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Lack of a desire to eat despite physiologic stimuli that would normally produce hunger.
Symptoms associated w/ it include: nausea, abd. pain, diarrhea, and psycholic distress
The reflux of chyme into the esophagus that is not expelled from the mouth r/t the closed esophageal sphincter. The chyme drops back into the stomach. This process can occur several time before vomiting occurs.
What are some of the causes of constipation?
low-residue diet, sedentary lifestyle, and insufficient hydration
megacolon, pelvic floor dyssynergia, abdominal muscle weakness, painful anal lesions, delayed spontaneous defecation, emotional depression, anticholinergics (antidepressants), cancer and cancer treatment, opiates, antacids (calcium carbonate, aluminum hydroxide), hypothyroidism, diabetic neuropathy.
What causes osmotic diarrhea?
A nonabsorbable substance in the intestine which draws water into the lumen by osmosis.
Magnesium, sulfate, phosphate, lactase deficiency (most common cause)
What causes secretory diarrhea?
Excessive mucosal secretion of chloride- or bicarbonate-rich fluid or inhibition of net sodium absorption primarily caused from bacterial enterotoxins (cholera, e. coli) and neoplasms (gastrinoma or thyroid carcinoma).
In secretory diarrhea, there can be large and small volume diarrhea. What causes each?
Large-volume: excessive motility caused by a lesion such as diabetic neuropathy.
Small-volume: usually caused by an inflammatory disorder of the intestine (ulcerative colitis or Crohn disease). Fecal impaction is another cause; the bowel produces excessive mucus and fluid to move the feces but it moves around it instead.
What causes motility diarrhea?
Resection of the sm. intestine, surgical bypass or an area of the intestine, or fistula formation between loops of intestine.
Prolonged diarrhea can cause what?
Dehydration, electrolyte imbalance, metabolic acidosis, and weight loss.
Generally the abd. organs are not sensitive to mechanical stimuli, such as cutting, tearing, or crushing. The organs are however, sensitive to _____.
stretching and distention
The onset of abdominal pain is associated with ____ ____. ____ ____ causes little pain.
Parietal abdominal pain arises from the ____ ____ which is more ____ and ____ than visceral pain.
localized and intense
Where is pain usually felt with visceral abdominal pain?
Near the midline in the epigastrium, midabdomen, or lower abdomen
How does referred pain of the gallbladder present?
Gallbladder pain starts out w/ vague discomfort in the rt epigastric region and then, as inflammation worsens, progress to a sharp, localized, referred pain between the shoulder blades.
Upper gastrointestinal bleeding occurs where and what is it commonly caused by?
Occurs in the esophagus, stomach, and duodenum.
Commonly caused by bleeding peptic ulcers but can also be caused by esophageal or gastric varices, a Mallory-Weiss tear, cancer, or angiodysplasias.
Lower gastrointestinal bleeding occurs where and what is it commonly caused by?
Occurs below the ligament of Treitz or from the small bowel (J or I), colon, or rectum.
Caused by polyps, inflammatory disease, diverticulosis, cancer, vascular ectasias, or hemorrhoids.
The digestion of blood proteins originating from massive upper GI bleeding is reflected by what lab result?
Why is Hgb and Hct values not the best indicator of acute GI bleeding?
B/c plasma and red cell volume are lost proportionately
What are the two general causes of dysphasia?
mechanical obstruction and functional disorder
Achalasia is a rare disorder that causes dysphasia. R/t denervation of smooth muscle in the mid and lower portions of esophagus and failure of lower esophageal sphincter to relax.
Treatment for GERD?
Proton pump inhibitors are the most effective monotherapy.
Also can use histamine-2 receptor antagonists or prokinetics, antacids, and alginate-antacids. Elevate HOB 6 inches, weight reduction and smoking cessation.
Laparoscompic fundoplication is the most common surgical intervention.
What ie eosinophilic esophagitis?
A rare, idopathic inflammatory disease of the esophagus characterized by esophageal infiltration of eosinophils associated with atopic diease, such as asthma and food allergies.
What is a sliding hiatal hernia?
