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Gastrointestinal
FA complete review part 3 Pathology 2
| Question | Answer |
|---|---|
| What are colonic polyps? | Growths of tissue within the colon |
| Gross description of colonic polyps | Flat, sessile, or pedunculated on the basis of protrusion into colonic lumen |
| List of Non-neoplastic colonic polyps: | 1. Hamartomatous polyps 2. Mucosal polyps 3. Inflammatory pseudopolyps 4. Submucosal polyps 5. Hyperplastic polyps |
| What conditions are associated with Hamartomatous polyps? | Peutz-Jeghers syndrome and Juvenile polyposis |
| Growths of normal colonic tissue with distorted architecture. | Hamartomatous polyps |
| Solitary colonic lesions/polyps that do not have significant risk of transformation. | Hamartomatous polyps |
| What kind of polyps are seen in Inflammatory bowel disease? | Inflammatory pseudopolyps |
| What is included as Submucosal polyps? | Lipomas, leiomyomas, and fibromas, among others. |
| What kind of polyp is a lipoma considered? | Submucosal polyp |
| What are the most common non-neoplastic polyps? | Hyperplastic polyps |
| Hyperplastic polyps: | Most common; Smaller and predominantly located in the rectosigmoid region |
| Where are most hyperplastic polyps located? | Rectosigmoid region |
| What are the two main types of Malignant polyps? | Adenomatous polyps and Serrated polyps |
| What gene mutations are associated with adenomatous polyps? | APC and KRAS |
| What neoplastic polyps are due to chromosomal instability pathway with mutations in APC and KRAS? | Adenomatous polyps |
| What are the three types of adenomatous polyps? | Tubular, Tubulovillous, and Villous adenomatous polyps |
| Which type of adenomatous polyps has the less potential for malignancy? | Tubular adenomatous polyps |
| Which type of adenomatous polyps is the most prone for malignancy? | Villous adenomatous polyps |
| Tubular < Tubulovillous < Villous | Increasing potential of adenomatous polyp malignancy |
| What is the most relevant symptom of Adenomatous polyposis? | Occult bleeding |
| Premalignant polyps? | Serrated polyps |
| CpG island methylator phenotype. Associated with: | Serrated polyps |
| What is CIMP? | Cytosine base followed by guanine, linked by a phosphodiester bond |
| CIMP is associated with ________________ polyposis. | Serrated |
| MMR gene mutation. Dx? | Serrated polyposis |
| What is the genetic result of silence MMR gene mutation? | Microsatellite instability and mutations in BRAF ---> Serrated polyps |
| Featured finding in biopsy of Serrated polyps? | "Saw-tooth" pattern of crypts |
| What is the cause for Familial adenomatous polyposis? | AD mutation of APC tumor suppressor gene on chromosome 5q21. |
| Mode of inheritance of FAP? | Autosomal dominant |
| What tumor suppressor gene mutation is involved in FAP development? | APC |
| On which chromosome is the APC gene mutated in FAP? | 5q21 |
| What polyposis syndrome is associated with a 2-hit hypothesis? | Familial adenomatous polyposis |
| What is the most significant complication of untreated FAP? | 100% progress to CRC (colorectal cancer) |
| What are some features of FAP? | 1. Thousands of polyps arise starting after puberty 2. Pancolonic 3. Always involves rectum |
| FAP + osseous and soft tissue tumors. Dx? | Gardner syndrome |
| What is Gardner syndrome? | FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium, impacted/supernumerary teeth. |
| FAP and malignant CNS tumor. Dx? | Turcot syndrome |
| What other type of tumor is associated in Turcot syndrome, along with FAP? | Malignant CNS tumor |
| What are the types of associated CNS tumors in Turcot syndrome? | Medulloblastoma and Glioma |
| What is Peutz-Jeghers syndrome? | AD syndrome featuring numerous hamartomas throughout GI tract, along with hyperpigmented mouth, lips, hands, and genitalia. |
| What type of polyps are associated with Peutz-Jeghers syndrome? | Hamartomatous polyps |
| What are associated risk of Peutz-Jeghers syndrome? | Breast and GI cancers |
| Mode of inheritance of Peutz-Jeghers syndrome? | Autosomal dominant |
