Lectures

Question 1

What is the hemoglobin curve called?

What tissue has the highest Hb saturation?

What tissue has the lowest Hb saturation?

If there is 100% saturation in the lungs, and 50% in the muscle, what percentage of oxygen was delivered?

What kind of shift helps dump oxygen in the muscle? This represents lower what?

Answer 1

Oxygen dissociation curve

Lungs

Muscle

50% (just subtract the difference)

Shift to the right, affinity

Question 2

What means increased WBC count?

What means increased platelet count?

Describe the symptoms of anemia.

Describe the cause and symptoms of uncompensated anemia.

Answer 2

Leukocytosis

Thrombocytosis

Dyspnea, fatigue, malaise, pallor, tachycardia

Severe rapid blood loss, Hypotension, tachycardia, confusion, organ failure

Question 3

Describe Warfarin, how it works, etc.

Answer 3

Used in rat poison, inhibits vitamin K, thus affecting 2, 7, 9, 10, it takes a few days for nonfunctional proteins to enter circulation, oral absorption (thus given as a pill), then it binds plasma proteins, thus hypoproteinemia makes it less effective, rapidly gets destroyed if it doesn’t bind plasma proteins.

Rifampin / barbiturates / phenytoin can shorten half life by increasing P450 enzymes, and so can alcoholism.

Question 4

Describe B12 and its absorption.

Answer 4

Cobalamin has binding proteins removed by pepsin in stomach, then salivary gland haptocorrin binds, then it enters duodenum where pancreas enzymes remove haptocorrin, then intrinsic factor from the parietal cells in the fundus of the stomach bind, binds to IF receptors in the ileum, and it is moved to liver by transcobalamin 2.

Question 5

Describe beta chain encoding and alpha chain encoding.

Describe the effect of removing these chains.

Answer 5

Beta chains are encoded by one gene on chromosome 11, whereas alpha chains are encoded by 2 genes on chromosome 16.

Removing alpha causes beta to aggregate together, and removing alpha causes beta to aggregate together into the beta tetramer called hemoglobin H, which destroys RBCs.

Question 6

Describe the function of 2,3-BPG.

Describe the function and structure of hemoglobin F.

Answer 6

2,3-BPG binds to the beta subunit of deoxyhemoglobin, removing it from the equilibrium, preventing oxygen from binding, thus decreasing the amount of oxyhemoglobin to reach a new equilibrium.

Fetal hemoglobin belongs to fetuses and contains a gamma subunit instead of a beta subunit, meaning it binds oxygen more tightly than the adult hemoglobin of the mother and attracts more oxygen in the lower partial pressure environment of the womb, which shifts oxygen dissociation curve to the left for higher affinity.

Question 7

What drains catchment areas?

Describe some of the common issues affecting lymph nodes.

Describe infections of the lymph nodes.

Answer 7

Afferent lymphatic vessels

Lymphadenitis can inflame lymph nodes, lymphadenopathy can make them grow, lymphangitis can inflame nearby lymphatic vessels, chronic issues tend to be painless whereas acute issues are painful by suddenly stretching the lymph node capsule.

Damaged afferent lymphatic vessels make you susceptible to lymph node infection, bacterial infections cause regional lymphadenopathy because bacteria are larger, whereas viruses can spread more easily and cause general lymphadenopathy.

Question 8

Describe B12 deficiency and its symptoms.

Answer 8

B12 deficient patients may feel numbness or tingling due to demyelination of the dorsal column, and experience dementia or psychosis. Therefore, you should always check a demented patient for B12 deficiency, which may help you recover some function with supplementation.

Like folic acid deficiency, B12 deficiency causes beefy red tongue (glossitis), macrocytic anemia with high MCV, and hyper-segmented neutrophils. But you cannot treat a B12 deficient patient by giving them folic acid.

Question 9

What two chemicals are required for DNA synthesis?

Describe iron administration.

Whose normal diet is insufficient to meet iron needs?

