celiac disease → dermatitis herpetiformis. PHYSICAL EXAMINATION
o Jaundice → pruritus. 1. General Principles
• Systemic diseases affecting GI tract: • Complements the history; guides urgency and differential
o Lupus → ischemic injury. diagnosis.
o Severe burns → stress ulcer. 2. Vital Signs
EVALUATION OF THE PATIENT WITH GI DISEASE • Fever: inflammation or neoplasm.
GENERAL APPROACH • Orthostasis: blood loss, dehydration, sepsis, autonomic
• Begins with careful history and physical examination. neuropathy.
• Subsequent investigations are based on findings and may 3. Extra-Abdominal Findings
assess: • Skin, eyes, joints: may indicate systemic disease (IBD,
o Gut structure, function, and luminal contents. vasculitis).
• When diagnostic tests are normal, validated symptom • Neck/swallow exam: for dysphagia.
profiles (e.g., Rome criteria) are used to diagnose • Cardiopulmonary exam: excludes cardiac/pulmonary
functional bowel disorders. causes of pain/nausea.
• Pelvic exam: identifies gynecologic sources.
HISTORY
• Rectal exam: detects blood, masses (appendicitis,
1. Importance and Purpose
neoplasm).
• Central to identifying likely etiology and pathophysiologic
• Peripheral neuropathy: in metabolic/motor disorders.
process.
4. Abdominal Examination
• Symptom timing, pattern, and duration help differentiate:
• Inspection: distention (obstruction, tumor, ascites),
o Acute processes: infection, inflammation, toxins,
ecchymoses (pancreatitis), vascular changes (liver disease).
ischemia.
o Chronic processes: chronic inflammation, • Auscultation:
neoplasia, functional disorders. o Absent bowel sounds: ileus.
2. Symptom Characterization o High-pitched sounds: obstruction.
o Bruit or rub: vascular disease or tumor.
• Luminal obstruction:
o Dysphagia, nausea/vomiting, bloating, • Percussion: liver span, shifting dullness (ascites).
distention, constipation, depending on site. • Palpation: organomegaly, masses, tenderness.
• Meal relation: o Visceral pain: diffuse tenderness.
o Worsened by meals: obstruction, ischemia, IBD, o Parietal pain/peritonitis: localized tenderness,
functional bowel disorders. guarding, rebound.
o Relieved by eating or antacids: ulcer disease.
, o Musculoskeletal pain: worsens with Valsalva or • Contrast radiography: mucosal detail, transit studies, pelvic
leg lift. floor evaluation.
o Esophagram: rings, strictures, achalasia.
TOOLS FOR PATIENT EVALUATION o Small-bowel contrast: tumors, strictures, fistulas.
1. Laboratory Testing o Contrast enema: if colonoscopy not possible.
• CBC and chemistries: • Ultrasound/CT/MRI:
o Iron deficiency: mucosal blood loss. o Detect mass lesions, gallstones, fluid collections,
o B12 deficiency: intestinal, gastric, pancreatic liver/pancreas abnormalities.
disease or malnutrition. o CT/MR colonography: colon cancer screening
o Leukocytosis: inflammation; leukopenia: viral (alternative).
illness. o MRCP: biliary/pancreatic ducts.
o Electrolyte and acid-base disturbances: from o CT/MR enterography: IBD activity.
vomiting/diarrhea. o Angiography: ischemia, tumor spread, biliary
o Pancreatic/liver chemistries: for hepatobiliary access.
disease. o PET and DOTA-octreotate PET-CT: detect
o Thyroid, cortisol, calcium: endocrine causes. neuroendocrine tumors.
o Pregnancy test: in women with nausea. • Scintigraphy:
• Serologic and tumor markers: o Bleeding scans: localize active hemorrhage.
o Celiac, IBD, connective tissue, paraneoplastic o Leukocyte scans: detect abscesses.
antibodies. o Biliary scans: for cholecystitis.
o Hormones: for endocrine neoplasia. o Transit studies: gastric emptying, intestinal/colonic
o Tumor markers: CEA, CA 19-9, α-fetoprotein. motility.
• Therapeutic monitoring: e.g., thiopurine metabolites in IBD. 5. Histopathology
• Research biomarkers: predict IBD course/treatment • Endoscopic biopsies: inflammatory, infectious, or
response. neoplastic diseases.