| A patient with colonic polyps and hyperpigmented mouth, lips, hands, and genitalia. Dx? | Peutz-Jeghers syndrome |
| A 3 year old with multiple hamartomatous polyps in colon, stomach, small bowel. Dx? | Juvenile polyposis syndrome |
| Juvenile polyposis syndrome is associated with increased risk of _________. | CRC (colorectal cancer) |
| What is the old name of Lynch syndrome? | Hereditary nonpolyposis colorectal cancer (HNPCC). |
| AD mutations of DNA mismatch repair genes with subsequent microsatellite instability. Associated colon pathology? | Lynch syndrome |
| Which part is always involved in Lynch syndrome? | Proximal colon |
| What are the associated cancers of Lynch syndrome? | Endometrial, ovarian, and skin cancers. |
| Approximate percent of Lynch syndrome cases progress to CRC? | 80% |
| What are risk factors of Colorectal cancer? | - Adenomatous and serrated polyposis - Familial cancer syndromes - IBD - Tobacco use - Diet of processed meat with low fiber |
| Presentation of Ascending Colorectal cancer? | Exophytic mass, iron deficiency anemia, and weight loss |
| What is the clinical presentation of Descending CRC? | Infiltrating mass, partial obstruction, colicky pain, and hematochezia. |
| Right sided CRC ---> | Bleeds |
| Left sided CRC ---> | Obstructs |
| Why do Left-sided CRC tend to obstruct more than right sided CRC? | Narrower lumen in the left sided |
| What is the typical finding of CRC by barium enema? | "Apple core" lesion |
| What is a good CRC tumor maker? | CEA |
| At what age should low-risk patients should start screening for CRC? | 50 years old |
| What hematologic condition should raise suspicion of CRC in men over 50 years old and postmenopausal women? | Iron deficiency anemia |
| A person with a first degree relative with Hx of CRC, should start monitoring at what age? | 40 years old, or at least 10 year prior to their relative's presentation. |
| At what age should the brother of a CRC patient, start monitoring, if the sibling presented CRC at age 45? | 35 years old |
| Most mutations of APC cause ---> | FAP |
| Sporadic mutations APC cause _____________. | Colorectal cancer (CRC) |
| What are the two pathways that may be involved in the development of CRC? | 1. Chromosomal instability Pathway 2. Microsatellite instability Pathway |
| What conditions are associated with the Chromosomal instability pathway? | 1. Mutations of APC --> APC 2. Sporadic CRC |
| What mutations are involved in the Microsatellite instability pathway? | Mutations or methylation of mismatch repair gentes (MLH1) |
| Sporadic CRC due to chromosomal instability pathway is caused via: | Adenoma-carcinoma sequence |
| Sporadic CRC due to Microsatellite instability pathway is caused via: | Serrated polyp pathway |
| What conditions are associated with the Microsatellite instability pathway? | Lynch syndrome and some sporadic CRC |
| What cancer has been linked or associated with overexpression of COX-2? | Colorectal cancer (CRC) |
| Which analgesics may used as chemopreventive in CRC? | NSAIDs |
| Why are NSAIDs chemopreventive of CRC? | Inhibits the overexpression of COX-2 |
| Mnemonic used to remember order of events causing CRC via the Chromosomal instability pathway? | AK-53 |
| What does the "AK-53" stand for? | Chromosomal instability pathway order of events: 1. Loss of APC gene 2. KRAS mutation 3. Loss of tumor suppressor genes (p53, DCC) |
| Which are the tumor suppressor genes involved in CRC development via the Chromosomal instability pathway? | p53 and DCC |
| What is caused by the loss of APC gene? | - Decreased intercellular adhesion - Increased proliferation of colon cells |
| What does a KRAS mutation cause in development of CRC? | Unregulated intracellular signaling |
| Increased tumorigenesis is seen at what point of CRC development? | At loss of tumor suppressor gene (p53, DCC) |
| What is cirrhosis? | Diffuse bridging fibrosis and regenerative nodules disrupt normal architecture of liver. |
| Cirrhosis increases the risks of developing which malignancy? | Hepatocellular carcinoma |
| What are the common etiologies for Cirrhosis? | Alcohol, non-alcoholic steatohepatitis, chronic viral hepatitis, autoimmune hepatitis, biliary disease, genetic/metabolic disorders. |
