Disorders of the Gastrointestinal System & Liver University of San Francisco Dr. M. Maag ©2003 Margaret Maag

2 Class 12 Objectives Upon completion of this lesson, the student will be able to –list the pathologies associated with GI motility. –determine the infectious agents associated with GI disorders. –predict those at risk for GI bleeding and the S & S these individuals could present. –analyze the clinical manifestations of severe liver impairment. –state the normal clotting mechanisms and the role vitamin K plays in blood clot formation. –state the cause(s) of DIC and list the S&S.

3 Pathologies of GI Motility Diarrhea Is an > in frequency, fluid and / or volume of stool –Osmotic: the presence of nonabsorbable substances in the intestine causing water to be drawn into the lumen by osmosis sorbitol-containing liquid medications; tube feedings lactose intolerance –Secretory: excessive mucosal secretion of fluid & electrolytes related to: gastroenteritis (E. Coli), rotavirus, laxative abuse, hyponatremia, fecal impaction

4 Pathologies of GI Motility Diarrhea Motile: > motility is d/t stimulation caused by inflammation or obstruction resection of small intestine, fecal impaction, early bowel obstruction (e.g. Bezor) Clinical Manifestations: crampy abdominal pain, > bowel sounds prolonged diarrhea leads to f & e imbalances and dehydration infants & elderly are at risk: check hydration & f/e status

5 Case Study A 72 year-old woman, who lives alone, has a history of laxative abuse. What type of diarrhea is she at risk for? What type of fluid imbalance is she at risk for? What would you expect her VS to be? Her electrolytes upon admission to the hospital are: Na+ = 155; K+ = 3.5; Cl- = 116; Hct = 45% Clinical manifestations? Treatment? Which acid-base disturbance is she at risk for? Why?

6 Pathologies of GI Motility Constipation Defined as infrequent or difficult defecation: most frequently c/o digestive disorder Etiology : functional disorder of bowel motility incidence is > in the elderly; diet poor in fiber & fluids; anatomic lesions; drug therapy d/t poor neural stimulation of GI motility, abdominal muscle weakness, bowel obstruction Mega colon, opiates, hypothyroidism, diabetic neuropathy, sedentary lifestyle, low residue diet

7 Pathologies of GI Motility GERD Reflux of gastric contents into lower esophagus resulting in clinical symptoms or structural alterations in the esophageal tissues (reflux esophagitis) 94% of the individuals have hiatal hernias a protrusion of some part of the upper portion of stomach through esophageal hiatus and then into the thorasic cavity Delayed gastric emptying is seen primarily in: diabetics, cigarette smoking, and ETOH abuse dysphagia, eructation, heartburn, GI bleeding, abdominal discomfort when lying down, dyspnea may be present Heartburn, ulcerations, precancerous lesions

8 Fecal Incontinence Inadequate control of defecation in an adult due to weak pelvic floor muscles and / or weakness of the external anal sphincter Common causes: Clostridium difficile responsible for nosocomial diarrhea Impaction, laxative abuse, hyperosmolar tube feedings Risk factors: older persons in long-term care institutions (Bliss, et al., 2000)

9 Intestinal Obstructions Large Bowel A large bowel obstruction is an emergency condition that requires early & prompt surgical intervention Etiology: infectious / inflammatory, neoplastic, or mechanical pathology (colorectal cancer) Rotation or twisting of the cecum or sigmoid colon will cause abrupt onset of symptoms Immediate abdominal distention –Decreases the ability to absorb F & E

10 Intestinal Obstructions Sigmoid volvulus usually seen in the older individual with a hx of straining at stool Symptoms: abdominal distention, nausea, vomiting, and crampy abdominal pain; check history of flatus and BMs Abrupt onset is indicative of an acute obstruction –Sudden onset due to torsion or hernia A chronic hx of constipation is related to a dx of diverticulitis or carcinoma Obstipation (no flatus or BM) & loss of weight = carcinoma

11 Intestinal Obstructions Paralytic ileus or “silent bowel” is most often seen after abdominal surgery & anesthesia bowel activity is < d/t lack of neural stimuli (“functional”) this can lead to “mechanical” obstruction d/t accumulation of feces Hernias: a loop of bowel protrudes through abdominal wall inguinal canal, umbilicus, or incisional scar tissue caused by heavy lifting, straining, or coughing

