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Brown blotches scattered throughout the esophagus B. Normal-appearing esophagus C. Red patches in the distal esophagus D. Reddish streaks throughout the pharynx and upper esophagus E.
White patches adherent to the esophagus [1. A pediatric feeding tube is passed orally to 20 cm without difficulty, with gastric secretions aspirated. Which of the following is the most likely diagnosis? Congenital heart disease B. Floppy epiglottis C. Respiratory distress syndrome D. Tracheoesophageal fistula E.
Zenker diverticulum Answers [1. Adenocarcinoma is the most common malignancy of the lower third of the esophagus and is strongly associated with Barrett esoph- agus. Squamous cell carcinoma is the most common type of cancer of the esophagus worldwide and usually affects the upper or middle region of the esophagus. This patient probably has HIV, and the clinical syndrome of painful and difficult swallowing is consistent with Candida esophagi- tis.
Endoscopy probably would reveal white plaques adherent to the esophagus. Other causes of esophagitis include herpes simplex infec- tion, cytomegalovirus CMV infection, and chemical-induced condi- tions such as those resulting from lye suicide attempt. The vast majority newborns with TE fistulae involve a nonpatent esophagus that is diagnosed by the inability to pass a feeding tube.
However, the baby in this case most likely has an unusual type of TE fistula H type in which the esophagus is patent but there is a con- nection between the esophagus and the trachea. When the baby feeds, the formula is aspirated into the tracheobronchial tree, leading to choking and cyanosis. This condition may be diagnosed with a radi- ologic contrast study and requires surgical correction. The gastrointestinal tract. Philadelphia, PA: Saunders, , — Liu C, Crawford JM.
Robbins and Cotran Pathologic Basis of Disease, 7th ed. Philadelphia, PA: Elsevier Saunders, —9. Rubin E. Essential Pathology, 3rd ed. The pain is worse at night and is somewhat better imme- diately after he eats. He has not had any fever, nausea, or vomiting. He takes approximately one mg acetaminophen tablet a week for headaches but does not take any other medications. Upper endoscopy reveals a 2-cm mucosal defect in the antrum of the stomach. There is mild edema in the adjacent mucosa, but there is no thickening of the edges of the ulcer.
Upper endoscopy reveals a 2-cm gastric ulcer. Peptic ulcers occur most frequently in the stomach and duodenum. Peptic ulcers are often remitting, relapsing lesions that may be seen in young adults but more often occur in middle-aged to older adults. They are usually chronic, solitary lesions caused by the action of gastric acid and pepsin, both of which are thought to be required for the development of peptic ulcers.
Helicobacter pylori infection of gastric mucosa is present in 90 to percent of patients with a duodenal ulcer and 70 percent of those with a gastric ulcer. Damage to the pro- tective mucus layer by bacterial urease and protease exposes the underlying epithelial cells to the influence of acid-peptic digestion and may lead to inflammation. The chronically inflamed mucosa is more susceptible to acid- peptic injury and thus more prone to ulceration.
Diaphragmatic hernias differ from hiatal hernias in that the defect in the diaphragm does not involve the hiatal orifice. Hypertrophy of the mus- cularis propria of the pylorus results in a palpable mass and obstruction with associated regurgitation and persistent projectile vomiting. Male infants are affected 3 to 4 times more often than are females. Treatment consists of surgical splitting of the muscle.
Pyloric stenosis may be acquired in adults with chronic antral gastritis or peptic ulcers near the pylorus. Other causes of acquired pyloric stenosis include gastric carci- nomas, lymphomas, and adjacent carcinomas of the pancreas.
Gastritis: Inflammation of the gastric mucosa. The inflammation may be predominantly acute, with neutrophilic infiltration, or chronic, with a predominance of lymphocytes and plasma cells. The classification and pathogenesis of acute and chronic gastritis are discussed below. Ulcer: A disruption of the mucosa extending through the muscularis mucosa into the submucosa or deeper. Ulcers may occur anywhere in the gastrointestinal tract but are seen most often in the stomach and duode- num, associated with peptic ulcer disease.