| Portal Hypertension definition: | Increase pressure in portal venous system |
| What are common etiologies of Portal hypertension? | Cirrhosis, vascular obstruction, and schistosomiasis |
| What is the MCC of portal hypertension in the western countries? | Cirrhosis |
| Common examples of vascular obstruction causing portal hypertension? | Portal vein thrombosis, Budd-Chiari syndrome |
| What are the effects of Portal hypertension? | 1. Esophageal varices ---> hematemesis 2. Gastric varices ---> Melena |
| What are common Integumentary manifestation of cirrhosis and portal HTN? | Jaundice, Spider angiomas, Palmar erythema, Purpura, and Petechiae |
| Neurologic symptoms in liver disease? | 1. Hepatic encephalopathy 2. Asterix |
| What is another way to refer to asterix? | "flapping tremor" |
| What are effects in the reproductive system of an indicitula with cirrhosis? | Testicular atrophy (if male), Gynecomastia (maes), and amenorrhea (female) |
| How is Spontaneous bacterial peritonitis also known as? | Primary bacterial peritonitis |
| What is a possible fatal bacterial infection in patients with cirrhosis and ascites? | Primary bacterial peritonitis |
| What are the most common organism that cause Primary Bacterial peritonitis? | Gram (-) organism (E. coli, Klebsiella), and less commonly gram (+) Streptococcus |
| Paracentesis with ascitic fluid absolute neutrophil count (ANC) > 250 cell/mm3. Dx? | Primary Bacterial peritonitis |
| What is the most common treatment for Spontaneous (primary) bacterial peritonitis? | 3rd generation cephalosporin (Cefotaxime) |
| How are serum markers of liver pathology categorized? | 1. Enzymes released in liver damage 2. Functional liver makers |
| Which are the enzymes released in liver damage? | 1. Aspartate aminotransferase and Alanine aminotransferase 2. Alkaline phosphatase 3. g-glutamyl transpeptidase |
| Examples of function liver markers: | Bilirubin, Albumin, Prothrombin time, and Platelets |
| ALT and AST levels in most liver disease? | ALT > AST |
| Which enzyme is more elevated, ALT or AST, in alcoholic liver disease? | AST |
| A higher level of AST than ALT in non-alcoholic liver disease indicates? | Progression to advanced fibrosis or cirrhosis |
| Which conditions have ALP (alkaline phosphatase) elevated? | 1. Cholestasis 2. Infiltrative disorders 3. Bone disease |
| Which enzyme is elevated with ALP in most cases except in bone disease? | g-glutamyl transpeptidase |
| Increased or Decreased. Bilirubin in liver disease? | Increased |
| How are the levels of Albumin altered in liver disease? | Decreased |
| Decreased levels of albumin indicate? | Advanced liver disease |
| Which functional serum markers are elevated in liver disease? | Bilirubin and Prothrombin time |
| Which functional serum markers are decreased in liver disease? | Albumin and Platelets |
| What does a decrease in platelets indicate about the liver? | Advanced liver disease and/or Portal hypertension |
| What is Reye syndrome? | Rare, and often fatal childhood hepatic encephalopathy. |
| What viral infections are often associated with Reye syndrome? | VZV and influenza virus treated with Aspirin. |
| What are findings of Reye syndrome? | - Mitochondrial abnormalities - Fatty liver (microvesicular fatty changes), - Hypoglycemia - Vomiting - Hepatomegaly - Coma |
| What medication intoxication causes Reye syndrome? | Aspirin |
| Result of treating fever or viral infections to children with aspirins? | Reye syndrome |
| How does aspirin cause Reye syndrome? | Decrease B-oxidation by reversible inhibition of mitochondrial enzymes. |
| List of Alcoholic-related liver diseases: | 1. Hepatic steatosis 2. Alcoholic hepatitis 3. Alcoholic cirrhosis 4. Nonalcoholic fatty liver disease 5. Hepatic encephalopathy |
| Macrovesicular fatty liver change that may be reversible with alcohol cessation. Dx? | Hepatic steatosis |
| What is the approximate AST to ALT level in Alcoholic hepatitis? | AST 2:1 ALT |
| What are the histological findings and changes in Alcoholic hepatitis? | - Swollen and necrotic hepatocytes with neutrophilic infiltration - Mallory bodies |