Answer 9

Vitamin B12, folate.

Pregnant women (2nd and 3rd trimester).

You can give it orally or parenterally, although oral is preferred. Furthermore, Fe2+ or ferrous iron is preferred because it is absorbed 3x greater than Fe3+ or ferric iron. We give ferrous sulfate pills (a type of salt) which is mostly absorbed in the upper small intestine right away. Stomach acidity helps keep it in the ferrous state, so antacids may reduce its bioavailability, and so will food, so we give it before meals.

Question 10

Describe the different forms of Von Willebrand disease.

Answer 10

There are three types, type 1 is autosomal dominant and decreased VWF, it is the most common, but it is not very severe as it causes heavy menses and nosebleeds, and they lack petechiae because they have sufficient platelets. Type 2a is just like type 1 and is also autosomal dominant but is due to having a correct amount of a structurally abnormal VWF. Type 3 is the most severe but is rarer because it is autosomal recessive. They have very low WVF this factor 8 is destabilized and they have symptoms of hemophilia A.

Question 11

Describe the ways of administering iron.

Describe the side effects.

Why would you give parenteral iron? Or if there is what? Name three preparations of parenteral iron.

Why are iron pills dangerous?

Answer 11

You want a steady supply of iron for hematopoiesis so you should give it several times per day. Large single doses have diminishing returns in how much reaches the blood because you saturate the uptake mechanisms, so spread it out. If they cannot tolerate oral iron due to malabsorption, give them parenteral iron in the form of sodium ferric gluconate, iron sorbitol, or iron sucrose.

Iron pills will give you heart burn and constipation.

They look red so kids will eat whole bottle and reach toxic levels.

Question 12

Describe how you can activate factor 9.

Describe how thrombin works.

Describe the pathways of the coagulation cascade.

Answer 12

Factor 7 can activate factor 9 via the alternate pathway, or factor 11 can activate it. Thrombin can directly activate factor 9, or it can indirectly activate factor 9 by activating factor 11.

Thrombin initiates a clotting positive feedback loop by turning on factors 7, 9, 11, and 5.

There are three pathways, the intrinsic pathway (12, 11, 9, 8), the extrinsic pathway (7), and both feed into the common pathway (10, 5, 2, 1). Note that factor 2 is also called thrombin and factor 1 is also called fibrinogen. There is also a fourth pathway, called the alternate pathway, which connects factor 7 to factor 9.

Question 13

Describe parvovirus B19.

Answer 13

Parvovirus B19 is a small ssRNA virus for whom young children are a reservoir. It is cytotoxic to erythroid progenitor cells and turns them into giant pro-normoblasts with nuclear inclusions that are visible in the bone marrow. It can cause pure red blood cell aplasia and therefore aplastic anemia. It can cause ‘fifth’ disease in school age children which gives them a slapped cheek rash and a reticulated (lake like) rash on their body.

Question 14

Describe the four cutaneous porphyrias.

Describe porphyria cutanea tarda.

Describe erythropoietic protoporphyria.

Answer 14

They are porphyria cutanea tarda, erythropoietic protoporphyria, congenital erythropoietic porphyria, and x-linked protoporphyria. These only cause skin lesions and do not cause neurological symptoms.

Porphyria cutanea tarda later is the most common porphyria and presents later in life. It results from a uroporphyrinogen decarboxylase deficiency, and is associated with hepatitis C.

Erythropoietic protoporphyria is due to a deficiency in ferrochelatase, which is the last enzyme in the pathway in the mitochondria, and can be precipitated by lead poisoning.

Question 15

Describe how you prepare for a transfusion.

Describe how blood bag usage is tracked.

When can you violate the FDA regulations?

Answer 15

Any hospitalized patient who is suspected of needing blood undergone typing and screening. Typing means finding their blood type (antigens on the cells) and screening means looking for antibodies in the blood. If an antibody is found, you must then figure out what it is targeting.

The transfusion rate describes the percentage of patients who receive blood, and the utilization rate describes the number of blood bags per patient.

