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77 Cards in this Set
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Esophagitis action?
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The action of gastric juicies is critical to the development of esophageal mucosal injury.
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Esophagitis features?
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Hyperkeratosis-- is thickening of the stratum corneum, often associated with a qualitative abnormality of the keratin,and also usually accompanied by an increase also in the granular layer.
Erosion Ulceration |
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Barrett esophagus is also known as?
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Gastroesophageal reflux disease (GERD).
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What is the most important factor for esophageal adenocarcinoma?
Why? |
Barrett esophagus (GERD)
Because distal squamous mucosa is replaced by metaplastic columnar epithelium. |
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What are the two criteria required for the diagnosis of Barrett esophagus?
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1. Endoscopic evidence of columnar epithelial lining above the gastroesophageal junction.
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Histologic evidence of intestinal metaplasia in the biopsy specimens from the columnar epithelium.
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Esophagitis action?
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The action of gastric juicies is critical to the development of esophageal mucosal injury.
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Esophagitis features?
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Hyperkeratosis-- is thickening of the stratum corneum, often associated with a qualitative abnormality of the keratin,and also usually accompanied by an increase also in the granular layer.
Erosion Ulceration |
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Barrett esophagus is also known as?
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Gastroesophageal reflux disease (GERD).
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What is the most important factor for esophageal adenocarcinoma?
Why? |
Barrett esophagus (GERD)
Because distal squamous mucosa is replaced by metaplastic columnar epithelium. |
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What are the two criteria required for the diagnosis of Barrett esophagus?
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1. Endoscopic evidence of columnar epithelial lining above the gastroesophageal junction.
2. Histological evidence of intestinal metaplasia in the biopsy specimens from the columnar epithelium. |
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What is the definitive morphological diagnosis of Barrett esophagus?
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Presence of intestinal globlet cells among columnar epithelium.
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The pathologic evaluation of barrett esophagitis is the presence of?
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Dysplasia- the precursor of malignancy.
Adenocarcinoma within areas of intestinal metaplasia. |
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Features of dysplasia in Barrett esophagus?
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Enlarged, crowned, and stratified hyperchromatic nuclei and loss of intervening stroma between adjacent glandular structures.
low and high grades. |
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What are mutagenic compounds for Squamous cell carcinoma?
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Alcohol
Tobacco usage These compounds work together. |
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What are the 6 clinical features of squamous cell carcinoma in the esophagus?
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1. Dysphagia--hard to move food through the esophagus
2. Obstruction 3. difficulty swallowing 4. weight loss 5. Hemorrhage and sepsis may accompany ulceration of the tumor 6. Aspiration of food via a cancerous tracheoesophageal fistula |
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Adenocarcinoma in the esophagus?
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Epithelial tumor with grandular differentiation.
Majority arise from Barrett mucosa. |
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Risk factors for Adenocarcinoma in the esophagus?
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Tobacco exposure and obesity
Helicobacter pylori |
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Clinical features of Adenocarcinoma in the esophagus?
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Occur in patients over 40
More common in white males Difficulty swallowing, progressive weight loss, bleeding, chest pain, and vomiting. Poor prognosis Regression may occur with low-grade dysplastic lesions. |
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Acute Gastritis?
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Inflammation of the gastric mucosa with a predominant neutrophilic infiltrate (usually transient).
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Chronic gastric?
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Inflammation of the gastric mucosa with a predominant lymphocyte and plasma cell infiltrate.
Chronic mucosal inflammation. Mucosal atrophy |
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Factors associated with acute gastritis?
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Heavy NSAID use
high EtOH consumption heavy smoking uremia--interference w/bicarb system severe stress cancer chemotherapy |
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Factors associated with chronic gastritis?
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Helicobacter pylori
gastric hyperacidity Autoimmune EtOH/tobacco Radiation |
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Helicobacter pylori?
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present in 90% of chronic gastritis.
Gram negative Flagella uses urease to buffer acid near the organism produces adhesin to bind to gastric epithelium (greater in blood type O) H. pylori doesn't invade gastric epithelium. |
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Chronic Gastritis with H. pylori Pathological features ?
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Intestinal metaplasia (columnar absorptive cells).
Regenerative changes are seen (increased mitosis) Lymphocytes and plasma cells are seen in the lamina propia. Mucosa may become thinned and flattened. Inflammation in the antrum, body-fundic mucosa. |
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Peptic Ulcer disease?
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A breach in the mucosa of the alimentary tract.