• Body fluid analysis: • Deep rectal biopsy: Hirschsprung’s, amyloidosis.
o Ascitic fluid: infection, malignancy, portal • Liver biopsy: abnormal chemistries, jaundice, viral hepatitis,
hypertension. post-transplant rejection.
o Urine: carcinoid, porphyria, heavy metals. • Image-guided biopsy: for intraabdominal masses
2. Luminal Contents inaccessible by endoscopy.
• Stool studies: 6. Functional Testing
o Cultures for pathogens; leukocytes, ova/parasites, • Manometry:
Giardia antigen. o Esophageal: achalasia.
o Duodenal aspirate: bacterial overgrowth, o Small intestinal: pseudoobstruction.
parasites. o Colonic: colonic inertia.
o Fecal fat: steatorrhea evaluation. • Wireless motility capsule: measures contractility and transit
o Fecal elastase: pancreatic insufficiency. through entire GI tract.
o Fecal calprotectin/lactoferrin: IBD marker. • Anorectal manometry: incontinence, constipation (outlet
o Stool electrolytes: osmotic vs. secretory diarrhea. dysfunction).
o Laxative screen: suspected abuse. • Biliary manometry: sphincter of Oddi dysfunction.
o FIT and stool DNA: colorectal cancer screening. • Endoluminal functional lumen imaging probe: evaluates
o Gastric acid output: excludes gastrinoma. sphincter distensibility (achalasia, gastroparesis, defecation
o Esophageal pH/impedance: refractory GERD. disorders).
3. Endoscopy • Breath tests:
• Indications: bleeding, pain, weight loss, diarrhea, fever, o Hydrogen: carbohydrate intolerance, bacterial
altered bowel habits. overgrowth.
• Types: o Urea breath test: H. pylori.
o Upper endoscopy: esophagus, stomach, o Gastric emptying breath test: gastroparesis.
duodenum.
o Colonoscopy: colon and distal ileum (IBD, cancer TREATMENT PRINCIPLES
screening). 1. Overview
o Sigmoidoscopy: distal colon in low-risk/younger • Treatment is etiology-specific and may include:
patients. o Diet modification, pharmacotherapy,
o Small-bowel techniques: push, capsule, or endoscopic/radiologic interventions, surgery,
double-balloon enteroscopy for obscure bleeding or psychological, and physical therapy.
Crohn’s. • Genetic testing may be indicated in hereditary GI disorders.
o EUS: malignancy staging, choledocholithiasis,
• Digital tools (e.g., smartphone apps) improve patient
pancreatitis, anal pathology.
adherence and education.
o ERCP: pancreatic/biliary evaluation and therapy.
• Advanced imaging: narrow-band imaging, NUTRITIONAL MANIPULATION
chromoendoscopy, confocal laser endomicroscopy, optical 1. Symptom-Relief Diets
coherence tomography, and AI-assisted dysplasia detection.
• Lactose restriction: lactase deficiency.
4. Radiography and Nuclear Medicine
• Liquid meals: gastroparesis.
GASTROINTESTINAL DISEASE absorption).
o Regulates acid production for digestion and
defense.
I. ANATOMIC CONSIDERATIONS 4. Small Intestine
• General Structure • Primary site of nutrient absorption.
o GI tract extends from mouth to anus. • Structural specialization:
o Composed of organs with distinct functional o Villus architecture maximizes surface area.
specializations. o Contains specialized enzymes and transporters.
o Sphincters separate regions and regulate flow • Duodenum:
between compartments. o Receives chyme, pancreatic juice, and bile.
• Gut Wall Organization o Pancreatic juice: enzymes + bicarbonate (optimizes
o Mucosa: pH for enzymatic activity).
▪ Acts as a barrier to luminal contents. o Bile: essential for lipid emulsification and
▪ Site of nutrient and fluid absorption. absorption.
o Smooth muscle (circular and longitudinal): • Regional specialization:
▪ Mediates propulsion and mixing of o Proximal intestine: rapid absorption of nutrients
luminal contents. and minerals.
▪ Controlled by the enteric nervous o Ileum: absorption of vitamin B12 and bile acids.
system (ENS). • Bile: also facilitates excretion of toxins, bilirubin, drugs, and
o Serosal layer: cholesterol.