Peptic ulcer disease: Peptic ulcers are chronic, usually solitary lesions of the gastrointestinal mucosa caused by the action of acid-peptic juices. Both acid and pepsin are necessary for peptic ulcer disease to develop. Hypertrophic gastropathy: A group of uncommon conditions character- ized by enlargement of the rugal folds of the gastric mucosa caused by hyperplasia of the mucosal epithelial cells. These three condi- tions may mimic gastric cancer on radiographic studies.
The excessive amount of acid secretion in the second and third conditions predisposes patients to peptic ulceration. The pyloric sphincter demarcates the antrum from the duodenum. Infoldings of mucosa and submucosa, or rugae, extend longi- tudinally and are most prominent in the proximal stomach. The secretion of gastric acid is proportional to the total number of parietal cells in the glands of the body and fundus of the stomach.
The secre- tory process may be divided into three phases: cephalic, gastric, and intestinal. Gastrin, which is released in response to vagal stimulation, is the most important mediator of gastric acid secretion. Histamine also stimulates acid secretion. Thus, surgical interruption of vagal stimulation and inhibition of histamine stimulation by blocking the H2 receptor on the parietal cell mem- brane are effective maneuvers for reducing gastric acid production.
Several factors act together to protect the stomach from digestion by gastric acid. Mucus secretion, bicarbonate secretion, the epithelial barrier formed by tight intercellular junctions, a rich mucosal blood flow that removes back-diffused acid, and reflex vasodilation in response to toxins or acid breach of the epithe- lial layer all contribute to the mucosal barrier.
Gastritis Inflammation of the gastric mucosa occurs in a variety of clinical situations and may be acute or chronic. Acute gastritis varies in severity; it may be asympto- matic, cause epigastric pain with nausea and vomiting, or present with massive hematemesis. In chronic gastritis, there are chronic mucosal inflammatory changes, usually without erosions, that may lead to mucosal atrophy and dysplastic epithelium, predisposing the patient to the development of carcinoma see Table Most cases of chronic gastritis are thought to be associated with chronic H.
Chronic gastritis that results from H. Most patients improve with antibiotic treatment, and relapses of chronic gastritis are associated with a recurrence of infection. Patients are at risk for developing peptic ulcer disease and gastric cancer, including adenocarcinoma and lymphoma. Patients with autoimmune gastritis diffuse atrophic gastritis may have nausea, vomiting, and upper abdominal pain.
Patients usually have autoanti- bodies to gastric parietal cells or intrinsic factor. Destruction of gastric glands of the fundus leads to loss of acid production achlorhydria and hypergas- trinemia.
Loss of intrinsic factor leads to pernicious anemia. Thus, patients with autoimmune gastritis may initially present with peripheral neuropathy symptoms from B12 deficiency in addition to their abdominal symptoms. Patients may also have other autoimmune disorders, such as Hashimoto thy- roiditis or Addison disease.
Peptic Ulcer Disease Peptic ulcers are usually solitary, arising from exposure of the mucosal epithe- lium to acid-peptic secretions. Peptic ulcer disease PUD occurs most often in middle-aged to older adults. The most common anatomic sites are the duo- denum and the stomach, in a ratio of see Table Helicobacter pylori can cause damage by 1 secreting urease, protease, and phospholipases, 2 attracting neutrophils that release myeloperoxidase, and 3 promoting thrombotic occlusion of capillaries, leading to ischemic damage of the epithelium.
Complications of PUD include anemia, hemorrhage, perforation, and obstruction. Malignant transformation is rare and is related to underlying chronic gastritis. Gastric Cancer Most 90 to 95 percent gastric malignancies are adenocarcinomas, with a smaller number of lymphomas, carcinoids, and spindle cell tumors. Although the incidence of gastric carcinoma has been decreasing in Western countries over the last 50 years, the prognosis is still poor, with a 20 percent 5-year survival.
Risk factors for gastric carcinoma include nitrates; smoked, salted, or pickled foods; lack of fresh fruits and vegetables; chronic atrophic gastritis; H. Two types of gastric carcinoma are recognized: the intestinal type and the diffuse type see Table These may represent two distinct forms of gastric carcinoma.