The musclaris mucosa is important because if an ulcer goes past it the infection will have access to the blood vessels. |
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Peptic ulcers are seen where? (decreasing frequency)
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Duodenum
Lesser curvature Body Antrum |
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What are the proposed factors by which H. pylori tip the balance of mucosal defenses?
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It generates a protease which breaks down glycoproteins in the gastric mucosa.
Elaborates a phospholipase which damages surface epithelial cells. Neutrophils in the area release myeloperoxidase which produces hypochlorus acid and monochloramine which destroys mammalian cells. |
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Complications of peptic ulcer disease?
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Hemorrhage
perforation Obstruction Malignancy |
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Idiopathic Inflammatory Bowel disease (IIBO)?
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Unknown cause, but theories suggest that a persistent infectious process may incite a chronic granulomatous vasculitits that lead to the development.
Abnormal host reactivity might account for the disease. Also gene abnormalities. |
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Crohn disease (CD)?
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A relapsing, inflammatory, granulomatous disease that may affect any portion of the gastrointestinal tract from the esophagus to anus but most often involves the small intestine and colon.
Extraintestinal inflammatory manifestation can occur. |
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Crohn disease (CD) is characterized by?
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The presence of non-caseating granulomas.
Skip lesions, cobestone, and linear ulcers. |
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Crohn disease (CD) morphology?
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String sign--thin stream of barium passing through the diseased segment.
Skip lesions--sharp, demarcation between diseased bowel and adjacent uninvolved segments. LInear ulcers--mucosal ulcers that coalesce into long serpentine ulcers. Superficial ulceration. Non-caseating granulomas present in all tissue layers of diseased and uninvolved segments of bowel. |
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Chronic Crohn disease clinical features?
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Pernicious anemia--autoimmune destruction of gastric parietal cells leads to a lack of intrinsic factor and Vit B12 deficiency.
Steatorrhea--absence of bile acids will cause the feces to turn gray or pale. |
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Complications of Crohn disease?
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Toxic megacolon.
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Ulcerative colitis (UC)?
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A relapsing inflammatory, non-granulomatous disease limited to the colon, with extraintestinal inflammatory manifestations.
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Ulcerative Colitis (UC) is characterized by?
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Ulceroinflamatory disease limited to the colon and ONLY the mucosa and submucosa (except in most severe cases).
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Ulcerative Colitis (UC) morphology?
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Pseudopolyps--created by isolated islands of regenerating mucosa that bulge upward.
Serosal surface is not involved. |
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Clinical features of Ulcerative Colitis (UC)?
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Bloody diarrhea with stringy mucus accompanied with abdominal pain/cramps relieved by defection.
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Tumors of the colon and rectum:
Hyperplastic polyps? |
Formed as a result of abnormal mucosal maturation, inflammation, or architecture.
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Tumors of the colon and rectum:
Adenomatous polyps? |
Exhibit dysplasia and are precursors of carcinoma.
Occur as the result of epithelial proliferation. occur in three types: Tubular, Villous, Tubulocillous adenomas or a mixture of both. |
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Adenoma-carcinoma sequence.
adenomatous polyps =>carcinoma? |
Abnormalities in tumor suppressor genes and genes responsible for repairing DNA.
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Tumors of the colon and rectum:
Most cancers occur in the? |
Sigmoid section of the colon.
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Tumors of the colon and rectum:
Tumors in the proximal portions (right side) of the colon tend to grow? |
Polypoid, exophytic, masses.
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Tumors of the colon and rectum:
Tumors in the distal portions (left side) of the colon tend to grow? |
Annular, encircling lessions that produce "napkin ring" constrictions of the the bowel.
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Tumors of the colon and rectum:
Invasive tumors incite? |
A Desmoplastic (fibrous tissue) stromal response making these tumors firm and hard.
Elevated above the epithelium. |
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Tumors of the colon and rectum:
Testing/ diagnosis? |
Fecal occult blood test: anemia assume cancer.
Iron deficiency in an older man means gastrointestinal cancer until proven otherwise. Change in bowel habits. May confirm by colonoscopy, biopsy, or carninoembroyonic antigen (CEA)--involved in cell adhesion |
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LIver cell Adenoma Characteristics?
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Yellow-tan bile-stained nodules.
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What are the four major factors for Heptocelluar CA?
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Viral infection (HBV, HCV)
Chronic alcoholism Non-alcoholic steatohepatitis (NASH) Food contaminants--Aflatoxins. |
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Hepatocellular CA features?
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Repeated cycles of cell death and regeneration.
HBV infection and host genome instability post HBV DNA integration--HBV X-protein. Carcinogen exposure--Aflatoxins. Cirrhosis (non-viral) |
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Microscopic morphology of Hepatocellular CA?