▪ Provides structural support. 5. Colon (Large Intestine)
▪ Allows external input (nerves, vessels). • Primary function: dehydration and storage of stool.
• Associated Systems • Fluid absorption: reduces ileal effluent (1000–1500 mL) to
o Pancreaticobiliary conduits: deliver bile and 100–200 mL stool output.
digestive enzymes into the duodenum. • Microbiome:
o Vascular supply: dynamically modulated by GI o Dense bacterial population.
activity. o Ferments undigested carbohydrates to produce
o Lymphatics: participate in immune surveillance short-chain fatty acids.
and lipid transport. o Modulates immune and metabolic functions.
o Nervous control: • Motility:
▪ Intrinsic (ENS): local regulation of o Proximal colon: mixing and absorption.
propulsion and secretion. o Distal colon: peristaltic contractions and mass
▪ Extrinsic (autonomic): provides movements for stool evacuation.
voluntary and involuntary control. o Transit time: >1 day in most individuals.
• Anus:
II. FUNCTIONS OF THE GI TRACT o Dual control: volitional and involuntary sphincters
A. Major Functions for continence and defecation.
• Assimilation of nutrients. 6. Ileocecal Junction
• Elimination of waste products. • Functions as a sphincter.
B. Regional Functions • Prevents coloileal reflux and excessive bacterial
1. Mouth contamination of small intestine.
• Mechanical processing and lubrication of food.
• Mixing with salivary amylase for starch digestion. III. EXTRINSIC MODULATION OF GUT FUNCTION
• Formation and propulsion of bolus toward esophagus. • Environmental Interface
2. Esophagus o Gut is in direct continuity with the external
• Propels food to the stomach via coordinated peristalsis. environment.
• Upper and lower esophageal sphincters: prevent air entry o Constant exposure to food antigens, drugs, and
and reflux. pathogens.
• Squamous mucosa: protective, minimal absorption. • Protective Mechanisms
• Peristaltic coordination ensures efficient swallowing. o Mucosal immune system:
3. Stomach ▪ Epithelial and lamina propria
• Functions: lymphocytes.
o Triturates and mixes food with gastric acid and ▪ Plasma cells and organized lymph nodes.
pepsin. o Paneth cells: secrete antimicrobial peptides.
o Acid sterilizes food and initiates protein digestion. o Liver (via portal circulation): detoxifies absorbed
• Regional specialization: substances.
o Proximal stomach: storage; receptive relaxation • Neural Control
after meals. o Intrinsic nerves (ENS): coordinate local motility
o Distal stomach: mixing and grinding; phasic and secretion.
contractions propel contents to pylorus. o Extrinsic pathways (vagal and splanchnic):
• Secretory roles: ▪ Modulate reflexes and regional activity.
o Brain-gut axis:
, ▪ Links emotional and cognitive centers • Microbiome dysbiosis: linked to IBD, celiac disease, IBS,
with gut function. and cancer.
▪ Stress may alter motility, secretion, and E. Impaired Gut Blood Flow
visceral sensitivity. • Ischemic injury:
o Causes: embolism, thrombosis, venous occlusion,
IV. OVERVIEW AND CLASSIFICATION OF GI DISEASES hypoperfusion.
GI diseases arise from structural, functional, immune, vascular, or o Results: mucosal necrosis, bleeding, perforation.
neoplastic abnormalities. • Chronic ischemia: may form strictures.
A. Impaired Digestion and Absorption • Radiation enterocolitis: reduced mucosal perfusion.
• Common causes: F. Neoplastic Degeneration
o Lactase deficiency (most common; benign gas and • Common malignancies:
diarrhea). o Colorectal cancer (most common in U.S.).
o Celiac disease. o Gastric cancer (prevalent in Asia).
o Bacterial overgrowth. o Esophageal carcinoma (linked to reflux, alcohol,
o Infectious enteritis. tobacco).
o Crohn’s ileitis. o Pancreatic, biliary, hepatic cancers (poor
o Radiation enteritis. prognosis).
• Consequences: malnutrition, anemia, dehydration, • Associated features:
electrolyte imbalances. o Weight loss, pain, jaundice, bleeding.
• Pancreatic disorders: o May present as adenocarcinoma, lymphoma, or
o Chronic pancreatitis or cancer → enzyme other histologic types.
deficiency and maldigestion. G. Functional (Nonorganic) Disorders
• Biliary obstruction: impaired fat digestion. • Examples: IBS, functional dyspepsia, functional heartburn.
