NURSING 632 Gastrointestinal patho | DIGESTIVE DISORDERS | (Burns, Inflammatory bowel disease, peptic ulcers, projectile vomiting) | best to ace your exam

Manifestations of GI disorders I. Basic Diagnostic Studies II. Dysphagia III. Hiatal Hernia IV. GERD V. Gastritis: Acute and Chronic VI. Peptic Ulcers: Gastric and Duodenal VII. Dumping Syndrom e VIII. Pyloric Stenosis IX. Gallbladder disorders X. Jaundice XI. Hepatitis XII. Cirrhosis & Alcoholic Liver Disease XIII. Pancreatitis XIV. Chronic Inflammatory Bowel Disease: Crohn’s & Ulcerative Colitis XV. Appendicitis XVI. Diverticulitis XVII. Colorectal Cancer XVIII. Intestinal Obstruction XIX. Peritonitis Manifestations of Digestive Disorders Anorexia: Loss of appetite. Often precedes Nausea / Vomiting. Non-specific (common in many disorders) Nausea: Unpleasant, subjective feeling stimulated by Distention, Irritation, Inflammation in the GI Tract Retching: Usually precedes Vomiting (nothing expelled) Vomiting (emesis): Forceful expulsion of chyme from the stomach Activated by vomiting center in the medulla oblongata Activated by: Distention/ irritation of the GI tract Response to unpleasant smells or tastes, or ischemia Pain and Stress Increased IntraCranial Pressure (ICP) “Projectile Vomiting” Stimulation of chemoreceptor trigger zone in medulla by drugs or toxins Character of vomitus diagnositic: Blood: (Hematemesis): “Coffee ground” Yellow/Green: Bile Diarrhea: Excessive frequency of stools (acute or chronic) Large-Volume diarrhea: water/infection or rapid transit Small-volume diarrhea: contains blood, mucus, or purulence Steathorrhea: foul-smelling, greasy, fat stools that float (fat not absorbed) Hematochezia (Blood in stool): Occult (hidden), Frank (seen), or Melena (red-tarry stool) Risks of Diarrhea: Dehydration 1. Hypovolemia: tissue Ischemia leads to anaerobic metabolism / lactic acidosis 2. Loss of HCO3: GI stores much of Bicarb, leading to further metabolic acidosis Malnutrition Burns 2011 Manifestations of Digestive Disorders Constipation: Less frequent bowel movements resulting in hard stools Acute or Chronic May alternate with Diarrhea in Irritable Bowel Syndrome (IBS) Causes of Constipation:  Inadequate Dietary Fiber intake Inadequate Fluid intake  Muscle weakness and Inactivity (Failure to respond to defecation reflex)  Neurologic Disorders Obstructions: Tumors or Strictures  Medications: Opiates, Iron Supplements, Bulk laxatives (without enough water) Chronic or Severe Constipation: May lead to….  Hemorrhoids Diverticulosis / Diverticulitis  Impaction or Obstruction Colon Cancer Fluid Balance Disorders: Dehydration and hypovolemia Electrolyte Imbalances Na+ Sodium is lost in BOTH Vomiting and Diarrhea Cl- Chloride is lost from Gastric secretions (Vomiting, NG suction). Lost through H-Cl K+ Potassium is lost with Diarrhea Acid-Base Imbalance: ***KNOW Vomiting: initially, Vomiting causes Metabolic ALKALOSIS (loss of H+) prolonged, Vomiting causes Dehydration, anaerobic metabolism, and ACIDOSIS Diarrhea: Loss of Bicarb (HCO3) and anaerobic metabolism (dehydration) lead to Metabolic ACIDOSIS Burns 2011 Radiographs Basic Diagnostic Tests X-ray (KUB (kindey, urine, bladder), Barium Swallows) CT Scan and MRI Endoscopy (upper GI), Colonoscopy (rectum, colon), Sigmoidoscopy (rectum, colon) Laboratory analysis of stool specimens or gastric washing Infection (O&P, Ova & Parasites) Blood (Hemoccult, Gastroccult) Tumors Malabsorption problems (steatorrhea in Cystic Fibrosis) Blood Tests Liver Function: Serum protein, coagulation, Liver enzymes (AST/ALT), Bilirubin Pancreatic Function: Pancreatic enzymes (Lipase, Amylase) Stool analysis of enzymes and fat content Other: Tumor markers Burns 2011 Dysphagia: Difficulty Swallowing Causes: Neurologic deficit CN V, VII, IX, X, XII Muscular disorder Achalasia Mechanical obstruction Congenital atresia Congenital fisula Compression Fibrosis Risks: Aspiration Burns 2011 Hiatal Hernia: Protrusion of (part of) stomach through opening (hiatus) of diaphragm Contributing Factors: Shortening of Esophagus Weakness of Diaphragm Increased abdominal pressure (pregnancy) Signs & Symptoms: Heartburn Frequent Belching or regurgitation Increased discomfort with coughing, lying down