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GI study guide.

Anatomy and physiology, Enzymes


1. Mouth: Buccal mucosa, Lips, hard Palate, Soft palate, teeth a. Salivary glands: secret amylase to breakdown carbohydrates 2. Esophagus: a. upper esophageal sphincter: at rest close to prevent air into esophagus b. Lower esophageal sphincter: at rest normally closed to prevent reflux 3. Stomach: a. parietal cells: hydrochloric acid, intrinsic factor b. chief cells: pepsinogen c. secretin: inhibits acid production 4. Pancreas: a. exocrine function: digestive enzymes such as Ductal cells and Acinar cells b. endocrine function: producing hormones such as insulin, glucagon, somatostatin 5. Liver a. storage of vitamins, minerals, iron magnesium, fat soluble vitamins A, D, E, K. b. Protective: Kupffer cells, engulfs harmful bacteria and anemic red cells, detoxifies blood c. metabolism: breakdown proteins removes ammonia (converts to urea) synthesis of plasma proteins: albulmin, prothrombin, and fibrinogen stores glycogen synthesizes, breaksdown, and stores fatty acids, triglycerides forms and secretes bile in response to gastrin, secretin, cholescystokinin 6. Gallbladder: Collects, concentrates, and stores bile. Is released when fat is present in duodenum 7. Small Intestines: movement, digestion, and absorption 8. Large Intestines: ascending, transverse, descending, sigmoid, rectum, anus a. blood supply: 20% total cardiac output Misc GI Diagnostics: 1. Prothrombin time: severe or acute liver disease leads to elevated prothrombin time 2. CBC: GI bleed is most common cause of anemia in adults 3. Calcium: is absorbed in GI tract, may detect malabsorption 4. Sodium, Potassium; absorbed in GI tract: vomiting and diarrhea may cause depletion 5. AST/ALT: enzymes found in liver. 6. Amylase, Lipase: elevations indicate pancreatitis 7. Ammonia: high levels indicate liver dysfunction 8. Bilirubin: pigment in bile. Elevations show impaired secretion from liver and bilary system 9. CA 19-9: diagnose GI cancer 10: Urine test: amylase, urobilinogen 11. Stool test:

a. fecal fat/steatorrhea: indicates malabsorption in small intestines b. clostridium difficile: toxin from bacteria causes severe diarrhea

Some of the major enzymes to know, please note these are not all of them, only the ones mentioned on the power points. Name Salivary Glands Parietal cells Chief Cells Gastrin (hormone) Where it is released Mouth Stomach Stomach Stomach Enzyme or hormone Enzyme:Amylase Enzyme:Hydrochloric acid Enzyme: Intrinsic factor Enyzme: Pepsinogen Hormone Function Breaks down carbs Digestion Absorbs b12 Digests proteins Releases parietal/chief cells when stomach is stretched Produce bicarbonate Secretes into small intestine for digestion Stimulates acinar cells Inhibits acid production Inhibits secretory mechanisms Digestion of fats

Ductal Cells Acinar Cells

Pancreas Pancreas

Enzyme Enzyme

Cholescystokinin(CCK) Secretin

Pancreas/small intestine Pancreas/small intestine Pancreas/small intestine Pancreas

Enzyme Hormone

Somatostatin Lipase

Hormone Enzyme

Pharmacology:
1. Antacids: interacts with acids at chemical level to neutralize a. aluminum, calcium salts, magaldrate, magnesium salts, sodium bicarb 2. H2 antagonists: prevents gastrin from stimulating the release of hydrochloric acid

a. cimetadine, famotidine, nizatadine, ranitidine 3. Proton Pump Inhibitor: inhibits final step of acid production, lowers acid in stomach a. lanzoprazole, omeprazole, esomeprazole, pantoprazole, rabeprazole 4. Antipeptic agents:coats injured area of stomach to prevent further injury from acid,such as an ulcer a. sulcrafate 5. Prostaglandins: inhibits secretion of gastrin, protects lining of stomach a. misoprostol 6. Digestive enzymes: salivart, creon, pancrease

Oral Cancer
Facts: 1. Most common sites: lips, lateral aspects of tongue, floor of mouth 2. risk factors: smokeless tobacco, tobacco, alcohol 3. curable if discovered early Patho 1. Squamouse cell carcinoma: surface of epithelium, slow growing, dysplagia 2. Basal cell carcinoma: primarily on lips, ulcer with raised border Clincial Manifestations 1. early: few to none in early stages 2. late: painless sore/mass that does not heal a. progression to tenderness, difficulty chewing, swallowing/speaking, coughing up tinged sputum, enlarged cervical lymph nodes Diagnostics: Oral exam, cervical lymph nodes, biopsy, CT scan Medical Management: 1. surgical resection a. hemiglossectomy: tongue b. total glossectomy: whole tongue c. Neck dissection with reconstructive surgery, nursing care postop: maintain airway, wound flap, hemorrhage, pain management. 2. radiation 3.chemo More on neck dissection: 1. radical: all lymph nodes removed 2. modified radical: less severe 3. complications: a. chyle fistula: milk like drainage from thoracic duct

b. hemmorage c. nerve damage

Mandibular Fractures:
1. Lower jaw fracture: a. Close fractures 2. Medical Management: a. Rigid fixation b. Bone grafting 3. Nursing Management: a. wire cutters at bedside b. oral suction c. exposed wires d. liquid diet e. airway

