A GI presentation refers to the clinical manifestation of gastrointestinal disorders, which can affect the digestive system's organs, including the esophagus, stomach, small intestine, large intestine, liver, pancreas, and gallbladder.
Common GI presentation...
Gastrointestinal (GI) Presentation:
A GI presentation refers to the clinical manifestation of gastrointestinal disorders, which can affect the digestive system's organs, including the esophagus, stomach, small intestine, large intestine, liver, pancreas, and gallbladder.
Common GI presentations include:
- Abdominal pain or discomfort
- Nausea and vomiting
- Diarrhea or constipation
- Blood in stool or vomit
- Weight loss or gain
- Changes in appetite or bowel habits
- Jaundice (yellowing of skin and eyes)
GI presentations can be caused by various factors, such as:
Accurate identification and evaluation of GI presentations are crucial for timely diagnosis and effective management of gastrointestinal disorders.
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UNIVERSITY OF CAPE COAST COLLEGE OF HEALTH AND ALLIED SCIENCES SCHOOL OF MEDICAL SCIENCES PHYSICIAN ASSISTANT STUDIES PROGRAMME GROUP SIX DISORDERS OF THE GASTROINTESTINAL SYSTEM 1
OUTLINE OF PRESENTATION This presentation looks at the pathologies of the various organs of the GIT: their basic principles, causes/pathogenesis, and symptoms. ORGANS OF THE GIT: MOUTH ESOPHAGUS STOMACH SMALL AND LARGE BOWEL APPENDIX EXOCRINE PANCREAS LIVER AND GALLBLADDER 2
ORAL CAVITY: DISEASES OF TOOTH AND SUPPORTING STRUCTURE: Caries – results from local demineralization of tooth structure (enamel & dentin) caused by acids generated during the fermentation of sugars by bacteria. Gingivitis – inflammation involving the squamous mucosa, or gingiva & associated soft tissues that surround the teeth. Periodontitis – inflammation that affects the supporting structures of the teeth (periodontal ligaments), alveolar bones, & cementum. With progression, periodontitis ligament & alveolar bone, & eventually tooth loss. All are associated with poor oral hygiene that affect the composition of gingival bacteria. 3
4 DENTAL CARIES
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ORAL INFLAMMATORY LESIONS: Aphthous Ulcers (Canker Sores) – extremely painful superficial mucosal ulcerations; more frequent in the 1 st two decades of life & often recur. Cause – unknown, but tend to be familial & may be associated with celiac disease, 6
PROLIFERATIVE & NEOPLASTIC LESIONS OF THE ORAL CAVITY: Fibrous Proliferative Lesions: Fibromas – are submucosal nodular fibrous tissue masses that are formed when chronic irritation results in reactive results in reactive connective tissue hyperplasia. Pyogenic Granuloma – an inflammatory lesion typically found on the gingiva of children, young adults, & pregnant women (pregnancy tumor). Leukoplakia & Erythroplakia: Leukoplakia – a white patch or plaque that cannot be scraped off. Erythroplakia – a red, velvety, sometimes ended lesion that is flat or slightly depressed relative to a surrounding mucosa. 7
8 FIBROMAS PYOGENIC GRANULOMA
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DISEASE OF THE SALIVARY GLANDS: Xerostomia – a dry mouth resulting from a decrease in the production of saliva. It is a major feature of autoimmune disorder Sjögren Syndrome. It can also be caused by radiation therapy; it is also observed as a side effect of many classes of medications: anti-cholinergic, anti-depressant, sedative, analgesics, etc. Complications – increased rate of dental caries & candidiasis; difficulty in swallowing & speaking. 10
Sialadenitis – inflammation of the salivary glands. Most common form of viral sialadenitis – Mumps; enlargement of all salivary glands. Bacterial sialadenitis – pathogens = S. aureus & S. viridans . 11
