GastroEnterology
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| How can we accurately diagnose liver disease? | Through history, physical, few lab tests (acc to findings), radiological tests (most imp is US), and finally liver biopsy if needed. Usually when we see symptoms we are at the late stages of liver disease |
| Describe briefly liver function and structure. | Largest organ, 1-1.5 KG, dual blood supply (20% hepatic artery and 80% portal vein) Made of hepatocellular part and cholestatic other part (stellate cells, kupfer cells...) Roles include protein synthesis (albumin, coagulation factors...)/ bile production/ nutrient regulation/ metabolism... |
| What are the most used liver function tests? | Serum Bilirubin (could give either conjugation problem- if conjugated bilirubin is low, not liver disease/ or excretion problem -if conjugated is high, live disease) Another test is albumin and prothrombin time to measure functionality of the liver (protein synthesis) Any frank liver failure will need a transplant immediately and cannot survive on any equipment |
| What are the present types of liver diseases? | Hepatocellular/ Cholestatic/ Mixed Hepatocellular could be injury/ inflammation/ necrosis Such as viral hepatitis and alcoholic liver disease Cholestatic could be problems in duct such as common duct stone, biliary cirrhosis, drug-induced, obstruction...) And mixed has both features like obstructive hepatitis. |
| How do risk factors for liver disease determine onset and prominence? | Age (20 years--> viral hepatitis, 60 years--> tumor, 40 years--> alcoholic...) sex Hx (drug users we can get hepC) |
| What are the typical symptoms of liver disease? | Most frequent: Fatigue Jaundice (could be acute (due to viral hepatitis, autoimmune, alcoholic, Wilson's, drug use in decreasing order) , or chronic (usually appears with poor prognosis in end stage disease)) Itching (Cholestatic pattern - ALP and bilirubin) RUQ pain Nausea and anorexia Intestinal bleeding abdominal distention (in chronic disease due to ascites) TO NOTE that the liver is a silent killer (usually px appear asymptomatic and symptoms only appear at late stages) |
| What are the things we look for during the diagnosis of liver disease? | Etiology (disease), Staging (fibrosis/ cirrhosis...), Category (hepatocellular, cholestatic) and grading (severe, acute, chronic...) |
| What are the constitutional symptoms in case of liver disease? | We have the non-specific symptoms ( fatigue, weakness, nausea, poor appetite, and malaise) and liver-disease specific symptoms ( liver-specific symptoms of jaundice, dark urine, light stools, itching, abdominal pain, and bloating.) Symptoms can also suggest the presence of cirrhosis, end-stage liver disease, or complications of cirrhosis such as portal hypertension |
| Describe the symptoms of liver disease one by one. | Fatigue (arises with activity, rarely present in morning at rest) Nausea (may be provoked by eating...) Vomiting (rarely persistent) Anorexia (with acute disease, rarely in chronic) Diarrhea (uncommon) RUQ pain (accompanied by tenderness over liver area, it arises from stretching Glisson's capsule, usually occurs for liver abscesses, venooclusive disease...) Itching (occurs with acute disease, early obstructive disease, and some hepatocellular disease, but mostly for cholestatic disease) |
| Talk about jaundice symptom of liver disease. | – hallmark symptom of liver disease patients – the most reliable marker of severity. – Jaundice is rarely detectable with a bilirubin level <43 μmol/L (2.5 mg/dL). (normal bilirubin is 1.5, jaundice appears if bilirubin between 1.5-2 at ear 2-2.5 at frenulum of tongue 2.5 and above in sclera, conjugtiva and skin |
| What are the risk factors for liver disease? | Alcohol use (females 22-30g, males 33-45g for more than 10 years cause chronic liver disease), medications, habits (Obesity), Sex, travel, exposure, drug use, surgery (due to anesthesia...), familial diseases (Wilson's, hemochromatosis, a1 antitrypsin (in case of hx of emphysema)) |