after eating, or bending over Dysphagia Mild, persistent chest pain after meals Two Types: Burns 2011 GERD: Gastro Esophageal Reflux Disease Periodic flow of gastric juice into the unprotected esophagus (past cardiac sphincter) Often seen in conjunction with hiatal hernia Delayed gastric emptying may be a factor Signs & Symptoms: Heartburn 30-60 minutes after eating, or at night Frequent reflux of gastric acid can lead to… Inflammation and ulceration of gastric mucosa (ulcer) Eventual fibrosis and stricture of esophagus Increased risk of esophageal cancer (Barrett’s Esophagus—precursor) Treatment: Type-2 Antihistamines: H-2 Blockers (Ranitidine, Cimetidine) – quick acting Proton Pump Inhibitors: PPI’s (omeprazole, desmeprazole) – takes a little longer Burns 2011 Gastritis: Acute and Chronic Definition: inflammation of the stomach Acute Gastritis: Gastritis mucosa appears inflamed, edematous. May be ulcerated or bleeding with severe damage or poor circulation:  Infection (bacterial or viral) Allergies (shellfish or drugs)  Spicy / irritating foods Excessive Alcohol intake  Ulcerative drugs (ASA, Ibuprofen) Corrosive / toxic subtances (battery acid)  Radiation or Chemotherapy Signs & Symptoms:  Anorexia Nausea / Vomiting Hematemesis (with ulceration) Can lead to: Dehydration Metabolic Acidosis Chronic Gastritis: Characterized by atrophy of the mucosa, with loss of secretory glands Achlorhydria Lack of Intrinsic Factor (Vit B12 Deficiency  Pernicious Anemia) Often Seen with:  Chronic Peptic Ulcers Alcohol Abuse Autoimmune disorders Elderly Signs & Symptoms: *Mild Gastric Discomfort *Anorexia *Food Intolerance (spicy) Can lead to: Peptic Ulcers Gastric Carcinoma Burns 2011 Peptic Ulcer Disease: Gastric & Duodenal Most Common: Proximal Duodenum (where low-pH stomach contents empties) Also present in the stomach or lower esophagus Characteristics: Single, small, round cavities with smooth margins that penetrate mucosa Once mucosa is penetrated, acid and pepsin cause further damage to impaired gastric tissue Ulcers can eventually erode through muscle layer causing gastric perforation!  Peritonitis, as gastric contents empty into sterile peritoneum Burns 2011 Peptic Ulcers: continued Pathophysiology: An area of inflammation surrounds the crater When the erosion invades a blood vessel, bleeding ulcer occurs. Bleeding may be:  Persistent loss of small amounts May manifest itself as Iron-deficiency anemia or occult blood in stool  Massive hemorrhage (depends on blood vessel eroded) Etiology:  Helicobacter Pylori (H.pylori) found in most cases  Inadequate blood supply (prolonged stress, glucocorticoid secretion or administration)  Ulcerative agents (ASA, Ibuprofen, Alcohol, Steroids)  Atrophy of gastric mucosa (chronic gastritis)  Increased acid-pepsin secretions:  Increased gastrin secretion (caffeine, ETOH, Increased vagal stimulation)  More common in Men, especially in Western Countries  More Common with Blood type O Signs & Symptoms: Epigastric pain / burning, especially 2-3 HOURS after eating or at night Pain often relieved by ingestion of food or antacids Heartburn / Nausea / Vomiting / Weight loss / *Iron Deficiency Anemia or occult blood in stool If severe, black tarry stools likely (melena) Burns 2011 Stress Ulcers: Peptic Ulcers: continued Etiology Severe Trauma Massive Burns (Curling’s ulcers)  Serious systemic problems (hemorrhage or sepsis) Pathophysiology: Multiple ulcers, usually gastric, form within hours of the precipitating event!  As blood flow is reduced to gastric mucosa from stress, there is reduced secretion of mucus and epithelial regeneration, which act as a protective barrier to the effects of acidic chyme  The acid barrier is lost; so, acid diffuses into the sensitive mucosa Treatment: Medications administered prophylactically to decrease acid release  Proton Pump Inhibitors (-prazoles; pantoprazole, esmoprazole) Peptic Ulcers: Healing – difficult to heal  Granulation tissue forms deep within cavity  Epithelial cell regenerates from the edges of the fragile granular tissue  Difficult due to constant exposure to irritants Often, granular tissue broken down by the acidic chyme Fibrous tissue forms at site, leading to scar tissue and impaired blood supply