Neoplasms – usually occur in adults, with a slight female predominance. Pleomorphic Adenoma – benign tumors that consist of a mixture of ductal (epithelial) & myoepithelial cells. Mucoepidermoid Carcinoma – composed of variable mixtures of squamous cells, mucus-secreting cells, & intermediate cells. It is the most common form of primary malignant tumor of the salivary glands. 12
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ODONTOGENIC CYSTS & TUMORS: Odontogenic cysts are derived from remnants of odontogenic epithelium present within the jaws. They can be inflammatory or developmental. Developmental: Dentigerous Cyst – originates around the crown of an encrypted tooth & is thought to be the result of degeneration of the dental follicle. Odontogenic Keratocysts – located within the posterior mandible; individuals between ages of 10 & 40 years of age. 14
15 DENTIGEROUS CYST
Inflammatory : Periapical Cyst – occur at the tooth apex as a result of long-standing pulpitis, which may be caused by advanced caries or trauma. Odontogenic Tumors – derived from odontogenic epithelium, ectomesenchyme, or both. Ameloblastomas – arise from odontogenic epithelium. Odontoma – most common type, arises from epithelium but shows extensive deposition of enamel & dentine. 16
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18 ATRESIA ESOPHAGEAL STENOSIS
ESOPHAGUS: OBSTRUCTIVE & VASCULAR DISEASES: Mechanical Obstruction: Atresia – thin noncanalized cord replaces a segment of the esophagus;; can result in aspiration, suffocation, pneumonia or severe fluid & electrolyte imbalances. Esophageal Stenosis – may be congenital or acquired; caused by fibrous thickening of the submucosa & atrophy of the muscularis propria. 19
20 ACHALASIA ESOPHAGEAL VARICES
Functional Obstruction: Esophageal dysmotility – characterized by discoordinated contraction or spasm of the muscularis; this spasm also can cause small diverticular to form; interferes with the efficient delivery of food & fluids to the stomach. Achalasia – characterized by the triad of ( i )incomplete LES relaxation, (ii) increased LES tone, & (iii) esophageal aperistalsis. Causes: - degeneration of nerves that innervate the esophagus -DM -amyloidosis -malignancy -sarcoidosis Esophageal Varices – dilated submucosal veins in the lower esophagus; it arises secondary to portal HPT. 21
22 EOSINOPHILIC ESOPHAGITIS BARRETT ESOPHAGUS
ESOPHAGITIS: GERD – reflux of gastric contents in the lower esophagus. Clinical Features – heartburn, dysphagia, regurgitation of sour-tasting gastric contents. Rarely, severe chest pain – chronic GERD. Complications – esophageal ulceration, hematemesis, melena, stricture development, Barrett esophagus; a precursor to esophageal carcinoma. Eosinophilic Esophagitis – a chronic immunologically mediated disorder. Symptoms – food impaction & dysphagia in adults, feeding intolerance or GERD-like symptoms in children. Barrett Esophagus – metaplasia of the lower esophageal mucosa from stratified squamous epithelium to nonciliated columnar epithelium with goblet cells. 23
Esophageal Lacerations, Mucosal Injury & Infections: Mallory-Weiss tears – often induced by severe retching or vomiting. Patients usually present with hematemesis. 24
ESOPHAGEAL TUMORS: Adenocarcinoma – a malignant proliferation of glands. Arises from preexisting Barrett esophagus; usually involves the lower 1/3 of the esophagus. Squamous Cell Carcinoma – malignant proliferation of squamous cells; most common type worldwide. Risk factors include the ff: ( i ) alcohol & tobacco (most common cause) (ii) very hot sub. (iii)achalasia (iv) esophageal injury Esophageal Carcinoma – presents late (poor prognosis) Symptoms – progressive dysphagia, weight loss, pain & hematemesis. 25
Autoimmune Gastritis – due to the autoimmune destruction of gastric parietal cells, located in the stomach body & fundus. Pathogenesis is mediated by T cells(type IV hypersensitivity). Clinical Features – atrophy of mucosa with intestinal metaplasia, megaloblastic anemia, achlorhydria with increased gastrin levels & antral G-cell hyperplasia, increased risk of gastric adenocarcinoma(intestinal type) 26 STOMACH:
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PEPTIC ULCER DISEASE - solitary mucosal ulcer involving proximal duodenum(90%) or distal stomach. Duodenal Ulcer – almost always due to H. pylori. Presents with epigastric pain that improves with meals Usually arises in the anterior duodenum; when present in posterior duodenum,, rupture may lead to bleeding from the gastroduodenal artery or acute pancreatitis Gastric Ulcer – usually due to H. pylori ; other causes: NSAIDs & bile reflux Presents with epigastric pain that worsens with meals Rupture carries risk of bleeding from left gastric artery 28
GASTRIC POLYPS & TUMORS: Gastric Polyps - Polyps are nodules or masses that project above the level of surrounding mucosa. Mostly affect individuals between 50 & 60 years of age. Gastric Adenocarcinoma: Most common malignancy of the stomach. Early symptoms resemble those of chronic gastritis, including dyspepsia, dysphagia, & nausea. Pathogenesis – ( i ) Mutations (ii) H. pylori (iii) Epstein-Barr virus(EBV) 29
30 GASTRIC POLYPS
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SMALL & LARGE INTESTINES: INTESTINAL OBSTRUCTION: Intussusception – telescoping of proximal segment of bowel forward into distal segment. Hirschsprung Disease – defective relaxation & peristalsis of rectum & distal sigmoid colon; associated with Down Syndrome. Clinical Features – failure to pass meconium; megacolon 32
Abdominal Hernia – occur through any weakness or defect in the wall of the peritoneal cavity. Volvulus – is the twisting of loop of intestine upon itself through 180° or more. Blood supply to the twisted intestine is cut. 33
34 ABDOMINAL HERNIA
35 VASCULAR DISORDERS OF BOWEL: Angiodysplasia – is a tortuous dilation of small vessels spanning the intestinal mucosa or submucosa. Lesions are multiple, most often involving the cecum or ascending colon.
Hemorrhoids – dilated anal & perianal collateral vessels that connect the portal & venous systems to relieve elevated venous pressure within the hemorrhoid plexus. Types: External Hemorrhoids Internal Hemorrhoids Clinical Features – ( i ) pain (ii)rectal bleeding, particularly bright red blood seen on toilet tissue. 36
DIARRHEAL DISEASE: Diarrhea is defined as the increase in stool mass, frequency, or fluidity, typically to amounts > 200g/day. In severe cases, stool vol. can exceed 14L/day. Some causes: Cystic Fibrosis, Celiac Disease 37
Lactase Deficiency – gives rise to osmotic diarrhea, because in its absence osmotically active lactose remains in the lumen. There are 2 types: Congenital Lactase Deficiency – caused by mutations in the gene encoding lactase. Manifests as explosive diarrhea with watery, frothy stools & abdominal distention after milk ingestion. Acquired Lactase Deficiency – caused by downregulation of lactase gene expression. Onset is sometimes associated with enteric viral or bacterial infections. 38
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INFLAMMATORY INTESTINAL DISEASE: Sigmoid Diverticulitis: diverticular disease refers to acquired pseudo-diverticular outpouchings of the colonic mucosa & submucosa. Associated with constipation, straining, & low-fiber diet ( i ) Hematochezia (ii) Diverticulitis (iii) Fistula[ colovesicular fistula] 40
Inflammatory Bowel Disease – is a chronic condition resulting from complex interactions b/n host immunity in genetically predisposed individuals resulting in inappropriate mucosal immune activation. It encompasses 2 entities; Crohn Disease & Ulcerative Colitis. Causes : ( i ) genetic (ii) mucosal immune responses (iii) epithelial defects Ulcerative Colitis - always involves the rectum and extends proximally in a continuous fashion to involve part or the entire colon that can be diffusely ulcerated. Clinical Features – bloody diarrhea with expulsion of stringy, mucoid material & lower abdominal material lower abdominal pain & cramps relieved by defecation 41