It is the most common type out of the two and it is characterized by the stomach sliding or moving into the thoracic cavity through the esophageal hiatus. This can occur in supine positions and then is reversed by standing.
What conditions exacerbate symptoms of a sliding hiatal hernia?
Factors that increase intra-abdominal pressure such as tight clothing, coughing, bending, ascites, obesity, or pregnancy. Associated with GERD.
What is a paraesophageal hiatal hernia?
The herniation of the greater curvature of the stomach through a secondary opening in the diaphragm in which it is possible for the entire stomach to pass into the thorax. GERD is uncommon. Strangulation of the hernia can occur and is an emergency.
Clinical manifestations of hiatal hernias?
Often asymptomatic. Various non-specific symptoms generally occur later in life which include GERD, dyphagia, heartburn, vomiting, and epigastric pain.
Treatment for sliding hiatal hernia?
Small, frequent meals and avoiding recumbent position after eating. Avoid things that increase inta-abdominal pressure. Elevate HOB
What is a pyloric obstruction?
The narrowing or blocking of the opening between the stomach and the duodenum caused by peptic ulcer disease or carcinoma near the pylorus.
What type of ulcers are more likely to obstruct the pyloris?
Duodenal ulcers are more likely to cause this in comparison to a gastric ulcer
S/S of a pyloric obstruction?
Early: vague epigastric fullness, nausea
As progresses: anorexia develops
Late and severe: gastric distention and atony and vomiting of undigested food (no bile)
What are the most common causes of small bowel obstructions?
Adhesions, secondary to previous abd. sx (50-70%)
Hernia, inguinal, ventral, or femoral (20-25%)
Tumors: may be associated with intussusception: 10%
Mesenteric ischemia: 3-5%
What are the most common causes of large bowel obstructions?
Colon/rectal cancer: 90%
Colonic volvulus 4-5%
Diverticular disease 3-5%
Other causes (inflammatory bowel disease, adhesions, hernia, adynamic ileus)
What are the S/S of colonic obstruction?
Usually presents as hypogastric pain and abd. distention. Pain can vary from vague to excruciating, depending on the degree of ischemia and the development of peritonitis
Acute gastritis is usually injury of the protective mucosal barrier caused by what?
Regurgitation of bile, drugs, alcohol, chemicals, H. pylori infection, and some systemic diseases.
How do NSAIDs cause gastritis?
NSAIDs such as aspirin, ibuprofen, naproxen, and indomethacin are known to cause erosive gastritis b/c they inhibit prostaglandins which normally stimulate the secretion of mucus.
Chronic gastritis tends to occur in which group of people and causes what symptoms?
Occur in older adults and causes chronic inflammation, mucosal atrophy, and epithelial metaplasia
There are two types of chronic gastritis, what are they and what causes them?
Chronic fundal gastritis:believed to be r/t autoimmune disorders
Chronic antral gastritis: four times more common than fundal gastritis. Factors associated w/ it include alcohol, tobacco, NSAIDs regurgitation of bile, and H. PYLORI.
Symptoms of gastritis can be managed with what?
smaller meals; soft, bland diet; and avoidance of alcohol and NSAIDs
What is peptic ulcer disease and what are the two major risk factors?
It is a break, or an ulceration, in the protective mucosal lining of the lower esophagus, stomach, or duodenum and the two major risk factors are H. pylori infection of the gastric mucosa and habitual use of NSAIDs.
Duodenal ulcers occur with ____ frequency than other types of peptic ulcers and tend to develop in _____ persons.
What are duodenal ulcers associated with (causes)?
Increased numbers of parietal cells in the stomach, elevated gastrin levels, and rapid gastric emptying
S/S of duodenal ulcers?
Chronic intermittent pain in the epigastric area. It begins 30 mins to 2 hrs after eating, when stomach is EMPTY. Pain is rapidly relieved by ingestion of food or antacids, creating a typical pain-food-relief pattern.
Treatment of duodenal ulcers is aimed at doing what?
What are the treatments?
Aimed at relieving the causes and effects of hyperacidity.
