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Gastrointestinal disease lecture(ppt)
 

Gastrointestinal disease lecture(ppt)

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Peptic ulcer disease
Chronic duodenal ulcer
Chronic benign gastric ulcer
Zollinger-Ellison syndrome
Gastritis
Gastric cancer
Post gastrectomy syndrome
Acute pancreatitis
Chronic pancreatitis
Insulinoma
Glucagonoma
Somatostatinoma

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  • Women who have had previous gall bladder disease more prone Ten percent mortality with uncomplicated; 60% with complications Meds that cause pacreatitis: BCP, thiazides, opiates, sulfa, steroids
  • Pancreatitis, Pancreas Hemorrhagic Pancreatitis and Fat Necrosis •Extensive necrosis has caused loss of the normal lobular surface markings of the pancreas •Chalky white surface(arrow) represents saponification- chelation of ca with fatty acids liberated by pancreatic enzymes •Hemorrhage caused by digestion of vessel walls by pancreatic enzymes is best seen at right
  • Turner’s sign

Gastrointestinal disease lecture(ppt) Gastrointestinal disease lecture(ppt) Presentation Transcript

  • Clinical Biochemistry Gastrointestinal Disease In the name of God
  • Clinical Biochemistry Gastrointestinal Disease By: Amir Nader Emami Razavi
  • Clinical Biochemistry Gastrointestinal Disease Gastrointestinal disease Peptic ulcer disease Chronic duodenal ulcer Chronic benign gastric ulcer Zollinger-Ellison syndrome Gastritis Gastric cancer Post gastrectomy syndrome Acute pancreatitis Chronic pancreatitis Insulinoma Glucagonoma SomatostatinomaJune 26, 2012 Total slide. 126 3
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 4
  • Clinical Biochemistry Gastrointestinal Disease Peptic Ulcer Disease (PUD) What is it? Group of chronic disorders characterized by ulcerating mucosal lesions in upper GI tract chronic inflammatory condition common forms are duodenal and gastric ulceration Where does it occur? Stomach, duodenum What causes PUD? H. pylori or drug induced (most commonly by chronic NSAID use)June 26, 2012 Total slide. 126 5
  • Clinical Biochemistry Gastrointestinal Disease Drugs that can cause PUD methotrexate cyclophosphamide azathioprine erythromycin iron corticosteriods potassium chloride NSAIDSJune 26, 2012 Total slide. 126 6
  • Clinical Biochemistry Gastrointestinal Disease Signs and Symptoms of PUD Can be symptomatic anorexia, nausea, vomiting, belching, bloating, heartburn, epigastric pain (pain in the upper abdomen) awakened at night (usu. around 3am,) duodenal ulcers epigastric pain, tenderness, burning, aching between xiphoid process and belly button relieved with food intake or antacids gastric ulcer diffuse pain over midepigastrium (midstomach) worsened by foodJune 26, 2012 Total slide. 126 7
  • Clinical Biochemistry Gastrointestinal Disease Characteristics and Comparisons Between Gastric and Duodenal Ulcers Gastric ulcer formation involves inflammatory involvement of acid-producing cells but usually occurs with low acid secretion. Duodenal ulcers are associated with high acid and low bicarbonate secretion. Increased mortality and hemorrhage are associated with gastric ulcers.June 26, 2012 Total slide. 126 8
  • Clinical Biochemistry Gastrointestinal Disease Pathology of Peptic Ulcer
  • Clinical Biochemistry Gastrointestinal Disease Normal StomachJune 26, 2012 Total slide. 126 10
  • Clinical Biochemistry Gastrointestinal Disease Esophagus & Stomach NormalJune 26, 2012 Total slide. 126 11
  • Clinical Biochemistry Gastrointestinal Disease Definition: Ulceration (breach in mucosa) due to acid & pepsin attack – peptic ulcer. Deeper than just mucosa Single, punched out, clean baseJune 26, 2012 Total slide. 126 12
  • Clinical Biochemistry Gastrointestinal Disease Etiology: Helicobacter pylori infection. Hyperacidity - eg. zollinger ellison. Drugs - anti-inflammatory (NSAIDs) & Corticostroids. Cigarette smoking, Alcohol, Rapid gastric emptying Personality and stressJune 26, 2012 Total slide. 126 13
  • Clinical Biochemistry Gastrointestinal Disease H. Pylori organisms- silver st.June 26, 2012 Total slide. 126 14
