Digestive Disorders.pdf

NURS 202 Pathophysiology Student Self Review: A&P ❖ Structure & Function of Digestive System...

NURS 202 Pathophysiology Student Self Review: A&P ❖ Structure & Function of Digestive System Lecture ❖ Alterations of Digestive Prepared by: Function Nicole L’Italien RN BScN MN NCBNP CNC Revised Jody Vaughan RN BScN MEd Fall 2016 Reproduction or use of contents without written permission prohibited ❖1 ❖2 Alterations of Digestive Function ❖3 Jody Vaughan 1  Disorders of the GI Tract ❖4 S&S of GI Dysfunction ❖5 S&S of GI Dysfunction ❖ Common S&S of many GI tract disorders include: ❖ Anorexia ❖ Nausea and vomiting (AKA ?) ❖ Abnormal BMs ❖ Constipation ❖ Diarrhea ❖ ABD Pain ❖ GI Bleeding ❖6 Jody Vaughan 2  S&S of GI Dysfunction Anorexia _____________ ❖7 S&S of GI Dysfunction Nausea & Vomiting Common stimuli include: ❖ Stomach or intestinal distension ❖ Torsion of an intra-abdominal organ(s) ❖ Motion ❖ Severe pain ❖ Stimulation of chemoreceptors in medulla ❖8 S&S of GI Dysfunction Constipation Infrequent or difficult BMs Can be caused by: ❖ Hypothyroidism ❖ Opiates * ❖ Aging * ❖ Neurogenic disorders of large intestine ❖ Low residue diet & Low activity level * ❖ Mechanical or functional (eg lesions) ❖ Constant/frequent suppression of stool * ❖9 Jody Vaughan 3  S&S of GI Dysfunction Diarrhea ↑ in the frequency, fluid consistency, and volume of BMs ❖ Acute or chronic ❖ Can be classified as ❖ Large volume ❖ Small volume ❖ 3 mechanisms: 1. Osmotic – H20 drawn into intestine (eg lactase/ pancreatic/celiac) 2. Secretory – secretion of water into the intestinal lumen exceeds absorption.(eg Colitis/ viral or bacterial infections) 3. Motility – impaired absorption (eg Small bowel resection) ❖10 S&S of GI Dysfunction ABD Pain Mechanical, inflammatory, or ischemic causes ❖ Mechanical - Stretching & distension activates nerve endings; traction on peritoneum increases tension ❖ Inflammatory - Biochemical mediators stimulate nerve endings; Edema & vascular congestion cause painful stretching (mechanical) ❖ Ischemic – Obstruction of blood flow (eg bowel obstruction) or a vessel thrombosis results in ischemia & metabolites that stimulate pain receptors ❖11 S&S of GI Dysfunction GI Bleeding ❖ Life threatening, depending on rate & volume of blood loss ❖ Origin of bleed can be 1. Upper GI 2. Lower GI ❖ Common terms associated with GI bleeding: ❖ Hematemesis ❖ Melena ❖ Hematochezia ❖ Occult bleeding ❖12 Jody Vaughan 4  S&S of GI Dysfunction GI Bleeding 1. Upper GI ❖ Esophagus, stomach, or duodenum ❖ Causes: bleeding varices, Mallory- Weiss tear, peptic ulcers (coming up) ❖ Common signs: ❖ Hematemesis or “Coffee ground” emesis ❖ Melena (more common) or hematochezia (less common but can occur ć rapid bleed) ❖13 S&S of GI Dysfunction GI Bleeding Mallory-Weiss Tear Bleeding from tears in the mucosa at the junction of the stomach and esophagus, usually caused by severe retching, coughing, or vomiting. What demographics are most at risk for this do you think? ❖14 S&S of GI Dysfunction GI Bleeding Esophageal Varices Extremely dilated sub- mucosal veins in the lower third of the esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis. ❖15 Jody Vaughan 5  S&S of GI Dysfunction GI Bleeding 2. Lower GI ❖ Jejunum, ileum, colon, or rectum ❖ Causes: polyps, inflammatory disease, cancer, hemorrhoids ❖ Common sign: ❖ Hematochezia ❖16 Peptic Ulcer Disease ❖17 Peptic Ulcer Disease (PUD) Erosion of the GI mucosa d/t the digestive action of HCl acid and pepsin ❖ Acute or chronic; superficial or deep Esophagus ❖ Superficial ulcers are not “true” ulcers Stomach ❖ True ulcers damage blood vessels or Duodenum perforate GI wall ❖ 3 types 1. Duodenal *** 2. Gastric 3. Stress ❖18 Jody Vaughan 6  Peptic Ulcer Disease Duodenal Ulcers (~80%) and Gastric Ulcers ❖ H. pylori causes more than 90% of duodenal ulcers and up to 80% of gastric ulcers. Damages mucosal cells & stimulates gastrin production/acid secretion Inhibits prostaglandins & ↓ mucus production Increases acid production ❖19 Peptic Ulcer Disease Signs and Symptoms ❖ Abdominal Pain - usually burning, gnawing epigastric pain (can be misinterpreted as hunger or indigestion); Gastric ulcer generally during meal; Duodenal ulcers generally feel better with eating, pain manifests 2-3 hours after meal. Why do you think this is so? ❖ Bloating and abd fullness ❖ N/V ❖ Anorexia and weight loss ❖ Hematemesis ❖ Melena ❖20 Peptic Ulcer Disease 3. Stress Ulcers ❖ An acute form of peptic ulcer ❖ Develop after severe illness, systemic trauma, neural injury ❖ Usually affects multiple sites of stomach or duodenum ❖ Classified as either: 1. Ischemic: Develop within hours of a major physiologic event (eg hemorrhage, multi-system trauma, sepsis, severe burns (Curling’s Ulcer) 2. Cushing: Associated with severe head trauma as a result of decreased mucosal blood flow and hypersecretion of acid ❖21 Jody Vaughan 7  Disorders of Motility ❖22 Dysphagia ❖23 Disorders of Motility Dysphagia Difficulty swallowing ❖ Can result from 1. Esophageal Mechanical Obstruction Tumors, pouchings, or strictures (intrinsic or extrinsic) 2. Impaired Esophageal Motility Neural (eg CVA) Muscular disorders that interfere with swallowing or peristalsis ❖24 Jody Vaughan 8  Gastroesophageal Reflux Disease (GERD) ❖25 Disorders of Motility Gastroesophageal Reflux Disease (GERD) Reflux of chyme (acid & pepsin) into esophagus ❖ LES doesn’t close properly, relaxes too much, or there is ineffective esophageal peristalsis ❖ Contributing factors: Vomiting, coughing, lifting, bending, and other activities that ↑ ABD pressure ❖ Severity depends on stomach content acidity & length of time chyme in contact with esophagus ❖ GERD can lead to Barrett’s Esophagus (esophageal metaplasia) 2° to chronic irritation ❖ Ever hear of silent reflux? Aka laryngopharyngeal reflux (LPR) ❖26 Hiatal Hernia Versus Abdominal Hernia ❖27 Jody Vaughan 9  Abdominal Hernia ❖28 Disorders of Motility Hernia ❖ Reducible ❖ Irreducible (Obstructed – intact blood supply; Incarcerated – adhesions btwn hernia wall and intestinal wall and can cut off blood flow; Strangulated – blood supply cut off=ischemia) Causes: ❖ Weakening of membranes or muscles (congenital, age, stretching muscles during pregnancy, previous surgery) ❖ Increased intra-abd pressure (pregnancy, ascites, COPD, straining during BMs, obesity) ❖ Note: Inguinal hernias are a protrusion of abdominal- cavity contents through the inguinal canal - up to 75% of all “abdominal” hernias ❖29 Disorders of Motility Hiatal Hernia Protrusion of upper portion of stomach through the diaphragm into the thorax 2 Types: 1. Paraesophageal (aka rolling): Stomach bulges up through opening in diaphragm (hiatus) alongside esophagus. Risk/major complication: strangulation 2. Sliding: Part of the stomach moves through diaphragm into thoracic cavity Sliding More common, not usually serious, Hernia usually asymptomatic. May have S+S heartburn, dysphagia – worse with reclining, bending, coughing ❖30 Jody Vaughan 10  Intestinal Obstruction ❖31 Disorders of Motility Intestinal Obstruction and Ileus A blockage that completely stops or seriously impairs the passage of intestinal contents in the small or large intestine Classified as either: 1. Simple: mechanical blockage (most common) (feces) ❖ Hernia, Torsion (Volvulus), Intussusception, Diverticulosis,Tumor 