Dissemination of gastric carcinoma, as well as other primary abdominal adenocarcinomas, to the ovaries is known as Krukenberg tumors. Upper endoscopy reveals chronic gastri- tis of the fundus with flattened gastric mucosa but no acute ulceration.
Which of the following is most likely to be associated with this finding? Autoantibodies to parietal cells B. Diet high in nitrites C. Hyperchlorhydria D. Hypoparathyroidism E.
Workup finds his serum gastrin levels to be markedly elevated, and an abdominal CT scan finds a large mass in the tail of the pancreas. A biopsy from this pancreatic mass finds an islet-cell adenoma that secretes gastrin. Which of the following is the best diagnosis? Hypertrophic-hypersecretory gastropathy B.
Linitis plastica C. Verner-Morrison syndrome E. She also has noticed loss of appetite and early satiety. Evaluation reveals an ulcerative mass located along the lesser curvature, and a biopsy shows an infiltrating adenocarcinoma. Further evaluation by abdominal CT imaging shows bilateral ovarian masses. Which of the following is this patient most likely to have?
Barrett mucosa B. Krukenberg tumor C. Primary ovarian neoplasm D. Uterine cancer Answers [2. Chronic atropic gastritis often is associated with autoantibodies to parietal cells.
Loss of these cells leads to decreased gastric acid hypochlorhydria and decreased intrinsic factor. Lack of intrinsic factor results in deceased or absent vitamin B12 absorption perni- cious anemia. Zollinger-Ellison syndrome refers to gastric gland hyperplasia sec- ondary to excessive gastrin secretion by a tumor gastrinoma , usu- ally found in the pancreas.
The excess gastrin increases the thickness of the gastric mucosa and increases the acid production by the stom- ach. This results in the formation of recurrent peptic ulcers, especially within the duodenum and jejunum. As a result, the classic clinical triad associated with the Zollinger-Ellison syndrome is the combina- tion of increased acid production by the stomach, peptic ulcers of the duodenum and jejunum, and an islet-cell tumor of the pancreas.
Del Valle J. Peptic ulcer disease and related disorders. Philadelphia, PA: Elsevier Saunders, —9, — He has not had diarrhea, nausea, vomiting, or other gastrointestinal symp- toms. He does not take any medications and denies using illegal drugs. He underwent a blood transfusion with several units in after an automobile accident.
Physical examination reveals generalized jaundice, a firm nodular liver edge just below the right costal margin, and a mildly protuberant abdomen with a fluid wave. He had a long asymp- tomatic period and now has signs of advanced liver disease.
His firm nodular liver probably represents cirrhosis, with scarring of the liver parenchyma along with regenerative nodules. His transaminases ALT and AST are only mildly elevated but these tests may be within normal limits, particularly early in the course of disease.
The fact that he has impaired hepatic synthesis of albumin and coagulation factors indicates that he has very advanced disease, especially in light of the enormous reserve and regenerative capacity of the liver. The accumulation of ascitic fluid in the peritoneum usually represents portal hypertension, an increase in pressure in the portal venous system that typically results from increased intrahepatic resistance to portal blood flow because of perisinusoidal deposition of collagen.
CLINICAL CASES 29 Definitions Cirrhosis: Although often used as a clinical description, cirrhosis is really a pathologic diagnosis that is characterized by disruption of normal liver architecture by interconnecting fibrous scars and the creation of parenchymal nodules by regenerative activity and the network of scars.
This pathologic process can be thought of as the final common pathway of many causes of chronic hepatic injury. The inciting factor causes hepatocyte necrosis and deposition of collagen. At some point the fibro- sis becomes irreversible, and cirrhosis then develops. Cirrhosis can be classified according to morphologic features micronodular, most often caused by alcohol, or macronodular, most often resulting from viral hepatitis or according to the etiology: alcoholic, cardiac, biliary, or drug induced.