  • Clinical Biochemistry Gastrointestinal Disease Pathogenesis: Helicobacter pylori infection Colonization of gastric mucous Urease ammonia neutralization of acid  Rebound acid production. Protease – Mucous break down. Weak mucosal resistance Acid & Pepsin digestion of mucosa Chronic UlcerationJune 26, 2012 Total slide. 126 15
  • Clinical Biochemistry Gastrointestinal Disease Etiology of PUD Normal Increased Attack Hyperacidity Weak defense Helicobacter pylori Stress, drugs, smokingJune 26, 2012 Total slide. 126 16
  • Clinical Biochemistry Gastrointestinal Disease Helicobacter pylori: Most common infection in the world (20%) 10% of men, 4% women develop PUD Positive in 70-100% of PUD patients. H.pylori related disorders: Chronic gastritis – 90% Peptic ulcer disease – 95-100% Gastric carcinoma – 70% Gastric lymphoma Reflux Oesophagitis. Non ulcer dyspepsiaJune 26, 2012 Total slide. 126 17
  • Clinical Biochemistry Gastrointestinal Disease Peptic Ulcer Morphology: 90% ulcers in first portion of duodenum or lesser curvature of stomach 80 to 90% cases single ulcer. Round Small ulcers with sharply punched out edges Small <2cm, clean base. Microscopy: 4 zones. Superficial necrotic layer. Inflammatory cells zone. Granulation tissue zone Collagenous scar layer.June 26, 2012 Total slide. 126 18
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 19
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 20
  • Clinical Biochemistry Gastrointestinal Disease Gastric peptic ulcerJune 26, 2012 Total slide. 126 21
  • Clinical Biochemistry Gastrointestinal Disease Gastric peptic ulcer:June 26, 2012 Total slide. 126 22
  • Clinical Biochemistry Gastrointestinal Disease Gastric Ulcer Gastric ulcer:June 26, 2012 Total slide. 126 23
  • Clinical Biochemistry Gastrointestinal Disease Duodenal Peptic UlcerJune 26, 2012 Total slide. 126 24
  • Clinical Biochemistry Gastrointestinal Disease Peptic ulcer - EndoscopyJune 26, 2012 Total slide. 126 25
  • Clinical Biochemistry Gastrointestinal Disease Gastric UlcerJune 26, 2012 Total slide. 126 26
  • Clinical Biochemistry Gastrointestinal Disease Gastric UlcerJune 26, 2012 Total slide. 126 27
  • Clinical Biochemistry Gastrointestinal Disease Gastric Ulcer Punched out ulcer Clean base Small single Radiating mucosal folds. Benign ulcer. No tumor.June 26, 2012 Total slide. 126 28
  • Clinical Biochemistry Gastrointestinal Disease Peptic UlcerJune 26, 2012 Total slide. 126 29
  • Clinical Biochemistry Gastrointestinal Disease Peptic Ulcer Microscopy:June 26, 2012 Total slide. 126 30
  • Clinical Biochemistry Gastrointestinal Disease PUD - Diagnosis Endoscopy Barium meal – contrast x-ray Biopsy – bacteria & malignancy H.Pylori: Endoscopy cytology Biopsy – Special stains Culture Urease Breath test.June 26, 2012 Total slide. 126 31
  • Clinical Biochemistry Gastrointestinal Disease CDU Camplications Hemorrhage Due to the ulcer’s eroding a blood vessel Perforation Through the anterior wall of the duodenal cap Causing peritonitis Penetration of the ulcer into the adjacent structures Such as pancrease , biliary tract , liver, colon, abdominal wall, or even long Luminal abstruction Caused by the gradual contraction of the ulser scarJune 26, 2012 Total slide. 126 32
  • Clinical Biochemistry Gastrointestinal Disease Gastric UlcerJune 26, 2012 Total slide. 126 33
  • Clinical Biochemistry Gastrointestinal Disease Points to Remember: A peptic ulcer is a sore in the lining of the stomach or duodenum due to attack by acid & Pepsin. The major cause - H. pylori bacterium. Others are NSAIDs. spicy food, stress are risk factors. H. pylori can be transmitted from person to person through close contact A combination of antibiotics and H pump inhibitors is the most effective treatment.June 26, 2012 Total slide. 126 34
  • Clinical Biochemistry Gastrointestinal Disease Helecobacter pyloriJune 26, 2012 Total slide. 126 35
  • Clinical Biochemistry Gastrointestinal Disease Toludine Blue stain – H pyloriJune 26, 2012 Total slide. 126 36
  • Clinical Biochemistry Gastrointestinal Disease Urease production testJune 26, 2012 Total slide. 126 37
  • Clinical Biochemistry Gastrointestinal Disease “You get ulcer, not from what you eat, but from what’s eating you..!”
