Gastrointestinal Diseases and Abnormalities in Adult-rev2

Penyakit dan kelainan sistem gastroenterologi dan pankreatobilier(Diseases and Abnormalities in the Gastroenterological and Pancreatobiliary System)

Marcellus Simadibrata K MD PhD SpPD KGEH FACG FINASIM

Department of Medical Education Faculty of Medicine University of IndonesiaDivision Gastroenterology Department of Internal Medicine Faculty of Medicine University of Indonesia

Lecture Module Gastrointestinal May 2013

Introduction

Gastrointestinal Diseases and Abnormalities: Upper and Lower border: Treitz ligament

Diseases in upper GI tract: Syndrome of dyspepsia, Gastroesophageal Reflux Disease(GERD), dysphagia, peptic ulcer, upper gastrointestinal bleeding(Hematemesis-Melena), polyp and cancer of the gaster/duodenum, cholangitis, bile duct Stone, pancreatitis.

Diseases in lower GI tract: diarrhea, irritable bowel syndrome, collitis infective-non Infective, Inflammatory Bowel Disease, polyp and cancer of the colon, hemoroid

Buku ajar Ilmu Penyakit Dalam. PIP Penyakit dalam jilid 1. 2005

Syndrome of Dyspepsia

Definition : persistent or recurrent upper abdominal pain or discomfort characterized by postprandial fullness, early satiety, nausea, and bloating.

Classification: Functional and organic , or ulcer and non ulcer(NUD)

Functional: dysmotility like, ulcer like, non-specific, (reflux like). Functional: no organic diseases.

Organic(with x-ray or endoscopy): peptic ulcer, cancer, severe gastritis-duodenitis.

Yamada T et.al. Textbook of Gastroenterology. 4th ed. Volume one.2003

PATHOGENESIS of Gastric mucosal Damage

Figure1. The Balance between aggressive and defensive factors

Aggressive factors Defensive factors Gastric acid Mucosal blood flow Pepsin Epithelial cell surface Bile reflux Prostaglandin Nicotine Phospholipid/surfactan NSAID Mucus Corticosteroid Bicarbonate Helicobacter pylori Motility Free radicals Mucosal impermeability to Stress H+ ion Intracellular pH regulation Growth factor

cited from Daldiyono & Shiessel R et.al.

Clinical features in syndrome dyspepsia NUD: 1. ulcerlike: dominant epigastric pain, relieved by

antacids or food 2. dysmotility like: epigastric discomfort aggravated

by food or associated with early satiety, fullness, nausea, retching, vomiting, or bloating.

3. nonspecific: symptoms does not fit the other categories

Ulcer: the same with NUD


Findings and diagnostic findings in syndrome dyspepsia

routine: blood, stool, amylase-lypase , liver function test . upper gastrointestinal endoscopy: if age > 45 years or

NSAID consumption or alarm symptoms: weight loss,hemorrhage, dysphagia, vomiting, jaundice. Biopsy for histopathological or helicobacter pylori.

Double contrast upper gastrointestinal barium radiography

Gastric scintigraphy: gastric gastroparesis/motility Helicobacter pylori serology examination. Ultrasound/CT-scan: to exclude gallbladder/biliary

stone/malignancies, pancreatitis.


Management of Syndrome Dyspepsia:

Avoid/stop -decrease the aggravating/agresive factors, increase the defensive factors.

Young patients < 45 years, no NSAID consumer nor alarm symptoms : empiric therapy 2-4 weeks: Ulcer like: antacids or h2 receptor antagonist or proton pump inhibitor. Dysmotility like: prokinetic or h2 receptor antagonist. Nonspecific: antifatulent antacids, simethicone, antianxiety-depression.

Peptic ulcer: H2RA or PPI with/without cytoprotector Upper GI malignancies: operation.


GASTROESOPHAGEAL REFLUX DISEASE (GERD)

DEFINITION: a pathologic consequences of the effortless movement of gastric contents to the esophagus, including symptoms or signs referable to the esophagus, pharynx, larynx, and respiratory tract.

CLINICAL FEATURES: Heartburn, substernal chest discomfort, regurgitation bitter or acid-tasting liquid, water brash or hypersalivary, solid dysphagia, odynophagia, oropharynx damage(sorethroat, erache, gingivitis, poor dentition, and globus), reflux damage of the larynx and respiratory tract (hoarseness, wheezing, bronchitis, asthma, pneumonia).