2. Functional: failure of motility (Paralytic Ileus) ❖ Neurological impairment (spinal cord injury, abd surgery, peritonitis, opiates, ↓K+) ❖32 Disorders of Motility Intestinal Obstruction and Ileus S&S of Vomiting & Distension dependent on obstruction location: ❖ Pyloric Early, profuse clear gastric emesis ❖ Proximal small intestine Mild distension; bile colored emesis ❖ Lower intestinal More pronounced distension, later vomiting with fecal type emesis Loss of F + E = imbalances and hypovolemia ❖33 Jody Vaughan 11  Disorders of Motility Intestinal Obstruction and Ileus S&S Obstruction ❖high-pitched (tympanic) bowel sounds – early – then diminished or absent ❖Severe colicky abd pain ❖Borborygmi Early paralytic ileus ❖Decreased or absent bowel sounds ❖Steady pain and distended abd ❖N/V Tests ❖Abdominal CT Scan ❖Abdominal x-ray ❖Barium Enema ❖Upper GI (upper to first part duodenum – barium and xray) and Small Bowel Series (distal duodenum to ileocecal valve) ❖34 Gangrenous Ileum ❖35 Disorders of Motility Intestinal Obstruction and Ileus Peritonitis ❖Inflammation of Peritoneal membrane 1. Chemical Irritation (bile, chyme in peritoneal cavity) Will lead to bacterial eventually due to inflammation -> increased permeability-> intestinal bacterial leak into cavity 2. Bacterial Invasion (necrosis or perforation of bowel wall) ❖36 Jody Vaughan 12  Disorders of Motility Intestinal Obstruction and Ileus Peritonitis S&S ❖ Abd distension and rigid, board- like abd ❖ N/V ❖ Pain ❖ Vasodilation -> hypovolemic shock ❖ Eventual septicemia ❖37 Malabsorption Syndromes ❖38 Malabsorption Syndromes Overview ❖ Absorption of nutrients in small intestine is impaired ❖ 2 general classes, usually interrelated: 1. Maldigestion Failure of chemical processes of digestion Caused by deficiencies of enzymes needed for digestion and/or inadequate secretion of bile salts/bile reabsorption 2. Malabsorption Failure of intestinal mucosa to absorb digested nutrients Caused by mucosal disruption (eg gastric/intestinal resections, intestinal disease) ❖39 Jody Vaughan 13  Pancreatic Insufficiency ❖40 Malabsorption Syndromes Pancreatic Insufficiency The deficient production of pancreatic enzymes (lipase, amylase, trypsin, chymotrypsin) by the pancreas ❖ Pancreatic enzymes digest fats, carbs, and proteins; fat maldigestion is the primary problem ❖ Causes: chronic pancreatitis, pancreatic carcinoma, pancreatic resection, cystic fibrosis ❖ There must be significant damage/loss of pancreatic tissue before insufficiency occurs ❖ Most common sign: steatorrhea ❖41 Lactase Deficiency ❖42 Jody Vaughan 14  ❖43 Malabsorption Syndromes Lactase Deficiency A genetic defect - lactase enzyme is lacking. This inhibits breakdown of lactose = prevents lactose digestion and absorption across intestinal wall. ❖ AKA Lactose Intolerance ❖ Undigested lactose stays in intestine → increases osmotic gradient = diarrhea S&S ❖ Cramping, bloating, diarrhea, flatulence ❖44 Celiac Disease ❖45 Jody Vaughan 15  Malabsorption Syndromes Celiac Disease Gluten-sensitive enteropathy and non-celiac gluten sensitivity (NCGS) Complex interaction involving dietary, genetic and immunological factors ❖ Patients with CD have an enzyme in the small intestine that breaks down the gliadin in a particular way that exposes the toxic portion of the protein, leading to antibody reaction to gliadin ❖ Leads to atrophy of villi in upper small intestine -> decr. surface area and malabsorption of nutrients. ❖ Inflammatory enteritis -> osmotic and secretory diarrhea ❖46 Malabsorption Syndromes Celiac Disease S&S (just to name a few – dozens have been documented) ❖ Cramping, bloating, diarrhea, steatorrhea ❖ Anemia, fatigue, infections, hair