| What liver disease is seen with (+) Mallory bodies? | Alcoholic hepatitis |
| What is the key histologic fining in alcoholic hepatitis? | Mallory bodies |
| What are Mallory bodies? | Intracytoplasmic eosinophilic inclusions of damaged keratin filaments. |
| Final and usually irreversible form of lliver disaase/damage. Dx? | Alcoholic cirrhosis |
| What is a histological feature in early Alcoholic cirrhosis? | Sclerosis around central vein |
| What are the final results/consequences of Alcoholic cirrhosis? | Portal hypertension and End-stage liver disease |
| Which liver disease is due to a metabolic syndrome? | Non-alcoholic fatty liver disease |
| Pathogenesis of Nonalcoholic fatty liver disease | Metabolic syndrome (insulin resistance) --> Obesity --> Fatty infiltration of hepatocytes --> cellular "ballooning" and eventual necrosis. |
| Which, AST or ALT, is higher in Nonalcoholic fatty liver disease? | ALT |
| Non-alcoholic fatty liver disease is _______________ of alcohol use. | Independent |
| What substance is in excess (or decreased secretion) in Hepatic encephalopathy? | NH3 |
| What is the pathogenesis of Hepatic encephalopathy? | Cirrhosis --> portosystemic shunts --> decreased NH3 metabolism which leads to neuropsychiatric dysfunction. |
| What are the Hepatic encephalopathy triggers? | 1. Increased NH3 production and absorption 2. Decreased removal of NH3 |
| What conditions lead to increased NH3 production and absorption? | Due to GI bleed, constipation, and infection. |
| What are conditions that decrease NH3 removal from body, leading to Hepatic encephalopathy? | Renal failure, diuretics, bypassed hepatic blood flow post-TIPS |
| What are the 2 medications used to treat Hepatic encephalopathy? | 1. Lactulose 2. Rifaximin |
| What is the mode of action of Lactulose? | Increase NH4+ generation |
| Mechanism of action of Rifaximin? | Decrease NH3-producing gut bacteria |
| What condition is treated with Lactulose and Rifaximin? | Hepatic encephalopathy |
| What is the MC primary malignant tumor of liver in adults? | Hepatocellular carcinoma (HCC) |
| What is the most common hepatitis virus associated with HCC development? | HBV |
| What are some common conditions leading to Hepatocellular carcinoma? | HCV, HBV, alcoholic and nonalcoholic fatty liver disease, autoimmune disease, hemochromatosis, Wilson disease, and alpha 1- antitrypsin deficiency |
| What are specific carcinogens leading to hepatocellular carcinoma? | Aflatoxin from Aspergillus |
| What is a common condition caused by HCC? | Budd-Chiari syndrome |
| What are some key findings of HCC? | Jaundice, hepatomegaly, ascites, polycythemia, and anorexia. |
| Which protein is elevated in HCC and is used as a diagnostic tool? | Increased alpha-fetoprotein (AFP) |
| Liver angiosarcoma is associated with exposure of which substances? | Arsenic, and vinyl chloride |
| Malignant liver tumor of endothelial origin. Associated with arsenic and vinyl chloride exposure? | Angiosarcoma |
| What is a Cavernous hemangioma? | Most common benign liver tumor |
| Benign liver tumor due to venous malformation in a 40 year old patient. Dx? | Cavernous hemangioma |
| Rare, benign liver tumor, often related to oral contraceptive or anabolic use. Dx? | Hepatic adenoma |
| What substance uses/therapies are associated with Hepatic adenoma development? | Oral contraceptive use and Anabolic use |
| What are the 3 main types of metastasis to liver? | GI malignancies, breast and lung cancer |
| Thrombosis or compression of hepatic veins with centrilobular congestion and necrosis. Dx? | Budd-Chiari syndrome |
| What veins are compressed or obstructed in Budd-Chiari syndrome? | Hepatic veins |
| Key physical finding in Budd-Chiari syndrome? | Absence of JVD |
| No JVD + Ascites, varices, abdominal pain and liver failure + Hx of DVT. Dx? | Budd-Chiari syndrome |
| What liver syndrome is associated with Nutmeg liver? | Budd-Chiari syndrome |
| What are some conditions associated with Buu-Chiari syndrome development? | Hypercoagulable states, polycythemia vera, postpartum state, and HCC. |