However, a single cause of hepatic injury can produce a variety of pathologic patterns, and any given morphology can result from a vari- ety of causes. See Figure Acute hepatitis: The influx of acute inflammatory cells, which may follow or precede hepatocyte necrosis. The morphologic changes in both acute and chronic hepatitis are common to the hepatitis viruses and can be mimicked by drug reactions.
Chronic hepatitis: It can be due to numerous causes, all of which result in hepatic inflammation and necrosis for at least 6 months, but without the nodular regeneration and architectural distortion of cirrhosis. Later, the vacuoles coalesce into macrovesicles, compressing and displacing the nucleus so that the hepatocyte resembles a lipocyte. Grossly, the liver becomes enlarged with a yellow, greasy appearance. Steatosis is usually reversible with discontinuation of the underlying cause, but it may lead to the develop- ment of fibrosis around the central veins and sinusoids and ultimately to cirrhosis.
The liver is organized into 1- to 2-mm hexagonal lobules, with cords or plates of hepatocytes radiat- ing out from the central vein, the terminal venules of the hepatic vein. At each corner of the hexagon are the portal tracts, composed of the terminal branches of the portal vein and the hepatic artery, as well as the bile duct. Arterial and portal venous blood flows through sinusoids, between the cords of hepatocytes, giving them a rich vascular supply 25 percent of cardiac output before draining into the central vein.
Bile is secreted into bile canaliculi between adjacent hepatocytes and flows into the canals of Herring and then to the lobular bile ducts. The organization of a lobule is shown in Figure The liver serves many functions, including maintenance of carbohydrate, lipid, and amino acid metabolism; synthesis of nearly all serum proteins; and detoxification and excretion of noxious substances in the bile.
One such sub- stance is bilirubin, a waste product that is the metabolite of the breakdown of heme from senescent red blood cells. It undergoes conjugation with glu- curonic acid in the hepatocyte to form conjugated or direct bilirubin, which is water-soluble and nontoxic, and then is excreted into the bile canaliculus.
When liver disease causes jaundice, affected individuals usually have reflux of conjugated bilirubin into the blood, which causes the visible icterus when deposited in tissues, as well as the dark urine resulting from urinary excretion of elevated levels of water-soluble conjugated bilirubin.
Figure Microscopic image of liver cirrhosis. Each virus can produce virtually indistinguishable clinical syndromes. Affected individuals often present with a prodrome of nonspecific constitu- tional symptoms, including fever, nausea, fatigue, arthralgias, myalgias, headache, and sometimes pharyngitis and coryza. This is followed by the onset of visible jaundice caused by hyperbilirubinemia, tenderness and enlargement of the liver, and dark urine caused by bilirubinuria.
The clinical course, out- comes, and possible complications vary with the type of virus causing the hep- atitis. A comparison of features of these five viruses is shown in Table Hepatitis A and hepatitis E are very contagious and are transmitted by the fecal-oral route, usually by contaminated food or water in areas where sani- tation is poor, and in day-care situations by children.
Hepatitis A is found worldwide and is the most common cause of acute viral hepatitis in the United States. Both hepatitis A and hepatitis E infections usually lead to self-limited illnesses and generally resolve within weeks. Almost all patients with hepatitis A recover completely and have no long-term complica- tions. Most patients with hepatitis E also have uncomplicated courses, but some patients, particularly pregnant women, have been reported to develop severe hepatic necrosis and fatal liver failure.
Hepatitis B is the second most common type of viral hepatitis in the United States, and it is usually sexually transmitted.
It also may be acquired parenterally, for example, through intravenous drug use, and during birth, from chronically infected mothers.
The outcome then depends on the age at which the infection was acquired. Up to 90 percent of infected newborns develop chronic hepatitis B infection, which places an affected infant at signifi- cant risk of hepatocellular carcinoma later in adulthood.
Among individuals infected later in life, approximately 95 percent recover completely without sequelae. Between 5 and 10 percent of patients will develop chronic hepatitis and may progress to cirrhosis.