  • Clinical Biochemistry Gastrointestinal Disease Hmmmm……… H.pylori
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 40
  • Clinical Biochemistry Gastrointestinal Disease Zollinger-Ellison syndrome Increased numbers of parietal cells with no change in surface and foveolar mucous cells.June 26, 2012 Total slide. 126 41
  • Clinical Biochemistry Gastrointestinal Disease Zollinger Ellison Syndrome Tumour Location Pancreas 50-60% Duodenum 40-50% 20-25% Related to MEN-1 50-70% Malignant (lymphnode metastases) Gastrinoma Triangle 80% Gastritis Symptoms Recurrent ulcers Diarrhea (malabsorption)June 26, 2012 Total slide. 126 42
  • Clinical Biochemistry Gastrointestinal Disease Zollinger-Ellison syndrome  0.1 to 1 percent of patients with peptic ulcer disease .  Underestimation! symptoms similar to typical peptic ulcer . symptoms may be controlled by standard doses of an antisecretory drug patients may not be tested for hypergastrinemia Gastrinomas can be either sporadic (80 percent) or associated with multiple endocrine neoplasia type 1June 26, 2012 Total slide. 126 43
  • Clinical Biochemistry Gastrointestinal Disease Signs of ZES  Multiple ulcers  Diarrhea  ulcer in atypical site  resistant ulcer  enlarged folds  severe esophagirtisJune 26, 2012 Total slide. 126 44
  • Clinical Biochemistry Gastrointestinal Disease Diarrhea in ZES The high rate of acid volume load that cannot be absorbed by the intestine The excess acid exceeds the neutralizing capacity of pancreatic bicarbonate . The exceptionally low pH of the intestinal contents inactivates pancreatic digestive enzymes, interferes with the emulsification of fat by bile acids, and damages intestinal epithelial cells and villi. The extremely high serum gastrin concentrations may inhibit absorption of sodium and water by the small intestine,June 26, 2012 Total slide. 126 45
  • Clinical Biochemistry Gastrointestinal Disease ZES diagnosis Exclude hyperacidity! >100mM/L in 12 hour overnight secretion of HCl Check gastrin, if >1000=ZES. <1000 but abnormal secretin test to be performed +200 pg/ml is ZES Secretin chalenge testJune 26, 2012 Total slide. 126 46
  • Clinical Biochemistry Gastrointestinal Disease ZES treatment any patient with a sporadic gastrinoma and without evidence of metastatic spread of disease should be offered exploratory laparotomy with curative intent laparotomy is not routinely recommended for patients with ZES as part of MEN 1 since the multifocal nature of the tumors in this disorder almost uniformly precludes cure of gastrin hypersecretionJune 26, 2012 Total slide. 126 47
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 48
  • Clinical Biochemistry Gastrointestinal Disease Definition The term gastritis is used to denote inflammation associated with mucosal injury Gastritis is mostly a histological term that needs biopsy to be confirmed Gastritis is usually due to infectious agents (such as Helicobacter pylori) and autoimmune and hypersensitivity reactions.June 26, 2012 Total slide. 126 49
  • Clinical Biochemistry Gastrointestinal Disease Definition Epithelial cell damage and regeneration without associated inflammation is properly referred to as “gastropathy”. Gastropathy may be referred without histological evidence and just according to gross appearance in endoscopy or radiology Gastropathy is usually caused by irritants such as drugs (eg, nonsteroidal antiinflammatory agents and alcohol), bile reflux, hypovolemia, and chronic congestion.June 26, 2012 Total slide. 126 50
  • Clinical Biochemistry Gastrointestinal Disease Acute Esophagitis & GastritisJune 26, 2012 Total slide. 126 51
  • Clinical Biochemistry Gastrointestinal Disease Gross–histologic correlation?June 26, 2012 Total slide. 126 52
  • Clinical Biochemistry Gastrointestinal Disease CLASSIFICATION GASTRITIS ACUTE COMMON CHRONIC STRESS BILE HP EMAG NSAID AMAGJune 26, 2012 Total slide. 126 53
