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Surgery Review 6
SR 6: Hepatopancreaticobiliary, spleen, hernia, transplant, wound healing
| Question | Answer |
|---|---|
| What is a replaced right or left hepatic artery? | Replaced right - originating off SMA (occurs in 17%) Replaced left - originating off left gastric (occurs in 10%) |
| Which segment of the liver drains directly into IVC? | Segment I - caudate lobe |
| What is Cantlie’s line? | Line drawn from gallbladder fossa to IVC separating right and left hepatic lobes |
| What are Kupffer cells? | Specialized macrophages in the liver responsible for clearing portal blood and immunosurveillance. Also responsible for early alcohol-induced liver injury |
| Describe the anatomical relationship of the portal triad | Portal vein posterior to CBD (on R) and hepatic artery (on L) |
| What are the boundaries of the Foramen of Winslow? | Anterior – portal triad, posterior – IVC, inferior – duodenum, superior – liver |
| Where is alkaline phosphatase located? | canalicular membrane |
| What is the only water soluble vitamin stored in the liver? | B12 |
| Which hepatocytes are most sensitive to ischemia? | Central lobular (acinar zone III) |
| What are the primary bile acids? | cholic and chenodeoxycholic |
| What are the secondary bile acids? | deoxycholic and lithocholic (dehydroxylated primary bile acids by bacteria in gut) |
| What is the main biliary phospholipid which solubilizes cholesterol and emulsifies fat in the intestine? | Lecithin |
| Where is jaundice first evident? | Under the tongue |
| Which hereditary hyperbilirubinemia is characterized by abnormal uptake and mildly high unconjugated bilirubin? | Gilbert’s disease |
| Which hereditary hyperbilirubinemia is characterized by inability to conjugate and deficiency of glucuronyl transferase causing high unconjugated bilirubin and life-threatening disease? | Crigler-Najjar disease |
| Which hereditary hyperbilirubinemia is characterized by immature glucuronyl transferase and unconjugated bilirubin? | Physiologic jaundice of newborn |
| Which hereditary hyperbilirubinemia is characterized by deficiency in storage ability and high conjugated bilirubin? | Rotor syndrome |
| Which hereditary hyperbilirubinemia is characterized by deficiency in secreation ability and high conjugated bilirubin levels? | Dubin-Johnson syndrome |
| Which viral hepatitis cannot cause chronic hepatitis and hepatoma? | Hepatitis A (but all viral agents can cause acute hepatitis and fulminant hepatic failure) |
| What is the most common viral hepatitis leading to liver transplant? | Hepatitis C |
| What is the only DNA hepatitis virus? | Hepatitis B |
| What is the treatment of hepatic encephalopathy? | lactulose, limit protein <70g/day, branched chain AA, dopamine receptor agonists. Rule out SBP and GI bleed |
| What is the treatment for esophageal varices? | sclerotherapy (90% effective), vasopressin, octreotide acutely, TIPS if refractory; nitro if CAD; propanolol may prevent rebleeding |
| What act as collaterals between the portal vein and the systemic venous system of the lower esophagus? | Coronary veins |
| What are the indications for TIPS? | protracted bleeding, progression of coagulopathy, refractory ascites, and visceral hypoperfusion |
| What is the cause of portal hypertension in children? | extrahepatic thrombosis of portal vein |
| What is Budd-Chiari syndrome? Treatment? | Occlusion of hepatic veins and IVC. Tx: portacaval shunt (needs to connect IVC above obstruction) |
| What is the treatment for hepatic adenoma? | Hepatic adenoma is an indication for resection – 10% rupture/bleed + malignant potential (some texts say may trial stopping OCPs first for regression) |
| What is the difference between a hepatic adenoma and focal nodular hyperplasia on colloid scan? | Hepatic adenomas do not have Kupffer cells, so have no uptake on sulfur colloid scan (cold), FNH will take up sulfur colloid |
| What is the treatment for hepatic hemangioma? | Do nothing unless giant or symptomatic/consumptive |
| What is the treatment of focal nodular hyperplasia? | Conservative treatment only, no malignancy risk, very unlikely to rupture |
| What is Kasabach-Merritt syndrome? | Consumptive coagulopathy or CHF due to hemangioma - usually in infants |
| What is the treatment of liver amebic abscess? | metronidazole, surgical only if free rupture |
| What is the treatment of hydatid cysts? | Surgical resection with albendazole or mebendazole before and after |
| What is the work-up of hydatid cysts? | Casoni skin test + Indirect hemagglutination. Do not aspirate (risk of anaphylactic shock) |
| What causes a maculopapular rash and increased eosinophils? | Schistosomiasis |
| What is the treatment of schistosomiasis? | praziquantal and control of variceal bleeding |