loss, acne, eczema ❖ Weight loss/gain, endocrine (hypothyroid) ❖ Peripheral neuropathy, mood changes, headaches/migraine, mental fog, anxiety, heart palpitations ❖ Osteoporosis ❖ Bone, joint and muscle pain ❖47 Inflammatory Bowel Disease What’s the difference between Irritable Bowel Syndrome (IBS) and Inflammatory Bowel Disease (IBD)? ❖48 Jody Vaughan 16  Ulcerative Colitis ❖49 Inflammatory Bowel Disease Ulcerative Colitis A chronic inflammatory disease that causes ulceration of colonic mucosa (usually rectum & sigmoid colon) ❖ Lesions usually appear b/t 20 - 40 yrs of age ❖ Cause: ? Maybe r/t dietary, genetic &/or immunological compromise ❖ Primary lesions form erosions which develop into ulcers. Abscess formation, necrosis, & ragged ulcerations of mucosa follows ❖ Mild or severe ❖ ↑ Risk of colon CA d/t chronic irritation ❖ Symptoms similar to Crohn’s disease ❖50 Inflammatory Bowel Disease Ulcerative Colitis S&S ❖ Mucosal bleeding, cramping, urge to defecate, frequent diarrhea (up to 20 times/day in severe cases) with bloody & purulent mucus. May have large volume watery diarrhea ❖ Intermittent periods of remission & exacerbation ❖ Dehydration ,weight loss, anemia, and fever may occur 2° to bleeding, fluid loss, and inflammation Diagnosing ❖ Hx, clinical manifestations, & imaging studies such as sigmoidoscopy, barium enema, X-rays. ❖51 Jody Vaughan 17  Crohn’s Disease ❖52 Inflammatory Bowel Disease Crohn Disease An inflammatory disorder affecting all of GI tract; Ascending & transverse colon most commonly affected ❖ Risk factors/causes relatively same as UC ❖ Affects all layers of colon: Inflammation begins in intestinal submucosa - then spreads into mucosa & serosa. Neutrophils & macrophages cause tissue injury ❖ Ulcerations may be “skip lesions” and appear as fissured ulcers (cobblestone pattern). Perianal fistulas may develop ❖ ↑ Risk for colon CA ❖53 Inflammatory Bowel Disease Crohn Disease S&S ❖ May have no specific symptoms other than an “irritable bowel” ❖ Diarrhea may be bloody with mucus (bloody less common than UC), tenderness in RLQ, wt loss ❖ Intermittent periods of remission & exacerbation ❖ May be anal involvement including fissure, abscess, fistulas Diagnosing ❖ Same as UC ❖54 Jody Vaughan 18  ❖55 Diverticular Disease ❖56 Inflammatory Bowel Disease Diverticular Disease Disease characterized by ‘pouchings’ of mucosa through muscle layers of colon wall. Most commonly in sigmoid area ❖ Diverticulosis: asymptomatic disease ❖ Diverticulitis: inflammation ❖ Most common in people > 60 ❖ Cause not known - ? ↓ fiber intake S&S ❖ Vague or absent; cramping of lower ABD, constipation, diarrhea, distension, or flatulence. Diverticula that cause abscesses can lead to fever, WBC ↑, tenderness of LLQ ❖57 Jody Vaughan 19  Appendicitis ❖58 Appendicitis Inflammation of vermiform appendix ❖ Most common surgical emergency of ABD ❖ Usually occurs b/t 20 & 30 yrs of age ❖ Exact cause ?; Common theory: lumen b/c obstructed with stool, tumors, or foreign Inflamed Appendix bodies which results in pressure, ischemia, infection and inflammation S&S ❖ Vague epigastric or periumbilical pain that worsens over 3 - 4 hrs. Pain may come and go, then shift to RLQ. Nausea, vomiting, Perforated Appendix anorexia and fever may develop, WBC may be ↑, rebound tenderness may be present ❖59 Disorders of the Accessory Organs of Digestion ❖60 Jody Vaughan 20  Disorders of the Accessory Organs of Digestion Overview ❖ Accessory organs of digestion secrete substances needed for digestion and metabolic functioning Liver Gallbladder Pancreas ❖61 Clinical Manifestations of Liver Disorders Of all the accessory organ disorders, acute