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Oral Pathology 773
Second Midterm
| Question | Answer |
|---|---|
| What are the four phases of normal hemaostasis? | Vascular phase, platelet phase, coagulation phase and fibrinolytic phase |
| What is the best indicator of normal hemostasis? | Hx of normal clotting after a recent challenge due to trauma or natural (better than any test) |
| What effect does nitrous oxide have on vessels? | Keeps them open |
| What does Von Willibrans factor do? | Prothrombotic when exposed to blood - Causes thromboxane A2 to be released which causes vasoconstriction |
| What is primary hemostasis? | The formation of a platelet plug |
| What do fibrin and fibrinogen do? | Fibrin stabilizes platelets, Fibrinogen makes the clot inactive (not sticky) |
| What are some causes of vessel defects? | Vit C dificiency (Scurvy - causes defective collagen), Bacterial, fungal and viral |
| What is the difference between thrombocytopenia and thrombocytopathy? | Thrombocytopenia - not enough platelets. Thrombocytopathy - poor quality platelets. |
| What drugs can cause thrombocytopenia? | Drug induced (Alcholol, thiazide diauretics), bone marrow failure, chemo/rad tx, Aplastic anemia, nutritional deficiencies and hypersplenism (CLL) |
| How does hypersplenism affect clotting? | Increased size of speeen leads to platelet trapping |
| What type of clotting disorders do DIC, Hemolytic uremic syndroms (HUS) and viral infections such as HIV and hepatitis cause? | thrombocytopenia |
| What type of clotting disorders do Uremia, bernard soulier, glanzman's thrombesthenia and von willebrand's disease cause? | Thrombocytopathy |
| How are lab values for Hemophilia A and B different from von willebrands disease? | Hemophilia A and B have a long PTT and a low factor 8 for A and low factor 9 for B. VWD have a normal platelet count but a long PTT. VWD also affects small vessels and capillaries. Hemophilia A/B affects large vessels. |
| How does the patient hx differ between hemophillia A, hemophillia B and Von Willebrand's Disease? | Hemophillia A/B has hemarthoses, large hematomas, ecchymoses and excessive bleeding with trauma. VWD petechiae and mucotaneous bleeding |
| What disease is the most common congenital deficiency of clotting. What factor is affected? | Von Willebrand's Disease. Factor 8 is low |
| What are the two types of von willebrand's disease? | type 1 - low concentrations of VW factor.(quantative defect). Type 2 - normal concentration but poor function. (qualitive defect) |
| How do broad spectrum antibiotics cause clotting disorders? | Kill gut bacteria resulting in low vitamin K production |
| How does saliva affect oral bleeding? | fibrinolytic activity - increases bleeding |
| What is the name of the antifibrinolytic agent that neutralizes fibrinolytic activity in the oral cavity? | Amicar - e-aminocaproic acid |
| What usually controls fibrinolytic activity after oral surgery? | plasma fibrinolytic inhibitors |
| What is DIC? | joint activation of fibrinolysis and coagulation (life threatening) |
| How are lab values affected with DIC? PT PTT D-Dimer, fibrinogen | Longer PT and PTT, positive D-Dimer and decreased fibrinogen |
| What causes DIC and how is it managed? | Sepsis, shock, obstetric problems. Manage by treating underlying disorder |
| Liver disease is associated with the malabsorption of what vitamin? | Vit K - reduces production of coagulation factors 2,7,9 and 10 |
| How is fibrinogen affected by liver disease? | reduced (factor 1) and factor 5 |
| How is coumadin monitored? Reversed? | Monitored by a PT-INR. Reversed by Vit K, FFP and rVIIa |
| How is heparin minitored? Reversed? | Monitored with aPTT. Reverse by stopping med (protamine reverses heparin effects) |
| How is low weight heparin monitored? Reversed? | Monitored with aPTT. Reverse by stopping med. Hard to reverse, may use factor rVIIa |
| How does malabsorption cause clotting disorders? | May interfer with bile acid metabolism. Bile is needed for vit K. Vit K is needed for clotting factors 2,7,9 and 10 |
| What 5 lab tests are used for coagulation disorders? | platelet count, platelet, function, PT, PTT, and fibrinogen levels |
| What are the three basic coagulation tests that should be used first? | Platelet count, PT/INR and a PTT |