  • Clinical Biochemistry Gastrointestinal Disease CLASSIFICATION Acute vs. chronic Acute refers to short term inflammation Acute refering to neurophilic infiltrate Chronic referring to long standing forms Chronic referring to mononuclear cell infiltrate especially lymphocyte and maccrophagesJune 26, 2012 Total slide. 126 54
  • Clinical Biochemistry Gastrointestinal Disease ACUTE GASTRITIS MORPHOLOGY Mucosal congestion, edema, inflammation & ulcerationJune 26, 2012 Total slide. 126 55
  • Clinical Biochemistry Gastrointestinal Disease Acute hemorrhagic erosive hemorrhagic and erosive lesions shortly after exposure of the gastric mucosa to various injurious substances or a substantial reduction in mucosal blood flowJune 26, 2012 Total slide. 126 56
  • Clinical Biochemistry Gastrointestinal Disease Acute hemorrhagic erosive nonsteroidal antiinflammatory drugs [NSAIDs], alcohol, or bile acids) or to mucosal hypoxia (such as in trauma, burns [Curlings ulcers] or sepsis) or to a combination of factors such as with antineoplastic chemotherapyJune 26, 2012 Total slide. 126 57
  • Clinical Biochemistry Gastrointestinal Disease Acute hemorrhagic erosive Gastric and duodenal ulceroinflammatory ulcers occurring during severe damage to the central nervous system (Cushings ulcers) are often considered in this groupJune 26, 2012 Total slide. 126 58
  • Clinical Biochemistry Gastrointestinal Disease Acute hemorrhagic erosive specific pathogenetic factor in NSAID-induced acute hemorrhagic and erosive gastropathy is the inhibition of prostaglandin production. Prostaglandins, especially those of the E class, protect against acute mucosal injury due to NSAIDs and other injurious substances by several mechanisms, including the stimulation of mucus and bicarbonate secretion, and maintenance of mucosal blood flowJune 26, 2012 Total slide. 126 59
  • Clinical Biochemistry Gastrointestinal Disease Acute hemorrhagic erosive Hemorrhagic or erosive gastropathy may be associated with the development of gastric or duodenal ulcers. Acute ulceration is most likely to occur in relation to shock-induced hemodynamic instability (ie, the stress ulcer syndrome).June 26, 2012 Total slide. 126 60
  • Clinical Biochemistry Gastrointestinal Disease Risk factors Prior history of an adverse GI event (ulcer, hemorrhage) increases risk four to fivefold Age >60 increases risk five to sixfold High (more than twice normal) dosage of a NSAID increases risk 10-fold Concurrent use of glucocorticoids increases risk four to fivefold Concurrent use of anticoagulants increases risk 10- to 15-foldJune 26, 2012 Total slide. 126 61
  • Clinical Biochemistry Gastrointestinal Disease HP and NSAID Patients with a history of uncomplicated or complicated peptic ulcers (gastric, duodenal) should be tested for H. pylori prior to beginning a NSAID or low dose aspirin. If present, H. pylori should be treated with appropriate therapy, even if it is believed that the prior ulcer was due to NSAIDsJune 26, 2012 Total slide. 126 62
  • Clinical Biochemistry Gastrointestinal Disease Helicobacter pylori Helicobacter pylori is a spiral shaped, gram negative bacterium measuring approximately 3.5 microns in length and 0.5 microns in widthJune 26, 2012 Total slide. 126 63
  • Clinical Biochemistry Gastrointestinal Disease Helicobacter pylori Urease appears to be vital for its survival and colonization; it is produced in abundance, making up more than 5 percent of the organisms total protein weight.June 26, 2012 Total slide. 126 64
  • Clinical Biochemistry Gastrointestinal Disease Helicobacter pylori urease forms ammonia and bicarbonate that neutralize gastric acid and form a protective cloud around the organismJune 26, 2012 Total slide. 126 65
  • Clinical Biochemistry Gastrointestinal Disease Helicobacter pylori spiral shape, flagella facilitate its passage through the mucus layerJune 26, 2012 Total slide. 126 66