You can violate the the FDA regulations when it is medically necessary, but you must write them a letter explaining why.

Question 16

Describe the progression of hematopoiesis up until birth.

Answer 16

At the beginning of gestation, the yolk sac produces blood. A few months in, the liver and spleen begin to produce blood. By the fourth month of gestation, the bone marrow will begin to produce blood cells and is the primary source of blood by birth.

Question 17

Describe fresh frozen plasma.

What will plasma from an A person contain?

Who can an O type person receive plasma from? Why?

Who can an A person get plasma from? What about a B person?

Who can an AB person get plasma from?

Answer 17

Fresh frozen plasma is frozen within 8 hours and can be stored for one year. It contains the cofactors and clotting factors necessary to treat a Coumadin overdose.

Anti-B antibodies.

Anyone, because foreign antibodies have nothing to attack.

(A or AB), (B or AB).

AB (because these donors don’t have any antibodies against A or B in the recipient).

Question 18

Describe the pathways and factors are measured by PTT.

Describe the pathways and factors measured by PT.

What can activate factor 11?

Describe the role of thrombin.

Answer 18

PTT measures all intrinsic and common factors (12, 11, 9, 8, 10, 5, 2, 1).

PT measures all extrinsic and common factors (7, 10, 5, 2, 1).

Factor 12 and thrombin can activate factor 11.

Thrombin activates platelets by giving their surface a negatively charge surface and by releasing calcium. It also triggers a positive feedback loop by activating factors 11, 9, 7, and 5.

Question 19

Describe VWF.

Answer 19

Von Willebrand factor exists as a very large multimer which is highly thrombogenic and must be cleaved by ADAMTS-13 before becoming less thrombogenic. VWF is stored in Weibel-Palade bodies in endothelial cells as well as alpha granules in platelets. It can also be found in the subendothelium and and plasma. VWF can bind collagen in the subendothelium as well as the GP 1b and GP IIb-IIIa receptors on platelets, and therefore sticks platelets to each other as well as collagen in the vessel wall. It also stabilizes factor 8 which would otherwise be rapidly destroyed.

Question 20

Describe beta thalassemia.

Answer 20

Beta chains are absent so alpha chains aggregate as insoluble clumps, which damages RBCs. The spleen then destroys them via hemolysis and causes Jaundice. This also forms hypochromic microcytes causing anemia. This hemolysis increases EPO release, triggering hypoproliferation that that expands the bone marrow and can break bones. This can even cause extramedullary hematopoiesis in the liver and spleen. It will also cause hepcidin to decrease which increases the iron in the plasma, causing iron overload known as secondary hemochromatosis.

Question 21

Describe a universal RBC donor.

Describe a universal plasma donor.

Describe cryoprecipitate.

Describe leukocyte reduction.

Answer 21

The type O blood type is a universal RBC donor because their cells lack antigens.

Type AB is a universal plasma donor because their plasma lacks antibodies against A or B antigens.

Cryoprecipitate is the miracle product for hemophiliacs because it contains factors VIII, VWF, and fibrinogen.

Leukocyte reduction means you remove leukocytes by irradiating blood products to prevent the spread of CMV into immunocompromised patients, or transfusion reactions to leukocyte antigens. This does not kill RBCs or platelets because they lack nuclei.

Question 22

Describe intravascular hemolysis.

What term means lots of Hb leaked into the blood?

What term means lots of Hb leaked into the urine?

What means hemosiderin leaked into the urine?

Answer 22

Intravascular hemolysis occurs inside of the vessel. When hemoglobin leaks out, haptoglobin binds it and gets depleted in the blood. The free hemoglobin gets oxidized to methemoglobin.

Hemoglobinemia.

Hemoglobinuria.

Hemosiderinuria.

Question 23

What rickettsia causes typhus? What spreads it? What war did this impact?

What else causes typhus? These all have what kind of rash?