or chronic liver disease leads to the most systemic & life threatening complications ❖62 Portal Hypertension ❖63 Jody Vaughan 21  ❖64 Clinical Manifestations of Liver Disorders Portal Hypertension Abnormally high blood pressure in the portal venous system. Most common cause is cirrhosis ❖ Caused by any disorder (and there are LOTS!) that obstructs/impedes blood flow through any part of the portal venous system or vena cava ❖ Obstructions can occur from thromboses, inflammation, or fibrosis (from cirrhosis, hepatitis, or parasitic infection) ❖ Portal outflow to vena cava can be impeded by hepatic vein thrombosis or impaired Rt ventricular contraction. Blood then backs up into the portal system, increasing pressure ❖65 Clinical Manifestations of Liver Disorders Portal Hypertension ❖ Patients with Portal HTN develop serious medical conditions that are hard to treat and may have poor prognoses: 1. Varices 2. Splenomegaly 3. Hepatic Encephalopathy 4. Ascites ❖66 Jody Vaughan 22  Clinical Manifestations of Liver Disorders Portal Hypertension…Varices 1. Varices ❖ What: distended tortuous collateral veins usually found in lower esophagus, stomach, and rectum ❖ Cause: prolonged elevation of pressure within the portal venous system ❖ S&S: Vomiting of blood from bleeding esophageal varices ❖67 Clinical Manifestations of Liver Disorders Portal Hypertension…Splenomegaly 2. Splenomegaly ❖ Enlargement of spleen caused by increased pressure in splenic vein ❖68 Clinical Manifestations of Liver Disorders Portal Hypertension… Hepatic Encephalopathy 3. Hepatic Encephalopathy ❖ Deterioration of brain cell functioning ❖ Occurs when: ❖ Blood is shunted through collateral vessels to systemic veins (blood bypasses liver = no detoxifying) OR ❖ Toxins in blood not removed adequately because liver fx impaired ❖ In other words…toxic substances in blood build up & affect brain cells ❖ NH4+ (produced in GI tract by bacterial degradation of amines, amino acids, purines, urea) is the primary culprit, as it does not get detoxified in the liver as it otherwise normally should ❖69 Jody Vaughan 23  Clinical Manifestations of Liver Disorders Portal Hypertension… Hepatic Encephalopathy Hepatic encephalopathy may occur as an acute, potentially reversible disorder. Or it may occur as a chronic, progressive disorder that is associated with chronic liver disease. Mild: ❖Breath with a musty or sweet odor ❖Changes in thinking; Confusion that is mild ❖Forgetfulness; Mental fogginess ❖Personality or mood changes ❖Worsening of handwriting or loss of other small hand movements More severe symptoms may include: ❖Abnormal movements or shaking of hands or arms ❖Agitation, excitement, or seizures (occur rarely) ❖Disorientation; Drowsiness or confusion ❖Inappropriate behavior or severe personality changes ❖Slurred speech ❖Slowed or sluggish movement ❖Patients with hepatic encephalopathy can become unconscious, unresponsive, and possibly enter a coma. ❖70 Clinical Manifestations of Liver Disorders Portal Hypertension…Ascites 4. Ascites ❖71 Clinical Manifestations of Liver Disorders Ascites ❖ Accumulation of fluid in the peritoneal cavity; “3rd spacing” ❖ Late stage manifestation of cirrhosis (coming up) & portal HTN ❖ Most common causes: ❖ Cirrhosis of the liver (most common) ❖ HF ❖ ABD malignancies ❖ Nephrotic syndrome ❖ Prognosis generally poor ❖72 Jody Vaughan 24  Clinical Manifestations of Liver Disorders Ascites ❖ 3 primary mechanisms produce ascites: 1. Portal HTN ** 2. Hepatocyte Failure (hepatocytes manufacture serum albumin….therefore….remember oncotic/osmotic pressure?) ** 3. Increased Hepatic Lymph Production (increased pressure in liver = increased lymph