| When should the blue tube be filled when getting blood samples? How soon should it be tested? | last. within 2 hours if room temp. within 4 hours if refridgerated |
| What are normal values for a platelet count? | 150k to 450k |
| What platelet count values are associated with spontaneous bleeding? Moderate risk? Prolonged bleeding after trauma? | spontaneous = <10k, Moderate = <20k, Prolonged = 20-50k |
| What platelet count value is associated with bleeding after a major trauma? Normal bleeding? | After trauma 80-100k, Normal = >100k |
| How many times the value needed to stop bleeding is kept in the body? | 3 times the amount needed |
| What is the normal range for a PT/INR? | 1-1.2 |
| What value of the PT/INR is associated with excessive bleeding? | 1.5 |
| What is the normal theraputic range for the PT/INR for patintes on coumadin? | 2-3.5 |
| What is the normal range for aPTT? | 22-37 seconds |
| What is the theraputic range for aPTT? | 1.5 times mean of normal (about 45 seconds) |
| How is low molecular wt heparin monitored? | Can cause excessive bleeding with a normal aPTT. Need to order factor 10a inhibition if monitoring therapy |
| What are 5 causes for a prolonged aPTT? | heparin, DIC, Hemophilia A and B, Aquired anti factor, Lupus inhibitors |
| What percent of normal do coagulation factors have to be before a PT or PTT with detect the disorder? | 30% of normal. |
| What coagulation disorders can have normal clotting tests? | Von Willebrands disease (sometimes), Rare fibrinolysis disorders, and factor 11 and 13 deficiencies |
| What is a normal value for fibfinogen? | 180-380 (measures the amount of available fibrinogen) |
| Excess bleeding occurs when fibrinogen is at what value? | <100 |
| quantitative fibrinogen problems are found in what 3 disorders? | liver disease, amniotic fluid embolism and DIC |
| What is dysfibrinogenemia? How is it Dx'ed | A mutant forms. Dx'ed by functinoal assays |
| Why isn't bleeding time used as a standard test for coagulation disorders? | Difficult to standardize. Fading from use. |
| What are platelet function screenings affected by? | function and count |
| What are the normal values for collagen/epinephrin (CEPI)? | 85-148sec |
| What are the normal values for collagen/ADP (CADP)? | 64-115sec |
| What do abnormal values for CEPI or CADP represent? | drug induced platelet dysfunction or intrinsic platelet dysunction |
| What are five meds that interfer with hemostasis? | ASA, anticoagulants, antibiotics, alcohol and anticancer. |
| What are 5 physical signs of coagulation disorders in the oral cavity? | Petechiae and ecchymosis, gingival hyperplasia, spontaneous gingival bleeding, ulceration of oral mucosa and lymphadenopathy |
| What PT-INR values and meds make patients high risk for anticoagulation disorders? | PT-INR >1.5-2 and ASA |
| What criteria makes a patient a high risk for bleeding disorders? | patients with known bleeding disorders and patients with known bleeding disorders with abnormal lab results |
| How are moderate coagulation risk patients managed? | adjust anticoagulants and ASA meds |
| How are high coagulation risk patients managed? | Hospitalization and close coordination with a hematologist. |
| What are patinets treated with if they have VWD and a mild risk of bleeding? major risk? | mild = DDAVP, major = Humate P |
| What percent of hemophilaics are type A and type B? | type A 80-85%, type B 10-15% |
| What is Humate P? What is it used to treat? | Factor 9 concentrate. Used to treate Hemophilia B. |
| What factor is deficient in hemophilia A? | Factor 8 |
| What lab results are used to Dx VWD? | Prolonged platelet function analysis (PFA), bleeding time and aPTT |
| What determines an abnormal platelet function analysis (aggregation study) | No agglutination with Ristocetin |
| What nutritional disease presents with gingival hemorragic areas | scurvy |
| Bernard Soulier autosomal disease is due to a lack of? | Gp1b (platelet receptor) |
| What is the difference between primary hemostasis and secondary hemostasis? | primary is due to a functional abnormality (defective platelet plug). Secondary is due to a lack of plasma clotting factors |
