Gastrointestinal Disorders: Symptoms, Complications, and Diagnosis, Exams of Pathophysiology

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Pathophysiology Ch 17: Gastrointestinal disorders

secretion, mechanical digestion, chemical digestion, absorption of nutrients (main function), propulsion, elimination - processes of the GI tract large double walled serous membrane in the abdominal cavity, parietal peritoneum-covers the abdominal wall and superior surface of bladder and uterus, visceral peritoneum-encases the organs, peritoneal cavity-potential space between the parietal and visceral peritoneum where a small amount of serous fluid is present, mesentery-double membrane layer of peritoneum that supports the intestines and conveys blood vessels and nerves to supply the wall of the intestine - peritoneum acid-digests food, bacteriocidal, converts pepsinogen to pepsin to form chyme; chief cells produce pepsin, pepsin-breaks down protein; production of intrinsic factor, secretes gastrin which is needed to produce IF; absorbs small and lipid soluble molecules; mucus-protects; prostaglandin also protects, produce mucus which protects the stomach - functions and contents of the stomach lower esophageal sphincter - LES duodenum, jejunum & ileum, major site for absorption of nutrients (most absorption occurs in ileum), digestion by pancreatic enzymes, intestinal enzymes and bile salts, villi and microvilli-greatly increase the absorbative SA of small intestine, carbs-monosaccharides and disaccharides, proteins-amino acids and peptides, fats-emulsified and broken down to fatty acids - small intestine cecum-pouch from where the appendix extedns, colon-general digestion and absorption ceases, rectum- stores feces & anus, colon: ascending, transverse, descending & sigmoid colon, absorption of large amounts of water and electrolytes takes place in large intestine, formation of solid feces - large intestine

resident bacteria assist with further breakdown of some food materials and convert bilirubin to urobilinogen giving feces the brown color, some bacteria is beneficial (synthesizes vitamin K), normal flora of stomach inludes strep, the stomach: relatively sterile-acid production, duodenum & jejunum: few bacterial growth-bile acid secretions, intestinal motility, antibody production; ileum & colon: most bacteria here-protects against infection, metabolism of bile salts, estrogens, androgens, lipids, carbs and drugs - intestinal bacteria overgrowth of bacteria such as H pylori (cause of peptic ulcer disease), E coli or clostridieum, perforation of intestine, or contamination from neighboring structures - infections in intestines from... metabolic factory of the body made up of lobes, lobules, hepatocytes, sinusoids, common bile duct and Kuppfer cells, largest organ of the body, Kuppfer cells-remove and phagocytize foreign material from GI before it reaches circulation - liver secretion of bile which is vital for digestion, synthesizes prothrombin, fibrinogen and clotting factors, metabolism of bilirubin, glycogenolysis-conversion of glucose to glycogen for future use, vascular and hematologic function-recycles damaged or old RBCs to recycle iron and protein, stores and releases blood, metabolism of nutrients, metabolic detoxification, storage of vitamins and minerals - liver functions stores and concentrates bile between meals, bile in liver travels from the hepatic duct to the duodenum or through cystic duct to gallbladder, "chole"=gall, "cyst"=bladder (cholecystitis), "lith"=stone (lithoripsy)

• gallbladder secretes digestive enzymes, electrolytes, water and alkaline fluids into small intestine, pancreatic enzymes hydrolyze carbs, proteins and fats, secreted from pancreas in inactive form and activated in the duodenum - exocrine pancreas

secretions into the intestine, often related to infections or a short transit time which limits reabsorption or to increased osmotic pressure of the intestinal contents causing them to retain water; small volume diarrhea often occurs in people with inflammatory bowel disease, stool may contain blood, mucus or pus, may be accompanied by abdominal cramps and urgency - diarrhea blood may occur in normal stools with diarrhea, constipation, tumors or inflammatory conditions frank blood-red blood often on the surface of the stool, usually results from lesions in the rectum or anal canal; occult blood-small hidden amounts of blood that aren't visible to the eye but are detectable with stool tests, may be caused by small bleeding ulcers in the stomach or small intestine; melena-dark colored (tarry) stool, may result from significant bleeding in upper digestive tract - blood in stool dehydration & hypovolemia-common complications of GI tract disorders, when vomiting and diarrhea occur fluid shifts from the blood into the digestive tract and if the loss persists eventually intracellular fluid is decreased, dehydration: electrolyte imbalance-Na, K, both lost in vomiting and diarrhea; hypovolemia-w/ impaired circulation and cellular dehydration may cause decreased function in all tissues and organs, hypervolemia; acid base balances-metabolic acidosis due to severe vomiting and diarrhea, infants and elderly more at risk because of the unique proportions and distributions of fluid in the body in these individuals and the decreased ability of their kidneys to compensate quickly for losses