Answer 23

Rickettsia prowazekii, lice, WW1 (because a guy named Prowazecki got typhus in WW1)

Rickettsia typhi, Black measles rash (same as Rocky Mountain spotted fever)

Question 24

What PBS cells appear in G6PD deficiency? What special stain shows what bodies? What are these made of?

How do bite cells form?

What lab can confirm the diagnosis of G6PD deficiency? This disease is a type of _______ hemolytic anemia. Does it cause chronic hemolysis? Why? Thus what two symptoms do they lack?

Answer 24

Bite cells, crystal violet stain, Heinz bodies, denatured hemoglobin chains

Spleen phagocytes remove the chunk containing a Heinz body

G6PD levels, episodic, no, exposure to the stressor is periodic, splenomegaly / gallstones

Question 25

For hemoglobin binding affinity, what word do you avoid using? What type of Hb has a weaker affinity? What type of Hb has a stronger affinity? What relaxes Hb even more? BPG binds what type of hemoglobin? So initially, BPG immediately removes what from the equation? So what decreases to equilibrate with the scarcer deoxyhemoglobin?

Answer 25

High Tensed Relaxed Binding of even more O2 Deoxyhemoglobin, deoxyhemoglobin, oxyhemoglobin

Question 26

What is plasma mostly made of? What three proteins are in plasma? How many RBCs are per cubic mm? How many platelets are per cubic mm? How many leukocytes / WBC?

Answer 26

Water Albumin, antibodies, fibrinogen 4-6 million RBCs 120-300 thousand 5-10 thousand

Question 27

What acute porphyria is AD? Mutation to what enzyme? Can also show lesions where? What acute porphyria results from ALA dehydratase deficiency? What element can precipitate an attack? Why?

Answer 27

Hereditary coproporphyrinogen (cops are dominant), coproporphyrinogen oxidase, skin Delta aminolevulinic acid dehydratase deficiency porphyria, lead, by inhibiting ALA dehydratase

Question 28

Viral hemorrhagic fevers are caused by what four families? Name two filovirus diseases. Name two flavivirus diseases. Many of the manifestations result from what two things? They cause ______ to synthesize what factor? This triggers what? It elevates _______, reduces the number of _______, and therefore causes severe what? What cells will be consumed?

Answer 28

Filoviruses, flaviviruses, arenaviruses, bunyaviruses Marburg / Ebola (Filo is ME) Yellow fever / dengue (the flavor of the yellow den) Direct viral tissue damage and host immune response, macrophages, cell surface tissue factor, coagulation cascade, D-dimer, platelets, bleeding Leukocytes

Question 29

What generalized lymphadenopathy has a pathogen from livestock? What dairy can transmit it? What cells ingest it? It is transported to where? It forms _____ with _______ infiltrates in tissues. It causes what specific type of fever? Where does the localized disease cause pain? What is the most sensitive culture for brucellosis? Why does PCR not work that well? What unique appearance will occur in the liver?

Answer 29

Brucellosis, unpasteurized dairy product Macrophages, lymph nodes, granulomas, inflammatory, undulent fever, joints Bone marrow, lack of standardization, snowflake calcification

Question 30

What are the progenitor cells for both blood lineages? What two major lineages are there? What stem cell corresponds to each lineage? What cells arise from the myeloid lineage? What are the only cells arising from the lymphoid lineage?

Answer 30

Hematopoietic stem cell Myeloid, lymphoid, early progenitor with myeloid potential, early progenitor with lymphoid potential Neutrophils, macrophages / monocytes, eosinophils, basophils, platelets, erythrocytes B cells, T cells, NK cells

Question 31

What does PTT stand for? You will activate what factor in a test tube? This activates what two pathways? Measures the time it takes to form what? What factors does PTT measure? What does PT stand for? You add what to activate factor 7? This triggers what two pathways? Measures time to form what? What factors does PT measure?