• Gastrinoma: excess acid damages mucosa, inactivates • Features:
pancreatic enzymes, accelerates transit. o No detectable structural or biochemical
B. Altered Secretion abnormalities.
• Hypersecretion: o Possible disordered motility or visceral
o Gastrinoma, G-cell hyperplasia, retained antrum. hypersensitivity.
o Results in duodenal ulcers, diarrhea. o Brain-gut dysregulation; may co-occur with
• Hyposecretion: psychological stress.
o Atrophic gastritis, pernicious anemia. H. Genetic Influences
• Secretory diarrhea causes: • Familial clustering in IBD, colorectal, esophageal, pancreatic
o Infectious (bacterial, viral, parasitic). cancers.
o SIBO, bile salt diarrhea, microscopic colitis. • Inherited dysmotility syndromes (rare).
o Endocrine tumors (VIPoma). • Functional disorders may show familial behavior patterns
C. Altered Gut Transit rather than true heredity.
• Mechanical obstruction:
o Esophagus: stricture, tumor, eosinophilic V. SYMPTOMS OF GI DISEASE
esophagitis. A. Abdominal Pain
o Stomach: peptic ulcer, carcinoma. • Visceral pain: midline, dull, poorly localized.
o Small intestine: adhesions, Crohn’s, radiation, • Parietal pain: sharp, localized.
drugs. • Inflammatory causes: peptic ulcer, appendicitis,
o Colon: carcinoma, IBD stricture, diverticulitis. diverticulitis, IBD, pancreatitis.
• Motor dysfunctions: • Noninflammatory: biliary colic, ischemia, neoplasia.
o Achalasia: impaired LES relaxation and peristalsis. • Common functional causes: IBS, functional dyspepsia.
o Gastroparesis: delayed gastric emptying (often B. Heartburn
diabetic). • Burning substernal discomfort; intermittent in 40% of adults.
o Intestinal pseudoobstruction: enteric
• Classic cause: acid reflux.
nerve/smooth muscle damage.
• Other causes: nonacid reflux, esophageal hypersensitivity.
o Slow-transit constipation: reduced colonic
C. Nausea and Vomiting
propulsion.
o Dyssynergic defecation: failure of anal relaxation. • Causes:
o GI obstruction, toxins, medications, infection, CNS
• Rapid transit disorders:
or endocrine disease.
o Dumping syndrome, hyperthyroidism, IBS,
o Chronic causes: gastroparesis,
functional dyspepsia.
pseudoobstruction, IBS.
D. Immune Dysregulation
o Functional syndromes: chronic nausea vomiting
• Celiac disease: gluten-triggered mucosal inflammation.
syndrome, cyclic vomiting, cannabinoid
• Eosinophilic GI diseases: eosinophilic hyperemesis.
esophagitis/gastroenteritis. D. Altered Bowel Habits
• IBD: ulcerative colitis and Crohn’s disease. • Constipation:
• Microscopic colitis: lymphocytic or collagenous infiltration. o Causes: obstruction, motility disorder, medications,
• Infectious enterocolitis: bacterial, viral, or protozoal. hypothyroidism.
, o Symptoms: infrequent stool, straining, incomplete • Pain timing:
evacuation. o Ulcer pain: intermittent, weeks–months.
• Diarrhea: o Biliary colic: sudden onset, lasts hours.
o Causes: infection, inflammation, malabsorption, o Pancreatitis: severe, lasts days–weeks.
medications. • Defecation and meals:
o IBS: alternating constipation/diarrhea, mucus in o Diarrhea after meals or pain relief after defecation
stool. → IBD or IBS.
o IBD: blood and pus in stool. • Stress: exacerbates functional bowel disorders.
o Steatorrhea: fat malabsorption. • Nocturnal pain (awakens from sleep): suggests organic
E. GI Bleeding disease.
• Upper GI bleeding: • Effect of fasting:
o Manifestations: melena, hematemesis. o Improves malabsorptive diarrhea,
o Causes: ulcers, esophagitis, varices, malignancy. o No effect on secretory diarrhea.