| If a px presents with hx of all hepatitis, liver disease and cancer what is the most suitable etiology? If also diabetes? | Most likely hepatitis (HepB- vertical transmission) With diabetes (hemochromatosis - iron overload) |
| Talk about the physical exam findings in liver disease | Usually normal unless acute and severe. Typical findings icterus/jaundice, Hepatomegaly, hepatic tenderness, Splenomegaly,Spider angiomata (red spots like web than when touched disappear- found normally 3-4 for women and none for men accompanied with estrogen) , palmar erythema (not necessarily for liver disease if accompanied with Dupuytren's contracture (thickening in palm tissue)--> alcoholic |
| What are the laboratory tests done for liver function? | ALT/ AST (when expect hepatocellular) ALP (when expect cholestatic) Bilirubin (could be both) Autoimmune and Ig tests, gamma GT Albumin and Prothrombin (Synthesis function) we move in a pattern of dx, first category then acute or chronic then stage |
| What does elevated prothrombin synthesis time indicate? | Either liver disease or vitamin K deficiency. To differentiate between the two we test factor V levels, if low then liver disease if high then vitamin K deficiency (since it is the only factor independent of vitamin K) |
| What are the imaging techniques used for liver disease? | Most important is the US for vessel issues and tumors use CT MRCP for biliary tree dx, and ERCP is more therapeutic for the biliary tree We also have elastography or fibroscan, which reveals fibrosis, and this technique will eventually replace biopsy as it show fibrosis and cirrohsis (however not inflammation) |
| What are interventional radio techniques? | Interventional Radio:– the biopsy of solitary lesions – performance of radiofrequency ablation and chemoembolization of cancerous lesions – insertion of drains into hepatic abscesse – measurement of portal pressure – creation of vascular shunts in patients with portal hypertension. |
| Talk about liver biopsy | Evaluate px with chronic liver disease, test severity, prognosis tx responsiveness (for autoimmune) to get dx use IgM and not all Ab. |
| What is acute pancreatitis? | Acute inflammation of pancreas involving other tissue organs. Clinically if 2 out of 3 criteria are found: 1-symptoms consistent with pancreatitis (sever pain) 2-Serum Lipase level more than 3X the normal value. 3-Pancreatitis seen on imaging usually CT or MRI |
| What are the two appearances of acute pancreatitis (natural history)? | 2 phases: interstitial and necrotizing. Interstitial: mild case involving 2/3 of pancreatitis, severity of the case depends on extra-pancreatic organs involved, presents with the normal signs of inflammation (fever, tachycardia, hypotension, respiratory distress, leukocytosis (SIRS -system inflammatory response syndrome) Necrotizing: severe, in 1/3 of cases, lasting weeks to months, mortality due to infection of necrosis and organ failure |
| What are the etiologies causing acute pancreatitis? | Obstruction (of wirsung, most important is gall stones, tumor maybe, parasites, diverticulia...) Alcohol or other toxins (not imp in lebanon, but major cause in US and europe) Metabolic abnormalities (TGs, DM, hypercalcemia (due to hyperPTH)) Infection (rare) Vascular (rare, more in gut and liver) Trauma (maybe unpredictable, pancreas can rupture) PostOp (cardiac surgery for example) Post ERCP (papillary injury causing inflammation) Sphincter of Oddi (dysfunction) Drug association (IBD - sulfasalazine, most important is furosemide (lasix)) |
| How does acute pancreatitis present clincally? | Abdominal pain, epigastric radiating dorsally, abrupt and sudden onset, knife like relieved with back flexion (max intensity 10-20 min, not as sudden as viscus)) most patients present with nausea |
| What are the physical exam findings of acute pancreatitis? | Nothing seen, maybe tenderness of abdomen, in severe pancreatitis, we see abdominal distention, tachycardia, HTN, may have fever (all these are due to extra-pancreatic organs) |