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Well and moderately differentiated tumors:
Trabeculated pattern Pseudoglandular pattern. |
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Jaundice definition?
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1. Excessive production of bilirubin (uc).
2. Reduced hepatic uptake (uc) 3. Impaired conjugation (uc) 4. Decreased hepatic excretion 5. Impaired bile flow. uc = unconjugated. |
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Neonatal Jaundice?
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Immaturity of the hepatic machinery involved in conjugating and excreting bilirubin.
Hereditary hyperbilirubinemias. |
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Crigler-Najjar syndrome type 1?
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Gene defect for the protein that encodes for UDP-glucuronosyltransferase enzyme.
Death within 18 months from kernicterus--staining of the nervous system when bilirubin is > 20mg/dL. |
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Viral Hepatitis?
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Infection of the liver caused by a group of viruses having a specific affinity for the liver.
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Serologic Diagnosis tests for Hep-A?
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IgM- HAV antibody in serum appears at onset of symptoms and confirms diagnosis.
IgM level declines after a few months. IgG HAV antibody appears as patient recovers and persists for life, conferring immunity. |
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Hep-B Serologic Diagnosis?
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HBsAg (surface antigen) appears before onset of symptoms.
HBeAg (polypeptide transcipt with a pre-core and core region), HBV DNA, DNA polymerase all signify active infection. IgM anti-HBc (core region) detectable as serum transaminases rise. |
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Hep C immunity?
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Elevated titers of anti-HCV IgG occurring after active infection do not confer effective immunity.
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Cirrhosis of the liver?
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among the top 10 causes of death in the western world.
End stage of liver disease. |
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Cirrhosis is caused by?
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Alcoholic liver disease
Viral hepatitis |
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Cirrhosis morphology?
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Bridging fibrous septa
Parenchymal nodules Total disruption of liver architecture |
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Cirrhosis Pathogenesis?
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The perisinusoual hepatic stellate cell (lto cell) is the major source of excess collagen in Cirrhosis.
Caused by: Inflammatory mediators cytokines Disruption of extracellular matrix Direct stimulation by toxins EtOH. |
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What are the three morphologihcal characteristics of Alcoholic liver disease?
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Hepatic steatosis
Alcoholic hepatitis Alcoholic Cirrhosis |
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Hepatic steatosis
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Micovesucular lipid accumulation
Liver becomes yellow, greasy, fractured easily It's reversible can progress to hepatitis |
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Alcoholic hepatitis?
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hepatocyte swelling and necrosis
Mallory bodies--tangled cytokeratin intermediate filaments. Neutrophil infiltration around dying hepatocytes Fibrosis in sinusoidal, pericenule, and periportal areas. can progress to cirrhosis |
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Alcoholic cirrhosis?
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Irreversible
Fibrous septa extend through sinusoids from central vein to portal regions, from portal tract to portal tract. Regenerative parenchymal trapped in fibrous septa form micronodules. As fibrous tissue deposition continues macronodules are formed. Bile stasis develops. |
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Clinical features of Alcoholic liver disease?
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Hepatorenal syndrome.
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Acute pancreatitis?
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Characterized by the acute onset of abdominal pain resulting from enzymatic necrosis and inflammation of the pancreas.
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#1 cause of acinar cell injury?
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Alcohol and drugs.
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Pancreatic duct obstruction leads to?
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Interstitial edema.
Hemorrhaging parenchymal necrosis. |
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Clinical features of acute pancreatitis?
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Increased serum lipase and amylase.
Fluid sequestration Respiratory distress syndrome Peripheral vascular collapse, Shock. acute renal tubular necrosis. |
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Chronic Pancreatitis?
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Characterized by repeated bouts of mild to moderate pancreatic inflammation with continued loss of parenchymal and replacement by fibrous tissue.
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Important factors which cause chronic pancreatitis?
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EtOH consumption
Ductal obstruction/stones Interstitial fibrosis |
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Clinical features of chronic pancreatitis?
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Jandice
Pseudocyst |
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What is a factor which causes pancreatic carcinoma?
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Inactivation of the p53 gene
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pancreatic carcinoma morphology?
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Adenocarcinomas have moderate to poor, aggressive and infiltative
May secrete mucin Evoke a desmoplastic reaction Grey-white gritty tissue mass. |
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Clinical signs of pancreatic carcinoma?
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Courvoisier sign--palpable distended gallbladder
Troussean sign--migratory thrombophlebitis |
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Diagnosis of pancreatic carcinoma?
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Tumor markers:
CEA C19-9 |
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