2026 Medicine 2: Approach to Patient with Gastrointestinal Diseases PDF

PCC SOM 2026 MEDICINE 2 M. 11.01 APPROACH TO PATIENT WITH GASTROINTESTINAL DISEASES ▪ The proximal colon mixes and absorbs fluid, while the...

PCC SOM 2026 MEDICINE 2 M. 11.01 APPROACH TO PATIENT WITH GASTROINTESTINAL DISEASES ▪ The proximal colon mixes and absorbs fluid, while the MEDICINE LECTURE distal colon exhibits peristaltic contractions and mass LECTURER: Dr. Arnel Jay Padua movements to expel the stool DATE: OVERVIEW OF GI DISEASES TOPIC OUTLINE ▪ GI disease develop as a result of abnormalities within or ANATOMIC CONSIDERATIONS outside of the gut and range in severity from those that FUNCTIONS OF THE GI TRACT produce mild symptoms and no long-term morbidity to OVERVIEW OF GI DISEASES those with intractable symptoms or adverse outcomes ▪ Disease may be localized to one organ or exhibit diffuse EVALUATION OF PATIENT WITH GI DISEASE involvement at many sites TREATMENT DISORDERS OF ESOPHAGUS CLASSIFICATION OF GI DISEASES ACHALASIA IMPAIRED DIGESTION AND ABSORPTION DIFFUSE ESOPHAGEAL SPASM ▪ Diseases of the stomach, intestine, biliary tree, and ANATOMIC CONSIDERATIONS pancreas can disrupt digestion and absorption. ▪ GI tract extends from the mouth to the anus and is ▪ Lactase deficiency – gas and diarrhea (most common) composed of several organs with distinct functions ▪ Celiac disease ▪ Sphincters assist in gut compartmentalization separating ▪ Bacterial overgrowth the organs ▪ Infectious enteritis ▪ Gut smooth muscle association with the enteric nervous ▪ Chron’s ileitis system mediates propulsion form on region to the next ▪ Radiation damage ▪ Interactions with other systems serve the needs of the ▪ Biliary obstruction gut and the body ▪ Chronic pancreatitis or pancreatic cancer Ø i.e., vascular supply (it tells the enteric system Ø impaired pancreatic enzyme release when we need more blood suppls), lymphatic channels (helps the GIT to fight of infections), ALTERED SECRETION intrinsic nerves (controls secretions, propulsions, ▪ Zollinger-Ellison syndrome and peristalsis) Ø excessive gastric acid secretion Ø prone to having PUD, GERD, and decreased FUNCTIONS OF THE GI TRACT absorption because it sometimes inactivates 2 Main Functions: enzymes from the pancreas (1) Assimilating nutrients ▪ G cell hyperplasia (2) Eliminating waste ▪ Retained antrum syndrome ▪ Some individuals with duodenal ulcers ▪ The stomach triturates and mixes the food bolus with ▪ Atrophic gastritis or pernicious anemia (caused by B12 pepsin and acid deficiency, folic acid may also cause this) – little or no Ø secretes intrinsic factor for vitamin B12 absorption ▪ Most nutrient absorption occurs in the small intestine gastric acid ▪ Pancreatic juice contains enzymes for carbohydrate, ▪ Inflammatory and infectious small-intestinal and protein, and fat digestion as well as bicarbonate to colonic diseases – produce fluid loss through impaired optimize the pH for enzyme activation absorption or enhanced secretion Ø Acute bacterial or viral infection, chronic Giardia or ▪ Bile secreted by the liver and stored in the gallbladder is cryptosporidia infections, small-intestinal bacterial essential for lipid digestion growth ▪ The proximal intestine is optimized for rapid absorption of most nutrients and minerals ALTERED GUT TRANSIT ▪ The ileum is better suited for absorbing vitamin B12 and bile acids (needed for B12 absorption) Mechanical Obstruction § Esophageal occlusion most often results from stricture ▪ The colon prepares waste for evacuation (due to acid exposure or eosinophilic esophagitis) or ▪ The colonic mucosa dehydrates the stool, decreasing neoplasm daily volumes of 1000-1500mL in the ileum to 100-200mL § Gastric outlet obstruction develops from peptic ulcer expelled from the rectum disease or gastric cancer Ø Colon possesses a