| What are the main risk factors for hepatocellular carcinoma? | Alcoholism, Hep B+C, hemochromatosis, PSC, aflatoxin, alpha-1-antitrypsin deficiency - PBC and Wilson's are not risk factors |
| What type of HCC has best prognosis? | Fibrolamellar (followed by clear cell and lymphocyte infiltrative) |
| What is the most potent risk factor for the development of HCC? | hepatitis B surface antigen positivity |
| What are risk factors for hepatic sarcoma? | PVC, thorotrast, arsenic |
| How does the gallbladder concentrate bile? | Active absorption of Na, Cl (H20 then follows) |
| What is bile conjugated to? | taurine and glycine |
| What are the boundaries of the triangle of Calot? | cystic duct, hepatic duct, and cystic artery (some texts say liver edge) |
| What is the blood supply to the common bile duct? | Right hepatic (lateral) and retroduodenal branches of GDA (medial) |
| What is the rate-limiting step in cholesterol formation? | HMG CoA Reductase |
| What causes gallstones in obese people? In thin people? | Obese – overactive HMG CoA reductase; thin – underactive 7-alpha-hydroxylase |
| What are the common causes of black gallstones? | Cirrhosis, hemolytic disorders, chronic TPN, ileal resection |
| What type of stones are generally primary CBD stones, formed in ducts? | Brown stones, caused by infection and subsequent deconjugation of bilirubin (E. coli most common) |
| What are the symptoms and treatment of cholangitis? | Fever, RUQ pain, jaundice, +/- hypotension, MS changes. Needs immediate IV Abx, IVF, emergent decompressions/drainage of CBD |
| What is the | 1 cause of benign biliary stricture? |
| What is the treatment of common bile duct strictures? | Hepaticojejunostomy. If early symptoms (<7 days), perform immediately; if late symptoms, perform 6-8 weeks after injury |
| What is the triad of hemobilia? | UGIB, RUQ pain, and jaundice - caused by fistula between biliary duct and hepatic arterial system |
| What is the treatment of hemobilia? | workup and treatment with arteriogram |
| What is the treatment of gallbladder adenocarcinoma? | Cholecystectomy adequate if confined to mucosa. If grossly visible tumor - regional lymphadenectomy, wedge segment V, skeletonize portal triad |
| What is the treatment of cholangiocarcinoma? | Upper 1/3 (Klatskin) – lobectomy and stenting of contralateral duct if localized, but usually unresectable; middle 1/3 – hepaticojejunostomy; lower 1/3 – whipple |
| What is the medical treatment of primary sclerosing cholangitis? | cholecystryramine, UDCA (urodeoxycholic acid) |
| What is the treatment of primary biliary cirrhosis? | Liver transplant |
| What is Mirizzi syndrome? | Compression and/or inflammation of common hepatic duct by a stone in the infundibulum of the gallbladder causing stricture and hepatic duct obstruction |
| What is the only pancreatic enzyme secreted in active form? | amylase |
| Which pancreatic cells receive a majority of the blood supply related to size? | Islet cells |
| What are the two types of pancreatic cells? | Acinar cells (98% of mass) – exocrine function and islet cells – endocrine function |
| What makes up the majority of the islet cells in the pancreas? | Insulin-producing B cells, located centrally make up 50-70% of the islet population |
| What do the delta cells of the pancreas produce? | somatostatin |
| What are the signs of annular pancreas? Treatment? | Double bubble on x-ray, prone to pancreatitis, possible obstruction. Treat obstruction with duodenojejunostomy, or duodenoduodenostomy and sphincteroplasty (do not resect pancreas) |
| What is the treatment of pancreas divisum? | sphincteroplasty and stent placement if symptomatic (if long-standing, may need longitudinal pancreaticojejunostomy) |
| What is the pathophysiology of acute pancreatitis? | impaired extrusion of zymogen granules and activation of degradation enzymes leading to autodigestion |
| What is ranson’s criteria? | Admit – GA LAW – Glucose >200, AST >250, LDH >350, age >55, WBC >16k; 48 hours – C HOBBS – Calcium <8, Hct drop >10%, oxygen < 60 mm, BUN > 5, base deficit > 4, sequestration of fluid > 6L |
| When do you operate on pancreatitis? | Only for infected pancreatitis, need to remove infected material, but generally leave sterile necrosis alone |
| What is the most important risk factor for necrotizing pancreatitis? | Obesity |
| What complications of pancreatitis are caused by the release of phospholipases and proteases? | phospholipases – ARDS and pancreatic/fat necrosis, proteases - coagulopathy |
| What is treatment of pancreatic pseudocyst? | Expectant management initally - 85% resolve on their own; If persistent and symptomatic or growing - internal drainage by cyst-gastrostomy, -duodenostomy, or –jejunostomy |
| Which pancreatic cells are usually preserved in chronic pancreatitis? | islet cells, whereas exocrine tissue gets calcified and fibrotic |
| What is the optimal treatment for bleeding gastric varices in chronic pancreatitis? | Splenectomy (chronic pancreatitis is the most common cause of splenic vein thrombosis) |