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Crohn Disease(Regional Enteritis) – occur in terminal ileum, ileocecal valve, & cecum. Clinical Features – intermittent attacks of relatively mild diarrhea, fever, & abdominal pain, Iron-deficiency anemia, hypoalbuminemia Some patients – right lower-quadrant pain & pain; mimic acute appendicitis or bowel perforation. Patients with colonic involvement – blood diarrhea & abdominal pain Extraintestinal manifestation - uveitis, migratory polyarthritis, sacroiliitis, ankylosing, spondylitis, erythema nodosum, & clubbing. 43
COLONIC POLYPS & NEOPLASTIC DISEASE: Neoplastic – most common = adenoma, has the potential to progress to cancer Adenomas – benign polyps that give rise to a majority of colorectal adenocarcinomas. Most adenomas, however, do not progress to adenocarcinoma. 44
Colorectal Carcinoma - carcinoma arising from colonic or rectal mucosa; most commonly arise from adenomas. Left-sided carcinoma – decreased stool caliber, left lower quadrant pain & blood-streaked stool Right-sided carcinoma – iron deficiency anemia(occult bleeding) & vague pain. 45
APPENDIX: ACUTE APPENDICITIS: It is associated with overt luminal obstruction, usually by a small, stone-like mass of stool, gallstone, tumor, or mass of worms. TUMORS OF THE APPENDIX: Most common tumor = carcinoid, or well-differentiated neuroendocrine tumor 46
Adenomas or non-mucin-producing adenocarcinomas may cause obstruction & enlargement that mimics the changes of acute appendicitis. PANCREAS ACUTE PANCREATITIS: is a reversible inflammatory disorder that varies in severity, from focal edema & fat necrosis to widespread hemorrhagic necrosis. Etiologic Factors: Metabolic – alcoholism hyperlipoproteinemia hypercalcemia drug (e.g., azathioprine) Genetic – mutations in the cationic trypsinogen (PRSS1) & trypsin inhibitor (SPINK1) genes. 47
Mechanical – gallstones trauma iatrogenic injury perioperative injury Vascular – shock atheroembolism polyarteritis nodasa Infectious – mumps coxsackievirus Idiopathic = 10 – 20% of cases of acute pancreatitis. Clinical Features: Epigastric abdominal pain that radiates to the back Nausea & vomiting Periumbilical & flank hemorrhage (necrosis spreads into the periumbilical soft tissue & retroperitoneum) Hypocalcemia(Calcium is consumed during saponification in fat necrosis) 48
Complications: Shock – due to peripancreatic hemorrhage and fluid sequestration. Pancreatic abscess – often due to E. coli; presents with abd pain, fever, & persistently elevated amylase CHRONIC PANCREATITIS: fibrosis of pancreatic parenchyma, most often secondary to recurrent acute pancreatitis. Causes: Alcohol(adults), Cystic fibrosis(children), Duct obstruction, idiopathic, Autoimmune pancreatitis Clinical Features: Repeated bouts of jaundice, vague indigestion, Persistent or recurrent abdominal & back pain 49
PANCREATIC NEOPLASMS Pancreatic Carcinoma – adenocarcinoma arising from the pancreatic ducts. It is most commonly seen in the elderly (avg. age = 70 years). Major risk factors = smoking & chronic pancreatitis Clinical Features: Epigastric abdominal pain & weight loss, obstructive jaundice with pale stools & palpable gallbladder, migratory thrombophlebitis Cystic Neoplasm – are diverse tumors that range from harmless benign cysts to invasive, potentially lethal cancers. 50
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LIVER: INFECTIOUS DISORDER: Bacterial, parasitic, & Helminthic Infections: Infectious organisms can reach the liver through several pathway: Ascending Infection – via the gut & biliary tract; partial or complete biliary tract obstruction. Vascular Seeding – most often through the portal system via the GIT; S. aureus in TSST, Treponema pallidum in secondary or tertiary syphilis, & S. typhi in typhoid fever. Direct Invasion – from an adjacent source(e.g., bacterial cholecystitis). Penetrating Injury 52