Pancreatitis
Functions of pancreas: 1. endocrine: insulin, glucagon, somatostatin 2. exocrine: amylase (carbs), trypsin (protein), lipase (fats) Pancreatitis: 1. associated with escape of activated pancreatic enzymes into the pancreas and surrounding tissue (normally enzymes are inactive until it reaches the small intestine, see below for more patho) 2. enzymes cause fat necrosis (autodigestion) and produce fatty deposits in abdominal cavity 3. most cases are a result of gallstones and alcohol abuse Patho: Bilary obstruction: 1. gallstones occlude common duct 2. obstruct flow of secretions 3. reflux of pancreatic secretions back into pancreatic duct 4. enzymes are activated, leads to autodigestion, vasodilation, increased vascular permeability 5. fluid electrolyte disturbance leads to fluid shift to interstitial space, leads to hypovolemic, leads to shock Clinical Manifestations: 1. Constant, knife like pain in right upper quadrant radiating to back 2. abrupt onset, no relief with emesis 3. increased pain with food or lying down 4. nausea/vomiting 5. jaundice

6. rigid abdomen, bruising around flank Assessment and diagnosis: 1. history of abdominal pain, risk factors physical exam 2. increase in serum amylase and lipase 3. urinary amylase, BUN, creatinine 4. WBC elevated (above 16,000) 5. fall in H/H (fall below 10) 6. Peritoneal fluid 7. Steatorrhea 8. CT with contrast 9. X-ray 10. hypocalcemia (calcium gets caught in fat necrosis), (fall below 8) 11. fluid shift (greater than 6L) 12. ERCG: provides detailed anatomy and pancreas and pancreatic and bilary ducts (for chronic pancreatitis) Complications: 1. fluid shift: need IV hydration 2. hypocalcemia: supplement with calcium gluconate 3. hyperglycemia 4. hypoxemia 5. ileus; intestinal obstruction 6. DIC: treat with FFP 7. Infection: IV antibiotics 8. pseudocysts Medical Management: a. NPO b. NG sunction c. H2 antagonists, proton pump inhibitors: to decrease acid d. Pain management e. intensive care ( for hemodynamic monitoring) f. respiratory care g. biliary drainage: to reestablish drainage from pancreas h. surgical intervention i. relieve pain and discomfort j. steroids k. insulin for hyperglycemia

Pancreatic Cancer:

Facts: 1. 5th leading cause of cancer deaths in U.S. 2. Occurs most frequently in 5th to 7th decade 3. 2 5% survival rate at 5 yeras Risk Factors: smoking, high fat diet, meat, exposure to industrial chemicals/toxins. Clincial Manifestations: 1. Early: vague, non specific, rarely diagnosed early 2. Late: metastasis to other organs, symptoms of obstruction Diagnostics: 1. CEA19-9 tumor marker 2. amylase, lipase 3. CT scan 4. ERCP 5. biopsy 6. paracenesis. Medical Management: 1. Surgical resection 2. chemo/radiation 3. palliative care

Disorders of the liver:


Functions: see above in anatomy section for details 1. storage: iron, magnesium, minerals, fat soluble vit. ect. 2. protection: detoxifies drugs, phagocytes, ect. a. first pass effect: the break down medications as they are ingested. 3. metabolism: breaks down proteins into albumin, amino acids, ect. Hepatic dysfunction: causes: 1. primary liver disease a. acute or chronic 2. obstruction of bile flow 3. derangements of hepatic circulation: this is really part of primary disease Symptoms of liver disease: 1. jaundice: a. hemolytic: from destruction of RBCs

b. hepatocellular: inability of damaged liver cells to clear bilirubin from blood c. obstructive: occlusion of bile duct d. hyperbilirubinemia 2. portal hypertension: when blood cant get through the liver because of liver disease, pressure builds up in veins between gut and liver (kinda like pulmonary hypertentionkinda) a. two major consequences: ascites: increase in fluid in abdomen (see below) varices: veins are not designed to handle the pressure build up, dissection and aneurysms occur. (see below for more patho) 3. Ascites (see below) 4. Esophageal varices: (see below) Ascites: 1. patho a. obstruction in liver b. increased cap pressure c. loss of albumin (responsible for holding water into vascular space through osmotic pressure) d. fluid shift into intraperitoneal space 2. Clinical Manifestations: a. increased abdominal girth b. rapid weight gain 3. medical management: a. diet b. diuretics c. bedrest d. paracentesis: to remove fluid to mainly aid in breathing e. transjugular intrahepatic portosystemic shunt (TIPS): to relieve pressure build up within liver, the shunt bypasses the liver entirely 4. Nursing: a. I and O b. abdominal girth measurement c. daily weights d. labs: ammonium levels e. frequent rest periods f. small frequent meals Esophageal varices: 1. patho: a. dilated veins found in submucosa of lower esophagus b. the veins that are created for collateral circulation are not designed to handle increase in pressure