| What is the number 1 risk factor for pancreatic adenocarcinoma? | tobacco |
| What is effective pain relief for non-resectable pancreatic CA? | Celiac plexus block (50% EtOH on both sides of aorta near celiac) |
| What % of nonfunctioning pancreatic tumors are malignant? | 90% |
| What is the most common islet cell tumor in the pancreas? In MEN I? | Insulinoma overall, gastrinoma in MEN I patients |
| What can help alleviate symptoms in a functional endocrine pancreatic tumor? | Octreotide, debulking surgery. Chemotherapy – 5FU and streptozocin |
| What are the signs of an insulinoma? Treatment? | Whipple's triad (symptoms of hypoglycemia, fasting glucose <45, improvement with glucose) Insulin to glucose ratio >0.4 Increased C-peptide and proinsulin; Tx = enucleation if <2cm, formally resect if >2cm (though 90% are benign) |
| What are the boundaries of the gastrinoma triangle? | (1) cystic/CBD junction (2) 3rd part of the duodenum (3) neck of the pancreas |
| What are the signs of gastrinoma? | Severe ulcer disease, diarrhea (lipase destruction by acid, malabsorption, increased secretion) |
| What test evaluates gastrinoma? | Secretin stimulation test - normal patients will decrease gastrin after secretin, though a baseline serum gastrin level >1000 is virtually diagnostic |
| What is the best test for localizing a gastrinoma? | Somatostatin receptor scintigraphy |
| What are the symptoms of a somatostatinoma? | gallstones steatorrhea pancreatitis diabetes |
| What are the symptoms of a glucagonoma? Treatment? | diabetes glossitis, DVT, stomatitis necrolytic migratory erythema (presenting problem in 70%) Rx = streptozocin/doxorubican (selectively destroy alpha cells) and octreotide (inhibits release), consider prophylactic anticoagulation |
| What are the symptoms of VIP-oma? | WDHA syndrome = watery diarrhea hypokalemia achlorydia |
| Describe the basic anatomy and physiology of the spleen | 85% red pulp – filter for RBCs, 15% white pulp – immunologic function (major site of bacterial clearance that lacks preexisting antibodies) |
| What are the effects of splenectomy on the immune system? | decreased tuftsin, properidin, and fibronectin (non-specific opsonins), decreased IgM production - susceptible to encapsulated organisms |
| What % of patients does splenectomy improve: hereditary spherocytosis? ITP? | 100% spherocytosis, 80% ITP |
| What is the treatment for TTP? | plasmapheresis (primary), steroids, ASA; not splenectomy |
| What is the pathophysiology of ITP? | Antiplatelet IgG originating in the spleen |
| For what condition is the risk of overwhelming postsplenectomy sepsis highest? | Thalassemia (also high with malignancies) |
| What hematologic disease has the highest morbidity after splenectomy? | Myeloid dysplasia |
| What vaccines are needed prior to splenectomy? | Pneumococcus, meningococcus, H. influenzae |
| What are the operative indications for splenic cysts? | Symptomatic or >10 cm |
| What is Felty’s syndrome? | rheumatoid arthritis, hepatomegaly, splenomegaly; splenectomy if symptomatic splenomegaly |
| What is the most common type of Hodgkin’s disease? Best prognosis? Worst prognosis? | Most common – nodular sclerosing, best – lymphocyte predominant, worst – lymphocyte depleted |
| What type of transplant is ABO blood compatibility not required for? | Liver |
| What type of cell mediates graft vs host disease? | T cells |
| What is the treatment for mild rejection? What about severe or secondary rejection? | Mild – pulse steroids, severe = OKT3 or other drugs |
| What is the number 1 and 2 malignancies following any transplant? | 1 = Skin cancer (squamous cell), 2 = Posttransplant lymphoproliferative disorder (PTLD) – EBV related – need to withdraw immunosuppresion |
| What is the mechanism of azathioprine (Imuran)? | 6MP derivative, purine analog that acts as an antimetabolite, decreases DNA synthesis which inhibits T cells |
| What is the mechanism of mycophenolate (cellcept)? | blocks purine synthesis to decrease T and B cell proliferation |
| How do steroids promote immunosuppresion? | inhibit genes for cytokine synthesis (IL-1, IL-6) and from macrophages |
| What is the mechanism of cyclosporine? | Calcineurin inhibitor – binds cyclophilin protein and inhibits mRNA encoding of IL-2, IL-3, IL-4 |
| What is the mechanism of FK506 (Prograf / Tacrolimus)? | Calcineurin inhibitor - binds FK binding protein, blocks IL-2 expressions/production from T cells, actions similar to cyclosporine but 10-100 times more potent |
| What is the mechanism of OKT3? | Monoclonal antibodies that block antigen recognition function of T cells by binding CD3; interferes with both class I and II MHC |
| What is the mechanism of sirolimus (Rapamune)? | mTOR inhibitor - inhibits the response of IL-2 thereby blocking the activation of T and B cells |