  • Clinical Biochemistry Gastrointestinal Disease Helicobacter pylori H. pylori then attaches to gastric epithelial cells by means of specific receptor-mediated adhesionJune 26, 2012 Total slide. 126 67
  • Clinical Biochemistry Gastrointestinal Disease Non HP gastritis Chemical gastritis (acute ・ chronic) Alcoholic gastritis Drug induced gastritis (e.g., NSAID) Reflux ( due to duodenal juice or bile) gastritis Other chemical gastritis Radiation gastritis Allergic gastritis Autoimmune gastritis Special forms of gastritisJune 26, 2012 Total slide. 126 68
  • Clinical Biochemistry Gastrointestinal Disease Stress ulcer pathophysiology Hypersecretion of acid –head trauma. Defects in gastric glycoprotein mucus –In critically ill patients, increased concentrations of refluxed bile salts or the presence of uremic toxins can denude the glycoprotein mucous barrier Ischemia – Shock, sepsis, and trauma can lead to impaired perfusion of the gut.June 26, 2012 Total slide. 126 69
  • Clinical Biochemistry Gastrointestinal Disease Stress ulcer risk factors Shock Sepsis Hepatic failure Renal failure Multiple trauma Burns over 35 percent of total body surface area Organ transplant recipients Head or spinal trauma Prior history of peptic ulcer disease or upper GI bleedingJune 26, 2012 Total slide. 126 70
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 71
  • Clinical Biochemistry Gastrointestinal Disease Gastric Neoplasia Benign Gastric polyps Ectopic pancreas Malignant Gastric Adenocarcinoma Gastric Lymphoma Gastric SarcomaJune 26, 2012 Total slide. 126 72
  • Clinical Biochemistry Gastrointestinal Disease WHO Classification 5 main categories Adenocarcinoma, Adenosquamous cell carcinoma, squamous cell carcinoma, undifferentiated carcinoma and unclassified carcinoma Adenocarcinoma – subdivided Papillary, tubular, mucinous, signet ring Further subdivided based on differentiationJune 26, 2012 Total slide. 126 73
  • Clinical Biochemistry Gastrointestinal Disease Cancer of Stomach 1. Incidence a. Worldwide common cancer, but less common in US b. Incidence highest among Hispanics, African Americans, Asian Americans, males twice as often as females c. Older adults of lower socioeconomic groups higher risk 2. Pathophysiology a. Adenocarcinoma most common form involving mucus- producing cells of stomach in distal portion b. Begins as localized lesion (in situ) progresses to mucosa; spreads to lymph nodes and metastasizes early in disease to liver, lungs, ovaries, peritoneumJune 26, 2012 Total slide. 126 74
  • Clinical Biochemistry Gastrointestinal Disease Cancer of Stomach 3. Risk Factors a. H. pylori infection b. Genetic predisposition c. Chronic gastritis, pernicious anemia, gastric polyps d. Achlorhydria (lack of hydrochloric acid) e. Diet high in smoked foods and nitrates 4. Manifestations a. Disease often advanced with metastasis when diagnosed b. Early symptoms are vague: early satiety, anorexia, indigestion, vomiting, pain after meals not responding to antacids c. Later symptoms weight loss, cachexia (wasted away appearance), abdominal mass, stool positive for occult bloodJune 26, 2012 Total slide. 126 75
  • Clinical Biochemistry Gastrointestinal Disease Cancer of Stomach 5. Collaborative Care a. Support client through testing b. Assist client to maintain adequate nutrition 6. Diagnostic Tests a.CBC indicates anemia b.Upper GI series, ultrasound identifies a mass c.Upper endoscopy: visualization and tissue biopsy of lesionJune 26, 2012 Total slide. 126 76
  • Clinical Biochemistry Gastrointestinal Disease Cancer of Stomach 7. Treatment a. Surgery, if diagnosis made prior to metastasis 1.Partial gastrectomy with anastomosis to duodenum: Bilroth I or gastroduodenostomy 2.Partial gastrectomy with anastomosis to jejunum: Bilroth II or gastrojejunostomy 3.Total gastrectomy (if cancer diffuse but limited to stomach) with esophagojejunostomyJune 26, 2012 Total slide. 126 77
  • Clinical Biochemistry Gastrointestinal Disease Fungating CarconomaJune 26, 2012 Total slide. 126 78