Answer 31

Partial thromboplastin time, factor XII, intrinsic and common, clot 12, 11, 9, 8, 10, 5, 2, 1 Prothrombin time, tissue factor, extrinsic and common pathways, clot 7, 10, 5, 2, 1

Question 32

How are hemophilia A and B inherited? What is missing in each? What does severity depend upon? Less than what percentage causes severe bleeding? What level causes moderate bleeding? What level causes mild bleeding? Patients present with easy what? And massive what? Why may they need knee replacements? This may also lead to what physical defect?

Answer 32

X linked recessive (due to a deficiency), factor 8 (A) and factor 9 (B) Factor levels 1%, up to 5%, over 5% Bruising, bleeding, repeated bleeding in their weight bearing joints, joint deformities

Question 33

What is slightly less severe than beta thalassemia major? It causes moderate what? What is the beta chain tetramer called? If young, they may also have what tetramer of the gamma chain? What two conditions are less severe? What kinds of cells will appear? They have what, but are not dependent on what? These can appear similar to what anemia? Beta thalassemia minor patient may have what compensatory hemoglobin form?

Answer 33

Alpha thalassemia (hemoglobin H disease) Hemolytic anemia, hemoglobin H, hemoglobin barts Beta thalassemia minor / alpha thalassemia minor (alpha thalassemia trait), microcytic hypochromic cells, anemia, transfusions, iron deficiency anemia HbA2 (because the body makes delta chains instead of beta chains)

Question 34

What is the mnemonic for microcytic anemia? Parvovirus can cause what three fetal complications? What does it not result in? What do you want to control in a parvovirus B19 infection? How can you fix fetal anemia? Where does malaria often occur? What three pathogens often cause malaria? What is the specific vector?

Answer 34

TAILS (thalassemia, anemia of chronic disease, iron deficiency anemia, lead poisoning, sideroblastic anemia) ***Micro-mouse has tails*** Miscarriage, death, fetal hydrops, does not result in neurological issues Fever, intrauterine blood transfusion Africa / Asia / Latin America, plasmodium falciparum / plasmodium vivax / plasmodium ovale, female anopheles mosquito

Question 35

Where is the blood factory? What type of bone marrow? What other name does this tissue have? What means blood cells are made outside of the bone marrow? What two organs are involved? What condition causes this? What clear cells fill up bone marrow? In the bone marrow, ____ cell colonies are surrounded by ______ cells such as _____ called nurse cells.

Answer 35

Bone marrow, red bone marrow, medulla ossium rubra Extramedullary hematopoiesis, liver and spleen, severe anemia Adipocytes Red, stromal, macrophages

Question 36

What is the first thing you look for in a PBS? What two things do you look for in RBCs? What index best measures the color of a RBC? Myeloblasts and metamyelocytes are not what? When does bone marrow begin producing blood? When do hematopoietic stem cells migrate to the bone marrow?

Answer 36

A reference cell (mature lymphocyte) Color / size Mean Corpuscular Hemoglobin Concentration Terminally differentiated Month 4, month 4

Question 37

What is a typical MCV value? What are high MCV RBCs called? What are low MCV RBCs called? Normal RBCs are the same size as what? What cells are smaller than this? What disease classically results in microcytes?

Answer 37

80-100 femptoliters Macrocytes Microcytes The nucleus of a small lymphocyte Microcytes Iron deficiency anemia

Question 38

What two specific thalassemia have a similar presentation? What thalassemia is lethal? Is there a form of beta thalassemia as lethal? Which (survivable) thalassemia is most severe? When does it become symptomatic? They require regular what? Marrow expansion creates deformities to what? What forms spikes on an X Ray? Beta major can also expand what two organs? You can measure for what compensatory hemoglobin?

Answer 38

Beta thalassemia minor / alpha thalassemia trait (alpha thalassemia minor) Alpha thalassemia hydrops fetalis, no Beta thalassemia major, infancy Transfusions, bones, cranium, spleen / liver, fetal hemoglobin

Question 39

What causes babesiosis? What is its vector? What is its reservoir? This it is similar to what disease? What disease has a similar location? Where in the world is it most common? What surgery increases risk? Why? What patients are most at risk? What microbiological stage identifies babesia? This has symptoms similar to what disease? Most infections are what? What type of unique fever? It infects what cells? Thus severe cases can cause what? What two drugs can treat it? Severely ill patients may require what procedure?