| What are the labs made to reveal acute pancreatitis? | Lipase (sensitivity>85%, and more specific than amylase) WBC we see leukocytosis Hyperglycemia, Liver enzymes elevated (we look at them to see gall stone or acute biliary pancreatitis) Hypocalcemia, the more severe the worse prognosis MCV increases (due to alcohol, we can also see gamma GT) |
| What are the diagnostic imaging techniques used for acute pancreatitis? | US (not for pancreas and more for gall bladder) CT and Endoscopic US (EUS) are more important, and we use Balthazar grades to assess the pancreatitis. EUS is a gastroscopy with an US inside, put on the wall of stomach to see the pancreas posteriorly. |
| What are the indicators of CT scan of pancreatitis? | (1) exclude other serious intra-abdominal conditions (e.g., mesenteric infarction or a perforated ulcer), (2) stage the severity of acute pancreatitis, and (3) determine whether complications of pancreatitis are present (e.g., involvement of the GI tract or nearby blood vessels and organs, including liver, spleen, and kidney). |
| How does pancreatic necrosis appear? | Pancreatic necrosis manifested as perfusion defects after IV contrast may not appear until 48 to 72 hours after onset of acute pancreatitis |
| What is Balthazar scale? | Grading from A to E (most severe) A: normal pancreas mild pancreatitis B: Enlargement of the gland C: B + peripancreatic inflammation D: C + single fluid collection E : D + perpancreatic fluid accumulation or gas... |
| Why is EUS used? | Not helpful if early, but reveals small tumors, pancreas divisum, bile duct stones... equivalent to ERCP and MRCP but more sensitive Best method evaluating necrotizing pancreatitis. If bilirubin increased --> do ERCP |
| What are the predictors of disease severity? | Our management of the disease is purely symptomatic Most important score of evaluation is SIRS (systemic inflammatory response syndrome) where we see if we have a sever acute pancreatitis by seeing other organs involvement, SIRSS 2 of 4 criteria (pulse >90 bpm, Rectal Temp <36 or >38, WBC <4000 or >12000, RR >20 or Pco2 <32 mmHg We also use scores like APACH (in ICU since it takes time (48 hours)) We could see CRP as well At a cutoff of 21 mg/dL, the sensitivity of CRP in detecting severe disease in patients with acute pancreatitis is only 60%, but the test is highly specific. At a lower cutoff (10 mg/L), CRP becomes highly sensitive, but the test specificity drops to 75%. |
| When should we manage SIRS? | 48 hours within the start of organ failure and SIRS (MR = 0% and else it becomes >36%) |
| What are risk factors of severe pancreatitis? | Old age, Obesity, Comorbidities, SIRS, inflammation, increased creatinine, extrapulmonary symptoms (pleural effusion, pulmonary infiltrate, extrapancreatic fluid accumulation) |
| What is the treatment of acute pancreatitis? | IV hydration, analgesics, NPO (stopping nausea), NG tube not used frequently, monitoring and Abx in case of biliary sepsis or infection pancreatic or extrapancreatic Nutrition: when there is no nausea or vomiting it is important to feed the patient to prevent floral translocation from gut to the site of pancreatitis and necrosis causing infectious necrosis. Surgery (Cholecystectomy (after ERCP to stop any new stone from happening - should happen in same hospitalization of pancreatitis), Necrosectomy or abscess drainage |
| What are the complications of acute pancreatitis? | Pseudocysts, Necrosis (sterile or infected), Abscesses, GI bleed, splenic complications, systemic failure THE MOST IMPORTANT ARE: Pseudocyst, Necrosis and Infected Necrosis |