  • Clinical Biochemistry Gastrointestinal Disease Gastric Surgical Procedures
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 80
  • Clinical Biochemistry Gastrointestinal Disease Post gastrectomy syndrome b. Complications associated with gastric surgery 1. Dumping Syndrome a.Occurs with partial gastrectomy; hypertonic, undigested chyme bolus rapidly enters small intestine and pulls fluid into intestine causing decrease in circulating blood volume and increased intestinal peristalsis and motility b.Manifestations 5 – 30 minutes after meal: nausea with possible vomiting, epigastric pain and cramping, and diarrhea; client becomes tachycardic, hypotensive, dizzy, flushed, diaphoretic c.Manifestations 2 – 3 hours after meal: symptoms of hypoglycemia in response to excessive release of insulin that occurred from rise in blood glucose when chyme entered intestineJune 26, 2012 Total slide. 126 81
  • Clinical Biochemistry Gastrointestinal Disease Post gastrectomy syndrome Treatment: dietary pattern to delay gastric emptying and allow smaller amounts of chyme to enter intestine Liquids and solids taken separately Increased amounts of fat and protein Carbohydrates, especially simple sugars, reduced Client to rest recumbent or semi-recumbent 30 – 60 minutes after eating Anticholinergics, sedatives, antispasmodic medications may be added Limit amount of food taken at one timeJune 26, 2012 Total slide. 126 82
  • Clinical Biochemistry Gastrointestinal Disease Post gastrectomy syndrome Common post-op complications Pneumonia Anastomotic leak Hemorrhage Relux aspiration Sepsis Reflux gastritis Paralytic ileus Bowel obstruction Wound infection Dumping syndromeJune 26, 2012 Total slide. 126 83
  • Clinical Biochemistry Gastrointestinal Disease Post gastrectomy syndrome Nutritional problems related to rapid entry of food into the bowel and the shortage of intrinsic factor Anemia: iron deficiency and/or pernicious Folic acid deficiency Poor absorption of calcium, vitamin D Radiation and/or chemotherapy to control metastasic spread Palliative treatment including surgery, chemotherapy; client may have gastrostomy or jejunostomy tube insertedJune 26, 2012 Total slide. 126 84
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 85
  • Clinical Biochemistry Gastrointestinal Disease PancreasJune 26, 2012 Total slide. 126 86
  • Clinical Biochemistry Gastrointestinal Disease Function Exocrine precursor digestive enzymes lipases Endocrine metabolic hormones Insulin from β cells Glucagon from α cellsJune 26, 2012 Total slide. 126 87
  • Clinical Biochemistry Gastrointestinal Disease Exocrine Pancreas The final product of the exocrine pancreas is a clear isotonic solution with a pH in the range of 8. The 2 distinct components of exocrine secretion are enzyme secretion and water+electrolyte secretion. Cholecystokinin is the most potent endogenous hormone known to stimulate enzyme secretion. Secretin is the most potent endogenous stimulant of pancreatic electrolyte secretion.June 26, 2012 Total slide. 126 88
  • Clinical Biochemistry Gastrointestinal Disease Endocrine Pancreas The release of insulin into the portal blood is controlled by the concentration of blood glucose, vagal interactions, and local concentrations of somatostatin. The major stimulus for glucagon release is a fall in serum glucose. Pancreatic polypeptide appears to function for regulation of pancreatic exocrine secretion and biliary tract motility. Somatostatin has a broad inhibitory spectrum of gastrointestinal activityJune 26, 2012 Total slide. 126 89
  • Clinical Biochemistry Gastrointestinal Disease Factors Leading to Pancreatitis Alcohol intake – usually 5 to 10 years Prior biliary disease Abdominal surgery or diagnostics Trauma Recent viral infections Medications Mostly middle aged menJune 26, 2012 Total slide. 126 90