Treatment: antacids, the eradication of H. pylori, ulcer-coating agents (sucralfate), anticholinergic drugs (inhibit gastric secretion, suppress gastric motility).
What are gastric ulcers? What are they commonly caused by?
Ulcers of the stomach that generally develop in the antral region and frequently caused by H. pylori which increases mucosal permeability to H ions.
What is the difference in S/S of a duodenal ulcer and a gastric ulcer?
Gastric ulcers also have the pattern of "pain-antacid-relief" AND "food-pain" but unlike duodenal ulcers, gastric ulcers tend to occur immediately after eating and tend to be CHRONIC rather than alternating between remission and exacerbation as duodenal ulcers.
Gastric ulcers usually occur between the ages of 50-70 and duodenal ulcers occur between 20-50 usually.
What are stress ulcers?
Acute form of peptic ulcers that tend to accompany the physiologic stress of severe illness; multisystem organ failure; or major trauma, including severe burns or head injury
How are stress ulcers classified and what causes each classification?
Ischemic ulcers or Cushing ulcers
Ischemic ulcers develop w/in hours of an event such as hemorrhage, severe burn, heart failure or sepsis that causes ischemia of the stomach and duodenal mucosa
Cushing ulcers are stress ulcers associated w/ severe head trauma or brain surgery which cause overstimulation of the vagal nuclei causing excessive acid secretion
What is dumping syndrome? What causes it?
It its the rapid emptying of hypertonic chyme from the surgically created, residual stomach into the small intestine 10-20 mins after eating (early dumping syndrome) or less commonly 1-3 hrs after eating (late dumping syndrome). It is often caused by a gastrectomy.
What are causes of malabsorption syndromes?
Inadequate digestion, pancreatic insufficiency, lactase deficiency, bile salt deficiency, and gluten-sensitive enteropathy.
What causes pancreatic insufficiency?
Chronic pancreatitis, pancreatic carcinoma, pancreatic resection, and cystic fibrosis.
Why is fat maldigestion the chief problem of pancreatic insufficiency?
Becausesalivary amylase and enzymes secreted by the intestinal brush border assist in carb and protein digestion, but not fats.
What are the most common signs of pancreatic insufficiency?
A large amount of fat in the stool and weight loss
Why are bile salts important to digestion?
Bile salts (conjugated bile acids) are necessary for the digestion and absorption of fats and fat soluble vitamins A,D,E, and K.
What are the causes of bile salt deficiency?
1) advanced liver disease
2) obstruction of the common bile duct
3) intestinal stasis which permits overgrowth of intestinal bacteria that deconjugate bile salts
4) diseases of the ileum which prevent the reabsorption and recycling of bile salts
What are the clinical manifestations of bile salt deficiency?
Increased fat in stools which leads to diarrhea and decreased plasma proteins and vitamin A,D,E, and K deficiencies
What are the S/S of vitamin A,D,E, and K deficiencies?
A: results in night blindness
D: results in decreased calcium absorption with bone demineralization (osteoporosis), bone pain, and fractures
E: uncertain effects but may cause testicular atrophy and neurologic defects in children
K: prolongs prothrombin time, leading to spontaneous development of purpura (bruising) and petechiae
What is ulcerative colitis?
A chronic inflammatory disease that causes ulceration of the colonic mucosa and extends proximally from the rectum into the colon.
What are some of the suggested causes of ulcerative colitis and which ones are most significant?
Dietary, infectious, genetic, and immunologic factors.
The most significant are the humoral and cellular immunologic factors associated with the disease
How does ulcerative colitis present in the colon?
Primary lesions are continuous with no skip lesions, limited to the mucosa, and not transmural. The rectum is almost always involved. The disease is most severe in the rectum and the sigmoid colon
What are the S/S of ulcerative colitis?
Large volumes of watery diarrhea, bleeding, cramping pain, and an urge to defecate.
What is the treatment for ulcerative colitis?
The first line treatment is 5-aminosalicylic acid. Steroids and salicylates suppress the inflammatory response. Immunosuppressive agents are used for chronic active disease.
Antibiotics, probiotics, nicotine
What is crohn disease?