| What is a pseudocyst? | Secondary to acute pancreatitis, takes 4 weeks to develop, secondary to pancreatitis or trauma. No distinct border, just a liquid with inflammatory tissue as a border. If asymptomatic just monitor (may resolve on its own) If symptomatic (see with EUS linear view to drain it with a needle, put a guidewire in the cyst and put a metallic stent half in the cyst and half to the intestine in order to drain it. In patients with known pseudocysts, new symptoms such as abdominal pain, chills, or fever should alert the clinician to the emergence of an infected pseudocyst or abscess. Treatment choices include surgical, radiologic, and endoscopic drainage |
| What is necrotizing pancreatitis? | Pancreatic necrosis is defined, in the absence of laparotomy or autopsy, by the presence of greater than 30% of nonenhancement of the pancreas on a contrast-enhanced CT scan May be infected or sterile |
| How does infection of pancreatic necrosis occur and how do abscesses form? | Bacterial translocation to necrotic tissue 10 days after hospitalization, recur with sepsis, fever, pain and leukocytosis, seen by CT guided FNA. Abx should be provided early debridement of pancreatic necrosis within the first 4 to 5 weeks of an attack will require surgery, WON can be treated laproscopically, percutaneously, or endoscopically |
| What are the findings of alcohol use on the liver? | Broad spectrum of symptoms according to consumption, ranging from asymptomatic to fatty liver and end-stage liver failure (jaundice, coagulopathy and encephalopathy) Moderate alcohol intake can cause vasodilation which is a cardiovascular benefit this makes the french paradox (less cardiovascular disease due to combination of alcohol and fat intake) It comes with socio-physical problems |
| What is the percentage of alcohol intake inducing liver cirrhosis? | For females: 20-40 g/day for males:60-80 g/day for over 10 years But may differ among individuals (only 10% of alcoholics will develop liver cirrhosis (acc to genetics, obesity (causing NASH), past hx, medications...) This quantity of alcohol intake is 1 L of wine or 8 beers. |
| Talk about the epidemiology of alcoholic liver disease. | One of the leading causes of global burden of disease and injury, it is the most widely abused substances worldwide 100,000 deaths/year is US, causes other conditions (psychotic, cardiomyopathy, amnesic syndrome, liver disease) In US it is the leading cause of death due to liver failure (in lebanon second cause) *it is a chronic disease - reliant in ethanol. |
| What are the percentages of alcohol in beverages? | Beer: 5%, wine: 12%, hard liquor (whiskey...): 40% But portions of consumed alcohol are practically the same (14g / serving) Regardless of type of alcohol consumed, more alcohol = more progressive disease. man <4 drinks/day or 14/week, woman <3/day or 7/week. |
| Talk about the risk of development of alcoholic liver disease. | Over 90% get liver steatosis, 10% get hepatitis. Risks of the disease are amount consumed, genetics, sex (female increased risk), obesity, chronic viral hepatitis, nutritional impairment and drugs intake |
| How does the liver metabolize alcohol? | Liver is principal alcohol metabolising organ, as ethanol is rapidly absorbed by the upper GI, it diffuses to liver via portal vein, then alcohol dehydrogenase degrades it converting it into acetaldehyde (affecting protein synthesis) damaging hepatocytes (excess free radicals) this excess leads to inability to prevent and repair damage + kupfer cell activated leading to hepatocellular death -->fibrosis. |
| What are the PE findings in alcoholic liver disease? | Acc to stage (normal, cirrhotic or decompensated) Ascites, clubbing, jaundice, neuropathy, palmar erythema. Most important pathogneomonic sign is Dupuytren's contraction (seen when hand shake) |
| What are the lab findings in alcoholic liver disease? | AST/ALT ratio >2 (both elevated) but less than 500 macrocytic anemia (increased MCV), leukocytosis (inflammation), increased bilirubin |
| What are all the liver consequences of alcoholism? | 90-100% of time leads to steatosis (fatty liver) which may lead to cirrhosis if no alcohol abstaining. Can also lead to acute hepatitis where frequent repeated attacks may also lead to cirrhosis. Acute hepatitis and steatosis are reversible (by abstaining from alcohol) while cirrhosis isn't (unless in very early stages) |