| Name 3 inherited coagulation disorders and the treatment for each. | Bernard Soulier (tx with platelet infusion), Glanzman's thrombesthenia (tx with platelet infusion), Von Willebrand's Disease (tx with DDAVP, Humate P) |
| What is the function of thromboxane A2? | vasoconstriction and increasing platelet aggregation. |
| How does ASA work on coagulation? | Blocks TXA2 |
| What agonists promote platelet aggregation | platelet activation, epinephrine, TXA2, Collagen, ADT and Thrombin (PET CAT) |
| What three values are off with DIC? | Low platelets, low fibrin, Long PTT |
| Metabolic functions of the liver include what 6 things? | Carb, fat and protein metabolism, Bile production, Nutrient and vitamin storage, detoxification of food and meds |
| The liver processes dietery facts and cholesterol into what substance for peripheral circulation? | lipoproteins |
| How does the liver help maintain blood sugar levels? | Through carbohydrate metabolism and glycogen storage |
| The liver is primarily responsible for the storage of? | Glycogen, fats, cholesterol, iron, copper, vitamins A, E, K and B12 |
| What is transferrin? | binding protein for iron (used in the liver) |
| What is Ceruloplasmin? | binding protein for copper (used in the liver) |
| What is alpha-1 antitrypsin? | a protease inhibitor made in the live |
| Name the plasma proteins synthesized in the liver? | albumin, coagulation factors (PT or INR), complement factors, lipoproteins (LDL, HDL), copper and iron binding proteins and protease inhibitors. |
| How is bilirubin produced? What is it bound to in the circulation? | Produced as a result of hgb breakdown, bound to albumin in circulation. |
| Bilirubin is taken up by what cells? and conjugated into what substance? | hepatocytes, glucuronic acid |
| How is bilirubin secreted? | in the bile |
| What is urobilinogen? How is it excreted? | Bilirubin that is unconjugated by gut bacteria. 80% excreted with feces, 20% absorbed back into circulation |
| What are the causes of unconjugated hyperbilirubinemia? | Hemolysis (excessive production), liver pathology (impaired conjugation) |
| What are the causes of conjugated hyperbilirubinemia? | Intrahepatic causes (impaired bile excretion), Extrahepatic causes (biliary obstruction) |
| What are the consequences of impaired bile secretion? | Jaundice, dark urine, pale stools, malabsorption of fat and sat soluble vitamins, itching due to increasing bile acids and liver cholestasis |
| What are the 5 causes of steatosis? | Alcoholic hepatitis, obesity, diabetes mellitus (type II), protein malnutrition, pregnancy, drug effect |
| How does alcoholic hepatitis affect portal areas and lobules and hepatocytes | Mixed and acute and chronic inflammation of portal areas and lobules, ballooning and degeneration of hepatocytes |
| What illness are Mallory's hyaline deposition, sinusoidal fibrosis and macrovesicular steatosis associated with? | Alcoholic hepatitis |
| Chronic hepatitis B, C and D are caused by what type of infection? | viral liver damage |
| Primary biliary cirrhosis and primary sclerosing cholangitis are caused by what type of disease? | autoimmune liver damage |
| Wilson's disease and alpha 2 antitrypsin deficiency are cause by? | toxic/metabolic damage to the liver |
| Esophageal varices is a common complication of? | chronic portal hypertension (cirrosis) - high risk of spontaneous life threatening hemorrhage |
| Name 4 metabolic and storage diseases that affect the liver. | Glycogen storage disease, Alpha-1-antitrypsin, hemochromatosis and Wilson's disease. |
| What is deficient in Von Gierke Disease? | glucose-6-phosphatase |
| Is alpha-1-antitrypsin deficiency disese autosomal dominant or recessive? What gene is affected? | recessive, over 75 polymorphs of the A1AT gene |
| Patients with alpha-1-antitrypsin deficiency that are Pi-ZZ homozygous have low serum levels of? | A1AT |
| What is A1AT's function? | inhibitor of neutrophil elastase which are released during inflammation |
| What happens to patients who smoke with alpha-1-antitrypsin deficiencies? | they develop emphysema |
| In aptients with an alpha-1-antitrypsin deficiency what does a Pi-Z mutation lead to? | blocks the exit of the inhibitor from the ER. |