dense bacterial colonization that § Small-intestinal obstruction most commonly results ferments undigested carbohydrates and short-chain from adhesions but may also occur with fatty acids § Chron’s disease, radiation or drug-induced strictures, and Ø Gut microbiome includes modulation of immune and less likely malignancy physiologic activity NOTE TAKER: Page 1 | 9  PCC SOM 2026 MEDICINE 2 M. 11.01 APPROACH TO PATIENT WITH GASTROINTESTINAL DISEASES § The most common cause of colonic obstruction is colon Colorectal most common and usually cancer, although inflammatory strictures develop in cancer presents after age 50 years in patients with inflammatory bowel disease (IBD), after the US certain infections such as diverticulitis, or with some drugs Gastric cancer prevalent Worldwide especially in certain Asian regions Characterized by impaired Esophageal develops with chronic acid reflux esophageal body peristalsis and cancer or after an extensive alcohol or Achalasia incomplete lower esophageal tobacco use history sphincter relaxation Small-intestinal are rare and occur with Symptomatic delay in gastric neoplasms underlying inflammatory disease Gastroparesis emptying of meals due to impaired gastric motility Pancreatic and elicit severe pain, weight loss, Intestinal Causes marked delays in small- biliary cancers and jaundice and have poor pseudo- bowel transit due to enteric nerve or prognoses obstruction intestinal smooth-muscle injury Hepatocellular usually arises in the setting of Occurs in post vagotomy dumping carcinoma chronic viral hepatitis or cirrhosis syndrome, with gastric secondary to other causes Rapid gastric hypersecretion, and in some cases of HepaB and HepaC – emptying causes liver cirrhosis functional dyspepsia and cyclic vomiting syndrome Anal cancers arise after prior anal infection or inflammation IMMUNE DYSREGULATION DISORDERS WITHOUT OBVIOUS ORGANIC ABNORMALITIES ▪ The mucosal inflammation of celiac disease results from dietary ingestion of gluten-containing grains ▪ IBS, functional dyspepsia, functional heartburn ▪ Food allergy also exhibit altered immune populations ▪ These disorders exhibit altered gut motor function; ▪ Eosinophilic esophagitis and eosinophilic gastroenteritis however, the pathogenic relevance of these are inflammatory disorders with prominent mucosal abnormalities is uncertain. eosinophils ▪ Exaggerated visceral sensory responses to noxious ▪ Ulcerative colitis and Crohn’s disease are disorders of stimulation may cause discomfort in these disorders uncertain etiology that produce mucosal injury primarily in the lower gut GENETIC INFLUENCES ▪ Alterations in the gut microbiome (termed dysbiosis) are ▪ Although many GI diseases result from environmental postulated to trigger flares of IBD, celiac disease, and IBS. factors, others exhibit hereditary components ▪ IBD, Colonic, esophageal, and pancreatic malignancies Inflammation or chronic swelling Inflammatory of the intestines SYMPTOMS OF GI DISEASES Bowel Disease e.g., Crohn’s DSE, Ulcerative Colitis ABDOMINAL PAIN ▪ Results from GI disease and extraintestinal conditions Inflammatory/ Chronic syndrome made up of a involving the genitourinary tract, abdominal wall, thorax, Irritable Bowel group of symptoms or spine. Syndrome ▪ Visceral pain generally is midline in location and vague in character, whereas parietal pain is localized and precisely IMPAIRED GUR BLOOD FLOW described. ▪ Rare cases of gastroparesis result from blockage of the ▪ Painful inflammatory diseases include peptic ulcer, celiac and superior mesenteric arteries. appendicitis, diverticulitis, IBD, pancreatitis, ▪ INTESTINAL AND COLONIC ISCHEMIA- more commonly cholecystitis, and infectious enterocolitis encountered; consequences of arterial embolus, arterial ▪ Noninflammatory visceral sources include biliary colic, thrombosis, venous