production) S&S ❖ Weight gain, ABD distension, increased ABD girth, “shiny” tight appearance of skin over ABD, dyspnea, increased RR with possible orthopnea, peripheral edema ❖73 Mechanisms of Ascites Caused by Cirrhosis ❖74 Jaundice ❖75 Jody Vaughan 25  A&P: Bilirubin Review Bilirubin is a byproduct of destroyed old RBCs Metabolism of Bilirubin: 1. Old RBCs are taken up & destroyed by macrophages: Lysis of RBCs releases Hgb 2. Hgb is then separated into its 2 component parts: Heme & Globin (turn into amino acids) 3. Through enzymatic processes, Heme is converted into bilirubin, and is then released into the plasma 4. In the plasma, bilirubin binds to albumin, forming unconjugated bilirubin. It is then transported to the liver 5. Liver hepatocytes then convert (conjugate) bilirubin 6. Conjugated bilirubin is excreted via bile to the intestines. Bacteria in the intestine break down bilirubin to urobilinogen for excretion in the feces (most) & urine (some) ❖76 Lipid soluble Water soluble ❖77 Therefore….. Unconjugated (indirect) bilirubin vs Conjugated (direct) bilirubin Prehepatic? Posthepatic? Lipid soluble? Water soluble? ❖78 Jody Vaughan 26  Clinical Manifestations of Liver Disorders Jaundice (Icterus) A yellowish pigmentation of the skin caused by hyperbilirubinemia (elevated plasma bilirubin) Can result from 1. Obstructive disorders of the bile ducts or impaired liver cells 2. Excessive hemolysis of RBCs (the body can’t keep up!) ❖79 Clinical Manifestations of Liver Disorders Jaundice (Icterus) A yellowish pigmentation of the skin caused by hyperbilirubinemia (elevated plasma bilirubin) Bilirubin test results are expressed as direct, indirect or total bilirubin. Total is a combination of direct and indirect bilirubin. Typically, you'll get results for direct and total bilirubin. ❖80 Clinical Manifestations of Liver Disorders Jaundice (Icterus) 1. Obstructive Jaundice Either extra or intrahepatic 1. Extrahepatic (outside the liver) (post-hepatic) ❖ Common bile duct occluded by gallstone, tumor, or compression from edema of pancreatitis ❖ Bilirubin is conjugated by hepatocytes but cannot flow into duodenum d/t obstruction ❖ Bilirubin then accumulates in liver → “backs up” and enters bloodstream = hyperbilirubinemia ❖ Stool may be light or clay colored d/t no urobilinogen excretion ❖81 Jody Vaughan 27  Clinical Manifestations of Liver Disorders Jaundice (Icterus) 1. Obstructive Jaundice 2. Intrahepatic ❖ Results from 1) Hepatocellular damage or 2) Obstruction of bile canaliculi (ducts) within liver 1. Hepatocellular damage: damaged hepatocytes leak conjugated bilirubin or they are unable to conjugate bilirubin = ↑ plasma concentrations of unconjugated and conjugated bilirubin 2. Obstruction of bile canaliculi = flow of conjugated bilirubin through liver & into common bile duct is diminished/impaired = ↑ plasma concentrations of conjugated bilirubin ❖82 Clinical Manifestations of Liver Disorders Jaundice (Icterus) 2. Hemolytic Jaundice (vs Physiological jaundice):prehepatic ❖ Excessive lysis of RBCs or absorption of a large hematoma ❖ Excess of unconjugated bilirubin exceeds hepatocytes’ ability to conjugate it = unconjugated hyperbilirubinemia ❖ Causes may include: RBC membrane defects, immune reactions (eg Lupus; transfusion of incompatible blood), severe infections, toxic substances in general circ, Rh incompatiblity ❖83 Disorders of the Liver ❖84 Jody Vaughan 28  Hepatitis ❖85 Disorders of the Liver Hepatitis “Liver Inflammation” Injury to the liver characterized by the presence of inflammatory cells in the tissue of the organ ❖ Acute or chronic forms ❖ Hepatitis can lead to fulminant hepatitis (coming up) ❖ Many different