12 Disorders of GI Bleeding Upper: includes the esophagus, stomach, duodenum peptic ulcer disease (PUD) or esophageal varices Lower: includes the jejunum, ileum, colon, rectum colorectal cancer, polyps, hemorrhoids, IBD Manifestations: hematemesis bright red blood in the stool (“hematochezia”) black,dark, tarry stools (“melena”) “occult” bleeding (invisible blood in the stool) Tx: find the underlying cause; fluid volume replacement; endoscopy or colonoscopy; medical and /or surgical tx

13 Disorders of GI Bleeding Results Shock will ensue if massive (25% EBL within hours) bleeding occurs Metabolic acidosis, prerenal failure, bowel infarction will occur < coronary & cerebral blood flow Death –See McCance, Figure 38-1, p. 1265

14 Peptic Ulcer Disease An inflammatory disorder causing deep erosion of stomach or duodenal mucosa by HCL & pepsin At risk: infection with H. pylori; > NSAIDS; > secretion of HCL as seen in Zollinger-Ellison syndrome Etiology: age, family hx –> mucolytic enzymes; may lead to pyloric obstruction, bowel perforation and ultimately peritonitis Sx: hallmark sign = upper gastric pain –Emergency:hematemesis, melena, occult blood, shock

15 Peptic Ulcer Disease Treatment includes: –< stress –< ETOH intake –screen for H. pylori (C-urea breath test) –frequent small meals –avoid calcium based antacids d/t > gastrin release –H2 blockers (Tagamet & Zantac) –Insert NG tube for severe bleeding and gastric lavage

16 Gastric, Duodenal, Stress Ulcers Gastric –> cancer risk –Lack of remission or exacerbation periods Duodenal –Younger age at onset –Strong familial history –Ulcerogenic drugs used –Nocturnal pain more prevalent Stress –Systemic trauma, severe illness, neural injury

17 Intestinal Bowel Disorders Ulcerative Colitis –Inflammatory disorder with eventual erosion of the colon Crohn’s Disease –Effects any part of the GI (mouth to anus) –Smoking, diet, and/or bacteria may influence –Cytokine-mediated damage

18 Gastric Cancer Adenocarcinoma is the primary malignant neoplasm 8th leading cause of mortality r/t cancer in US Epidemiology: year olds; 2 times greater incidence in men vs. women Risk factors: H. pylori, < socioeconomic class, consumption of pickled foods, improper food storage, radiation exposure Etiology:chronic inflammation, dietary influences, genetic & environmental factors

19 Gastric Cancer Sx: Vague early sx with weight loss; indigestion; abdominal distention; mild pain induced with or without food; chronic blood loss leads to anemia; occult blood in stool Tx: reduce risk factors; total or partial gastrectomy; lymph node resection; chemotherapy & radiation 15% of cases lend a 5-year survival rate

20 Peritonitis Etiology: Inflammation of peritoneal membrane sterile: rupture of biliary system; hemorrhagic pancreatitis, endometriosis, surgical procedures infectious: bacteria from ruptured bowel or appendix; introduction of bacteria from abdominal trauma or invasive procedures (e.g. peritoneal dialysis) Sx: Circulatory volume collapse, septic shock causing a high mortality rate, absent bowel sounds, pain, abdominal distention & rigidity, > nausea & vomiting, paralytic ileus Tx: antibiotics, NG tube, IV fluids, surgical repair of etiology

21 Colorectal Cancer “Patients with long-standing ulcerative colitis have been shown to be at increased risk of developing colorectal cancer” (Medscape, 1999) Involves a primary malignant tumor of the rectum or colon 2nd leading cause of cancer death in US > incidence in 50 year olds > fat and poor fiber diet; > ETOH consumption; cigarette smoking; obesity; sedentary life style Exact etiology unknown…> incidence with polyps

22 Colorectal Cancer Symptoms: –fecal occult blood or ulcerative lesions manifest as anemia or rectal bleeding distention, abdominal pain, vomiting, constipation –metastatic disease: weight loss, anorexia, possible palpable mass Prevention: ASA may < risk; routine monitoring for guaic (+) Tx: colostomy repair; permanent colostomy for rectal tumors

Liver Disorders

24 Portal Hypertension Fibrosis of the liver structures causes an increased resistance to blood flow within the liver, therefore an elevation in the portal venous pressure –This > in pressure can cause esophageal varices and hemorrhoids and 3rd spacing of fluid into peritoneal cavity (ascites) “Hepatic encephalopathy” can occur d/t the toxic effects of altered metabolism –cerebral edema & IICP can result from severe cases

25 Ascites A common feature of liver failure. Basic mechanisms include: –an increase in portal hypertension –sodium and water retention –decreased blood oncotic pressure secondary to a low serum albumin level