• fluid and electrolyte imbalances mechanical: pain from stretching or distention-adhesions from scar tissue, tumors, swelling of organs, impacted feces; inflammatory: biochemical mediators of inflammatory response stimulate nerve endings causing pain; ischemia: from bowel distention, thrombosis, tumors - causes of abdominal pain burning sensation-frequently accompanies inflammation and ulceration in upper digestive tract; dull, aching pain-typical result of stretching of liver capsule caused by swelling; cramping or diffuse pain- characterisic of inflammation distention or stretching of intestines; colicky, often sever pain-results from recurrent smooth muscle spasms or contraction, occurs in response to severe inflammation or obstruction - visceral pain

somatic pain receptors directly linked to spinal nerves-may cause reflex spasm of overlying abdominal muscles, characterized by a steady, intense, often well localized abdominal pain which indicates involvement or inflammation of parietal peritoneum, this forms the basis for the "rebound tenderness" that is identified over an area of inflammation when pressure is released (to elicit response pressure is applied slowly to the abdomen by the fingers and then suddenly released resulting in a sharp pain at the site) - somatic pain common phenomenon, pain perceived at a site different from origin, results when visceral and somatic nerves converge at one spinal cord level, source of visceral pain is perceived as the same as that of the somatic nerve, may assist or delay diagnosis depending on problem - referred pain H. pylori, aspirin, alcohol, ischemia, regurgitation of bile, NSAIDS (non-steroidal anti-inflammatory drugs)

• breaks in mucosal barrier caused by... upper GI bleed: esophagus, stomach or duodenum caused by bleeding varices, peptic ulcers, Mallory- Weiss tear; lower GI bleeding: jejunum, ileum, colon, rectum caused by polyps, cancer, inflammatory disease, hemorrhoids; color: "frank red" or "coffee ground" - GI bleeding blood in stools (red, black, occult), decreased Hct & Hgb, increased HR, decreased BP, changes in level of consciousness, vomiting blood (hematemesis), diarrhea (blood irritates GI tract) - S/S of GI bleeding difficulty swallowing, may result from neurological deficit, muscular disorders or a mechanical obstruction mechanical obstructions: congenital atrasia-developmental defect in which the upper and lower esophageal segments are separated, the upper section ends in a blind pouch, in many cases there is a connecting fistula from one of the segments to the trachea; stenosis or narrowing of esophagus, can be secondary to fibrosis; diverticula-outpouchings of esophageal wall, accumulated food in pouch obstructs flow of food down esophagus; tumors-may be external or internal, external are located outside the esophagus and compress it - dyspahgia

most are due to H. pylori infection (90%), occur most commonly in the proximal duodenum (duodenal ulcers), also found in the antrum of the stomach (gastric ulcers), development begins w/ breakdown of mucosal barrier which results from an imbalance between the mucosal defense system and forces that are potentially damaging to it (acid): decreased mucosal defense is more common in gastric ulcer development, increased acid secretion predominant factor in duodenal ulcers - gastric and duodenal ulcers hemorrhage: due to erosion of blood vessels, common complication, may be the 1st sign of peptic ulcer; perforation: ulcer erodes completely through the wall allowing chyme to enter the peritoneal cavity, results in chemical peritonitis; obstruction: may result later due to the formation of scar tissue - complications w/ PUD increased acid and pepsin secretion major causes: H. pylori, NSAIDs complications: intestinal obstruction causing bleeding, perforation and death - duodenal ulcers not as common as duodenal ulcers causes: H. pylori, NSAIDs associated w/: chronic gastritis, decreased prostaglandin synthesis, duodenal reflux of bile and pancreatic enzymes - gastric ulcers an acute peptic ulcer related to severe illness, trauma or neural injury, usually multiple sites, prophylaxis: protonix, other proton-pump inhibitors (PPIs) - stress ulcers Sx: epigastric burning or aching 2-3 hours after eating meals and at night-pain is relived by ingestion of food, heartburn, N/V, weight loss, iron deficiency anemia, occult blood in stool Tx: combination of antimicrobial and proton pump inhibitors or H2 blockers (Tagamet, Prilosec), antacids, reduction of exacerbating factors, surgical intervention-vagotomy to reduce acid production, gastrectomy or pylorplasty if perforated - PUD-Sx, Tx