| Mottled liver appearance, is termed _______________ ____________. | Nutmeg liver. |
| What causes a1-antitrypsin deficiency? | Misfolded gene product protein aggregates n hepatocellular ER leading to cirrhosis with PAS (+) globules in liver |
| Which two organs are affected by alpha 1- antitrypsin deficiency? | Lungs and liver |
| What does alpha 1-antitrypsin (ATT) deficiency cause in the lungs? | Uninhibited elastase in alveoli which causes decreased elastic tissue causing Panacinar emphysema |
| Which enzyme deficiency leads to liver cirrhosis with PAS (+) globules? | Alpha 1- antitrypsin (ATT) |
| What is jaundice? | Abnormal yellowing of the skin and/or sclera due to bilirubin deposition |
| What are the most common conditions/pathologies that cause increased bilirubin levels? | Hemolysis, Obstruction, Tumor, and Liver disease |
| What are the main conditions leading to increased levels of Conjugated (direct) bilirubin? | 1. Biliary tract obstruction 2. Biliary tract disease 3. Excretion defects |
| What are common biliary tract obstructions that cause Conjugated hyperbilirubinemia? | Gallstones, Cholangiocarcinoma, pancreatic or liver cancer, liver fluke. |
| Which are the MC biliary tract diseases that increment conjugated bilirubin? | 1. Primary Sclerosing Cholangitis 2. Primary Biliary Cholangitis |
| What are common excretion defects leading to Conjugated (direct) hyperbilirubinemia? | Dubin-Johnson syndrome and Rotor syndrome |
| Crigler-Najjar disease causes _________ hyperbilirubinemia. | Unconjugated (indirect) |
| What conditions are associated with development of Unconjugated (indirect) hyperbilirubinemia? | Hemolytic, physiologic (newborns), Crigler-Najjar, and Gilbert syndrome. |
| What conditions lead to Mixed (direct and indirect) hyperbilirubinemia? | Hepatitis, and cirrhosis |
| What is the MC reason for pediatric liver transplantation? | Biliary atresia |
| What is the most common cause of physiologic neonatal jaundice? | Immature UDP-glucuronosyltransferase --> unconjugated hyperbilirubinemia --> jaundice/kernicterus. |
| When is physiologic neonatal jaundice first noticed? | After the first 24 hours of life, and resolves in 1-2 weeks |
| Treatment for Physiologic neonatal jaundice? | Phototherapy (non-UV) isomerizes unconjugated bilirium to water-soluble bilirubin |
| What kind of bilirubin, direct or indicred, is accumulated in Physiologic Neonatal jaundice? | Unconjugated (indirect) bilirubin |
| What are the common signs and sympotso that indicate possible Biliary atresia? | Persistent jaundice after 2 weeks of life, darkening urine, acholic stools, and hepatomegaly |
| What are the labs found in Biliary atresia? | Increased direct bilirubin (conjugated hyperbilirubinemia) and increased GGT. |
| Mode of inheritance of all Hereditary hyperbilirubinemia? | Autosomal recessive |
| Which hyperbilirubinemias have excess Unconjugated bilirubin? | Gilbert syndrome and Crigler-Najjar syndrome |
| Which two known hyperbilirubinemias have excess Conjugated bilirubin? | Dubin-Johnson syndrome and Rotor syndrome |
| What is the reason for Gilbert syndrome development? | Mildly decreased UDP-glucuronosyltransferase conjugation and impaired bilirubin uptake. |
| What enzyme is decresed in Gilbert syndrome? | UDP-glucuronosyltransferase |
| Which is a benign Unconjugated hyperbilirubinemia syndrome? | Gilbert syndrome |
| What type of triggers or events lead to jaundice in Gilbert syndrome? | Stress, illness, or fasting. |
| Absent UDP-glucuronosyltransferase. Dx? | Crigler-Najjar syndrome |
| Which Crigler-Najjar type is more severe? | Type 1 |
| Crigler-Najjar type 2 responds well to ____________________, which increase liver enzyme synthesis. | Phenobarbital |
| If a patient with Crigler-Najjar syndrome responds well to Phenobarbital, it indicates that it is type _____. | 2 |
| What are the findings associated with Crigler-Najjar syndrome? | Jaundce, Kernicterus, and UNCONJUGATED hyperbilirubinemia |
| Bilirubin deposition in the brain. | Kernicterus |
| How does Phenobarbital has proven to work in Type II Crigler-Najjar syndrome? | Increases liver enzyme (UDP-glucuronosyltransferase). |