| What is the mechanism of Zenapax? | Human monoclonal antibody against IL-2 receptors; used with induction and to treat rejection |
| What causes hyperacute rejection? | pre-formed antibodies activate complement cascade and thrombosis of vessels occur |
| What test can identify patients who will develop hyperacute rejection? | Crossmatch |
| What causes acute rejection? | Due to HLA mismatch, foreign MHC antigens of graft cells activate host T cells |
| During what timeframe is acute rejection at highest risk to occur? | 1 week to 3 months |
| What is the mechanism of chronic rejection? | Fibrosis of blood vessels of transplanted tissue - loss of blood supply, partially a type IV hypersensitivity reaction |
| What is the number 1 complication of a kidney transplant? | Urine leak – treat with drainage and stenting |
| What is the cause of post-op oliguria in a kidney transplant recipient? | ATN |
| What does new proteinuria in a kidney transplant recipient suggest? | Renal vein thrombosis |
| What is the empiric treatment for an increase in Cr in a kidney transplant recipient? | U/S with duplex (to rule out vascular problem or ureteral obstruction) and biopsy; decrease CSA or FK (nephrotoxicity); pulse steroids |
| What are contraindications to liver transplant? | Current alcohol abuse or acute ulcerative colitis |
| What disease is most likely to recur in new liver allograft? | Hepatitis C – reinfects essentially all grafts |
| What is the treatment for a patient with hepatitis B undergoing liver transplant? | HBIG (hep B immunoglobulin) and lamivudine (protease inhibitor) postoperatively |
| What is the number 1 predictor of primary nonfunction in a transplanted liver? | Macrosteatosis – if 50% of cross section is macrosteatatic, there’s a 50% chance of primary nonfunction |
| What is the number 1 post-op complication of a liver transplant? | Bile leak – treat with PTC tube and stent |
| What is the most common cause of biliary complications post transplant? | Ischemia – check hepatic arterial flow |
| How does chronic rejection manifest in a liver transplant? | Vanishing bile ducts |
| What donor vessels are needed for pancreatic transplant? | Donor celiac and SMA for arterial supply, donor portal vein for venous drainage |
| What does a biopsy showing perivascular infiltrate with increased grades of myocyte inflammation and necrosis on a heart transplant patient suggest? | Acute rejection |
| What is the number 1 cause of early mortality in lung transplant? | Reperfusion injury |
| How long can you store a donor heart? Lungs? Kidney? Liver? | Kidney = 48 hrs, Liver = 24 hours, Heart/Lungs = 6 hours |
| What is the number 1 viral infection post-transplant? | CMV |
| Which risk is higher in patients on immunosupression: viral or bacterial infection? | Viral > bacterial because immunosuppression is largely cellular and not humoral |
| What is the order of cells to a healing wound? | Platelets, PMNs, macrophages (essential), fibroblasts (dominant by day 5), lymphocytes |
| What is the function of fibronectin? | Chemotactic for macrophages; anchors fibroblasts |
| What is the most important factor in healing closed incisions? | tensile strength – depends on collagen deposition and cross-linking of collagen |
| What is the strength layer of the bowel? | submucosa |
| What is the most important factor in healing open wounds (secondary intention)? | epithelial integrity – depends on granulation tissue, migration from wound edges |
| What cells provide wound contraction and are responsible for healing by secondary intention? | Myofibroblasts |
| What is the primary collagen in a scar? | Type I |
| When does a healing wound reach its maximum tensile strength? | 8 weeks (but this is only 80% of original strength) |
| What is the time frame of collagen production in a wound? | Begins day 3, max at day 21, then constant amount but more crosslinking, strength |
| What counteracts the effects of steroids on wound healing? | Vitamin A |
| What is the principal collagen in a healing wound? | Type III (this is the collagen of granulation tissue) |
| What type of collagen is low in Ehlers-Danlos syndrome? | Type III |
| What is the defect in Marfan’s syndrome? | fibrillin |
| What is the most common cause of leg ulcers? | 90% are caused by venous insufficiency |
| At what point does chemotherapy have no effect on wound healing? | Fourteen days |
| What is the cause of keloid scar? | failure of collagen breakdown and increased collagen production |
| Which type of scar extends beyond original margins: keloid or hypertrophic? | Keloid |
| What is the treatment for a hypertrophic or keloid scar? | Both can benefit from steroids, silicone, and pressure dressings; keloid can also be treated with XRT |
| What is fetal wound healing characterized by? | increased hyaluronic acid synthesis |
Created by:
jclanton82
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