Complications:  Hemorrhage (with blood vessel ulceration)  Bacterial peritonitis (with gastric muscle perforation into peritoneum)  Obstruction: if ulceration / fibrous tissue narrows passageway, such as duodenum Burns 2011 Dumping Syndrome: Loss of Gastric Emptying Control Pathophysiology: Large amounts of ingested food is quickly “dumped” into the intestines Hyperosmolar chyme draws more fluid from the vascular compartment  Causes abdominal distention and increased motility  Fluid and electrolytes are then lost in diarrhea Hypoglycemia results 2-3 hours after meals from “dump” loss Signs & Symptoms: Cramps Nausea Diarrhea Hypovolemia: tachycardia, dizziness Hypoglycemia: 2-3 hours after eating Etiology: Gastric Resection:  Loss of pyloric sphincter in surgery (usually controls slow chyme release into duodenum Burns 2011 Pyloric Stenosis Definition: Narrowing or obstruction of the pyloric stenosis, inhibiting free-emptying Etiology: Developmental Defect (infants) Acquired: Usually a result of scar tissue (ulcers) Signs & Symptoms: Developmental: Episodes of Regurgitation Projectile vomiting after eating Dehydration Small, infrequent stools Failure to thrive / failure to gain weight Irritability (malnutrition, hunger) Acquired: Persistent feeling of “fullness” Increased vomiting Contains food from recent and past meals Burns 2011 Gallbladder Disorders: Cholecyst Cholelithiasis: “Gallstones” Formation of gallstones, which are masses of solid material /calculi formed in bile  Form in bile duct, gallbladder, cystic duct  Consist of cholesterol, bile pigment (bilirubin), Calcium salts Signs & Symptoms: Often asymptomatic Often precipitated by fatty meal Sudden waves of pain (biliary colic) in RUQ / epigastrium that  Often radiates to back / Rt shoulder Nausea / Vomiting Jaundice: indicates bile backed up into the liver, and thus blood (posthepatic jaundice) Leukocytosis / Fever Pathophysiology: Presence of stones may cause inflammation in the gallbladder wall (cholecystitis) Infection can result from E. coli & enterococcus When a stone obstructs bile flow: biliary colic: severe spasms An obstruction at the sphincter of Oddi: can cause pancreatitis secretions backup into pancreas cause self-digestion Burns 2011 Gallbladder Disorders: Continued Cholelithiasis / Cholecystitis: (continued) Etiology: Cholesterol Stones:  More common in women  Hypercholesterolemia  Obesity  Multiparity or Oral Estrogen Contraceptive use Bile Stones: Hemolytic anemia sufferers  Alcohol Cirrhosis – effects liver  Biliary tract infection Other Gallbladder Conditions: Cholangitis: inflammation of gallbladder and cystic duct Choledocholithiasis: Obstruction of the biliary tract (duct) by gallstones Burns 2011 Jaundice: (hyperbilirubinemia “icterus”) Definition: Yellowish color of the skin and tissues that results from high levels of serum bilirubin  Usually evident in the sclera first Classifications of Jaundice:  Prehepatic: Etiology is “before liver”  Excessive RBC destruction (hemolytic anemias)  Liver Function is normal! But is unable to handle workload of unconjugated bilirubin Ex: hemolytic anemias, blood reactions, newborn hemolysis  Intrahepatic: Etiology is “liver disease”  Impaired uptake of bilirubin in blood  Decreased conjugation of bilirubin by hepatocytes  Posthepatic: Etiology is “after liver”  Obstruction of bile flow into gallbladder or duodenum  Bile “traffic jam” stops liver bilirubin flow  Subsequent backup of bile into the blood Burns 2011 Etiology: Hepatitis: Inflammation of the liver Idiopathic: (fatty liver) Infection: both local and systemic Toxicity: Drug (Acetaminophen) or chemicals (inhalants, ETOH) Viral Hepatitis: infection by a group of viruses that specifically target the hepatocyte Hepatitis A (HAV) Hepatitis B (HBV) Hepatitis C (HCV) Hepatitis D (HDV) Pathophysiology: May be asymptomatic carriers (HBV, HCV, HDV) Liver cells are damaged by: 1) Direct Action of Virus (Hepatitis C) 2) Cell-mediated immune response to the virus (Hepatitis B) Cell injury leads to inflammation / necrosis in liver Depending on cell damage: 1) Cells may regenerate, or… 2) May develop fibrous tissue that affects hepatic function Chronic Inflammation with HBV, HCV, HDV (inflammation/necrosis