Answer 39

Babesia, deer tick, white footed mouse (babies are small like mice), Lyme disease, Lyme disease, U.S. and europe Splenectomy, cannot filter blood, immunocompromised, merozoite form (tetrad structure), malaria, subclinical, fever spikes RBCs, anemia, clindamycin and quinine Transfusion

Question 40

What strange metric indicates levels of RBC production? What does myeloid represent? What does erythroid represent? What is a normal M/E ratio? If the ratio is 1:1, what does this mean? What are the three prongs of trilineage hematopoiesis? What does each prong mean?

Answer 40

Myeloid to erythroid ratio (M/E ratio) Granulocytes and their precursors, erythrocytes and their precursors 2-3/1, the body is making too many RBCs Erythroid / myelocytic / megakaryocytic ``` Erythroid = RBC Myelocytic = WBC Megakaryocytic = platelets ```

Question 41

What blood cell has a C shaped band? When is it seen? A blast should never be found where? It may contain red lines called what? What is the safest place to perform a bone marrow aspirate?

Answer 41

Band cell Bacterial infection (Bandteria) In the peripheral blood Auer rods Iliac crest

Question 42

What two organs synthesize heme? It starts and ends in what organelle? But where do some intermediate steps occur? What cells lack mitochondria? What final enzyme turns protoporphyrin 9 into heme? What element does this require? Therefore, heme is just iron added to what?

Answer 42

Bone marrow and liver, mitochondria, cytosol, erythrocytes Ferrochelatase, iron Protoporphyrin 9

Question 43

What is one broad cause of anemia? This causes a low what? The body cannot do what? What is another broad cause of anemia? This causes high what? The body tries to do what?

Answer 43

Impaired production / hypoproliferative Low reticulocyte index (under 2%), compensate for anemia (you will have a low RI even though the bone marrow becomes hypercellular) Destruction of cells / blood loss High reticulocyte index (over 2%), compensate for anemia

Question 44

What does HS stand for? These mutations occur in what proteins? What pattern of inheritance is this? HS causes what major symptom? What two things does this, like all hemolytic anemias, cause? What will the PBS show? What metric is increased? Why? Splenomegaly prevents it from filtering out what? What test can measure HS? But what technique is better? What virus can cause aplastic crisis? Why do they feel bad? What can treat an aplastic crisis?

Answer 44

Hereditary spherocytosis Ankyrin / spectrin / band 3, band 4.2 (as the RBC surface proteins will make RBCs look like spheres) Autosomal dominant, hemolytic anemia Jaundice, splenomegaly Spherocytosis, MCHC, cell is smaller so density of Hb is higher, Howell-Jolly bodies Osmotic fragility test, quantitative flow cytometry, parvovirus B19, their anemia prevents them from compensating for decreased RBC production due to the virus Blood transfusion

Question 45

What mutation can increase clotting? What specific type of mutation? This makes factor 5 resistant to what? Thus they often form what? What mutation can increase prothrombin levels? This also increases the risk of what? Both the Leiden and prothrombin mutation heterozygotes have what effect? What if they are homozygous? Rare deficiencies in _____, _____, or ______ can also prevent the inhibition of clotting. What is the most common clotting cascade mutation?

Answer 45

Factor V Leiden mutation, point mutation (arginine to glutamine), protein C, deep vein thromboses G20210A, deep vein thrombosis Slight increased risk of DVT, severe risk of thrombosis Antithrombin III, protein C, protein S Factor V Leiden mutation

Question 46

What virus causes the owl’s eye inclusion? It is what type of virus, just like what? What are most cases? What type of mononucleosis? How is this lymphadenopathy different from that of EBV? What is the most common congenital viral infection in the U.S.? What % have symptoms at birth? What is the most common neurological sequela? It will cause hemorrhage of what? This can lead to what? What antiviral is ineffective?