causes of hepatitis, such as: ❖ *Viruses/Infections ❖ Toxins ❖ Drugs (esp those that are hepatotoxic) ❖ Autoimmune processes/diseases ❖ Alcohol ❖ Hereditary causes ❖86 Disorders of the Liver Viral Hepatitis Viral hepatitis (all types) cause ❖ Varying degrees of hepatic cell injury and tissue necrosis ❖ Autolysis (self-destruction of cells) ❖ These changes are completely reversible when acute phase of disease subsides S&S ❖ Fatigue, anorexia, headache, joint and muscle pain, N/V, fever, RUQ pain, dark urine, clay color stools, jaundice. ❖87 Jody Vaughan 29  Disorders of the Liver Viral Hepatitis Viral hepatitis ❖88 Fulminant Hepatitis ❖89 Disorders of the Liver Fulminant Hepatitis Fulminant Hepatitis ❖ Can result as a severe complication of Hep B (most common) or C or other liver disease ❖ Causes acute and massive widespread & severe hepatic necrosis & liver failure – usu within 8 wks ❖ Cause unknown: Hepatocytes become grossly edematous & patches of necrosis & inflammatory cell infiltrates disrupt liver tissue and therefore liver function ❖ Very poor prognosis; treatment usually palliative ❖90 Jody Vaughan 30  Cirrhosis ❖91 Disorders of the Liver Cirrhosis ❖ An irreversible, slowly progressive chronic inflammatory disease of the liver that disrupts liver structure and function ❖ Replacement of liver tissue by fibrotic cells, scar tissue and regenerative nodules (lumps that occur as a result of a process in which damaged tissue is regenerated) ❖ Distortion of vascular bed impedes blood flow (L/T portal hypertension) ❖ Process of cellular injury is dependant on type/cause of cirrhosis. Pathogenesis remains yet to be completely understood ❖ 4 types… ❖92 Disorders of the Liver Cirrhosis 1. Laennec’s – AKA alcoholic or nutritional cirrhosis – chronic alcoholism and malnutrition 2. Postnecrotic cirrhosis – MOST COMMON worldwide – usu. complication from viral hepatitis; may occur from drugs/toxins 3. Biliary cirrhosis – prolonged bile duct obstruction or inflammation 4. Cardiac cirrhosis – prolonged venous congestion in liver from right sided heart failure ❖93 Jody Vaughan 31  Disorders of the Liver Cirrhosis S&S ❖ Anorexia ❖ Indigestion ❖ N/V ❖ Abd pain ❖ Bruising ❖ Easy bleeding ❖ Jaundice ❖ Pruritis ❖ Lethargy ❖94 Disorders of the Gallbladder ❖95 Gallbladder Common Bile Duct ❖96 Jody Vaughan 32  Cholelithiasis cho·le·li·thi·a·sis ❖97 Disorders of the Gallbladder Cholelithiasis Presence of gallstones in the gallbladder ❖ Cause of gallstone formation not known ❖ Develops when balance of cholesterol, bile salts, and calcium is disrupted ❖ Bile secreted by liver is supersaturated with cholesterol = precipitation = stone formation ❖ Cholesterol Stones (80%) ❖ Pigment Stones (bilirubin) ❖ Mixed Stones (bile salts, bilirubin, calcium salts) ❖98 Disorders of the Gallbladder Cholelithiasis ❖ Risk factors: Obesity; middle age; female, fertile (4 F’s); gallbladder or pancreatic disease; rapid wt loss/crash diets; conditions that encourage stasis of/decreased bile flow (immobility etc) ❖ S&S: Cardinal: Epigastric discomfort, fatty food intolerance Others: heartburn, flatulence, epigastric pain, pruritis, jaundice. Pain usually “colicky” ❖99 Jody Vaughan 33  Cholecystitis cho-le-cyst-itis ❖100 Disorders of the Gallbladder Cholecystitis Inflammation of gallbladder or cystic duct ❖ Acute or chronic ❖ Usually caused by lodging of a gallstone in cystic duct ❖ Obstruction leads to inflammation & distension of gallbladder ❖ Pressure against distended gallbladder wall impairs blood flow → ischemia, necrosis, perforations. ❖ S&S: pyrexia, ↑ WBC, rebound tenderness, ABD muscle rigidity (guarding) ❖101 Disorders of the Pancreas ❖102 Jody Vaughan 