| What is hepatic steatosis? | Fatty liver, not exclusive for ALD. accumulation of TGs in hepatocytes, 90-100% of heavy drinkers have it, short term exposure to over 80g/day for several days may cause it. Reversible, no clinical symptoms (maybe hepatomegaly), normal liver test or elevated. it occurs due to macrovesicular fatty infiltrate, can be due to other causes than alcohol (starve, pregnancy, drug, viral hep, Reye...) |
| What is alcoholic hepatitis? | Fatty liver + hepatitis (steatohepatitis), precursor of cirrhosis. results from alcohol abuse, can be subclinical. 40% of them will lead to cirrhosis within 1-2 years Clinically its heavy alcohol intake with lab findings (viral/ use drugs..) Presents Asymptomatic - majority, or symptomatic liver failure Elevated ALP, gGT, bilirubin, CRP, ESR needs urgent treatment (corticosteroids for 3 weeks) Obligatory: liver cell necrosis, mallory body, neutrophil infiltrate, perivenular inflammation |
| What is alcoholic cirrhosis? | Irreversible, 50g/day alcohol intake for 10 years causing it, both steatosis and hepatitis and fibrosis, if unchecked makes hepatic fibrosis. May be micronodular (chronic) or macronodular (acute) or mixed. Similar to normal cirrhosis but increased ration of AST/ALT Needs long-term management (abstinence, nutrition, liver transplant urgent |
| An alcoholic patient comes with epigastric pain, what is the differential ? | Acute pancreatitis due to alcohol, we confirm it by lipase test |
| An alcoholic pt presents with jaundice, what is the course of action? | LFT (Bi, ALT, AST, gGT, ALP, INR, ALB), CBC, Virals serology (for hep B and C) |
| What is fulminant hepatic failure? | Rapid development of acute liver injury with impaired function and encephalopathy (w/in 8 weeks if healthy liver or 2 weeks with underlying liver disease) Death is caused by brain edema (which occurs in FLF) |
| What is the difference between FHF and sub FHF? | Cerebral edema in FHF only, Renal failure and HTN portal in sub HFH only. |
| What are the major causes of FHF? | Acetaminophen toxicity (should be directly treated with N-acetylcysteine), hepA, autoimmune (make ANA), hepB,C,D, Wilson's disease, fatty infiltrate, Reye, pregnancy. Vascular (portal thrombosis, veno-occlusion, ishemic hepatitis) Miscellanous (sepsis, heat stroke, autoimmune) |
| What are the signs and symptoms of FHF? | Acute liver failure symptoms (malasie, nausea, jaundice, ecchymoses) Hepatic encephalopathy (stages, 1 ->daynight sleep reverse, 2 slowed response, 3 confusion, 4 coma) Cerebral edema, sepsis, renal failure, circulatory issues, GI bleed, |
| What are the lab findings of FHF? | CBC, LFT, Viral serology, EEG done. If INR high and encephalopathy --> transplant |
| What are the treatments of FHF? | Liver transplant (stage 3 or 4) complication treatments (encephalopathy -->mannitol (ammonia within gut lumen) Restrict protein diet, abx. Cerebral edema (astrocyte edema/ neurosymptoms --> treated by elevated head position and manitol 0.5-1g/lg |
| A patient 65 years old is admitted to the ER for cardiogenic shock, we see on labs ALT 2000 and AST 1500, what is the course of action and differential? | This may be liver shock, which is caused by hypotension, hepatocytes get destroyed and liver enzymes are very very high. it is reversible and self-limited resolves after correcting BP (unless pt has chronic liver disease) If it occurs with CLD --> this may be a cause for liver decompensation. |
| A pt comes to ER with 3000 ALT, what is the course of action? | If INR high and hepatic encephalopathy directly go for transplant as pt will die within 24-48 hours |
| What is drug induced hepatitis? | Hepatotoxicity by drugs, most common cause of FHF more than 90% are subclinical (mostly Abx and antihyperlipidema) Can vary from subclinical to acute injury (cyto or chole) to chronic injury to vascular or granuloma or neoplasia. Most elevations are benign and resolve when offending agent is done. |
