Patho Chapter 36

B - Bacterial infections lead to secretory diarrhea. A nonabsorbable substance in the intestine leads to osmotic diarrhea. Hypotonic diarrhea is not a form of diarrhea. Food is not mixed properly, digestion and absorption are impaired, and motility is increased, leading to motility diarrhea.

A - A nonabsorbable substance in the intestine leads to osmotic diarrhea. Infections lead to secretory diarrhea. Hypotonic diarrhea is not a form of diarrhea. Food is not mixed properly, digestion and absorption are impaired, and motility is increased leading to motility diarrhea.

A - Visceral pain arises from a stimulus (distention, inflammation, and ischemia) acting on an abdominal organ. Somatic is a form of parietal pain. Parietal pain, from the parietal peritoneum, is more localized and intense than visceral pain, which arises from the organs themselves. Referred pain is visceral pain felt at some distance from a diseased or affected organ.

C - Esophageal varices is the most common disorder associated with upper GI bleeding. Diverticulosis could lead to bleeding, but it would be lower GI rather than upper. Hemorrhoids can lead to bleeding, but they would be lower GI. Cancer could lead to upper GI bleeding, but peptic ulcers and varices are identified as more common.

C - Bleeding from the upper GI tract can also be rapid enough to produce hematochezia (bright red stools). Melena is a black or tarry stool. Occult bleeding is hidden bleeding. Hematemesis is vomiting blood.

C - Gastroesophageal reflux is due to loss of muscle tone at the lower esophageal sphincter. The resting tone of the lower esophageal sphincter (LES) tends to be lower than normal from either transient relaxation or weakness of the sphincter. Gastroesophageal reflux is not due to fibrosis, stimulation of sympathetic nerves, or reverse peristalsis.

D - Regurgitation, dysphagia, and epigastric discomfort after eating are common in individuals with hiatal hernia. Pyloric stenosis is manifested by projectile vomiting. Gastric cancer is not manifested by heartburn. Achalasia is a form of functional dysphagia caused by loss of esophageal innervation.

B - Strangulation of the hernia is a major complication. Neither hemorrhage, peritonitis, nor ascites is associated with paraesophageal hiatal hernia complications.

C - The pylorus is the opening between the esophagus and the duodenum; the obstruction is pyloric. Ileocecal obstruction is in the small intestine. Hiatal hernia is related to the esophagus. Hiatal obstruction is related to the esophagus.

A - Large intestine obstruction usually presents with hypogastric pain and abdominal distention. Neither diarrhea, epigastric pain, nor rectal bleeding occurs.

B - Chronic gastritis is classified as type A (fundal) or type B (antral), depending on the pathogenesis and location of the lesions. Gastritis is not classified by severity, age, or symptoms, but by location.

A - Pernicious anemia can develop because the damage to the mucosa makes the intrinsic factor less available to facilitate vitamin B12 absorption in the ileum. None of the other options would result from this damage.

B - Peptic ulcer disease is caused by breaks in the mucosa and the presence of corrosive substances. High gastrin occurs, but the disease is due to breaks in the mucosa. Vagal activity increases. Gastric erosions occur, but they are not due to high ammonia.

A - Duodenal ulcers occur with greater frequency than other types of peptic ulcers and are commonly caused by H. pylori infection and NSAID use. Neither antacids nor caffeinated beverages contribute to ulcer formation. Fiber is important, but consuming limited fiber will not contribute to ulcer formation.

B - A Cushing ulcer is a stress ulcer associated with severe head trauma or brain surgery that results from decreased mucosal blood flow and hypersecretion of acid caused by overstimulation of the vagal nerve. Cushing ulcers are not associated with infections or H. pylori. Curling ulcers develop secondary to burns.

B - The primary clinical manifestation of stress-related mucosal disease is bleeding, which is uncommon, but occurs more readily with the presence of coagulopathy and more than 48 hours of mechanical ventilation. None of the other options is associated with stress ulcers.

A - Clinical manifestations of bile salt deficiency are related to poor intestinal absorption of fat and fat-soluble vitamins (A, D, E, and K). Neither water-soluble vitamins nor minerals require bile salts for absorption; thus, they are not affected. Protein breakdown is facilitated by bile, but its absorption is not dependent upon it.

C - One of the complications is anemia due to iron malabsorption, which may result from decreased acid secretion. Diarrhea, not constipation, occurs. The reflux would be alkaline, not acidic. Hiccups are not associated with gastrectomy.

A - Ulcerative colitis is characterized by abdominal pain, fever, elevated pulse rate, frequent diarrhea (10-20 stools/day), urgency, obviously bloody stools, and continuous, crampy pain. Hiatal hernia is most often asymptomatic and would not be manifested by abdominal pain. Pyloric obstruction would be manifested by forceful or projectile vomiting. Achalasia would be manifested by difficulty or uncomfortable swallowing.

C - Pancreatic insufficiency is the deficient production of lipase by the pancreas. Pancreatic insufficiency is not associated with the deficient production of insulin, amylase, or bile.