thrombosis, or hypoperfusion from mesenteric ischemia, and neoplasia. dehydration, sepsis, hemorrhage, or reduced cardiac ▪ The most common causes of abdominal pain are IBS and output functional dyspepsia. ▪ COMPLICATIONS: mucosal injury, hemorrhage, or even perforation HEARTBURN ▪ A burning substernal sensation, is reported NEOPLASTIC DEGENERATION intermittently by 40% of the population ▪ All GI regions are susceptible to malignant ▪ Results from excess gastroesophageal acid reflux, but degeneration to varying degrees. some cases exhibit normal esophageal acid NOTE TAKER: Page 2 | 9  PCC SOM 2026 MEDICINE 2 M. 11.01 APPROACH TO PATIENT WITH GASTROINTESTINAL DISEASES exposure and are caused by reflux of nonacidic material or heightened sensitivity of esophageal nerves. NAUSEA AND VOMITING ▪ Are caused by GI diseases, medications, toxins, infection, endocrine disorders, labyrinthine conditions, and central nervous system disease. ▪ Mechanical obstructions ▪ Disorders of propulsion including gastroparesis and intestinal pseudo-obstruction elicit similar symptoms. EVALUATION OF THE PATIENT WITH GI DISEASE ▪ Are commonly reported by patients with IBS and functional disorders of the upper gut ▪ Evaluation of the patient with suspected GI disease begins with a careful history and examination ALTERED BOWEL HABITS HISTORY § Common complaints of patients with GI disease: ▪ Symptom, timing, patterns Ø Constipation ▪ Short duration symptoms commonly result from acute Ø Diarrhea infection or inflammation, toxin exposure, or ischemia ▪ Irritable Bowel Syndrome (IBS) produces ▪ Long-standing symptoms point to chronic inflammation, constipation, diarrhea, or an alternating bowel neoplasia, or functional bowel disorders pattern. ▪ Ulcer pain occurs intermittently over weeks to months, GI BLEEDING whereas biliary colic has a sudden onset and lasts up to several hours ▪ Hemorrhage may develop from any gut organ. ▪ Acute pancreatitis pain is severe and persists for days to ▪ Upper GI bleeding presents with melena or weeks hematemesis while lower GI bleeding produces passage ▪ Meals elicit diarrhea while defecation relieves of bright red or maroon stools. discomfort in some cases of IBD and IBS o Upper GI Bleeding: Melena ▪ Functional bowel disorders are exacerbated by stress o Lower GI Bleeding: Hematochezia ▪ However, briskly bleeding upper sites can elicit ▪ Diarrhea from malabsorption usually improves with voluminous red rectal bleeding, whereas slowly bleeding fasting, whereas secretory diarrhea persists without oral ascending colon sites may produce melena. intake ▪ Chronic occult GI bleeding may present with iron ▪ Obstructive symptoms with prior abdominal surgery deficiency anemia. raise concern for adhesions ▪ Loose stools after gastrectomy or cholecystectomy JAUNDICE suggest dumping syndrome or post cholecystectomy diarrhea. ▪ Results from prehepatic, intrahepatic, or post-hepatic disease. ▪ Symptom onset after travel prompts consideration of infection (e.g., Travelers diarrhea) ▪ Post-hepatic causes of jaundice include biliary diseases, ▪ Medications produce pain, altered bowel habits, or GI like choledocholithiasis, acute cholangitis, primary bleeding (e.g., NSAIDS) sclerosing cholangitis, other strictures, and neoplasm, ▪ Celiac disease is prevalent in people of northern and pancreatic disorders, like acute and chronic European descent, whereas IBD is more common in pancreatitis, stricture, and malignancy. Jewish populations ▪ A sexual history may raise concern for infection or OTHER SYMPTOMS immunodeficiency. ▪ Dysphagia, odynophagia, and unexplained chest pain suggest esophageal disease ROME CRITERIA ▪ Weight loss, anorexia, and fatigue present with neoplastic, Ø Symptom criteria to improve diagnosis of functional inflammatory, motility, pancreatic, and psychiatric bowel disorders and