dumping syndrome anemia: iron malabsorbed-related to decreased acid production or no duodenum, iron and/or vitamin B12 or folate deficiencies weight loss: inadequate food intake, can't tolerate carbs or normal sized meals - post gastrectomy syndromes control of gastric emptying is lost, large quantities of ingested food are rapidly "dumped" into the intestine, rapid emptying of hypertonic chyme into duodenum 10-20min after eating S/S: cramping pain in abdomen (immediate), diarrhea (immediate), hypoglycemia (2-3hrs after meal)- sweating, weakness, tremors prevention: small high protein meals low in simple carbs, drink fluids after you eat not with meals - dumping syndrome-S/S cholelithiasis-formation of gallstones which are masses of solid material or calculi that form in bile S/S: biliary colic-severe abdominal pain, jaundice, heartburn, food intolerances (fats, cabbage...) cholecystitis-inflammation of gallbladder and cystic duct, usually from gallstones stuck in cystic duct S/S: abdominal pain, fever, increased WBC, rebound tenderness pain may be referred to shoulder - gallbladder disorders-S/S chronic pancreatitis, pancreatic cancer, removal of pancreas, cystic fibrosis - pancreatic insufficiency caused by... inflammation of the pancreas resulting from autodigestion of the tissues, medical emergency; common causes: alcoholism, biliary tract obstruction; obstruction of outflow of pancreatic enzymes, enzymes are activated prematurely leading to autodigestion S/S: severe abdominal pain radiating to the back, vomiting, abdominal distention shock symptoms (low BP, pallor, sweating, rapid but weak pulse) due to hypovolemia, fever, paralytic ileus Tx: rest the pancreas, pain medication, antibiotics, stop drinking 20% mortality-higher in the ederly -

portal hypertension, ascites, hepatic encephalopathy, jaundice, hepatorenal syndrome, esophageal varicies, spenomegaly - clinical manifestations of liver disorders obstructed blood flow through portal system; causes: thrombosis, inflammation, fibrous changes in liver... - portal hypertension increased portal vein pressure causes development of collateral vessels; like varicose veins-distended, tortuous collateral veins, usually in lower esophagus, stomach and rectum; mortality from ruptured esophageal varices from 30-60% - esophageal varices accumulation of fluid in peritoneal cavity, increased pressure in tributaries of portal vein -> hydrostatic pressure increases -> pushes water out into peritoneal cavity S/S: weight gain, abdominal distention, shortness of breath, spider angioma, bacterial peritonitis (complication), hypovolemia - acites-S/S, process blood shunted around liver (not through), goes straight into vena cava, toxins, hormones and harmful substances bypass liver detoxification, harmful substances reach the brain via circulation, due to high ammonia levels, leads neurological syndrome, impaired brain function and electroencephalogram (EEG) changes, may develop quickly or slowly S/S: changes in personality and memory, irritability, confusion, flapping tremor of hands, stupor, convulsions, coma, death - hepatic encephalopathy-S/S yellow/green pigmentation of skin related to increased bilirubin in blood reasons for increase: disorders of bile ducts or liver cells or increased breakdown of RBCs, sign of many different types of primary disorders classified into groups: prehepatic jaundice-results from excessive destruction of RBCs and is characteristic of hemolytic anemia or tranfusions, posthepatic jaundice- caused by obstruction of bile flow into the gallbladder or duodenum and subsequent backup of bile into the blood - jaundice

viral hepatits, cirrhosis, fulminant hepatits - disorders of the liver inflammation of the liver 6 strains: A (HAV), B (HBV), C (HCV), D (HDV), E (HEV)-all can cause acute hepatitis Hep A (infectious hepatitis) - fecal/oral transmission - most common: incubation 2 to 6 weeks, acute but self limiting infection and no carrier or chronic state Hep B&C are both blood born: can also cause chronic hepatitis, liver cancer and liver failure, longer incubation-2 months, Hep C transmitted by blood transfusions - viral hepatits Prodromal phase (preicteric): 2 weeks after exposure; fatigue, malaise, N/V, headache, pain, fever..., very infectious-elevated liver enzymes AST and ALT Icteric: 1-2 weeks later; jaundiced, dark urine, clay colored stools, enlarged liver Recovery (posticteric): 6-8 weeks after exposure; S/S diminish, liver still enlarged and tender; liver back to normal 2-12 weeks after onset of S/S - phases of hepatitis A virus (HAV) rest, low fat diet, increased carbs (if bile flow obstructed), antiviral drugs for chronic hepatitis, strict hand washing (virus can be passed via feces for up to 3 months after onset of S/S) - Tx for hepatits A progressive destruction of liver tissue, irreversible, inflammatory disease, damages liver structure and function, diffuse fibrosis (scarring) and loss of lobular organization, nodules of regenerated heaptocytes are present between fibrous bands ("cobbly" appearance), develops slowly, toxins can speed up the damage, types: alcoholic liver disease (largest group), biliary cirrhosis-associate w/ immune disorders and those causing obstruction of bile flow, postnecrotic cirrhosis-linked w/ chronic hepatitis or long term exposure to toxic materials - cirrhosis of the liver fatty liver: mildest form, asymptomatic, reversible when drinking stops