| Genetic hemochromatosis is caused by an autosomal recessive or dominant process that leads to an excess absorption of? | recessive, iron |
| What causes genetic hemochromatosis? | mutation in the HFE gene |
| What happens when iron accumulates in the liver due to genetic hemochromatosis? | hepatotoxicity, fibrosis and cirrhosis. Iron also accumulates in the heart (CHF) and pancreas (diabetic) |
| How is the immune system affected in genetic hemochromatosis? | impaired function |
| Who does genetic hemochromatosis affect? | males over 40 |
| What lab tests are abnormal with genetic hemochromatosis? | ferritin and transferrin-iron saturation |
| What is the treatment for genetic hemochromatosis? Life expectancy? | treat with phlebotomy. Normal life expectancy if iron levels can be returned to normal |
| What causes Wilson's Disease? | Excessive copper accumulation due to genetic defects in ATP driven Copper transporter |
| What are some symptoms of Wilson's Disease? | Kayser-Fleischer rings in the corneas, bronze skin and low serum ceruloplasmin |
| What age groups are affected by Wilson's Disease? | ages between 5 and 30 |
| Wilson's disease may develop in patients due to what other diseases? | Liver failure, cirrhosis or neurodegenerative diseases |
| What type of infection is caused by Echinococcus granulosus? How is it spread? What symptoms occur? | Cestode (tapeworm) infection. Canine feces. Ingested eggs invade liver, lungs and bone. Cysts form in the liver and lungs. |
| What happens 6 months after an echinococcus granulosus infection? | daughter cysts form and contain scolicies (hook like attachments). Cysts may rupture and cause anaphylaxis |
| How is Hep A spread? What type of virus is it? What are the clinical symptoms? Is it a chronic or acute infection? | Fecal oral route (contaminated water or shellfish), ssRNA (piconavirus), no symptoms common or self-limiting hepatitis with jaundice, few life threatening fulminant cases. acute infection only |
| What blood tests are used to reflect ongoing hepatocellular necrosis? | AST and ALT |
| What does the direct bilirubin blood test reflect in hepatitis A? | impairment of bile excretion |
| What to the Gamma-glutamyl transferase (GGT) and alkaline phosphatase reflect in hepatitis A? | Damage to bile canaliculi |
| What do circulating immunoglobulins to viral proteins reflect in hepatis A? | stage of infection |
| What test can always be done to see if a person has had a previous hepatitis A infection? | Elevated IgG remains elevated |
| Which hepatitis virus is a calcivirus? Is it ss or ds? What is the route of transmission? Chronic or acute? | Hepatitis E, ssRNA, fecal oral transmission, acute only (can cause fulminant hepatitis) |
| Which hepatitis is the most dangerous for pregnant women? Why? | Hepatitis E because it can cause death in 20% |
| Is hepatitis B acute or chronic? ss or ds? What age groups are at highest risk? | Chronic, dsDNA virus. 90% infants at birth, 30% kids 1-5 y/o, 6% after 5 y/o. Death due to liver disease in 15-25% |
| What type of hepatitis causes "ground glass" hepatocytes? | Chronic hepatitis B |
| Which virus is a "delta" virus that is dependent on hep B proteins for replication? | Hep D |
| What situation of hep D infection has a 90% recovery chance? What about 80% chance of chronic disease complicated by cirrhosis with a 7-10% chance of fulminant hepatic failure? | If simultaneous coinfection with B then 90% chance of full recovery. If hep D infects a person with established hep B then 80% chance of chronic with cirrhosis and 7-10% hepatic failure. |
| Is hepatitis C a ss or ds? How is it transmitted? | ssRNA, Transmitted by IV drugs 38%, sex/household exposure 10%, work 2%, transfusions/dialysis very low risk |
| What is the most common hep disease leading to liver transplant? | Hep C |
| What are the chances of getting hep C from a needle stick? | 1.8% |
| How long can a hep C virus survive on a surface at room temp? | 16 hours to 4 days |
| What are the chances of a chronic hep C infectin? | 85% |
| Pegylated interferon and ribavirin is used to treat what type of hepatitis? How effective is treatment? | Hep C. 40-80% (up to 50% in patients infected with genotype 1 (most common in US)). Up to 80% in patinets with genotypes 2 and 3. |