Answer 46

Cytomegalovirus, heroesvirus, Epstein Barr virus Asymptomatic CMV mononucleosis Not limited to the cervical area (because it is generalized) Congenital CMV, 10%, sensorineural hearing loss Retina, blindness, acyclovir

Question 47

To measure hemoglobin, you ___ the cells, free ______ is oxidized to ________, which binds with ______ ions to form _______, and you measure its absorbance with what wavelength?

Answer 47

Lyse, hemoglobin, methemoglobin, cyanide, cyanomethemoglobin, 540 nm

Question 48

Name four iron studies. What measures the iron-transferrin complex? What kind of disease decreases this number? What measures the maximum possible ability to carry iron? How does iron deficiency anemia affect this number? Why? What is a normal transferrin saturation? How does iron deficiency anemia affect this? Why? What two results are highly specific for iron deficiency anemia?

Answer 48

Serum iron, TIBC (total iron binding capacity), % saturation, ferritin Serum iron, iron deficiency anemia TIBC (measures the empty car), increases this number, more of the transferrin is unbound 33%, lowers this, less transferrin is bound to iron High TIBC (high transferrin) with a low saturation

Question 49

A ton of reticulocytes in your blood will correct what? These alone may increase what index? Increased homocysteine leads to increased what and what? A defect to what causes macrocytic anemia? What kind of anemia has a globin chain defect? What kind of anemia has IL6 activation?

Answer 49

Hemolytic anemia, MCV Atherosclerosis and clotting DNA synthesis Thalassemia Anemia of chronic disease

Question 50

What is the RBC expiration date? What is the platelet expiration date? Where does blood flow in the US? How regulated is it? Who can’t give blood based on travel? Or if you have been what? You then screen for what? What gets lots of extra processing? What does not get much extra processing?

Answer 50

42 days, 5 days, central US to the coast, extremely regulated Traveled to malaria endemic area in a year Incarcerated more than 72 hours Viral markers Plasma, red blood cells

Question 51

What is a big risk of heparin? For severe bleeding, what is the antidote? This binds to the _____ charged _______ groups. This only works for what type of heparin? What should stop treatment immediately? Never do what?

Answer 51

Bleeding, protamine sulfate, negatively, sulfate, large MW heparin Signs of thrombocytopenia (platelet drop below 50%), never give them heparin ever again

Question 52

What lab should you always order for bleeding? This will also let you check for what? Or insufficient what? What two tests assess coagulation issues? If either is increased, perform what study? What does this involve? How will you know if the patient is factor deficient? What can you infer if mixing does not result in improvement? Why may a patient with hemophilia develop factor inhibitors? What disease can naturally produce inhibitors of these factors? What are these inhibitors often composed of?

Answer 52

CBC, anemia, platelets PT (INR) and PTT Mixing study, mix patients sample with normal plasma Mixing will correct PT and PTT, the patient has a factor inhibitor Antibodies against medically administered recombinant factors, lupus, autoantibodies

Question 53

What does ITP mean? What is the best sign of this? What will a PBS show? What will a BMB show are still normal? This is always a diagnosis of what? Why? They will have what visible symptom? Bleeding from where? Platelet count below what can cause what two bleeds? Children often have what type of ITP? Why? Why is this not as dangerous? What can reduce this immune response? What organ often destroys platelets? Thus what surgery can help treat acute ITP?

Answer 53

Immune thrombocytopenic purpura, decreased platelet count, larger platelets (platelets swell due to damage from antibodies), megakaryocytes (these are normal because the antibodies are only targeting platelets in the blood) Exclusion (as are most idiopathic autoimmune disorders), many things can cause thrombocytopenia Petechiae, nose and gums, 5,000, subarachnoid or intraparenchymal hemorrhage Acute, they get sick which triggers autoimmunity, self limiting, steroids, spleen, splenectomy

Question 54

What is the major non-dietary source of iron? What molecule stores most iron? Which cells have it? What two areas in particular? ______ in the liver consume old ______, turn their _______ into amino acids and capture heme. This heme is then harvested for what two things? The porphyrin becomes what? The iron becomes stored where? Or it may be released into what carrier?