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AUTOIMMUNE HEPATITIS – chronic, progressive hepatitis with all features of autoimmune diseases. Triggers – viral infections drug or toxin exposure 2 types: Type 1 – more common in middle-age & older individuals. Type 2 – usually seen in children and teenagers 54
ALCOHOLIC & NONALCOHOLIC FATTY LIVER DISEASE: Alcoholic Liver Disease – result from excessive alcohol consumption. Nonalcoholic Fatty Liver Disease – a common condition in which fatty liver disease develops in individuals who do not drink alcohol. It is associated with insulin resistance, metabolic syndrome, type 2 diabetes mellitus[or FHx of it], obesity, dyslipidemia, or HPT. Clinical Features – ( i ) tender hepatomegaly (ii) cirrhosis (iii) alcoholic hepatitis (iv) malaise (v) fever (vi) anorexia (vii) weight loss (viii) upper-abdominal discomfort (ix) steatosis 55
CIRCULATORY DISORDERS: classified according to whether the disorder leads to abnormalities in the inflow, flow-through, or outflow of blood. Impaired Blood Flow into the Liver: Hepatic Artery Compromise Portal Vein Obstruction & Thrombosis: Manifestations: esophageal varices splenomegaly intestinal congestion Impaired Blood Flow Through the Liver Hepatic Venous Outflow Obstruction Manifestations: ascites(cirrhosis), esophageal varices, hepatomegaly 56
NODULES & TUMORS: Cavernous Hemangiomas Hepatocellular Adenomas – most common symptom is pain Malignant Neoplasms Hepatocellular Carcinoma(HCC) – incidence is high in countries with high rates of chronic HBV infection; Aflatoxin increase risk of HCC. Clinical Features -ill-defined upper-abdominal mass, jaundice, fever, & esophageal variceal bleeding 57
Cholangiocarcinoma(CCA) – arises from intrahepatic & extrahepatic bile ducts. Risk factors – infestation by liver flukes, hepatolithiasis, fibropolycystic liver disease. Clinical Features: Involvement of the brainstem produces cranial signs(ataxia, nystagmus, & internuclear ophthalmoplegia) Spinal cord lesions give risk to motor & sensory impairment of trunk & limbs, spasticity & loss of bladder control. Unilateral visual impairment due to involvement of the optic nerve 58
GALLBLADDER: 59 CHOLELITHIASIS:
CHOLECYSTITIS: inflammation of the gallbladder; it may be acute, chronic, or acute superimposed on chronic, & almost occurs in association with gallstones. It can be acute or chronic[repeated bouts of acute cholecystitis, or de novo] Clinical Features: pain in upper abd that radiates to right shoulder, nausea, fever, leukocytosis CARCINOMA OF THE GALLBLADDER: It is the most common malignancy of the extrahepatic biliary tract. The most important risk factor is gallstones. 60
CHOLESTATIC SYNDROMES: JAUNDICE – refers to yellow discoloration of skin, sclerae, & tissues caused by hyperbilirubinemia; usually > 2.5mg/dL. It is most often associated with hepatocellular disease, biliary obstruction, or hemolytic anemia. Congenital Hyperbilirubinemias: Gilbert Syndrome Dubin -Johnson Syndrome Crigler -Najjar Syndrome Type 1 CHOLESTATIC – a condition caused by extrahepatic or intrahepatic destruction obstruction of bile channels or by defects in hepatocyte bile secretion. Patients may have jaundice, pruritus, skin xanthomas, or symptoms related to intestinal malabsorption; fat-soluble vitamins A,D, or K. 61
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REFERENCES: Sattar, A. H. (2021). Fundamentals of Pathology. (9 th ed.). Pathoma LLC. Schneider, A.S. & Szanto , P. A. (2014). BRS Pathology. (5 th ed.). Lippincott. Kumar, V., Abbas, A. K. & Aster J. C. (2018). Robbins Basic Pathology. (10 th ed.). Elsevier Inc. 63