Also, a chronic carrier state may be seen in which the virus continues to replicate but does not cause hepatic damage in the host. Hepatitis C is transmitted parenterally by blood transfusions or intra- venous drug use and rarely by sexual contact. It uncommonly is diagnosed as a cause of acute hepatitis, often producing subclinical infection, but frequently is diagnosed later as a cause of chronic hepatitis. The natural history of infec- tion is not completely understood, but 50 to 85 percent of patients with hep- atitis C will develop chronic infection.
Hepatitis D is a defective RNA virus that requires the presence of the hepatitis B virus to replicate. It can be acquired as a coinfection simultane- ously with acute hepatitis B or as a later superinfection in a person with a chronic hepatitis B infection.
Hepatitis Serologies Clinical presentation does not reliably establish the viral etiology, and so sero- logic studies are used to establish a diagnosis. If anti-hepatitis C antibody is present, acute hepatitis C is diagnosed, but the test may be nega- tive for several months.
The hepatitis C polymerase chain reaction PCR assay, which becomes positive earlier in the disease course, often aids in the diagnosis.
Acute hepatitis B infection is diagnosed by the presence of hepati- tis B surface antigen HBsAg in the clinical context of elevated serum transaminase levels and jaundice. There is often an interval of a few weeks between the disappearance of HBsAg and the appearance of anti-HBsAb, which is referred to as the window period. Hepatitis B pre- core antigen HBeAg represents a high level of viral replication.
It is almost always present during acute infection, but its persistence after 6 weeks of ill- ness is a sign of chronic infection and high infectivity. Persistence of HBsAg or HBeAg is a marker for chronic hepatitis or a chronic carrier state; elevated or normal serum transaminase levels distinguish these two entities see Table Hepatitis B serology.
There may be hepatocyte swelling called ballooning degeneration, as well as liver cell necrosis, including frag- mentation and condensation of hepatocytes, forming intensely eosinophilic Councilman bodies, which are characteristic of viral hepatitis. Formation of ropelike eosinophilic structures within hepatocytes, called Mallory bodies, is typical of alcoholic hepatitis.
Another finding in acute hepatitis is an inflam- matory infiltrate in the portal tracts. Chronic hepatitis C is characterized by the formation of lymphoid aggregates in the portal tracts as well as fatty changes in hepatocytes. Ground glass cells often are seen in chronic hepatitis B. If inflammation is limited to the portal tracts, the disease is milder and the prognosis is better. When it spills over into the peri- portal parenchyma, destroying the limiting plate piecemeal necrosis or extend- ing across lobules, such as the portal area to the central vein, which is termed bridging necrosis, the disease is more progressive and the prognosis is poorer.
Complications of Chronic Hepatitis Many patients with chronic hepatitis have stable disease, but a significant fraction develops ongoing fibrosis and ultimately cirrhosis, as was described previously. The fibrosis causes increased intrahepatic resistance to portal venous blood flow and thus increased pressure in this venous system.
Portal hypertension in turn leads to the development of ascites, or the accumulation of intraperitoneal fluid, and the formation of collateral venous circulation, such as esophageal varices, which often produce life-threatening hemorrhages. Finally, patients with chronic hepatitis and cirrhosis of almost any cause, especially hepatitis B or hepatitis C, are at increased risk for developing hepatocellular carcinoma.
The pathologic fea- tures of these conditions were described previously. The major points to note here are that fat begins to accumulate within hepatocytes after even a moder- ate intake of alcohol and, with continued exposure, continues to accumulate until the liver may be 3 to 4 times its normal mass.
Up to the point where fibro- sis appears, the fatty change is reversible with abstention from alcohol. Alcoholic hepatitis is characterized by acute hepatocyte necrosis, particularly after bouts of heavy drinking, and is usually reversible.
It typically includes some sinusoidal and perivenular fibrosis and, if superimposed on fatty liver, often progresses to cirrhosis. Acetaminophen Toxicity A relatively common and treatable form of hepatotoxic exposure that other- wise may lead to hepatic failure and death is acetaminophen poisoning. A minor metabolite of acetaminophen is produced by cytochrome P 2E1 in the form of a hepatotoxin, which normally is detoxified by binding to glu- tathione.