| What are the side effects of interferon? | fever, chills, headache, muscle and joint aches, tachycardia and depression |
| What are the side effects of ribavirin? | anemia |
| Name three liver autoimmune diseases. | Autoimmune hepatitis, primary biliary cirrhosis (PBC) and primary sclerosing cholangitis(PSC) |
| What age group and sex is most affected by autoimmune hepatitis? | children and adults. males more than females |
| What Hx is most common with people who get autoimmune hepatitis? | Hx of thyroid, rheumatoid and other autoimmune diseases |
| What are the clinical symptoms for autoimmune hepatitis? | fatigue, fever, RUQ pain, elevated serum transaminase level, elevated IgG, marker Ab's ANA and ASMA |
| What is the treatment for autoimmune hepatitis. How long does it take? Why? | Give corticosteroids. Takes years of immunosuppression to prevent cirrhosis. |
| What causes primary biliary cirrhosis? What do these changes lead to? What sex is affected? age group? | Granulomatous destruction of medium sized bile ducts leading to chronic cholestasis, fibrosis and cirrhosis. Females 9 to 1 male. Age 40-50 |
| How is primary biliary cirrhosis detected and what is the treatment? | Detect with anti-mitochondrial antibodies. Treat with Ursodeoxycholic acid (bear bile) and transplantation |
| How is primary sclerosing cholangitis different from primary biliary chrrhosis? | PSC occurs at a younger age (25-35), affects more males 2:1. No treatment except transplant. Affects large bile ducts not the medium |
| What percent of patinets with primary sclerosing cholangitis will develop chronic ulcerative cholitis and chrones disease? | Cholitis 70%, Chrons 10% |
| Which ducts are affected with primary sclerosing cholangitis? | large bile ducts including extrahepatic ducts |
| What does primary sclerosing cholangitis do to the liver? | Causes obstructive cholestasis, ribrosis and cirrhosis |
| How old are people who get primary sclerosing cholangitis? | 25-35 |
| What is the treatment for primary sclerosing cholangitis? | No treatment. Only liver transplant |
| What age group and sex are affected by focal nodular hyperplasia? Symptoms? Risk for malignancy? | Young and middle age adults, females more than males, symptoms painless and less than 5mm nodules, No malignancy risk because it's not a neoplasm |
| What is hepatic adenoma associated with? What age and sex are affected? | Usually associated with birth control use greater than 5 years. Usually occurs in young women |
| Hepatic adenoma has been associated in men who do what? What symptoms does this disease cause? | Use anabolic steriods. Causes RUQ pain. |
| Can hepatic adenoma progress to carcinoma? | No it's not associated with hepatocellular carcinoma. Rarely may rupture capsule and cause hemoperitoneum |
| What is the most common primary malignant tumor of the liver? What are the risk factors? | Hepatocellular carcinoma. Cirrhosis, chronic hep B, aflatoxins produced bo mold in spoiled food (may cause p53 gene mutation) |
| What is the treatment for hepatocellular carcinoma? | surgery. Chemo and Rad usually have little effect |
| What is cholangiocarcinoma and where does it occur? | Adenocarcinoma of the bile duct that may occur anywhere in the biliary tree. |
| What are the risk factors for cholangiocarcinoma? | Primary sclerosing cholangitis, anomaly of the extra-hepatic ducts, Opisthochis sinensis (liver fluke) |
| What are the symptoms of cholangiocarcinoma? | jaundice, weight loss and RUQ |
| What is the treatment of cholangiocarcinoma? | surgery - chemo and rad usually ineffective |
| What is a Klatskin tumor? | A cholangiocarcinoma of the hepatic ducts |
| What is the most common site for gallstones? | gallbladder |
| What are the symptoms of cholecystitis? | RUQ pain, fever, nausea and vomiting |
| What people are most affected by gallstones? | most common in females of child bearing age, fat people, gallstones are present in 20% of women and 8% of men |
| What causes obstructive jaundice and pancreatitis? | Gall stones pass into the common bile duct and obstruct the ampulla of Vater |
| What three enzymes are secreted by the exocrine pancreas? | proteases, amylases and lipases |
| Are the ducts of acini associated with the endocrine or exocrine pancreas? | exocrine |