It is an idiopathic inflammatory disorder that affects any part of the gastrointestinal tract from the mouth to the anus.
Although crohn disease can affect any part of the GI tract, where is it most likely to be located?
The distal small intestine and proximal lg colon (ileocolon)
What are some of the risk factors for crohn disease?
Family history, tobacco use, Jewish ethnicity, urban residency, and the CARD15/NOD2 gene mutation.
How does crohn disease progress and present in the GI tract?
Begins in the intestinal subucosa and spreads across the intestinal wall to involve the mucosa and serosa in areas overlying lymphoid tissue. It commonly presents with skip lesions.
What is the typical chronic lesion of crohn disease?
A granuloma having cobblestone projections of inflamed tissue surrounded by areas of ulceration.
What are common complications of crohn disease?
Lumen narrowing with inflammation, edema, and fibrotic strictures which usually require surgical resection.
What are the most common signs of crohn disease?
Abdominal pain and diarrhea are most common with passage of blood and mucus
What is the treatment for crohn disease?
Similar to that of UC. Immunomodulatory agents, TNF-alpha-blocking agents, and surgery
What is diverticulosis and diverticulitis?
Diverticulosis is asymptomatic diverticular disease.
Diverticulitis represents inflammation.
Most common in those over 60.
Where is it most commonly located and what are the S/S?
The left colon
When the diverticula are not inflamed, s/s are usually vague or absent.
Diverticulitis presents with fever, leukocytosis, and tenderness fo the lower left quadrant.
What are the s/s of apendicitis? What are the most serious complications?
Pain may be vague at first, move then to RLQ with rebound tenderness. N/V, anorexia, fever, and leukocitosis.
The most serious complications are perforation, peritonitis, and abscess formation.
What are the manifestations of liver disease?
Portal HTN, splenomegaly, ascites, hepatic-encephalopathy, jaundice, and hepatorenal syndrome
What is portal hypertension?
Abnormally high blood pressure in the portal venous system primarily caused by resistance to portal blood flow. It can be caused by intrahepatic, pasthepatic, or prehepatic causes. It is the most serious complication of liver disease.
What is hepatopulmonary syndrome?
Pulmonary htn associated w/ the release of vasodilators that effect pulmonary arterioles and is associated with portal htn and severe liver disease. Vasodilators are being released to decrease portal htn.
What are the long term causes of portal htn?
Varices: particularly in the lower esophagus and stomach but also in the rectum
Splenomegaly: caused by increased pressure in the splenic vein
Ascites: caused by increased hydrostatic pressure in the mesenteric tributaries of the portal vein
Hepatic encephalopathy: characterized by central nervous system disturbances w/ astrocyte cchanges that lead to alterations of consciousness
S/S or portal htn?
Most common is the vomiting of blood from bleeding esophageal varices. Slow, chronic bleeding from varices causes anemia or melena
What is the most common manifestation of congestive splenomegaly caused by portal htn?
Cirrhosis is the most common cause of ____ and ____ is the most common complication of cirrhosis.
ascites and ascites
What are the clinical manifestations and treatment of ascites?
S/S: weight gain, abd. distention, and increased abd. girth.
Treatment: paracentesis to relieve discomfort, dietary salt restriction and potassium-sparing diuretics.
Monitor serum electrolytes: hyponatremia and hypokalemia are common
What is hepatic encephalopathy and what is its pathophysiology?
It is a complex neurologic syndrome characterized by impaired cognitive function, flapping tremor (asterixis), and electroencephalogram (EEG) changes.
Liver dysfunction and collateral vessels that shunt blood around the liver to the systemic circulation permit neurotoxins and other harmful substances absorbed from the GI tract to circulate freely to the brain. The most hazardous substances are end products of intestinal protein digestion, particularly ammonia.
The astrocyte is the most vulnerable b/c it is the site of ammonia detoxification in the brain.
S/S of hepatic encephalopathy: initial and late symtoms?
Initial: subtle changes in personality, memory loss, irritability, lethargy, and sleep disturbances are common.