• Lower GI bleeding: 3. Association with Other Factors
o Manifestations: hematochezia (bright red blood). • Post-surgical adhesions: suggest obstruction.
o Causes: hemorrhoids, diverticulosis, IBD, ischemic • Post-gastrectomy/cholecystectomy: dumping or
or infectious colitis, neoplasm. postcholecystectomy diarrhea.
• Occult bleeding: may present as iron deficiency anemia. • After travel: infectious cause.
F. Jaundice • Medications: may cause pain, altered bowel habits, or
• Posthepatic causes: bleeding.
o Biliary obstruction (stones, tumors, cholangitis, • Ethnicity:
PSC). o Celiac disease → northern European descent.
o Pancreatic disease (pancreatitis, stricture, cancer). o IBD → Jewish populations.
G. Other Symptoms • Sexual history: infection or immunodeficiency risk.
• Dysphagia, odynophagia → esophageal disease. 4. Functional Bowel Disorders
• Globus sensation → functional or pharyngoesophageal • Diagnosed using symptom-based criteria (e.g., Rome
causes. criteria).
• Weight loss, anorexia, fatigue → malignancy, • Sensitivity/specificity ~55–75% vs. structural findings.
inflammation, dysmotility. • Caution needed in high-risk patients to avoid missing
• Systemic manifestations: organic disease.
o IBD → arthritis, eye/skin/hepatobiliary disease.
o Celiac disease → dermatitis herpetiformis. PHYSICAL EXAMINATION
o Jaundice → pruritus. 1. General Principles
• Systemic diseases affecting GI tract: • Complements the history; guides urgency and differential
o Lupus → ischemic injury. diagnosis.
o Severe burns → stress ulcer. 2. Vital Signs
EVALUATION OF THE PATIENT WITH GI DISEASE • Fever: inflammation or neoplasm.
GENERAL APPROACH • Orthostasis: blood loss, dehydration, sepsis, autonomic
• Begins with careful history and physical examination. neuropathy.
• Subsequent investigations are based on findings and may 3. Extra-Abdominal Findings
assess: • Skin, eyes, joints: may indicate systemic disease (IBD,
o Gut structure, function, and luminal contents. vasculitis).
• When diagnostic tests are normal, validated symptom • Neck/swallow exam: for dysphagia.
profiles (e.g., Rome criteria) are used to diagnose • Cardiopulmonary exam: excludes cardiac/pulmonary
functional bowel disorders. causes of pain/nausea.
• Pelvic exam: identifies gynecologic sources.
HISTORY
• Rectal exam: detects blood, masses (appendicitis,
1. Importance and Purpose
neoplasm).
• Central to identifying likely etiology and pathophysiologic
• Peripheral neuropathy: in metabolic/motor disorders.
process.
4. Abdominal Examination
• Symptom timing, pattern, and duration help differentiate:
• Inspection: distention (obstruction, tumor, ascites),
o Acute processes: infection, inflammation, toxins,
ecchymoses (pancreatitis), vascular changes (liver disease).
ischemia.
o Chronic processes: chronic inflammation, • Auscultation:
neoplasia, functional disorders. o Absent bowel sounds: ileus.
2. Symptom Characterization o High-pitched sounds: obstruction.
o Bruit or rub: vascular disease or tumor.
• Luminal obstruction:
o Dysphagia, nausea/vomiting, bloating, • Percussion: liver span, shifting dullness (ascites).
distention, constipation, depending on site. • Palpation: organomegaly, masses, tenderness.
• Meal relation: o Visceral pain: diffuse tenderness.
o Worsened by meals: obstruction, ischemia, IBD, o Parietal pain/peritonitis: localized tenderness,
functional bowel disorders. guarding, rebound.
o Relieved by eating or antacids: ulcer disease.
, o Musculoskeletal pain: worsens with Valsalva or • Contrast radiography: mucosal detail, transit studies, pelvic
leg lift. floor evaluation.
o Esophagram: rings, strictures, achalasia.
TOOLS FOR PATIENT EVALUATION o Small-bowel contrast: tumors, strictures, fistulas.