Pathophysiology of GERD

Spectrum Of Endoscopic Findings with GERD

Normal esophagus Grade 3 esophagitis

Grade 4 esophagitis Barrett’s esophagus

MANAGEMENT of GERD

Lifestyle modification: Head elevation, stop smoking/alcohol, reduce meal size and intake of fat/carminative/chocolate/coffee, carbonated beverages, tomato juice, citrus products, stop medications reducing LES pressure (anticholinergics, theophylline etc.)

Medication therapy: - Acid suppressive drugs: 1. Proton pump inhibitor(PPI)( omeprazole, lansoprazole, rabeprazole, pantoprazole, esomeprazole): drug of choice 2. H2 receptor antagonists(cimetidine, ranitidine, famotidine, nizatidine): mild-moderate 3. Liquid Antacids: good for mild - Prokinetics agents: metoclopramide, domperidone, cisapride Surgical treatment. Endoscopic fundoplication.


PEPTIC ULCER DISEASE(PUD)-1 DEFINITION: PUD Mucosal break gaster and duodenum,

diameter more than 0,5 cm. Refractory ulcer duodenal ulcer 8 weeks therapy ineffective or gastric ulcer lack response to 12 weeks treatment.

PATHOGENESIS: Imbalance, aggressive factors >>> defensive factors(see dyspepsia).

Simadibrata M. Penatalaksanaan tukak peptik MKI 2007Yamada T et.al. Textbook of Gastroenterology. 4th ed. Volume one.2003

CLINICAL FEATURES of PUD

Abdominal pain 94%: epigastric in location, does not radiate, occurs 2-3 hours postprandially, and relieved by food or antacids. Some time awakens the patient between midnight and 3 AM.

Some patients have no symptoms Complications: hemorrhage(melena)(15%),

perforation(7%), penetration, and obstruction(2%).


FINDINGS ON DIAGNOSTIC TESTING of PUD routine blood(Hb, leukocyte) & stool(occult blood test) Upper gastrointestinal barium radiography: gastric &

duodenal ulcer Upper gastrointestinal endoscopy: gastric & duodenal

ulcer, biopsy for histopathological examination: benign/malignant disease, Helicobacter pylori infection

Helicobacter pylori testing: serology, culture/CLO test/histopathology examination from upper GI endoscopy examination, C-Urea Breath test, Stool’s H.pylori antigen

Serum gastrin and gastric acid secretion testing: hypergastrinemia in gastrinoma


MANAGEMENT of PUD-1 Non pharmacological management: - stomach diet, - avoid/stop aggressive factors: stress etc. Pharmacological management: - H2 receptor antagonist. - Proton pump inhibitors. - Cytoprotective Agents: Sucralfate, Misoprostol, Bismuth subsalicylate, Tephrenone and Rebamipide


Helicobacter pylori Eradication(KSHPI)

Tripple therapy(1 or 2 weeks): 1. PPI+Amoksisilin+Klaritromisin

2. PPI+Metronidazol+Klaritromisin 3. PPI+Metronidazol+Tetrasiklin (alergy to chlarithromisin) Quadruppel therapy(1 or 2 weeks): 1. If

fail of therapy combination 3 drugs: Bismuth+PPI+Amoksisilin+Klaritromisin Bismuth+PPI+Metronidazol+Klaritromisin 2. Hight resistency areas: PPI+Bismuth+Tetrasiklin+Metronidazol

PPI 2 x/d; Omeprazol/Esomeprazol 20 mg, Lansoprazol 30 mg, Pantoprazol 40 mg, Rabeprazol 10 mg. Amoksisilin: 2 x 1000 mg/d, Klaritromisin 2 x 500 mg/d, Metronidazol 3

x 500 mg/d, Tetrasiklin 4 x 250 mg/d, Bismuth 4 x 120 mg/d.

KSHPI, Konsensus infeksi Helicobacter pylori di Indonesia 2003

DYSPHAGIA DEFINITION: - Dysphagia sensation of food being hindered in

its passage from the mouth to the stomach. - Odynophagia pain on swallowing. - Globus sensation perception of a lump,

tightness, or fullness in the throat that is temporariloy relieved by swallowing.