Late: confusion, flapping tremor of the hands, stupor, convulsions, and coma.
What are the two causes of jaundice?
1: Hepatobiliary mechanisms (intrahepatic and extrahepatic obstructive jaundice)
2: Hematologic mechanisms
What differences in serum bilirubin is observed for each cause of jaundice?
1: In hepatobiliary jaundice, the bilirubin has been conjugated by the liver so elevated levels of serum conjugated bilirubin will be present
2: In hematologic caused jaundice, there will be elevated serum levels of unconjugated bilirubin. Hemolysis occurs faster than the liver can process the bilirubin
What is hepatorenal syndrome (HRS)?
It is functional kidney failure (prerenal renal failure) caused by advanced liver diases, particularly cirrhosis with portal hypertension.
What are the causes of hepatorenal syndrome?
1: The diseased liver fails to remove excessive angiotensin, vasopressin, prostaglandins, and catecholamines from the blood which travel to the kidneys and cause vasoconstriction.
2: Vasoconstriction also may be a compensatory response to portal hypotension and valdiation in the splanchnic circulation
3: Systemic vasodilation caused by increases in nitric oxide and other substances also may contribute to vascular alterations and renal failure in advanced liver disease
Manifestations of hepatorenal syndrome?
Oliguria, jaundice, ascites, gastrointestinal bleeding
Sodium and water are retained, hypotension occurs r/t peripheral vasodilation due to advanced liver disease.
Discuss the basics about each viral hepatitis.
HAV: Usually transmitted fecal-oral route and risk factors include crowded, unsanitary conditions and food and water contamination
HBV: Transmitted through contact w/ infected blood, body fluids, and contaminated needles. Maternal transmission possible. Vaccine available to prevent Hep B.
HCV: Responsible for most cases of post-transfusion hepatitis. Implicated in infections r/t IV drug use. 50-60% result in chronic hepatitis
HDV: Depends of hepatitis B for replication
HEV: fecal-oral transmission, prevalent in developing countries.
HGV: transmitted parenterally and sexually
What are the pathologic lesions of hepatitis?
Hepatic cell necrosis, scarring, Kupffer's cell hyperplasia, and infiltration by monocytes.
What are the abnormal lab values found in acute viral hepatitis?
Elevated serum aspartate transaminase (AST) and alanine transaminase (ALT).
The clinical manifestations of the various types of heatitis are very similar. The clinical course of hepatitis usually consists of which four phases?
Incubation, prodromal, icteric, and recovery
Discuss the prodromal phase of viral hepatitis.
Begins about 2 wks after exposure and ends w/ appearance of jaundice. Fatigue, anorexia, malaise, nausea, vomiting, headache, hyperalgia, cough, and low-grade temp precede the onset of jaundice. Infection is HIGHLY TRANSMISSIBLE during this phase.
Discuss the icteric phase.
Begins about 1-2 wks after the prodromal phase and lasts 2-6 wks. Hepatocellular destruction causes jaundice or icterus. This us the actual phase of illness. Liver is enlarged, smooth, and tender, and percussion over the liver causes pain.
Discuss the posticteric or recovery phase of viral hep,
Begins w/ resolution of jaundice at about 6-8 wks after exposure. In most cases liver function returns to normal w/in 2-12 wks after the onset of jaundice.
What is fulminant hepatitis?
A clinical syndrome resulting in severe impairment or necrosis of liver cells and potential liver failure. May occur as a complication of hep C or B (particularly B). Also Acetaminophen overdose (leading cause of acute liver failure in the U.S)
What is cirrhosis?
An irreversible inflammatory disease that disrupts liver structure and function and is one of the leading causes of death in the U.S.
What are the four types of cirrhosis?
1) Alcoholic cirrhosis, laennec cirrhosis, portal cirrhosis, fatty cirrhosis
2) Biliary cirrhosis (intra or extrahepatic obstruction of bile flow), Primary and secondary biliary cirrhosis
3) postnecrotic cirrhosis
4) metabolic cirrhosis
What are the causes of alcoholic cirrhosis?
toxic effects of chronic, excessive alcohol intake; acetaldehyde formed by alcohol metabolism damages hepatocytes
What is the pathophysiology of alcoholic cirrhosis?