Hepatotoxicity is most likely to develop in patients with single very large ingestions such as suicide attempts or patients with enhanced activity of this cytochrome, as well as those with depleted levels of glutathione, such as chronic alcoholics.
Blood levels of acetaminophen correlate with the severity of hepatic injury. Patients with toxic levels of acetaminophen may be treated with doses of N-acetylcysteine, which replaces glutathione stores, allowing detoxification of the metabolite.
The disease classically was referred to as bronze diabetes because of the deposition of iron causing skin pigmenta- tion, diabetes, as well as micronodular cirrhosis, with increased levels of fer- ritin and hemosiderin within hepatocytes.
It now can be diagnosed before the occurrence of end-organ damage resulting from iron deposition by screening for transferrin saturation greater than 45 percent and confirmed by HFE genotyping. In some patients, the abnormal A1AT is synthesized in the liver but cannot be secreted, and so it accumulates in cytoplasmic globules. The spectrum of liver diseases ranges from neonatal hepatitis, to childhood cirrhosis, to adult cirrhosis.
Thus, patients with A1AT deficiency will often develop emphysema due to increased levels of elastase in the lungs in addition to cirrhosis. Wilson Disease Wilson disease is an inherited disorder of copper metabolism in which there is accumulation of copper in multiple tissues, including liver, brain, and eye. Clinical manifestations may include acute or chronic hepatitis, fatty liver, and cirrhosis, along with extrapyramidal movement disorders or psychiatric dis- turbances.
Diagnosis is made by finding Kayser-Fleischer rings in the cornea, which are pathognomonic, or by low levels of serum ceruloplasmin a serum copper-transport protein , as well as increased levels of hepatic or urinary copper. It is nearly always a self-limited infection without a chronic or car- rier state.
It is an RNA virus that usually is acquired from contaminated food and water. It typically is associated with the formation of Mallory bodies on biopsy. When it is acquired in adulthood, more than 85 percent of patients develop chronic hepatitis.
Her liver biopsy shows hepatocyte necrosis and inflam- matory portal tract infiltrate. Which of the following tests is most likely to yield the diagnosis?
Staining of liver specimen with Prussian blue B. Ophthalmologic slit-lamp examination E. Serum acetaminophen level [3. A liver biopsy reveals liver cell drop-out along with focal inflammation and ballooning degeneration of hepatocytes. A few intensely eosinophilic oval bodies are found. What are these microscopic bodies called?
Councilman bodies B. Cowdry A bodies C. Mallory bodies D. Psammoma bodies E. Russell bodies Answers [3. Acute hepatitis B infection is characterized by the presence or shedding of HbsAg, followed by a rise in anti-Hbc IgM. Adult infec- tion has a much better prognosis only 5 to 10 percent of patients develop chronic hepatitis compared with perinatal infection more than 90 percent develop chronic infection.
Councilman bodies can be seen in viral hepatitis; Mallory bodies are characteristic of alco- holic hepatitis. The pathologic findings of acute hepatitis are nonspecific. The dis- tinguishing feature in this case is the presence of hemiballism, an extrapyramidal movement disorder, suggesting Wilson disease. Kayser-Fleischer rings are green to brown deposits of copper in the Descemet membrane near the corneal limbus and are diagnostic. Councilman bodies are intensely eosinophilic bodies that may be seen in liver biopsy specimens from individuals with viral hepatitis.
These Councilman bodies are in fact necrotic hepatocytes that have undergone T-cell induced apoptosis. These apoptotic cells are cleared rapidly, and there may not be as many present in a liver biopsy spec- imen as were originally present. The liver and biliary tract. Crawford JM. Approach to Reading. Psychotherapy25 Part 2. Show more. Show less. About the Authors. Each case includes a complete discussion, clinical pearls and references.
This is a very high yield text which teach how to improve their diagnostic and problem-solving skills as they work through sixty high-yield clinical cases. The new edition is well updated with new Case Correlations feature which highlights differential diagnosis and related cases in the book.
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