| Are the islets of langerhans associated with the endocrine or exocrine pancreas? | endocrine |
| What is secreted by the endocrine pancreas (islet of langerhans)? | insulin, glucagon and somatostatin |
| What are the symptoms of pancreatitis? | severe mid abdominal pain, sometimes radiating to the back, nausea vomiting and fever |
| What lab changes are related to pancreatitis? | elevated serum amylase and lipase. In severe cases decreased serum calcium, elevated WEC and hyperglycemia |
| Three tumors of the pancreas include | Mucinous cystic neoplasm, pancreatic neuroendocrine neoplasm and ductal adenocarcinoma |
| How serious are nucinous cystic neoplasms? What people are affected? | 90% benign. Affects middle aged females |
| What is the prognosis and metastatic effect of pancreatic neuroendocrine tumors? | hard to predict prognosis. Mets to abd and liver. Many patients live for years with metastatic disease. |
| What type of tumor is insulinoma, glucagonoma, somatostatinoma, gastrinoma and VIPoma associated with? | pancreatic neuroendocrine tumor |
| What percent of pancreatic neuroendocrine tumors are functional? | 50% |
| What are the symptoms of pancreatic ductal adenocarcinoma? | Weight loss, jauncide, back pain , trousseau's syndrome |
| What type of pancreatic cancer accounts for 5% of all cancer deaths? | pancreatic ductal adenocarcinoma |
| What is the 5 year survival rate for pancreatic ductal adenocarcinoma? Treatment? | <5%. Surgical tx. Rad and Chemo not effective |
| What is the difference between type 1-4 diabetes? | type 1 loss of islet of langerhans cells, type 2 peripheral resistance to insulin, type 3 genetic, type 4 gestational |
| What are the causes of secondary diabetes? | Pancreatectomy, chronic pancreatitis, hemochromatosis |
| What should the plasma glucose level be in a fasting state? random state? | fasting 7.0mmol/L. Random 11.1mmol/L according to the ADA. However, the WHO says a normal fasting is 7.8mmol/L |
| Name three potential causes for type 1 diabetes? | genetic, viral or toxin exposure |
| What cells are destroyed in type 1 diabetes? | beta cells of the islets of langerhans are destroyed by T cells |
| What condition is caused by a lack of beta cells in the pancreas? | insufficient insulin - acute symptoms with chronic complications |
| What happens to glucose, fatty acids, ketone bodies and acid levels during type 1 diabetes? | elevated blood glucose due to decreased uptake, increased free fatty acids and fatty acid oxidation, ketone bodies are present, acidosis occurs |
| What are the common symptoms of type one diabetes? | hyperglycemia, polyuria, glucosuria, polydipsia, volume depletion |
| Which type of diabetes is associated with HLA-DR genotype? | type 1 |
| Which type of diabetes is associated with polygenic inheritance? | type 2 |
| Which type of diabetes is ketoacidosis common? | type 1 |
| Islet cell antibodies occur in which type of diabetes? | type 1 |
| Type 2 diabetes has a strong link with what predisposition? Affects what percent of the population? | fat people, 6% |
| What is the genetic predisposition for type 2 diabetes? | 90% in identical twins |
| Retinopathy, neuropathy, renal glomerular disease, small vessel disease (arteriosclerosis), and predispositions to infection are all associated with what disease? | type 1 and type 2 diabetes |
| What is the target control value for HbA1C? | 6 (135) or 7 (170) |
| What level of HbA1c is considered elevated? | at 8 (205 or higher) |
| What are the treatments for type 1 and type 2 diabetics? | type 1 - insulin and diet. Type 2 - diet and exercise, pill to decrease insulin resistnace and insulin |
| Name two meds that can cause lymphadenopathy. | Allopurinol (Zyloprim) and PCN |
| Is all lymphadenopathy lymphoma? | no |
| KNOW Give examples of general catagories of lymphadenitis and list examples of each. | Viral - Ebstein Barr Virus (mono), Parasitic (toxoplasmosis), bacterial (cat scratch disease) |
| What is Bartonella henselae responsible for? | Cat scratch disease. Low IgM sensitivities. IgG not a good indicator of disease |
| What lab tests are used to ID Cat Scratch Disease? | IgM low sensitivities. Bug ID Bartonella henselae. Other tests are negative |