| What are the two types of Conjugated hyperbilirubinemia? | Dubin-Johnson syndrome and Rotor syndrome |
| What is the most common cause of Dubin-Johnson syndrome? | Conjugated hyperbilirubinemia due to defective liver excretion |
| Rotor syndrome is due to : | Impaired hepatic uptake and excretion by the liver. |
| Gross view of Dubin-Johnson syndrome? | Black (dark) liver |
| Which is most severe, Dubin-Johnson or Rotor syndrome? | Dubin-Johnson syndrome |
| What is the cause of Wilson disease? | Autosomal recessive mutations in hepatocyte copper-transporting ATPase |
| What does the mutation causing Wilson disease results in? | Decreased copper incorporation into apoceruloplasmin and excretion into bile leading to decreased serum ceruloplasmin. |
| Which metal is accumulated in Wilson disease? | Copper |
| Which gene and chromosome suffer mutations in Wilson disease? | ATP7B gene; chromosome 13 |
| Which organs get copper accumulated in Wilson disease? | Liver, brain, cornea, and kidneys |
| Copper in urine. Dx? | Wilson disease |
| What key finding in Wilson disease? | Kayser-Fleisher rings |
| What are Kayser-Fleischer rings? | Deposits in Descemet membrane of cornea |
| What are complications of Wilson disease? | 1. Liver disease (failure, cirrhosis) 2. Neurologic disease (dysarthria, dystonia, tremor, Parkinsonism) 3. Psychiatric disease 4. Kayser-Fleischer rings 5 Hemolytic anemia 6. Renal disease (Fanconi syndrome) |
| What are the Liver complications of Wilson disease? | Hepatitis, liver failure, and cirrhosis |
| What is the treatment of Wilson disease? | Chelation with penicillamine or trientine, and oral zinc |
| Penicillamine is used to treat __________ ____________. | Wilson disease |
| What type of anemia is seen in Wilson disease? | Hemolytic anemia |
| Gene mutated in Hemochromatosis? | HFE |
| HFE gene is located in which chromosome? | Chromosome 6 |
| HLA associated with Hemochromatosis? | HLA-A3 |
| What are the most common mutations in Hemochromatosis? | C282Y mutation > H63D mutation in HFE gene, located in chromosome 6 |
| Abnormal iron sensing and increased intestinal absorption. Dx? | Hemochromatosis |
| What is a common secondary cause of Hemochromatosis? | Chronic transfusion therapy (B-thalassemia) |
| Which organs accumulate/deposited most iron in Hemochromatosis? | Liver, pancreas, skin, heart, pituitary, and joints |
| Modes to identify Hemosiderin? | MRI or Biopsy with Prussian blue stain |
| Why is a young healthy woman with a slow Hemochromatosis progression? | Iron loss through menstruation |
| What metal is accumulated or deposited in organs in Hemochromatosis? | Iron |
| What is the classic triad of Hemochromatosis? | Cirrhosis, Diabete mellitus, and skin pigmentation |
| "bronze diabetes" . Dx? | Hemochromatosis |
| What are secondary complications or symptoms of Hemochromatosis? | - Restrictive and/or Dilated cardiomyopathy - Hypogonadism - Arthropathy |
| Arthropathy in Hemochromatosis? | Calcium pyrophosphate deposition; especially in metacarpophalangeal joints. |
| What is a common cause of death in Hemochromatosis? | Hepatocellular carcinoma |
| What is the treatment for Hemochromatosis? | 1. Repeated phlebotomy 2. Chelation with deferoxamine 3. Chelation with oral deferiprone |
| Deferasisox, Deferoxamine, and deferiprone are: | Iron chelating agents used in Hemochromatosis treatment |
| At what level is Iron overload considered relevant for Hemochromatosis diagnosis? | Total body iron > 20 grams |
| What is the classic type of cardiomyopathy seen as a complication of Hemochromatosis? | Restrictive |
| What are the shared signs and symptoms of all biliary tract diseases? | Pruritus, jaundice, dark urine, light-colored stool, and hepatosplenomegaly. |
| What are the LFTs in Biliary tract diseases? | - Increased conjugated bilirubin, - Increased cholesterol - Increased ALP |
| What are some common biliary diseases? | 1. Primary Sclerosing Cholangitis 2. Primary Biliary cholangitis 3. Secondary Biliary cholangitis |