Fatty liver, inflammation (alcoholic steatohepatitis), and derangement of the lobular architecture by necrosis and fibrosis (cirrhosis) with obstruction of biliary and vascular channels
What is the cause of primary and secondary biliary cirrhosis?
Primary: unknown, possible autoimmune mechanisms
Secondary: Obstruction by neoplasms, strictures, or gall-stones
What is the pathophysiology of primary and secondary cirrhosis?
Primary: inflammation and scarring of lobular bile ducts
Secondary: Inflammation and scarring of bile ducts proximal to the obstruction
What are the causes of postnecrotic cirrhosis?
Viral hepatitis caused by hepatitis A,B, or C virus; drugs or other toxins; autoimmune destruction
What is the pathophysiology of postnecrotic cirrhosis?
Replacement of necrotic tisue with cirrhotic tissue, particularly fibrous, nodulr scar tissue
What are the causes of metabolic cirrhosis?
Metabolic defects and storage disease, such as alpha1-antitrypsin deficiency, glycogen storage disease, hemochromatosis, Wilson disease, galactosemia
What is the pathophysiology of metabolic cirrhosis?
Inflammation and scarring w/ specific morphologic changes r/t cause.
What does cirrhosis cause?
hepatomegaly, splenomegaly, ascites, gastrointestinal hemorrhage, portal htn, hepatic encephalopathy, and esophageal varices.
What are the most common and distressing symptoms of primary and secondary biliary cirrhosis?
jaundice and pruritis. RUQ pain is also common
What is cholelithiasis and cholecystitis?
Cholelithiasis is the formation of gallstones
Cholecystits is th einflammation of the gallbaldder or cytic duct
What are the two types of gallstones and which is most prevalent?
Cholesterol and pigmented stones. Cholesterol stones are most common. Pigmented stones occur later in life and are associated with cirrhosis.
How do cholesterol gallstones form?
From bile that is supersaturated with cholesterol produced in the liver
What are the s/s of cholelithiasis?
Epigastric and rt hypochondrium pain and intolerance to fatty foods are the cardianl symptoms of cholelithiasis. The pain, often called biliary colic, is most characteristic and is caused by the lodging of one or more gallstones in the cystic or common duct. Pain usually radiates to the mid-upper back.
What are the s/s of cholecystitis?
Similar to that of cholelithiasis. The person will usually also have fever, leukocytosis, rebound tenderness, and abd. muscle guarding.
Pancreatitis is associated with clinical conditions?
Alcoholism, obstructive biliary tract disease, peptic ulcers, trauma, hyperlipidemia, and certain drugs.
Why does acute pancreatitis develop?
B/c of an injury or disruption of the pancreatic ducts or acini that permits leakage of pancreatic enzymes into pancreatic tissue. The leaked enzymes initiate autodigestion and acute pancreatitis. Bile reflux into the pancreas occurs if gallstones obstruct the common bile duct
What happens when autodigestion of the pancreas occurs?
The activated trypsin, elastase, and lipases destroy tissue and cell membranes, which causes edema, vascular damage, hemorrhage, and necrosis. Toxic enzymes are also released into the blood-stream and cause injury to vessels and other organs such as the lungs and kidneys.
What are the serum diagnostic findings for chronic pancreatitis?
Elevated serum amylase and lipase are characteristic diagnostic features and serum lipase is more specific and sensitive.
What is the cardinal symptom of acute pancreatitis? What are some of the other symptoms?
Mild to severe epigastric or midabdominal pain. The pain may radiate to the back.
Fever and leukocytosis accompany the inflammatory response. N/V are caused by hpermotility or paralytic ileus. Hypotension and shock frequently occur b/c plasma volume is lost as enzymes and kinins released into the circulation increase vascular permeability and dilate vessels.
What is the goal of treatment for acute pancreatitis?
To stop the process of autodigestion and prevent systemic complications. Narcotics for pain relief, parenteral fluids to restore blood volume and prevent hypotension and shock.
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