Greater than 6 months)  Eventually causes permanent liver damage and cirrhosis  Increased incidence of hepatocellular cancer Signs & Symptoms: Stage 1: (Pre-Icteric) Fatigue Malaise Anorexia Malaise Sometimes RUQ pain Stage 2: (Icteric) Jaundice Clay stools Dark urine Pruritic skin Hepatomegaly Severe Cases: Blood clotting prolonged (prothrombin / fibrinogen) Stage 3: (Post-Icteric / “Recovery”)  Marked reduction in symptoms versus Liver Failure (Icteric) Burns 2011 Cirrhosis Definition: Progressive destruction of liver tissue  Leads to eventual liver failure when 80-90% of liver destroyed  25,000 deaths annually  50% are Alcohol-related Classified by the structural changes or cause of the disorder  Alcoholic Liver Disease  Biliary Cirrhosis  Postnecrotic cirrhosis  Metabolic cirrhosis Pathophysiology: Extensive diffuse fibrosis and loss of lobular organization  Regenerated tissue can be non-functional because of vascular disorganization Effects of cirrhosis evolve from two factors: 1) Loss of liver function 2) Interference with blood and bile flow in liver  Decreased removal and circulation of bilirubin  Decreased bile production; Impaired absorption of nutrients (especially fat-soluble vitamins) KADE  Decreased blood clotting factors (fibrinogen & prothrombin) and plasma proteins (Albumin)  Impaired glucose / glycogen metabolism (hypoglycemic risk)  Inadequate storage of Iron and Vitamin B12 (Folate)  Decreased Aldosterone & Estrogen activity  Decreased removal of toxic substances such as Ammonia and Drugs Burns 2011 Alcohol Liver Disease: Cirrhosis: continued Pathophysiology: There are several steps to Alcohol Liver Disease… Alcohol and metabolites (acetyladehyde) are toxic to the liver Malnutrition may aggravate liver damage. First, “Fatty liver”. Accumulation of fat cells in liver Hepatomegaly. Asymptomatic Second, “Alcohol Hepatitis”. Inflammation and cell necrosis; Fibrous tissue forms Lastly, “End-Stage Cirrhosis”. Hepatitis Symptoms become exacerbated Significant replacement of hepatocytes with fibrotic tissue Portal Hypertension: Congestion of liver “traffic jam” causes increased pressure, edema. Impaired digestion and absorption Signs & Symptoms: Fatigue, anorexia, indigestion, weight loss Portal Hypertension & low Albumin: Ascites General edema Esophageal varices, hemorrhoids Decreased clotting factors and immunity Anemia (marrow shift to RBC’s) Leukopenia / Thrombocytopenia Splenomegaly (RBC destruction) Increased bleeding / purpura Hepatic encephalopathy: High Ammonia (CNS toxin) Tremors, confusion, coma, death Increased Aldosterone / Estrogen / Androgen production Gynecomastia, impotence, irregular menses Fluid Retention Jaundice (Intrahepatic): elevated unconjugated bilirubin Pruritis Burns 2011 Cirrhosis: Summarized Burns 2011 Acute Pancreatitis Definition: inflammation of the pancreas from autodigestion of the tissues May be Acute or Chronic Acute: Medical Emergency Pathophysiology: Premature activation of proenzyme trypinogen into trypsin Trypsin converts other proenzymes into active pancreatic enzymes, Amylase & Lipase Trypsin, Amylase, Lipase digest the pancreas (instead of intestinal contents) Autodigestion  Causes massive inflammation, bleeding, and necrosis Etiology: Gallstones Alcohol abuse Signs & Symptoms: Severe epigastric or abdominal pain radiating to the back.  Pain Increases when supine (flat) Signs of shock (tachycardia, hypotension) Low-grade Fever Abdominal distention and decreased bowel sounds Diagnostic Tests: Amylase (12-24 hours) Lipase (approx 1 week) Hypocalcemia Leukocytosis Burns 2011 Chronic Inflammatory Bowel Disease: Crohn’s Disease & Ulcerative Colitis Etiology: Genetic Factor appears to be involved  Familial: More common in whites, namely Ashkenazi Jews (Eastern Europe) Onset of Development:  Crohn’s Disease: Adolescence  Ulcerative Colitis: Young Adults (20-30) Both characteristically have exacerbations and remissions and diversity in presentation Crohn’s Disease  “Skip lesions” Site: Distal ileum Signs/Sx: Soft, semi-formed stools Melena, if ulcers RLQ pain Anemia, Fatigue, Weight loss Complications: Hypoproteinemia Avitaminosis Malnutrition Steatorrhea—fatty stools Adhesions (thick walls) Fistulas Burns 2011 