c. these veins can bleed easily d. patient will cough up tons of blood, (remember: GI responsible for 20% of cardiac output) 2. clinical manifestations: a. hematemesis: vomiting of blood b. melena: black stools c. shock d. mental physical deterioration 3. nursing: monitor H and H, transfuse as necessarily, monitor for bleeding 4. Diagnostics: a. endoscopy b. portal system pressures 5. medical management: a. vasopressin: causing vein constriction b. balloon tamponade: not as common, but this is be on the test. c. endoscopy d. surgury: TIPS procedure, portocaval shunt, splenorenal shunt, H-graft mesocaval shunt Cirrhosis of liver: chronic disease, normal liver tissue is replaced by fibrotic tissue, this disrupts liver function 1. Alcohol is primary cause 2. men more than women 3. three types of cirrhosis a. alcoholic: most common b. post necrotic: secondary to viral hepatitis, have intermittent function of the liver c. biliary: obstruction of bile ducts, this is usually acute, not chronic d. cryptogenic: idiopathic (we dont know what happens, yay!) 4. Compensated: early disease a. enlarged liver b. abdominal pain c. intermittent mild fever 5. decompensated: late disease a. ascites b. liver shrinks c. portal htn d. varicies e. wasting syndrome f. bruising g. high risk for infection 6. Diagnostics: a. labs: ALT, AST, Bilirubin,ammonium levels : all go up. HandH and Electrolytes go down b. liver biopsy: need to lie on right side on a pillow that provides pressure

c. CT, MRI, ultrasound, radio-isotope liver scan 7. Medical management: a. treatment is symptomatic b. ETOH abstinence c. Medications: PPI, H2 blockers, antacids d. nutrition: low protein, high calorie diet Hepatic Encephalopathy: accumulation of ammonia and toxic metabolites in blood and brain, often associated with portal hypertension 1. patho: a. liver cells unable to convert to ammonia to urea b. causes brain dysfunction and damage c. by product of protein metabolism is ammonia 2. Clinical manifestations a. dementia type symptoms b. mood changes ect. c. asterixix: flapping tremor of hands 3. Assessment and diagnostics: a. ammonia level elevation b. EEG: shows generalized slowing c. fetor hepaticus: sweet slightly fecal odor to breath 4. Medical management; a. lactulose: promotes excretion of ammonia b. beomycin: suppress gi bacteria that produce ammonia c. avoid sedatives, tranquilizers, analgesics, tylenol, small frequent meals

Gastric cancer
Facts: 1. more men than women 2. diet of smoked foods, without fruits and vegs 3. chronic inflammation 4. poor prognosis, even at early stages 5. associated with pyloric obstruction, bleeding, severe pain, gastric perforation Patho: 1. adenocarcinoma most common, 86% occur in lining of stomach 2. can occur anywhere in stomach 3. tumor infiltrates surrounding mucosa Clinical manifestations 1. early: usually asymptomatic, pain relieved with antacids

2. late: dyspepsia (indigestion), anorexia, abdominal pain, constipation, anemia, weight loss, get full quickly from eating 3. commonly goes to liver, pancreas, esophagus, colon. Assessment and diagnostics: 1. EGD with biopsies, cytology 2. stools for occult blood 3. complete blood count Medical management: 1. surgery, removal of tumor a. complications: anastamosis leak, blood clots, bowel obstruction, B12 def, esophagitis, osteoporosis 2. pallative care common because the body loses the ability to absorb nutrients, and dumping/wasting syndrome develops Nursing care: 1. TPN post op, monitor electrolytes ect. a. high risk for infection due to high glucose of TPN b. need glucose checks 2. treatment of surgical wound

Colon cancer:
1. Patho: a. risking from lining of colon b. usually starts as benign polyp c. transforms to malignancy d. invades, destroys normal tissues 2. facts: a. third leading cause of cancer that is at primary site, not metastasized b. family history, chronic inflammation, high fat low fiber diets are all risk factors c. 95% adenocarcinoma 3. clinical manifestations: a. number one: change in bowel habits b. blood in stools c. unexplained anemia d. weight loss and fatigue e. right sided: dull abdominal pain, melana(black stools) f. left sided: associated with obstruction, abdominal pain, cramping, narrowing stools, constipation, distention, bright red blood. g. rectal lesion: painful straining at stool, rectal pain, feeling of incomplete evacuation

4. assessments/diagnostics a. stools for occult blood b. colonoscopy c. labs: CEA, usually done after cancer treatment to see if tumor has been eradicated 5. complications: obstruction, hemorrhage, perforation, sepsis, shock 6. Medical management: surgery is number one choice 7. Nursing management: a. nutrition: TPN or IVF until bowel function returns b. slow advancement of diet c. trail and error to find foods that control constipation or diarrhea 8. chart 38-10 on irrigating colostomy

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