CATEGORY: Dysphagia divided into: 1. Illnesses involving oral preparation, oral transfer, or pharyngeal phases of swallowing

2. conditions involving dysfunction of the

esophageal phase


Table 1. Causes of dysphagia Oropharyngeal dysphagia Neuromuscular diseases Cerebrovascular accident Parkinson’s disease Wilson’s disease Amyotrophic lateral sclerosis Brain stem tumors Bulbar poliomyelitis Peripheral neuropathy Myasthenia gravis Muscular dystrophies Polymyositis Metabolic myopathy Amyloidosis Systemic lupus erythemathosus Local mechanical lesions Inflammation(pharyngitis, abscess, tuberculosis, radiation, syphilis) Neoplasm Congenital webs Plummer-vinson syndrome Extrinsic compression(thyromegaly, cervical spine hyperostosis, adenopathy) Oropharyngealk resection Upper esophageal sphincter(UES) disorders Hypertensive UES Hypotensive UES Abnormal UES relaxation(cricopharyngeal achalasia, central nervous system, lymphoma, Oculopharyngeal muscular dystrophy, cricopharyngeal bar, Zenker’s diverticuum, familial Dysautonomia)Esophageal dysphagia Motility disorders Achalasia Scleroderma Diffuse esophageal spasm Nutcracker esophagus Hypertensive lower esophageal sphincter Nonspecific esophageal dysmotility Other rheumatologic conditions Chagas’ disease Intrinsic mechanical lesions Benign stricture(peptic, lye, radiation) Schatzki’s ring Carcinoma Esophageal webs Esophageal diverticula Benign tumors Foreign bodies Extrinsic mechanical lesions Vascular compression Mediastinal abnormalities Cervical osteoarthritis

DIAGNOSIS of Dysphagia

History: distinguish oropharyngeal / esophageal in location and if it is structural or neuromuscular in origin. Etc.

Physical examination: The head and neck sensory and motor function of the cranial nerves, masses, adenopathy, or spinal deformity. Examine systemic disease.

Additional testing: Barium swallow radiography, Upper endoscopy and biopsy, UES manometry.


Management of Dysphagia

The management depend on the cause. Neuromuscular disease—myotomy(surgical) Benign strictures—dilatation by bougienage Early malignancies –surgically resected Unresectable malignancies – dilatation, cautery, laser or stenting Achalasia—medications(calcium channel antagonists), botulinum

toxin injection into the LES, by endoscopic dilation, and by surgical myotomy.

Other primary esophageal dysmotilities respond to nitrates, calcium channel antagonist, surgical myotomy.


ACHALASIA-1

The most easily recognized & best-defined motor disorder of the esophagus

Incidence 1 per 100.000 population per year in US. Classification: Primary & Secondary. Neuropathology: LES failure to relax completely &

aperistalsis smooth muscle esophagus damage innervation loss of ganglion cells within myenteric(Auerbach) plexus, degeneration vagus nerve & degeneration dorsal motor nucleus vagus.


ACHALASIA-2

Clinical manifestation: dysphagia(100% solid & half liquid), regurgitation, chest pain, weight loss& aspiration pneumonia.

Esophagogram: esophageal dilatation with distal stenosis bird beak(paruh burung)/rat tail(ekor tikus).

Esophagoscopy: esophageal dilatation /atony with food residue/saliva.

Treatment: Dilatation(bougie, pneumatic-balloon), Botulinum toxin injection, Operation.


UPPER GASTROINTESTINAL

BLEEDING(HEMATEMESIS-MELENA)

DEFINITION: Upper gastrointestinal bleeding/ hematemesis melena refers to bleeding source from the upper gi tract. The blood in stool – tarry stools, the blood vomiting—black tarry vomiting

EPIDEMIOLOGY: - The frequent cause of upper gi bleeding in Indonesia is rupture of esophageal varices. - The frequent cause of upper gi bleeding in Europe is peptic ulcer.


Bad Predictor in upper gastrointestinal bleeding Age > 60 years Other comorbid Hypotension or shock Coagulopathy Bleeding onset in hospital Transfusion requirement > 6 unit Fresh bleeding from stomach Recurrens bleeding from the same lesion

Triadapafilopoulos G. Aliment Pharmacol Ther 2005;22(suppl.3): 53-8

WORKUP/DIAGNOSIS of Hematemesis Melena Resuscitation History Physical examination Upper gi endoscoopy Scintigraphy and angiography: the rate of blood loss

must exceed 0.5 ml per minute. Other radiographic studies: for aortoenteric fistula

abdominal computed tomographic or magnetic resonance imaging studies


MANAGEMENT of Hematemesis Melena

Blood Transfusion Medications: PUD/gastritis: H2RA, or PPI; varices or portal

gastropathy: vasopressin / terlipressin / somatostatin or octreotide . Angiodysplasia: intravenous or oral estrogens with or without progesterone.