| Unknown cause of concentric "onion skin" bile duct fibrosis leading to alternating strictures and dilation with "beading" of intra- and extrahepatic bile ducts on ERCP, magnetic resonance cholangiopancreatography (MRCP) | Pathology of Primary Sclerosing Cholangitis |
| Epidemiology of Primary sclerosing cholangitis | Classically in middle-aged men with IBD |
| What are the key features of intra and extrahepatic ducts in PCS? | Alternating structures and dilation with "beading" |
| What condition is seen with concentric "onion skin" bile duct fibrosis? | Primary sclerosing Cholangitis |
| Which biliary tract disease is (+) p-ANCA? | Primary sclerosing Cholangitis |
| What is a biliary conditions caused by Primary Sclerosing Cholangitis? | Secondary biliary cholangitis |
| What IBD is associated strongly with primary sclerosing cholangitis? | Ulcerative colitis (UC) |
| What malignancies are at risk of development in patient with Primary Sclerosing cholangitis? | Cholangiocarcinoma and gallbladder cancer |
| What is the MC Biliary tract disease is most commonly seen in middle-aged women? | Primary biliary cholangitis |
| What is the pathology of Primary Biliary cholangitis? | Autoimmune reaction --> lymphocytic infiltrate + granulomas --> destruction of lobular bile ducts |
| Biliary disease seen with destruction of lobular bile ducts due to lymphocytic infiltrate and granulomas? | Primary Biliary cholangitis |
| Primary biliary cholangitis is (+) ___________________________ antibody. | Antimitochondrial antibody |
| Increased IgM is seen which Biliary tract diseases? | Primary sclerosing cholangitis and Primary biliary cholangitis |
| What are autoimmune disorders associated with Primary Biliary cholangitis? | Sjogren syndrome, Hashimoto thyroiditis, CREST , rheumatoid arthritis, and celiac disease |
| How is Secondary biliary cholangitis complicated? | Development of Ascending cholangitis |
| What is the initial problem in Secondary biliary cholangitis? | Extrahepatic biliary obstruction leading to increased pressure in intrahepatic ducts |
| A patient with gallstone, or any other obstructive lesion, is more susceptible to develop which biliary tract disease? | Secondary biliary cholangitis |
| What are the most common causes of Gallstones? | 1. Increased cholesterol and/or bilirubin, 2. Decreased bile salts 3. Gallbladder stasis |
| Common term of Cholelithiasis? | Gallstones |
| What are the two types of Gallstones? | 1. Cholesterol stones 2. Pigment stones |
| What are common associations for cholesterol gallstones synthesis? | Obesity, Crohn disease, advance age, estrogen therapy, multiparity, and rapid weight loss, and Native American origin. |
| 80% of cholesterol gallstones are __________________. | Radiolucent |
| What causes the opacity of cholesterol gallstones? | Calcifications |
| What are the main risk factors for Gallstones? | Female Fat Fertile (multiparity) Forty (40s year old) |
| What is the most common complication of Gallstones? | Cholecystitis |
| Black pigment gallstones are due to: | Calcium bilirubinate and hemolysis |
| Which pigment gallstone type is radiolucent? | Brown; due to infection |
| Dark pigment gallstone is _____________. | Radiopaque |
| What pathologies or conditions associated of Pigment gallstones? | Crohn disease, chronic hemolysis, alcoholic cirrhosis, advanced age, biliary infections, and total parental nutrition. |
| Neurohormonal activation triggers contraction of gallbladder, forcing stone into cystic duct. | Biliary colic |
| What is a common neurohormonal activation for a biliary colic? | CCK after a fatty meal |
| Presence of gallstone in the common bile duct. Dx? | Choledocholithiasis |
| What is the MC type of Cholecystitis? | Calculous cholecystitis |
| Calculous cholecystitis is due to: | Gallstone impaction in the cystic duct resulting in inflammation and gallbladder wall thickening |
| What are the major causes of Acalculous cholecystitis? | Gallbladder stasis, hypoperfusion, or infection (CMV) |
| What is the Murphy sign? | Inspiratory arrest on RUQ palpation due to pain |
| What sign is associated with Cholecystitis? | Murphy sign |
| Where does pain radiate in a person with (+) Murphy sign? | Right shoulder |