chronic inflammation, inflammation starts in rectum and progresses through the colon (S intestine rarely involved), ulceration of colon mucosa (rectum, sigmoid colon), tissue destruction interferes w/ absorption of fluid and electrolytes in colon, lesion affects mucosa only and is continuous and diffuse, more common in younger people (20-40 years) S/S: fever, increased HR, 10-20 stools/day (diarrhea), frequent watery stools marked by blood and mucus, weight loss, anemia, cramping pain, rectal bleeding complications: edema, strictures and fibrosis result in obstruction, cancer - ulcerative colitis-S/S, complications occurs in large and small intestines but mostly in S intestine (affects terminal ileum and sometimes colon); aggravated by stress (not caused by it); inflammation occurs in a distribution called "skip lesions" w/ affected segments separated by areas of normal tissue-begin in submucosa and go into mucosa and serosa (affects all layers), damaged wall impairs the ability of small intestine to process and absorb food and inflammation interferes w/ digestion and absorption leading to malnutrition; loose, semi-formed, non-bloody diarrhea; granuloma, fistula, fissure, and abscess formation are common, stricture and obstruction are common, problem: lesions develop into holes and inflammation spreads to lymph tissue, risk of developing into colon cancer S/S: diarrhea, cramping abdominal pain, soft or semi-formed stool, melena may occur if ulcers erode blood vessels, anorexia, weight loss, anemia, fatigue - crohn's disease (enteritis)-S/S diverticuli=pouches form in colon mucosa and pouch outward diverticulosis=asymptomatic condition of having diverticuli diverticulitis=inflamed or infected diverticuli S/S: may be vague or absent or mild to severe, lower abdomen pain, abdominal cramping, diarrhea, constipation, distention, gas, fever, leukocytosis, tenderness in lower left quadrant (LLQ) complications: hemorrhage, peritonitis, bowel obstruction, fistula formation - diverticular disease-S/S, complications inflammation of appendix S/S: abdominal pain and tenderness esp. in lower right quadrant (RLQ), N/V, diarrhea, fever complications: perforation, peritonitis, abscess formation - appendicitis-S/S, complications

risk factors: tobacco use, alcoholism, GERD S/S: chest pain, pain on swallowing spreads quickly - esophageal cancer-S/S causes: H. pylori, heavily salted or preserved foods, tobacco, alcohol, low intake of fruits and vegetables S/S: none at first; anorexia, weight loss, vomiting, change in bowel habits, anemia, S/S usually occur after tumor penetrates muscle layers and has spread to other tissues Tx: surgery - stomach cancer-causes, S/S, Tx advanced age, high fat diet, low fiber diet, cigarette smoking, obesity, low levels of physical activity, ulcerative colitis for more than 10 years, colon polyps, family history of colorectal cancer or polyps - colon and rectal cancer risk factors can be a sporadic event or associated w/ genetic or environmental factors, most are moderately differentiated adenocarcinomas, polyps are pre-cancerous growths that closely associated w/cancer development S/S: change in bowel habits, anemia, lower GI bleeding, abdominal pain, palpable mass, abdominal distention, N/V, blood in stool if tumor creates a partial obstruction, may see ribbon stool-obstipation (severe or complete constipation) if lower rectum, Sx of obstruction depends on location - colorectal cancer-S/S usually secondary to cancer in other organs; other factors: chronic hepatitis (B&C), cirrhosis; cancer may invade hepatic and portal veins, spread to heart, lungs, etc S/S: N/V, abdominal fullness, jaundice, pain, weight loss, anorexia Tx: surgery, chemotherapy - liver cancer-S/S, Tx