Therapeutic endoscopy: thermal and nonthermal methods. Emergency upper endoscopy ; esophageal banding or

sclerotherapy. Mechanical compression: ballon tamponade/Senstaken-

Blakemore tube or Linton-nachlas , then followed by sclerotherapy or ligation.

Therapeutic angiography Surgery:if endoscopy fails


LOWER GASTROINTESTINAL BLEEDING DEFINITION: Lower gastrointestinal

bleeding refers to bleeding source from the lower gi tract. The blood in stool – red fresh bloody stools.


ETIOLOGY/CAUSES/DIFFERENTIAL DIAGNOSIS LOWER GI BlEEDING

Diverticulosis Angiodysplasias Hemorrhoids Anal fissures Neoplasms Inflammatory bowel disease Ischemic colitis Infectious colitis Radiation induced colitis Meckel’s diverticulum Intussusception Aortoenteric fistula Solitary rectal ulcera NSAID-induced cecal ulcers


DIAGNOSIS/WORKUP

Resuscitation: correction of volume deficits & stabilization of hemodynamic variables. If suspected upper gi bleeding ngt, Laboratory studies

History & Physical examination: GI diseases such as IBD, malignancy(weight loss, anorexia, lymphadenopathy, or palpable masses) etc

Additional testing: Endoscopy, Scintigraphy & angiography, Other radiologic studies(Barium enema).


MANAGEMENT LOWER GI BLEEDING-1 Medications. Therapeutic endoscopy. Therapeutic angiography. Surgery


ACUTE ABDOMEN

DEFINITION: Acute abdomen refers to any acute intra & extra abdominal disease processes. Many cases require urgent surgical management, although some can be managed nonsurgically.


ETIOLOGY/CAUSES/DIFFERENTIAL DIAGNOSIS OF ACUTE ABDOMEN

Gastrointestinal Appendisitis Perforated peptic ulcer Intestinal ischemia Diverticulitis Inflammatory bowel disease Meckel’s diverticulitis Pancreaticobiliary tract, liver, spleen Acute pancreatitis Calculous cholecystitis Acalculous cholecystitis Acute cholangitis Hepatic abscess Ruptured hepatic tumor Splenic rupture Urinary tract Renal/ureteral stone Gynecologic Ectopic pregnancy Tuboovarian abscess Ovarian torsion Uterine rupture Ruptured ovarian cyst or follicle Retroperitoneum Abdominal aortic aneurysm Supradiaphragmatic Pneumothorax Pulmonary embolus Acute pericarditis Empyema


WORKUP/DIAGNOSIS ACUTE ABDOMEN-1 History: Acute appendicitis: periumbilical pain, low-grade fever, anorexia

with/without vomiting followed by movement of the pain into the right lower quadrant McBurney’s point.

Constipation: obstructive conditions, inflammatory disorders produce ileus.

Watery diarrhea: gastroenteritis, Bloody diarrhea: infectious colitis, inflammatory bowel disease,

mesenterial ischemia. Jaundice: hepatic and pancreaticobiliary disease, sepsis. Urinary abnormality : urologic disease. Physical examination: Appendicitis acute: local peritonitis at McBurney’s point, psoas

sign(+). Perforation: general/local peritonitis, disappear of liver percussion

dullness. Bruits mesenteric thrombosis. Ectopic pregnancyunilateral adnexal mass with blue cervical

discoloration.


WORKUP/DIAGNOSIS ACUTE ABDOMEN-2 Initial studies: Blood testing: anemia, leukocytes, or leukopenia, serum

electrolytes, blood urea nitrogen, and creatinine, pregnancy test,

Peritonitis abdominal radiographs(3 positions abdominal xray)

Gas in the biliary tree – fistula or cholangitis. Ileus diffusely dilated loops of the small intestine & colon.

Free subdiaphragmatic air 75% patients with ulcer perforation.