1. Laboratory Testing o Contrast enema: if colonoscopy not possible.
• CBC and chemistries: • Ultrasound/CT/MRI:
o Iron deficiency: mucosal blood loss. o Detect mass lesions, gallstones, fluid collections,
o B12 deficiency: intestinal, gastric, pancreatic liver/pancreas abnormalities.
disease or malnutrition. o CT/MR colonography: colon cancer screening
o Leukocytosis: inflammation; leukopenia: viral (alternative).
illness. o MRCP: biliary/pancreatic ducts.
o Electrolyte and acid-base disturbances: from o CT/MR enterography: IBD activity.
vomiting/diarrhea. o Angiography: ischemia, tumor spread, biliary
o Pancreatic/liver chemistries: for hepatobiliary access.
disease. o PET and DOTA-octreotate PET-CT: detect
o Thyroid, cortisol, calcium: endocrine causes. neuroendocrine tumors.
o Pregnancy test: in women with nausea. • Scintigraphy:
• Serologic and tumor markers: o Bleeding scans: localize active hemorrhage.
o Celiac, IBD, connective tissue, paraneoplastic o Leukocyte scans: detect abscesses.
antibodies. o Biliary scans: for cholecystitis.
o Hormones: for endocrine neoplasia. o Transit studies: gastric emptying, intestinal/colonic
o Tumor markers: CEA, CA 19-9, α-fetoprotein. motility.
• Therapeutic monitoring: e.g., thiopurine metabolites in IBD. 5. Histopathology
• Research biomarkers: predict IBD course/treatment • Endoscopic biopsies: inflammatory, infectious, or
response. neoplastic diseases.
• Body fluid analysis: • Deep rectal biopsy: Hirschsprung’s, amyloidosis.
o Ascitic fluid: infection, malignancy, portal • Liver biopsy: abnormal chemistries, jaundice, viral hepatitis,
hypertension. post-transplant rejection.
o Urine: carcinoid, porphyria, heavy metals. • Image-guided biopsy: for intraabdominal masses
2. Luminal Contents inaccessible by endoscopy.
• Stool studies: 6. Functional Testing
o Cultures for pathogens; leukocytes, ova/parasites, • Manometry:
Giardia antigen. o Esophageal: achalasia.
o Duodenal aspirate: bacterial overgrowth, o Small intestinal: pseudoobstruction.
parasites. o Colonic: colonic inertia.
o Fecal fat: steatorrhea evaluation. • Wireless motility capsule: measures contractility and transit
o Fecal elastase: pancreatic insufficiency. through entire GI tract.
o Fecal calprotectin/lactoferrin: IBD marker. • Anorectal manometry: incontinence, constipation (outlet
o Stool electrolytes: osmotic vs. secretory diarrhea. dysfunction).
o Laxative screen: suspected abuse. • Biliary manometry: sphincter of Oddi dysfunction.
o FIT and stool DNA: colorectal cancer screening. • Endoluminal functional lumen imaging probe: evaluates
o Gastric acid output: excludes gastrinoma. sphincter distensibility (achalasia, gastroparesis, defecation
o Esophageal pH/impedance: refractory GERD. disorders).
3. Endoscopy • Breath tests:
• Indications: bleeding, pain, weight loss, diarrhea, fever, o Hydrogen: carbohydrate intolerance, bacterial
altered bowel habits. overgrowth.
• Types: o Urea breath test: H. pylori.
o Upper endoscopy: esophagus, stomach, o Gastric emptying breath test: gastroparesis.
duodenum.
o Colonoscopy: colon and distal ileum (IBD, cancer TREATMENT PRINCIPLES
screening). 1. Overview
o Sigmoidoscopy: distal colon in low-risk/younger • Treatment is etiology-specific and may include:
patients. o Diet modification, pharmacotherapy,
o Small-bowel techniques: push, capsule, or endoscopic/radiologic interventions, surgery,
double-balloon enteroscopy for obscure bleeding or psychological, and physical therapy.
Crohn’s. • Genetic testing may be indicated in hereditary GI disorders.
o EUS: malignancy staging, choledocholithiasis,
• Digital tools (e.g., smartphone apps) improve patient
pancreatitis, anal pathology.
adherence and education.
o ERCP: pancreatic/biliary evaluation and therapy.
• Advanced imaging: narrow-band imaging, NUTRITIONAL MANIPULATION
chromoendoscopy, confocal laser endomicroscopy, optical 1. Symptom-Relief Diets
coherence tomography, and AI-assisted dysplasia detection.
• Lactose restriction: lactase deficiency.
4. Radiography and Nuclear Medicine
• Liquid meals: gastroparesis.