26 Cirrhosis Focal or diffuse inflammation and liver cell necrosis that causes severe changes in the structure and function of liver cells Inflamed liver cells compress the liver lobule and cause increased resistance to blood flow and portal hypertension –Liver tissue is regenerated, but not in the normal fashion –Fibrotic changes are irreversible, causing liver dysfunction

27 Cirrhosis Alcoholic: results from long-term alcohol abuse; most common cause in the USA Biliary: caused by a < in bile flow; commonly caused by long-term obstruction of bile ducts Cardiac: caused by long-term right-sided CHF –results in < oxygenation of liver cells Postnecrotic: result from hepatoxins, chemicals, or infection with Hepatitis B or C –massive death of liver cells & associated with cancer

28 Viral Hepatitis Inflammation of the liver followed by the necrosis of hepatic cells –Caused by infection with one or more hepatoviurses Types: A, B, C, D, E & G Little is known about the blood-borne “G” –Hepatic inflammation may occur d/t toxins, autoimmunity, and metabolic disorders htmhttp:// htm

29 Viral Hepatitis HAV is found primarily in contaminated food and water –Transmitted by the enteric route (oral-fecal) –Poor hand washing or unsanitary food preparation –During the viremic phase of acute infection it can be spread via blood exposure (unusual) –Virus infects the liver and is excreted via the feces –Most contagious before presentation of S & S –Prevalence of immunity to HAV has decreased to < 25% of US adults (DiCarlo, 1999)

30 Hepatitis A Virus Hepatitis A antibodies show up in the blood 2-6 weeks following exposure & remain indefinitely in the blood Clinical manifestations: fever, chills, brown urine, anorexia, irritability, clay-colored feces, N&V, headache Liver function tests & coagulation tests are abnormal

31 Hepatitis B Virus HBV is transmitted via blood & body fluids –“Infected adults have a 50% chance of developing acute symptoms, but only a 10% chance of developing chronic infection” (DiCarlo, 1999) –In the US, 60% of hepatitis B virus infections are sexually transmitted unprotected sex with multiple partners –A vaccine has been available since 1982 immunity develops in more than 90%

32 Hepatitis B Virus Hepatitis antigen-antibody complexes can be detected from 1-10 weeks after exposure to the virus Incubation period for HBV can last from 6 weeks to 6 months; clinical S & S of the acute phase are the same as HAV Patients have an > chance of “fulimant hepatic failure”…a sudden degeneration of the liver & loss of all normal liver functions

33 Hepatitis C Virus HCV is a blood-borne type of hepatitis –Formerly known as non-A, non-B hepatitis –Common among hemophiliacs & IV drug abusers –40% of the cases are idiopathic –Incubation period of 6-7 weeks and acute infection results in a 30-40% chance of jaundice –70% will develop some form of chronic hepatitis (DiCarlo, 1999) –Sexual transmission accounts for 15-20% of the infections in the US (DiCarlo,1999)

34 Other Types of Viral Hepatitis HDV is also known as the “delta virus” –It is a blood-borne virus that must coexist with HBV in order to exert its viral activity –This covirus heightens the course and outcome of illness with HBV HEV is the “enteric” form of non-A, non- B hepatitis –is generally seen in underdeveloped countries

35 Precautions Use of gloves while handling all items contaminated with client’s body secretions Use of disposable patient care items, such as thermometers, dishes, eating utensils Use of private bathroom and room for clients who are incontinent of feces. Double bagging and labeling of linen or any hospital equipment that is contaminated with feces or blood (Hartshorn, 1997, p. 462)

36 Clotting Factor Defects Review normal function of clotting factors Inherited disorders: deficiencies of clotting factors –Hemophilia's –Willebrand disease Acquired cases –Deficient synthesis of clotting factors by liver –Liver disease, dietary deficiency of Vitamin K Factor 7 is first to decline  then factor 2 and 10 –Thrombocytopenia may occur due to splenomegaly  liver disease and portal hypertension

37 Disseminated Intravascular Coagulation Acquired complex clinical syndrome –Due to > protease activity in the blood caused by > release of thrombin –Acute, severe,life-threatening process –Massive hemorrhage and thrombosis –Becomes a chronic, low-grade condition Minor lab abnormalities with sub acute hemorrhage and microcirculatory thrombosis May involve many organs

38 References Bliss, D. Z., Johnson, S., Savik, Clabots, C. R., & Gerding, D. N. (2000). Fecal incontinence in hospitalized patients who are acutely ill. Nursing Research, 49(2), Hansen, M. (1998). Pathophysiology: Foundations of disease and clinical intervention. Philadelphia: Saunders.