Decision to operate immediately Imaging studies: CT-scan, ERCP/MRCP


MANAGEMENT OF ACUTE ABDOMEN

Urgent surgery Conservative management


DIARRHEA

DEFINITION: Stool soft or watery with a daily stool weight of > 200 g(250g). Frequency more than 3 times/day


CAUSES/DIFFERENTIAL DIAGNOSIS OF DIARRHEA High output osmotic Nonabsorbed solutes Saline and phosphate laxatives Sorbitol, fructose, lactulose Disaccharidase deficiency Lactase deficiency Isomaltase-sucrase deficiency Trehalase deficiency Small intestinal mucosal disease Celiac spure Tropical sprue Viral gastroenteritis Whipple’s disease Amyloidosis Intestinal ischemia Lymphoma Giardiasis Pancreatic insuffciency Chronic pancreatitis Pancreatic carcinoma Cystic fibrosis Reduced intestinal surface area Small intestinal resection Enteric fistulae Jejunoileal bypass Bile salt malabsorption Bacterial overgrowth Ileal resection Crohn’s disease Defective transport Congenital chloridorrhea High-output secretory Laxatives Bisacodyl Phenolphthalein Ricinoleic acid Dioctyl sodium sulfosuccinate Bacterial toxins Vibrio cholerae Toxigenic Eschericia coli Clostridium perfringens Hormonally induced Vasoactive intestinal polypeptide Serotonin Calcitonin Glucagon Gastrin Substance P Prostaglandins

Defective neural control Diabetic diarrhea Bile acid diarrhea Ileal resection Crohn’s disease Bacterial overgrowth Post cholecystectomy Mucosal inflammation Collagenous colitis Lymphocytic c olitis Villous adenoma High output injury Inflammatory bowel disease Crohn’s disease Ulcerative colitis Acute infections Viruses(rotavirus, Norwalk agent) Parasites(Giardia, Cryptosporidium, Cyclospora) E.coli Shigella Salmonella Campylobacter Yersinia enterocolitica Entamoeba histolytica(amebiasis) Chronic infections E.histolytica(amebiasis) Clostridium difficile Ischemia Atherosclerosis Vasculitis Normal output Motility disorders Irritable bowel syndrome Endocrinopathies Hyperthyroidism Proctitis Ulcerative proctitis Infectious proctitis Fecal incontinence Surgical and obstetrical trauma Hemorrhoids Anal fissures Perianal fistulae Anal neuropathy(diabetes


CLASSIFICATION

Time: acute less than 15 days chronic more than 15 days

Organic diseases: Organic and functional Infective/infectious causes: Infective/infectious and

non-infective/infectious Stool: soft, watery, bloody or steatorrhea, bloody ,

nonsteatorrhea nonbloody Pathomechanism: osmotic, secretory, increased

motility, mucosal inflammation,


DIAGNOSIS OF DIARRHEA-1 - History: Duration of diarrhea, recent travel, sexual practices, ingestion

of well water and poorly cooked food and shellfish, and exposure to high-risk persons in day care centers, hospitals, mental institutions, and nursing homes.

The characteristics of the diarrhea causative organism. Watery diarrhea+nausea, little paintoxin producing bacteria. Invasive bacteria pain, bloody diarrhea. Viruses watery diarrhea, pain significant, fever, mild-

moderate vomiting. Homosexual men, prostitutes, iv drug abusers diarrhea

through oral-fecal transfer. Antibiotic associated colitis recent antibiotic use. Recent medications: antacids containing magnesium,

antirrhytmias, antihypertensives, diuretics, central nervous system drugs, antiarthritis, cholesterol lowereing medications and theophylline.


DIAGNOSIS OF DIARRHEA-2 – Physical Examination Abdominal tumor/mass, dehydration, fever etc. Hypotension, decreased skin turgor, dry mucous membranes

dehydration need intravenous hydration. Emaciation, cheilosis and glossitis severe malabsorption. Dermatitis herpetiformis celiac sprue, Pyoderma gangrenosusm inflammatory bowel disease, Sclerodactily scleroderma. Arthritis inflammatory bowel disease or Whipple’s disease. Resting tachycardia hyperthyroidism, pulmonic stenosis and

tricuspid regurgitation carcinoid syndrome. Peripheral or autonomic neuropathy visceral neuropathy in

diabetes and intestinal pseudo-obstruction. Neuropsychiatric findings Whipples disease. Abdominal mass malignancy, Crohn’s disease, diverticulitis. Localized abdominal tenderness inflammatory condition. A digital rectal examination perianal disease with Crohn’s disease,

reduced sphincter tone incontinence. Occult or gross fecal blood infectious, inflammatory and neoplastic

conditions.


DIAGNOSIS OF DIARRHEA-3 - Acute diarrhea

Routine stool examination. Complicated and prolonged infection, unresponsive to

supportive care routinestool culture for Salmoneella, shigella, or Campylobacter organisms.

Special culture techniques Yersinia, Plesiomonas organisms and enterohemorrhagic E.coli.

Stool samples for parasitic disease—ova & parasites: Giardia, Cryptosporidium, E.histolytica or Strongyloidesorganisms.