| What is Gallstone ileus? | Fistula between gallbladder and GI tract --> stone enters GI lumen which leads obstructs at ileocecal valve |
| Where is the MC place were a fistula will produce gallstone ileus? | Ileocecal valve |
| Calcified gallbladder due to chronic cholecystitis. Dx? | Porcelain gallbladder |
| What is the common treatment of Porcelain gallbladder? | Prophylactic cholecystectomy due to high rates of gallbladder cancer |
| What is Ascending cholangitis? | Infection of biliary tree usually due to obstruction that leads to stasis/bacterial overgrowth. |
| What is the Charcot triad of cholangitis? | Jaundice, fever, and RUQ pain |
| What is Reynolds pentad? | Charcot triad plus altered mental status and shock (hypotension) |
| Charcot triad + Altered mental status + Shock = | Reynolds pentad |
| Autodigestion of pancreas by pancreatic enzymes surrounded by edema. Dx? | Acute pancreatitis |
| What are the causes of acute pancreatitis? | I GET SMASHED: Idiopathic Gallstones Ethanol Steroids Mumps Autoimmune disease Scorpion sting Hypercalcemia/Hypertriglyceremia ERCP Drugs |
| What are common drugs that are linked to development of acute pancreatitis? | Sulfa drugs, NRTIs, and Protease inhibitors |
| Complete 3 item list for diagnose of Acute pancreatitis: | 1. Acute epigastric pain often radiating to the back 2. Increased serum amylase or lipase to 3x upper limit 3. Characteristic imaging findings |
| Which serum level is more specific when diagnosis acute pancreatitis? | Lipase |
| What are some common complications of acute pancreatitis? | 1. Pseudocyt 2. Abscess 3. Necrosis 4. Hemorrhage, infection and organ failure 5. Hypocalcemia |
| What is characteristic of a pseudocyst due to acute pancreatitis? | Lined by granulation tissue, not epithelium |
| What lines the pseudocyst due to acute pancreatitis? | Granulation tissue |
| How does acute pancreatitis cause hypocalcemia? | Due to precipitation of Ca2+ soaps |
| Pathology of chronic pancreatitis? | Chronic inflammation, atrophy, and calcification of the pancreas |
| Which are the two major causes of chronic pancreatitis? | Alcohol abuse and genetic predisposition |
| What condition poses a genetic predisposition to the development of chronic pancreatitis? | Cystic fibrosis |
| Complications of chronic pancreatitis? | Pancreatic insufficiency and Pseudocysts |
| How is Pancreatic insufficeny clinically presented? | Steatorrhea, fat-soluble vitamin deficiency, and diabetes mellitus |
| Which, acute or chronic pancreatitis, always have elevated amylase and lipase serum levels? | Acute pancreatitis |
| Where does Pancreatic adenocarcinoma arise from? | Pancreatic ducts |
| Which part of the pancreas are tumor likely to be located? | Head of Pancreas |
| What is the result of tumors in the head of pancreas? | Obstructive jaundice |
| What is the most specific tumor serum marker of Pancreatic adenocarcinoma? | CA 19-9 |
| (+) CA 19-9. Dx? | Pancreatic adenocarcinoma |
| WHat are common risk factors of Pacreatic adenomcarcinoma? | Tobacco use, Chronic pancreatitis Diabetes Age > 50 years Jewish and African-American males |
| What are the most significant clinical features of Pancreatic adenocarcinoma? | - Abdominal pain radiating to the back, - Weight loss - Migratory thrombophlebitis |
| What is another term used for Migratory thrombophlebitis seen in Pancreatic adenocarcinoma? | Trousseau syndrome |
| Redness and tenderness on palpation of extremities | Trousseau syndrome |
| What are the two signs/syndromes that are present in Pancreatic adenocarcinoma? | Trousseau syndrome and Courvoisier sign |
| What is Courvoisier sign? | Obstructive jaundice with palpable, non-tender gallbladder |
| What is the treatment (s) for Pancreatic adenocarcinoma? | 1. Whipple procedure 2. Chemotherapy 3. Radiation therapy |
| What is the Whipple procedure? | Complex operation to remove the head of the pancreas, the first part of the small intestine (duodenum), the gallbladder and the bile duct. |
| What part of the pancreas is often removed by the Whipple procedure? | Head of Pancreas |
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