Colorectal Cancer In U.S., ranked highly lethal in those Over 50 Death can be prevented by early detection and treatment of precancerous polyps Fecal Occult Blood tests after Age 40 Sigmoidoscopy & Colonoscopy every 3-5 years after 50 Pathophysiology: Most develop from adenomatous polyps, getting larger and dysplastic (malignant) Can be on any portion of colon Carcinoma invades wall, mesentary, and lymph nodes causing metastasis to liver Staging based on TNM system (Tumor, Node, Metastasis) Etiology: Primary in persons >55 year More common in Western Hemisphere Risk Factors:  Familial multiple polyposis  Long-term ulcerative colitis  Diet high fat high red meat low fiber Burns 2011 Chronic Inflammatory Bowel Disease: Ulcerative Colitis Pathophysiology: Inflammation of the mucosa and submucosa at th ebase of the crypts of Lieberkuhn (mucus-secreting cells of colon) Starts in the Rectum and advances superiorly up colon The tissue is friable and ulcerations develop Granular tissue is susceptible to bleeding In severe episodes: Toxic megacolon as inflammation blocks peristalsis  Obstruction and dilation of colon (usually transverse colon) Signs & Symptoms: Diarrhea Frequent, watery, blood-containing Abdominal cramping Tenesmus: rectal spasms Rectal bleeding (anemia) Fever Weight loss Often requires bowel resection Burns 2011 Appendicitis Definition: Inflammation and infection of the vermiform appendix Incidence: Occurs in 10% of population; common in Young Adults Pathophysiology: Obstruction of the appendiceal lumen is commonly the initiating factor Fluid builds up inside appendix and microorganisms proliferate Appendiceal wall becomes inflamed and exudate forms ischemia leads to necrosis Bacteria may escape through inflamed wall and cause local bacterial peritonitis  peritonitis may spread along peritoneal membrane if not resolved If left, the appendix will undergo necrosis and –possibly—perforation Signs & Symptoms: General umbilical pain  localizes to RLQ (McBurneys Point) Low-grade fever & leukocytosis Nausea / Vomiting Rebound tenderness RLQ Peritoneal irritation signs (Psoas / Obturator) Rupture may relieve pain temporarily Peritonitis  Boardlike abdomen  Tachycardia  Hypotension Resolution: Appendectomy Burns 2011 Intestinal Obstruction Burns 2011 Diverticulosis: (Diverticulitis) Definition: Diverticulum is a herniation or “pouching out” of the mucosa through the colon wall Frequently occurs at Sigmoid Colon Diverticulosis: asymptomatic diverticular disease. Pouches there; no problems. Diverticulitis: inflammation of the diverticula causing pain, cramping. Pathophysiology: Gaps form between the bands of longitudinal muscles in colon wall In the presence of high pressure, weak areas of the wall bulge outward forming a pouch Causes: Chronic constipation Irregular bowel habits Aging Complications: Obstruction Perforation with peritonitis Abscess formation Signs & Symptoms: Mild:  Abdominal pain Diarrhea  Constipation Flatulence Acute Diverticulitis:  Statis of feces in the pouch  LLQ pain (Sigmoid colon)  Mild fever / leukocytosis  Nausea / Vomiting  May lead to obstruction / perforation Burns 2011 Abdominal Obstruction: Dangerous Cycle 1. Obstruction Occurs 2. Fluid/gas build up 3. Distention / colic 4. Vomiting / dehydration / electrolytes imbalance 5. Wall pressure = More fluid shifts in 6. Third-spacing / hypovolemic Shock 7. Edema and Ischemia / more edema and less peristalsis 8. Increased permeability of intestinal wall allows bacteria to cross intestinal wall 9. Leads to peritonitis 10. More hypovolemic shock! Burns 2011 Peritonitis: Inflammation of the peritoneal membrane Caused by: Chemical Irritation Bacterial invasion of the peritoneal cavity (peritoneal cavity is normally sterile)  Trauma  Surgery  Appendicitis  Bowel Obstruction Chemical Peritonitis: Enzymes released with pancreatitis  pepsin, amylase, lipase Urine from a ruptured bladder Chyme from a perforated ulcer Bile escaping from a perforated gallbladder Blood Bacterial Peritonitis Trauma Appendicitis Intestinal Obstruction / Ischemia Abdominal surgery Pelvic Inflammatory Disease (PID) Infection from the uterus into the fallopian tubes Provides direct-access to peritoneum Burns 2011 Show Less