| What lab tests are used to ID toxoplasma lymphadenitis? | IgM titer positive for anti-toxoplasma. IgM antibodies indicate reproductive tachyzoites associated with acute infection. |
| What lab tests are used to ID mono? | Monopositive screening test. IgG and IgM antibodies to the capsid antigen. |
| How is malignancy determined with lymphomas? | Immunohistochemistry (p310), Kappa light chain positive. needle biopsy, cytology, flow cytometry |
| What are the WHO classifications of lymphoma? | Bcell - immature, mature and plasma cell neoplasms. Tcell - immature and mature. Hodgkin's Lymphoma |
| Follicular lymphoma, mantle cells lymphoma, marginal zone lymphoma, Burkitt's lymphoma, small lymphocytic lymphoma are all Bcell or Tcell lymphomas? | Bcell |
| What cells are indicators for Hodgkin's Lymphoma? | Reed Sternberg cells |
| What are the cell findings for Hodgkin's Lymphoma? | Nodular sclerosis (grade 1 and 2), lymphocyte rich, mixed cells, lymphocyte depleted |
| KNOW Name a high grade lymphoma. | Burkitt's and diffuse large B cell |
| KNOW Name the translocation typically found on Burkitt's lymphoma. | t(8,14) |
| KNOW What is the name for the low power microscope pattern seen in Burkitt's lymphoma? | Starry sky, tingle body macrophage |
| KNOW Name a low grade lymphoma | Follicular lymphoma, small lymphocytic lymphoma, marginal zone lymphoma |
| KNOW an intermediate grade lymphoma | mantle cell lymphoma |
| KNOW what are some characteristics of multipul mylenoma? | Night sweats and weight loss >10 lbs |
| KNOW Is back pain a common presenting symptom with multipul mylenoma? | Yes |
| KNOW Do myeloma patients typically have or develop lytic bone lesions? | Yes |
| KNOW What kind of test are used to diagnose multiple myeloma? | Protein and Immunofixation Electrophoresis |
| KNOW Are there light chains in the cytoplasm of plasma cells? | Yes, excretion of light chains causes tubular damage in the kidneys |
| KNWO What is meant by B symptoms in Hodgkin's Lymphoma? | Fever, night sweats and weight loss |
| KNOW Is nodular lymphocytic predominant Hodgkin's considered classic Hodgkin's? | No |
| KNOW How are the different grades of Bcell lymphoma determined? | By the appearance of the cells. Grade 1 small cell. Grade 2 mixed small and large cell. Grade 3 large cell |
| KNOW some favorable prognostic indicators in ALL - age, sex, WBC values, day 14 and cytogenetics | All Favorable - age 1-10, female, wbc <10, free of disease on day 14, hyperdiploidy |
| KNOW some unfavorable prognostic indicators in ALL - age, sex, WBC values, day 14 and cotogenics | All unfavorable - age less than 1 or greater than 10, male, wbc >50, residual disease after day 14, hypodiploidy |
| KNOW lymphoblastic leukemias have what cell types? | Early T and B cells |
| KNOW Do early B cells express light chains? TdT? | No light chains but have TdT |
| KNOW What is the difference between acute lymphoblastic leukemia and lymphoblastic lymphoma? | ALL is d/t B and T cells, and is in the blood and marrow. LL is 85% T cell and is in the lymph |
| KNOW Do cells in T lymphoblastic lymphoma express TDT? Light chains? | Yes they express TDT but not light chains |
| Define leukemia | colonal expansion of blast cells in bone marrow, blood or other tissue |
| What is pancytopenia? what symptoms are associated with it? | Low rbc, wbc and platelets (leukemia). Associated with weakness, fatigue, infections |
| Define Acute lymphoblastic leukemia (ALL) | Colonal expansion of lymphoblasts with lots of blood and marrow involvement |
| Is ALL caused mostly by B or T cells? | 85% B cells |
| What are the presenting symptoms of ALL? | Fever, bleeding, spleenomegaly, hepatospleenmegaly, bone pain, altered wbc counts, 5% CNS involvement |
| Define acute myelogenous leukemia | a colonal expansion of meyloid blasts in the blood, bone marrow or other tissues |
| What cells are included in meyloid blasts? | early granulocytes, megakeratinocytes, red cell precursors |
| What transmutations are present in AML? | t(15,17), inv 16 and t(8,21) |
| How many blasts do I need for leukemia? | 10–19% myeloblasts in the blood or bone marrow |
| How are the subtypes of AML decidec upon? | by evaluating cells from the bone marrow. M0 - M7 classifications |
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