  • Clinical Biochemistry Gastrointestinal Disease Pathophysiology Inflammation from an insult or injury Causes activation of pancreatic enzymes Enzymes autodigest and cause fibrosis Leads to thrombi and necrosis of tissue Fat necrosis occurs Fats bind to calcium Results in hypocalcemiaJune 26, 2012 Total slide. 126 91
  • Clinical Biochemistry Gastrointestinal Disease More Patho Necrosis of blood vessels Fibers in blood vessels and ducts are dissolved Vasodilation starts due to vessel damage Results in bleeding and hemorrhage May be acute or chronic May be mild to necrotizingJune 26, 2012 Total slide. 126 92
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 93
  • Clinical Biochemistry Gastrointestinal Disease Acute Pancreatitis Nonbacterial inflammatory disease caused by activation, interstitial liberation, and autodigestion of the pancreas by its own enzymes.June 26, 2012 Total slide. 126 94
  • Clinical Biochemistry Gastrointestinal Disease Acute Pancreatitis Aetiology Gallstones and Alcohol account for 90% Hyperlipidemia Hypercalcemia Familial Pancreatic duct obstruction Tumour Pancreas divisum Viral infection Scorpion venom Drugs IdiopathicJune 26, 2012 Total slide. 126 95
  • Clinical Biochemistry Gastrointestinal Disease Acute Pancreatitis Symptoms and signs Midepigastric abdominal pain, radiating to the back Nausea and vomiting Fever and tachycardia Epigastric tenderness Abdominal distention Bluish discoloration in the flank (Grey Turner’s sign)June 26, 2012 Total slide. 126 96
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 97
  • Clinical Biochemistry Gastrointestinal Disease Acute Pancreatitis Diagnosis It is supported by appropriate laboratory determinations and radiographic findings Serum amylase is the most widely used lab test Hyperamylasemia is commonly observed within 24 hrs. of the onset and gradually returns to normalJune 26, 2012 Total slide. 126 98
  • Clinical Biochemistry Gastrointestinal Disease Acute Pancreatitis Diagnosis Elevated amylase levels may occur in other acute abdominal conditions, though levels rarely exceed 500 IU/dL Urinary amylase excretion is increased and this may be very helpful in cases where the serum amylase level has returned to normal. Other lab. Findings Moderate leukocytosis Mild bilirubin elevation (<2mg/dL) Raised Haematocrit Hypocalcaemia (Calcium being complexed with fatty acids)June 26, 2012 Total slide. 126 99
  • Clinical Biochemistry Gastrointestinal Disease Acute Pancreatitis Glasgow prognostic systemJune 26, 2012 Total slide. 126 100
  • Clinical Biochemistry Gastrointestinal Disease Acute Pancreatitis Treatment Goals of medical treatment Reduction of pancreatic secretory stimuli Correction of fluid and electrolyte derangementsJune 26, 2012 Total slide. 126 101
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 102
  • Clinical Biochemistry Gastrointestinal Disease Chronic Pancreatitis Is an entity encompassing recurrent or persistent abdominal pain of pancreatic origin combined with evidence of exocrine and endocrine insufficiency and marked pathologically by irreversible parenchymal destruction. It is associated with alcohol abuse, Hyperparathyroidism, congenital anomalies of the pancreatic duct and pancreatic trauma. It may also be idiopathic.June 26, 2012 Total slide. 126 103
  • Clinical Biochemistry Gastrointestinal Disease Chronic Pancreatitis Patients typically present in the fourth or fifth decade with a history of alcohol abuse and with epigastric or back pain. Anorexia and weight loss may be present. 1/3 of pts. Have insulin-dependent diabetes 1/4 of pts have steatorrhea. Narcotic abuse is commonJune 26, 2012 Total slide. 126 104
  • Clinical Biochemistry Gastrointestinal Disease Chronic Pancreatitis pancreatic calcifications in ~50% pancreatic parenchymal nodularity, calcifications and pancreatic ductal dilatation.June 26, 2012 Total slide. 126 105
  • Clinical Biochemistry Gastrointestinal Disease Signs and Symptoms of Chronic Pancreatitis Abdominal pain: intense, burning, Abdominal tenderness Ascites Steatorrhea JaundiceJune 26, 2012 Total slide. 126 106