C - Appendicitis is manifested originally with periumbilical pain that then migrates to the right lower quadrant pain with rebound tenderness. A low-grade fever is common. Colon cancer may be asymptomatic, followed by bleeding. Pancreatitis is manifested by vomiting. Hepatitis would be manifested by upper abdominal pain, not lower.

D - The most common cause of chronic mesenteric ischemia is atherosclerosis. Neither poor nutrition nor anemia leads to vascular insufficiency. An aneurysm would lead to acute vascular insufficiency.

A - Occlusion of blood flow is often precipitated by embolism. This type of occlusion is not associated with pancreatitis, chronic malnutrition, or hypovolemic shock.

B - Ischemia and necrosis (intestinal infarction) alter membrane permeability. Initially, there is increased motility, nausea, and vomiting. Mucosal alteration causes fluid to move from the blood vessels into the bowel wall and peritoneum. Fluid loss causes hypovolemia. Arterial insufficiency is not related to liver failure. Bleeding may occur, but hypovolemia is related to fluid shifts. Fluid shifts lead to hypovolemia; it is not due to overstimulation of the parasympathetic nerves.

B - Leptin, a product of the obesity gene (Ob gene), acts on the hypothalamus to suppress appetite and functions to regulate body weight within a fairly narrow range. Leptin levels increase as the number of adipocytes increases; however, for unknown reasons, high leptin levels are ineffective at decreasing appetite and energy expenditure, a condition known as leptin resistance. Leptin resistance fails to inhibit oriexigenic hypothalamic satiety signaling and promotes overeating and excessive weight gain. Insulin becomes resistant, not present in excess. Leptin resistance, not adipocyte failure, leads to obesity. Malabsorption does not lead to obesity, but primarily to weight loss.

B - Portal hypertension occurs secondarily to cirrhosis of the liver. Portal hypertension is not associated with thrombosis of the spleen, left ventricular failure, or renal stenosis.

C - Vomiting of blood from bleeding esophageal varices is the most common clinical manifestation of portal hypertension. Neither rectal, duodenal, nor intestinal bleeding is a common clinical manifestation of portal hypertension.

C - Hepatic encephalopathy effect on the liver prevents end products of intestinal protein digestion, particularly ammonia, from being converted to urea by the diseased liver. Impaired ammonia metabolism leads to the symptoms of hepatic encephalopathy. Symptoms are primarily neurologic, not jaundice oriented. Manifestations associated with hepatic encephalopathy are not associated with hyperbilirubinemia and jaundice, fluid, and electrolyte imbalances or decreased cerebral blood flow.

B - Excessive hemolysis (breakdown) of red blood cells can cause hemolytic jaundice (prehepatic jaundice). Red blood cell breakdown is not associated with the other forms of jaundice.

B - The icteric phase is manifested by jaundice, dark urine, and clay-colored stools. The liver is enlarged, smooth, and tender, and percussion causes pain. Fatigue and vomiting occur during the prodromal stage. Resolution occurs in the recovery phase. Fulminant liver failure does not involve icterus.

C - The clinical manifestations of alcoholic steatohepatitis include jaundice, hepatomegaly, and testicular atrophy. These symptoms are not a result of a bacterial or viral infection, or a drug overdose.

A - Alcoholic cirrhosis is caused by the toxic effects of alcohol metabolism on the liver. Alcohol is transformed to acetaldehyde, and excessive amounts significantly alter hepatocyte function and activate hepatic stellate cells, a primary cell involved in liver fibrosis. Bile toxicity does not cause alcoholic cirrhosis. Acidosis does not cause alcoholic cirrhosis. Fatty infiltrations do not cause alcoholic cirrhosis.

D - The majority of gallstones are composed of cholesterol. The other options are not found in high quantities.

D - Jaundice is due to obstruction of the common bile duct. This form of jaundice is not due to obstruction of the intrahepatic canaliculi, gallbladder, or the cystic duct.

B - Cholecystitis can be acute or chronic, but both forms are almost always caused by a gallstone lodged in the cystic duct. Accumulation of bile in the hepatic duct would not lead to cholecystitis. Neither the accumulation of fat nor a viral infection leads to cholecystitis.

C - In pancreatitis there is backup of pancreatic secretions and activation and release of enzymes (activated trypsin activates chymotrypsin, lipase, and elastase) within the pancreatic acinar cells. The enzymes become activated, triggering the resulting autodigestion, inflammation, and oxidative stress. The tissue damage associated with pancreatitis is not due to insulin toxicity or to hydrochloric acid reflux.

C - Epigastric or midabdominal pain ranging from mild abdominal discomfort to severe, incapacitating pain is one of the manifestations of pancreatitis. Right lower pain would be a symptom of appendicitis. Right upper quadrant pain would be manifestation of liver inflammation. Suprapubic pain would be related to full bladder or colon problems.

A - Adenocarcinomas are more prevalent in males and are associated with cigarette smoking, obesity, and gastroesophageal reflux disease (GERD). Intestinal parasites, ingestion of salty foods, or the use of antacids does not lead to adenocarcinoma of the esophagus.