| What are drugs causing acute liver injury? | Cytotoxic (acetaminophen, phenytoin, methyldopa) Cholestatcic (TMB-sulfa (bactrim), rifampin, erythromycin, amiodarone, chloropromazine) Mixed (phenytoin, increased risk of chronic disease) Steatosis (tetracyclin, amiodarone, microvesicular) |
| What are drug induced chronic liver injuries? | Autoimmune like, viral like, necroinflammatory, steatosis (glucocorticoids...), fibrosis (amiodarone, methotrexate, methyldopa) Intrahepatic cholestasis (ampicillin, amoxicillin-clavulanate, erythromycin, tetracyclin. Biliary sclerosis, vascular disease (veno-occlusive vit A or COC, or azathioprine) |
| How is the dx of drug induced hepatitis? | Can be very difficult, due to multiple meds taken. To ensure it is right, exposure should precede injury, liver diseases all negative, improve after stopping the drug. |
| How is the treatment of drug-induced hepatitis? | Withdrawal of drug |
| A 45 year old pt comes to ER for jaundice upon workup CBC normal and LFT elevated, all labs serology, ANA, meds, cirrhosis are negative what is cause? | Herbs (aleovera (can cause irreversible injury and renal injury)) |
| What is chronic pancreatitis? | It is defined histologically as chronic irreversible damage of the pancreas, chronic inflammation, causing fibrosis (cell damage) and eventually duct and parenchymal damage (of pancreatic glands) It can be defined clinically as abdominal pain + exocrine and endocrine insufficiency) |
| Suppose we have an alcoholic pt with acute pancreatitis, what should we expect? | We expect him to have chronic pancreatitis |
| Why is chronic pancreatitis a syndrome? | Since we can't obtain pancreatic tissue easily, we call it a syndrome with features including exposure to risk factors, genetic background, symptoms of exocrine and endocrine insufficiency, and structural changes of pancreas seen on imaging |
| What are the clinical presentations of chronic pancreatitis? | Abdominal pain (most common, occurs at beginning of the evolution and stops at the end, epigastric radiating to the back, may be associated with nausea and vomiting, and if severe causes loss of apetite) Steatorrhea (no lipase activity, occurs when pancreatic enzyme secretion is less than 10% max output, get diarrhea and weight loss+ fat-soluble vitamin deficiency (A,E and D) and maybe osteoporosis and osteopenia, also caused by celiac disease) DM (40-80% of pt, if we see pancreatic calcifications early onset and tail resection, less insulin -->give IV insulin) |
| What are the tests done for diagnosis of chronic pancreatitis? | Direct test (secretin-CCK (not used anymore)) Indirect test (fecal fat excretion most important and used, elastase in stool (not used in lebanon)) |
| What are the imaging findings of chronic pancreatitis? | On Xray (we see calcifications due to alcoholic pancreatitis (lethiasis of enzymes with calcium ions and thus close channels leading to necrosis, done laterally or obliquely on pt) US not used CT (sensitive and specific) MRCP (best, see fibrosis of wirsung, we can see cavities due to acinar cell destruction by IV secretin admin where it fills the defect) ERCP (we may see dilation, irregular path and calcifications) EUS (detailed later) |
| What are the gradings of chronic pancreatitis by ERCP? | Cambridge grading (according to pancreatic duct and side branch involvement. Normal, Equivocal (if main duct normal and <3 side are abnormal), mild (main normal and >3 side are abnormal), moderate (main abnormal and >3 side abnormal), severe (main abnormal with at least one of large cavity (>10mm), obstruction, filling defects, severe dilatation)) |
| What are the gradings of chronic pancreatitis seen on US or CT? | Normal Equivocal (either mild dilation of duct, or gland enlargement) Mild/Moderate (equivocal + >4mm dilatation or duct irregularity or cavities <10mm or parenchymal heterogeneity or focal necrosis) Severe (mild + more severe cavities/ duct dilatation/ calcification/ obstruction...) |