34  ❖103 Acute Pancreatitis ❖104 Disorders of the Pancreas Acute Pancreatitis Inflammation of the pancreas ❖ Most highly associated with alcoholism (pancreatic cells metabolize ethanol = toxic metabolites form in pancreas = obstructions) & biliary tract obstruction (most common) ❖ Cause is unknown: ? Injury to acinar cells or activation of pancreatic enzymes in pancreas rather than intestines auto digests the pancreas → inflammation & tissue death ❖ If these enzymes enter into bloodstream, damage to other organs can ensue, resulting in possible end stage multi- organ dysfunction ❖105 Jody Vaughan 35  ❖106 Disorders of the Pancreas Acute Pancreatitis Signs and Symptoms ❖Common symptoms of an acute attack include: ❖Severe abdominal pain, often spreading through into the back ❖Bloating ❖Fever ❖Sweating ❖Nausea ❖Vomiting ❖Collapse ❖107 Chronic Pancreatitis ❖108 Jody Vaughan 36  Disorders of the Pancreas Chronic Pancreatitis Inflammation of the pancreas ❖ Results from structural or functional pancreatic impairments ❖ IDDM aka Type 1 DM may develop from loss of islet cells if much of the pancreas has been damaged 2 major types: ❖ Chronic Obstructive Results from cancer or biliary tract disease, esp inflammation of sphincter of Oddi as seen with Cholelithiasis ❖ Chronic Calcifying Results from chronic inflammation and scarring of pancreas and pancreatic duct (eg chronic ETOH misuse) ❖109 Disorders of the Pancreas Chronic Pancreatitis Signs and Symptoms ❖ Recurrent or even constant abdominal pain, which may be severe ❖Steady weight loss, caused by the body’s inability to properly digest and absorb food ❖IDDM ❖Chronic pancreatitis can contribute to the development of pancreatic cancer. ❖110 Cancer of the Digestive System ❖111 Jody Vaughan 37  Cancer of the GI Tract ❖112 Cancer of the Esophagus ❖113 Cancer of the GI Tract CA of the Esophagus ❖ Relatively rare ❖ Usually over 60 yrs age ❖ Risk factors: smoking, alcohol use, reflux esophagitis , obesity, nutritional deficiencies ❖ Usually squamous cell carcinoma; can occur anywhere along esophagus ❖ Recall Barrett’s Esophagus ❖114 Jody Vaughan 38  Cancer of the Stomach ❖115 Cancer of the GI Tract CA of the Stomach ❖ Risk factors: infection with Helicobacter pylori, food additives and preservatives, smoked foods, chronic gastritis, low intake of fruits/veggies, family hx ❖ Incidence greater in men ❖ S&S develop only after tumor has penetrated wall of stomach: Weight loss, upper ABD pain, vomiting, hematemesis, anemia ❖116 Cancer of the Colon & Rectum ❖117 Jody Vaughan 39  Cancer of the GI Tract CA of the Colon & Rectum ❖ 2nd most common cause of CA death ❖ Usually occurs > 50 years age ❖ Frequently develops from polyps ❖ Genetic & environmental causes/risk factors: ❖ Alterations in tumor suppressor gene ❖ Family hx ❖ Diet (high fat, low fiber & calcium) S&S ❖ Pain, palpable mass, anemia, blood in stool (ascending colon) ❖ Progressive ABD distension, pain, vomiting, constipation, cramping, bright red blood covering stool (descending colon) ❖118 End of Lecture Jody, ❖119 Resources & References Gould, B. & Dyer, R. (2011). Pathophysiology for the health professions (4 th ed.). St. Louis: Elsevier. Gutierrez, K. & Peterson, P. (2002). Real world nursing survival guide: Pathophysiology. Philadelphia: Saunders. Hogan, M. (ed). (2008). Pathophysiology: Reviews & rationales (2 nd ed.). Upper Saddle River: Pearson. McCance, K. & Heuther, S. (2006). Pathophysiology: The biological basis for disease in adults and children (5th ed.). St. Louis: Mosby. Porth, C. (2007). Essentials of pathophysiology: Concepts of altered health states (2 nd ed.). Philadelphia: Lippincott. ❖120 Jody Vaughan 40