Recent antibiotic use –Stool C.difficile culture and toxin determination.

20-40% acute infectious diarrhea remain undiagnosed despite laboratory evaluation.


DIAGNOSIS OF DIARRHEA-4- Chronic diarrhea

Stool examination for leukocytes, fat (Sudan stain) for fat malabsorption, parasites and stool culture.

Antibiotic use culture C.difficile. Serum electrolyte Erythrocyte sedimentation rate systemic inflammatory

disease. Serum albumin and globulin reduced malabsorption,

malnutrition, or protein losing enteropathy. Additional blood testsfor malnutrition: carotene, iron,

folate, vitamin B12, cholesterol, alkaline phosphatase and prothrombin time.

Flexibel sigmoidoscopy exclude proctitis, pseudomembranes and melanosis coli due to laxative abuse.

Biopsy for normal appearance microscopic and collagenous colitis or irritable bowel syndrome.


MANAGEMENT OF DIARRHEA

Intravenous resuscitation Agents for mild diarrhea: antidiarrheal, bismuth subsalicylate,

diphenoxylate, codeine. Antibiotics for acute infectious diarrhea Therapy for osmotic diarrhea: carbohydrate malabsorption

lactase deficiency or fructose or sorbitol intolerance dietary modification, lactase supplements

Therapy of secretory diarrhea somatostatin analog(octreotide), parenteral calcitonin, indomethacine.

Therapy for inflammatory diarrhea anti-inflammatory drugs(aminosalicylate and corticosteroid. Refractory cases azathioprine, 6mercaptourine, methotrexate.


Polyp and Cancer of the gaster/duodenum Definition: tumor of the gaster/duodenum,

benign and malignant(cancer) Management: polypectomy per endoscopic or

operation


Cholangitis

Definition: Infection of the common bile duct due to obstruction like biliary stone or cholangiocarcinoma or papillary tumor.

Management: - Antibiotic - ERCP diagnostic and therapetic(sphincterotomy + stone extraction or stenting) - Operative: laparoscopic cholecystectomy & stone extraction or laparotomy biliodigestive procedure


Bile duct Stone

Definition: Stone of the common bile duct. Management:

ERCP or operation


Pancreatitis

Definition: Inflammation or infection of the pancreas

Classification: Acute and Chronic Management:

1. Conservative: Fasting, total parenteral nutrition, antibiotics, octreotide/somatostatin, anti TNF).

2. Surgery


Acute pancreatitis with pancreatic enlargement& Peripancreatic edema & pseudocysts

Diagnosis of Acute Pancreatitis

• Clinical Features: abdominal pain, vomiting• Elevation of plasma amylase - lipase recommendation grade A 3 or 4 x normal (must not always rely on this value)• Plain radiograph• Abdominal Ultrasonography: pancreatic swelling(25-50% patients), CBD/gall bladder stones, dilatation of the CBD• Abdominal CT-scan(recommendation grade C)• Abdominal Magnetic Resonance Imaging(MRI)• CBD stones: ERCP & MRCP


Severity of Acute Severity of Acute pancreatitispancreatitis Mild ( Edema type ): fat necrosis of the

pancreatic superficial & interstitial edema Severe( Hemorrhagic-Necrotic type): diffuse

fat necrosis of pancreatic superficial and parenchymal. Necrotic and bleeding of the pancreatic parenchymal.


Etiologic factor & Pathogenesis in Acute PancreatitisEtiologic factor & Pathogenesis in Acute PancreatitisEtiologic factor(Biliary, alcoholism, unknown etc)

Initial process(bile reflux, duodenal refux etc)

Initial damage of the pancreas(edema, vascular injury, acinar pancreatic duct rupture) Digestive enzyme activation Trypsin

Phospholipase A Elastase Lypase Chymotrypsin Kallikrein

Autodigestive

Pancreatic necrosis

Lankisch.Acute Pancreatitis. Springer Verlag 1987

Irritable Bowel Syndrome Definition: Symptoms of lower gastrointestinal like

diarrhea, constipation or combination with abdominal cramps/pain. No organic abnormality found in colonoscopy.

Pathogenesis: stress, hypersensitivity, abnormal serotonin, abnormal motility etc.

Management:

- Diet rich of fibre

- Anti Anxiety-Depression

- Constipation: Prokinetic , 5 HT 4 agonist

- Diarrhea: Antispasmodic, anticholinergic


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Gastrointestinal Diseases and Abnormalities in Adult-rev2