| What are the observations of EUS in chronic pancreatitis? | See advanced chronic pancreatitis, imp since we see parenchyma not just the duct. Highly accurate |
| When do we use hormonal stimulation test of pancreas? | In case all imagings are - done in a specialized center Rk: ERCP not used diagnostically. |
| What are the etiologies of chronic pancreatitis? | Alcoholic Pancreatitis (50% of cases, even if acute he should stop since it will progress to chronic pancreatitis) Smoking increases it alot, hypercalcemia, hyperTG are more for acute not chronic pancreatitis) Genetics (hardly seen) Autoimmune Obstructive (not imp) |
| What is alcoholic pancreatitis? | Occurs for men, 5 years of drinking 4-5 drinks per day + genetics + risk factors like smoking... Many have an early phase of recurrent acute pancreatitis attacks which lasts 5 years and develops into chronic pancreatitis (abdominal pain recurrent attacks) |
| What are the treatment options of chronic pancreatitis? | Medical (analgesic (may get addicted), stop tobacco and alcohol, pancreatic enzyme and some somatostatin (octreotide)) Endoscopy (according to pathophysio, sphincterotomy, stent placement, duct stone removal) Surgery (last option, open all wirsung (wirsungojejenostomy) |
| What are pseudocysts? | They occur in 25% of chronic pancreatitis pt, most commonly occurs with abdominal pain, persistent elevation of lipase enzyme, dx by imaging ez, complications occur for 20-40% of pt (include large peripancreatic vessels, infection, duodenum and stomach involvement, hemorrhage, fistula formation |
| What are the autoimmune pancreatitis? | They could cause acute or chronic pancreatitis, two types 1 and 2 differ on many aspects |
| What is the difference between autoimmune pancreatitis 1 and 2? | Histology (no damage of ductal epithelium in 1 while in 2 we have destruction) IgG4 (present in type 1 and absent in 2) Age (60-70 in 1 and 40-50 in 2) Gender (male for 1 and both for 2) Clinical presentation (more obstructive jaundice in 1 and more acute pancreatitis pain in 2) Pancreatic imaging (more diffuse enlargment in 1 and more focal enlargement in 2) Other organ involvement (more in 1 than 2) other diseases (strictures, pseudotumors in 1 and IBD in 2) Relapses (frequent in 1 and rare in 2) |
| How is the epidemiology of pancreatic cancer? | Disease of aging, occurs after age of 45 usually, most important risk factor is cigarette smoking. Other risk factors include other cancers (FAMMM, heriditary pancreatitis, breast cancer...) |
| How is the pathology of pancreatic cancer? | Ductal adenocarcinoma (85-90%) of pancreatic tumors. 70% in head (common bile duct affected causes jaundice, usually small tumor maybe resectable <3cm w/no metastasis), 5-10% body and 10-15% tail (stomach cause) |
| How is the invasion of pancreatic cancer? | Head tumors can obstruct common bile duct and pancreatic duct, leads to jaundice and chronic obstructive pancreatitis. We see duct dilation, fibrous atrophy of pancreatic parenchyma. Some tumors can involve ampulla of vater/ duodenum, and retroperitoneal tissue involvement is almost always present at time of dx can result in invasion of SMA and nerves/portal vein. Neoplasms of tail can cause invasion of spleen, stomach, splenic flexure of colon or left adrenal gland, if advanced metastasis to lymph nodes, liver and peritoneum are common. Also pleura and lungs and bone are less commonly involved |
| What are the clinical symptoms of pt with unresectable (palliated) and resectable pancreatic cancer? | Paliated more severe abdominal pain and weight loss, while for resectable tumors we see more jaundice. age almost same 65 years old, men more than women in both and mostly affects white race 91%. |
| How is the dx of pancreatic cancer done? | Imaging (not biopsy). US (transabdominal frequently used (no one does it in lebanon)) CT (method of choice for dx, best one, limitation if tumor <2cm (not seen), tells extensions in early phases delineates the tumor and in late phases enhances vascular relationships and liver metastasis) sensitive 97%) |