to minimize the numbers of conditions unnecessary diagnostic tests performed ▪ IBD is associated with hepatobiliary dysfunction, skin and eye lesions, and arthritis Ø Exhibit sensitivities and specificities of only 55– 75% ▪ Celiac disease may present with dermatitis herpetiformis indicating the need for careful test selection in patients ▪ Jaundice can produce pruritus at high risk of organic disease. ▪ Severe burns may lead to gastric ulcer formation NOTE TAKER: Page 3 | 9  PCC SOM 2026 MEDICINE 2 M. 11.01 APPROACH TO PATIENT WITH GASTROINTESTINAL DISEASES PHYSICAL EXAMINATION ▪ Abnormal vital signs provide diagnostic clues and determine the need for acute intervention ▪ Fever suggests inflammation or neoplasm. ▪ Orthostasis is produced by significant blood loss, dehydration, sepsis, or autonomic neuropathy. ▪ Neck examination with swallowing assessment evaluates dysphagia. ▪ Lung and cardiac examinations evaluate for cardiopulmonary disease as causes of abdominal pain or nausea ▪ Pelvic examination tests for a gynecologic source of abdominal pain ▪ Rectal examination may detect blood, indicating mucosal injury or neoplasm or a palpable inflammatory mass in appendicitis ▪ Metabolic conditions and gut motor disorders have associated peripheral neuropathy ▪ Abdominal inspection may reveal distention ▪ Specialized CT or MR enterography quantifies IBD from obstruction, tumor, or ascites or vascular intensity abnormalities with liver disease ▪ Angiography excludes mesenteric ischemia and ▪ Ecchymoses develop with severe pancreatitis determines spread of malignancy ▪ Loss of bowel sounds signifies ileus, whereas high- ▪ Positron emission tomography can distinguish malignant pitched, hyperactive sounds characterize intestinal from benign disease in several organ systems. obstruction ▪ Percussion assesses liver size and detects shifting HISTOPATHOLOGY dullness from ascites ▪ Endoscopic mucosal biopsies evaluate for ▪ Palpation assesses for hepatosplenomegaly and inflammatory, infectious, and neoplastic disease neoplastic or inflammatory masses ▪ Deep rectal biopsies facilitate diagnosis of ▪ Intestinal ischemia elicits severe pain but little Hirschsprung's disease or amyloid tenderness ▪ Liver biopsy is performed for abnormal liver chemistries, ▪ Patients with visceral pain may exhibit generalized in unexplained jaundice, following liver transplant to discomfort, whereas those with parietal pain or exclude rejection, and to characterize inflammation in peritonitis have localized pain with involuntary guarding, chronic viral hepatitis prior to initiating antiviral therapy. rigidity, or rebound. FUNCTIONAL TESTING TOOLS FOR PATIENT EVALUATION RADIOGRAPHY/NUCLEAR MEDICINE ▪ Tests of gut function provide important data when ▪ Contrast enemas are performed when colonoscopy is structural testing is nondiagnostic unsuccessful or contraindicated ▪ Functional testing of motor activity is provided by ▪ Ultrasound and computed tomography (CT) evaluate newer high resolution manometric techniques regions not accessible by endoscopy or contrast studies, ▪ Esophageal manometry is useful for suspected achalasia, including the liver, pancreas, gallbladder, kidneys, and whereas small-intestinal manometry tests for pseudo- retroperitoneum and are useful for diagnosing masa obstruction and colon manometry evaluates for colonic lesions, fluid collections organ enlargement, and, in the inertia case of ultrasound, gallstones ▪ Anorectal manometry ▪ CT and magnetic resonance (MR) colonography have ▪ Biliary manometry been considered as alternatives to colonoscopy for colon ▪ Urea breath testing cancer screening ▪ MR methods image the pancreaticobiliary ducts to exclude neoplasm, stones, and sclerosing cholangitis, and the liver to characterize benign and malignant tumors NOTE TAKER: Page 4 | 9  PCC SOM 2026 MEDICINE 