  • Clinical Biochemistry Gastrointestinal Disease More S & S of Chronic Dark urine Signs and symptoms of diabetes Dyspnea Orthopnea Weight lossJune 26, 2012 Total slide. 126 107
  • Clinical Biochemistry Gastrointestinal Disease Diagnostics Elevated amylase, lipase, and urine amylase Elevated glucose, bilirubin, alkaline phosphatase Elevated WBCs Hypocalcemia HypomagnesiaJune 26, 2012 Total slide. 126 108
  • Clinical Biochemistry Gastrointestinal Disease Chronic Pancreatitis Medical Treatment Control of abdominal pain Treatment of endocrine and exocrine insufficiencyJune 26, 2012 Total slide. 126 109
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 110
  • Clinical Biochemistry Gastrointestinal Disease Insulinoma •Characteristic clinical manifestation is fasting hypoglycemia with symptoms • insulinomas arise from cells of ductular/acinar system of the pancreas
  • Clinical Biochemistry Gastrointestinal Disease Insulinoma Incidence 0.4/100,000 person-yrs (4 cases/million/year) So rare that few institutions have accrued enough experience to provide dataJune 26, 2012 Total slide. 126 112
  • Clinical Biochemistry Gastrointestinal Disease Insulinoma Symptoms Confusion, visual changes, unusual behavior Sympathoadrenal symptoms include palpitations, diaphoresis, and tremulousness Amnesia as wellJune 26, 2012 Total slide. 126 113
  • Clinical Biochemistry Gastrointestinal Disease Insulinoma Information based on a collection of 224 patients out of Olmsted County, Minnesota Of those 224, 8% had MEN neoplasia Tumor distribution: 87% had single benign lesions 7% benign tumors-multiple 6% had malignant insulinomasJune 26, 2012 Total slide. 126 114
  • Clinical Biochemistry Gastrointestinal Disease Insulinoma Established by demonstrating inappropriately high serum [insulin] during a spontaneous or induced episode of hypoglycemia Virtually all insulinomas are islet cell tumors After diagnosis, imaging used to localize tumorJune 26, 2012 Total slide. 126 115
  • Clinical Biochemistry Gastrointestinal Disease Insulinoma/diagnosis Serum glucose Male<55mg/dl Female<35mg/dl Plasma insulin level >15 mu/l Plasma proinsulin level >40 pmol/lJune 26, 2012 Total slide. 126 116
  • Clinical Biochemistry Gastrointestinal Disease Insulinoma/treatment Surgical removal partial pancreatectomy enucleation of insulinoma surgeon’s choiceJune 26, 2012 Total slide. 126 117
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 118
  • Clinical Biochemistry Gastrointestinal Disease Glucagonoma Syndrome Glocagenoma Syndrome Tumour Location Pancreas >90% malignant Symptoms Necrolytic migratory erythema Weight loss Anemia Trombosis Impaired glucose tolerance DiarrhoeaJune 26, 2012 Total slide. 126 119
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 120
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 121
  • Clinical Biochemistry Gastrointestinal Disease Glocagenoma Syndrome/Diagnosis Histopathology Agyrophil staining, CgA, glucagon:500pg/ml glicentin Tumour Markers p-CgA, p-glucagon Radiology Octreoscan, Endoscopic ultrasound, CT-angiography, MRIJune 26, 2012 Total slide. 126 122
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 123
  • Clinical Biochemistry Gastrointestinal Disease Somatostatinoma Syndrome Somatostatinoma Syndrome Tumour Location Duodenum Pancreas Colon/Rectum >80% mixed tumours Symptoms Gallstones Steatorrhea Impaired glucose tolerance Often “non-functioning” tumours!June 26, 2012 Total slide. 126 124
  • Clinical Biochemistry Gastrointestinal Disease Somatostatinoma Syndrome/Diagnosis Histopathology Argyrophil staining, CgA Somatostatin Tumour Markers p-CgA, p-Somatostatin (s-Gastrin, p-Glucagonom, mixed tumour) Radiology Endoscopic ultrasonography CT-angiography, MRI Colonoscopy US (liver metastases)June 26, 2012 Total slide. 126 125
  • Clinical Biochemistry Gastrointestinal DiseaseJune 26, 2012 Total slide. 126 126