| What does CT tells us regarding resectability? | Longstanding CT is done to see resectability, sees distant metastasis (liver...), encasement of celiac axis/SMA, occlusion of portal vein/SMV. If tumor in tail/body usually easier to resect since no vessels are involved, while in head, bulb, duodenum and stomach are involved, so we remove them monoblock (all together) + remove SMA + SMV (which can be reconstructed) 10-15% are resectable, and 40% 5 year death. |
| What are the ERCP findings in case of pancreatic cancer? | Double duct sign (strictures in biliary and pancreatic ducts. We can get tissue samples from ERCP (ampullomas, duodenal biopsy) by endoscopic forceps. Tumors of distal bile duct maybe sampled by brush biopsy. ERCP is unnecessary most of the time. |
| What is the significance of EUS in pancreatic cancer? | EUS most accurate but costly, but equally dx as CT (if not CT more after advances in it seeing vascularization and resectability) Most sensitive method is EUS, and give ability to make FNA/FNB which is safe, reliable w/ no false-positive results (97% specificity). EUS guided FNA proves malignancy and rules out other diseases (sarcoidosis/TB) and distinguish adenocarcinoma from other tumors (neuroendcrine/ lymphomas) But usually we don't need biopsy for resection. |
| When do we use EUS? | Not necessary for all pt (if resectable by CT no need) Stage IV disease, EUS-FNA is excellent option to dx primary tumors, and allows stratificetion of pt for resection vs neoadjuvant tx for borderline disease. |
| What is the dx use of CA 19-9? | Major tumor marker in presence of jaundice (cholangitis) but can give false-positive, and negative BGs can give false negatives as well. Studies shown CA19-9 in pancreatic cancer in 85% (Cut off 37 U/ml), normalization of CA19-9 after resection and pt w/ CA19-9 above 90 didn't benefit from chemo |
| What is the significance of MRI in pancreatic cancer? | Not that much used, but can be useful in tumor evaluation, MRCP non invasive |
| What is the use of PET-CT in pancreatic cancer? | No improvement in comparison with multidetector CT, assesses recurrence after resection, or benefit in assessing tumor response to neoadjuvant chemo |
| How is diagnostic workup of pt with pancreatic cancer? | Minimal workup include PE, CT/MRI of abdomen/pelvis. Borderline cases use EUS w/CT. For dx and staging, use laparoscopy for all pt w/ tumors in body and tail and pt w/tumors larger than 2cm in head |
| How is the staging of pancreatic cancer? | TNM T: tumor (TX (not assessed), T0(no tumor), Tis (carcinoma in situ) T1 (limited to pancreas <2cm), T2 (limited to pancreas >2cm), T3 (beyond pancreas but not SMA/ celiac axis), T4 (invades all)) N (lymph node metastasis, NX(can't be assessed), N0 (no metastasisi) N1 (metastasis)) M (distant metastasis same as N) Staging according to AJCC staging Stage 0 (Tis, N0,M0), Stage IA (T1, N0,M0, Stage IB (T2, N0,M0), Stage IIA (T3, N0,M0), Stage IIB (T1/T2/T3, N1,M0), Stage III (T4, N1, M0), Stage IV (Any T, any N, M1) |
| What are the groups of patients in pancreatic cancer staging? | Group1 (metastatic, no surgery benefit, short survivial chemo) Group2 (Locally advanced unresectable w/no metastasis, benefit chemo neoadjuvant and can be surgical after chemo) Group3 (borderline resectable, more likely benefit neoadjuvant chemo) Group4 (Resectable) |
| What are the indications of surgery for pancreatic cancer? | Only about 15-20% of pt are candidates to pancreatectomy (since mostly advanced disease stage) Contraindications include encasement/ occlusion of SMV/portal vein, extension to celiac axis/SMA/vena cava. Preop biliary stent is not recommended (if resectable) if non-resectable biliary stent is recommended as paliative tx. |
| How is prognosis after surgery of pancreatic cancer? | Poor prognosis, 5 year survival 25%, usually 12-24 months. Surgery alone isn't enough, still needs immunotherapy/ molecular targetted therapy. |