2 M. 11.01 APPROACH TO PATIENT WITH GASTROINTESTINAL DISEASES TREATMENT NUTRITIONAL MANIPULATION THERAPIES DIRECTED TO ECTERNAL INFLUENCES § Treatments that only reduce symptoms ▪ Psychological therapies including psychotherapy, § Therapies correct pathologic defects behavior modification, and hypnosis, have shown § OR replace normal food intake with enteral or parenteral efficacy in functional bowel disorders formulations DISORDERS OF THE ESOPHAGUS PHARMACOTHERAPY § Over the counter (OTC) agents ANATOMY AND PHYSIOLOGY: ESOPHAGUS § Prescription drugs § Transport food and fluid between these ends, otherwise § Complementary and alternative medicine treatment remaining empty Ø Through peristalsis movement due to enteric TREATMENT OF GUT DYSBIOSIS nervous system § Stop reflux of acid or bolus of food ▪ Some cases of diarrhea predominant Ø IBS respond to non-absorbable antibiotics PARTS OF THE ESOPHAGUS: ▪ Oral antibiotics also are the mainstay of managing § Upper esophageal sphincter intestinal bacterial overgrowth § Inter-sphincteric esophagus ▪ Probiotics containing active bacterial cultures and § Lower esophageal esophagus prebiotics that selectively nourish non- noxious commensal bacteria are used as adjuncts in some LAYERS OF THE ESOPHAGUS (OUTER TO INNER): cases of infectious diarrhea and IBS § Adventitia or the serosa ▪ Transplantation of donor feces into the colon by § Two (2) muscular layers after the adventitia colonoscopy or enema has become accepted and Ø Inner Circular muscle effective treatment for recurrent, refractory Ø Outer Longitudinal muscle Clostridium difficile colitis. INTERVENTIONAL ENDOSCOPY OR RADIOLOGY TECHNIQUES § Submucosa: manage secretions of GIT § Mucosa ▪ In addition to its diagnostic role, endoscopy has Ø The mucosa is composed of stratified therapeutic capabilities in many settings nonkeratinized squamous epithelium. Continues ▪ Control of bleeding onto the GIT (stomach) and becomes stratified ▪ Removal of masses columnar epithelium Ø i.e., polyps, debulking of lumen narrowing malignancies ▪ Sphincterotomy in choledocholithiasis ▪ Mucosal resections ▪ Ablation ▪ insert gastric feeding tubes ▪ radiofrequency therapy, transoral fundoplication, endoscopic stapling, and anti- reflux mucosectomy have been devised ▪ Angiographic embolization or vasoconstriction ▪ CT and ultrasound help drain abdominal fluid collections SURGERY ▪ Is performed to cure disease, control symptoms without cure, maintain nutrition, or palliate unresectable neoplasm ▪ Medication-unresponsive ulcerative colitis, diverticulitis, cholecystitis, appendicitis, and intra- abdominal abscess are curable with surgery, ENTERIC NERVOUS SYSTEM whereas symptom control without cure is only MYENTERIC (AUERBACH’S) possible with Crohn's disease § In between the outer longitudinal muscle and the inner ▪ Surgery is mandated for ulcer complications such as circular muscle bleeding, obstruction, or perforation and intestinal § Peristalsis or the contraction of the esophageal walls obstructions that persist after conservative care § Controls the lower esophageal sphincter NOTE TAKER: Page 5 | 9  PCC SOM 2026 MEISSNER’S (SUBMUCOSAL) MEDICINE 2 M. 11.01 APPROACH TO PATIENT WITH GASTROINTESTINAL DISEASES § In between the submucosa and inner circular muscle § Regulates the configuration of the luminal surface § Controls glandular secretions § Alters electrolyte and water transport DIAGNOSTIC TESTS § Regulates local blood flow BARIUM SWALLOW § Main screening for achalasia ACHALASIA § Bird’s beak appearance: pathognomonic radiographic sign PATHOPHYSIOLOGY OF ACHALASIA § Due to the destruction of the myenteric (Auerbach’s) plexus § The myenteric plexus contains ganglion cells Ø 2 types are excitatory and inhibitory cells EXCITATORY CELLS INHIBITORY CELLS § Release § Release Nitric Oxide Acetylcholine and sometimes the à ACH is the Vasoactive intestinal neurotransmitter the peptide (VIP) controls the contraction § Allows the LES to Relax of lower esophageal sphincter (LES) § The problem in achalasia is that the inhibitory cells are ESOPHAGEAL MANOMETRY destroyed § Next to be requested after barium swallow Ø No Nitric Oxide → No relaxation § Gold standard test for achalasia Ø This becomes an unchallenged AcH action → Nothing counteracts the contractions from the AcH → Esophagus remains contracted. § Once the patient eats there may be regurgitation of food and sometimes dysphagia because the food is stuck on the contacted part § Symptoms: Ø Regurgitation Ø Dysphagia Ø Rumination Ø Weight loss: Lack of nutrition, limited food intake § Solids and liquids are affected on achalasia § As the condition progresses, the patient still tries to eat but the esophagus turns into a sigmoid-like shape (bird’s beak) as it becomes dilated NOTE TAKER: Page 6 | 9  PCC SOM 2026 MEDICINE 2 M. 11.01 APPROACH TO PATIENT WITH GASTROINTESTINAL DISEASES PSEUDOACHALASIA ▪ The same s/s and picture of achalasia however the ▪ Attribulate to abnormal esophageal contraction with cause is not destruction of the inhibitory cells normal deglutitive LES relaxation ▪ Pathophysiology: Ill defined Etiologic entities: ▪ Signs and Symptoms (almost similar to achalasia): ▪ MALIGNANCY Ø Severe chest pain Ø Most common causes: esophageal CA, Ø Dysphagia gastrointestinal CA (any CA adjacent to LES), Ø Heart burn lymphoma Ø Regurgitation Ø Impinges on the LES and may also cause ▪ Triggers: destruction of the ganglion cells Ø Hot and cold fluids ▪ STRICTURES Ø Heightened emotion/ emotional stress Ø May be from ischemia, infectious esophagitis ▪ SCLERODERMA DIAGNOSTICS Ø It is an autoimmune disease Ø Skin and mucosal layers are stretched out Should be done during the chest pain We can use endoscopic studies to rule these out but you can only episodes because if after see a constricted LES from the inside. We also request for other “Corkscrew or Rosary beads” Barium studies which will look for other causes of achalasia, (i.e., CT scan) swallow pattern in barium swallow due to contractions but in many instances, these abnormalities are indicative of TREATMENT achalasia ENDOSCOPIC THERAPY Endoscopy To rule out structural abnormalities ▪ Botulinum toxin injection Ø Inhibits Ach release a variety of defining features have Ø May develop tolerance with repetitive injections been proposed including – less effective uncoordinated (“spastic”) activity in ▪ Pneumatic dilatation the distal esophagus, spontaneous Ø 30-98% success rate and repetitive contractions, or high- Ø Most common complication: Perforation - 0.5-5% Esophageal amplitude and prolonged ▪ Endoscopic myotomy Manometry contractions. Ø 90% success rate *Stimulation test: use of SURGERY Ergonovine to stimulate the DES ▪ Heller myotomy with fundoplication (not common in clinical practice) ▪ Medical therapy: Ø Calcium Channel blockers (CCB) Occurrence of contractions in the o Nifedipine is usually used distal esophagus with short latency o MOA: allows smooth muscle relaxation High- relative to Ø Nitroglycerine (NTG) resolution the time of the pharyngeal Ø Sildenafil manometry contraction, a dysfunction indicative of impairment of inhibitory myenteric DIFFUSE ESOPHAGEAL SPASM plexus neurons DES is substantially less common than achalasia TREATMENT 1. Nitrates e.g., Nitroglycerin 2. Calcium Channel blockers (CCB’s) 3. PPIs to reduce acid reflux NOTE TAKER: Page 7 | 9  PCC SOM 2026 MEDICINE 2 M. 11.01 APPROACH TO PATIENT WITH GASTROINTESTINAL DISEASES CHECKPOINT NOTE TAKER: Page 8 | 9  PCC SOM 2026 MEDICINE 2 M. 11.01 APPROACH TO PATIENT WITH GASTROINTESTINAL DISEASES NOTE TAKER: Page 9 | 9  2026 MEDICINE 2 M. 11.01 APPROACH TO PATIENT WITH GASTROINTESTINAL DISEASES NOTE TAKER: Page 10 | 9