Answer 54

Recycling by the body Ferritin, all cells, bone marrow and liver Macrophages, erythrocytes, globin, iron and porphyrin Bilirubin, ferritin or hemosiderin, transferrin

Question 55

What transporter removes iron from the cell? Once in the blood stream, what must be done to free iron? It binds what transporter protein? It can then be stored where, or utilized where? What cell utilizes it in the bone marrow? What allows this cell to uptake the ferric/transferrin complex? What liver hormone blocks ferroportin? This causes iron to be lost how?

Answer 55

Ferroportin, oxidized to the ferric state, transferrin In the liver, bone marrow Erythroid precursor, receptor Hepcidin, as ferritin sloughed off in the intestine

Question 56

What type of heparin has a more predictable kinetic profile? Which one is most common? Because this lacks the added chain, what does not not attract well? But what can still bind regardless of the extended tail chain? Thus low MW heparin binds what more than what? What is the smallest of low MW heparin? It is just the what? Heparin is not absorbed where? Must be given how? Unfractionated heparin has a half life dependent on what? It this good? If someone has a PE, give them _______ for immediate inhibition of ________, and then wean them to ______ anticoagulants.

Answer 56

Low molecular weight heparin, enoxaparin (low MW) Thrombin (II), factor X, factor X more than factor II Fondaparinux, core pentasaccharide GI tract, parenterally, dose, no (very hard to use) Heparin, coagulation, oral

Question 57

Vitamin B12 and folic acid are both required for what? Folic acid becomes what specific form? It carries what group? It adds a methyl to what group to form what amino acid? What is the left over folic acid version called? What is this form essential for? It specifically turns what into what?

Answer 57

DNA synthesis, methyltetrahydrofolate, methyl group, homocysteine, methionine (thus folate deficiency causes a homocysteine buildup) Tetrahydrofolate (lacking the methyl group), DNA synthesis, deoxyuracilmonophosphate to deoxythymidinemonophosphate (you need TETra to make the THYmidine)

Question 58

Drugs that do what can increase the effectiveness of warfarin? Why? What deficiency also helps warfarin be more effective? What does warfarin toxicity cause? What is the ideal INR target for warfarin? What INR can be risk of bleeding? Give them what immediately? How long may this take to work? So what can you give them that works immediately? Warfarin can also cause what major issue? What kind of drug has a half life of months? How do you solve an overdose?

Answer 58

Drugs that displace warfarin from the plasma proteins, increased concentration of free warfarin, vitamin K deficiency Bleeding, 2 to 3, greater than 5, vitamin K (to generate more normal coagulation factors), 48 hours, plasma transfusion Birth defects, superwarfarin, regular vitamin K

Question 59

What indicates a normal beta chain allele? What means no beta chains are made at all? What means you have some beta chains? These are collectively called what? What are the possible genotypes for beta thalassemia minor? What are the possible genotypes for beta thalassemia major?

Answer 59

B, B0, B+, beta thal alleles 1. B, B+ 2. B, B0 (All have at least one normal copy) 1. B+, B+ 2. B+, B0 3. B0, B0 (No normal copies at all)

Question 60

What anemia is due to too few RBCs being produced? This will have a reticulocyte index below what? This may be due to deficiencies of what nutrients? What does severe blood loss count as?

Answer 60

Hypoproliferative anemia 2% Iron deficiency, folate deficiency Destructive / hemolytic anemia

Question 61

All anemias cause ______ bone marrow, with what single exception? Would iron deficiency anemia increase RI? Why? So what index is decreased? What anemia can cause neurological issues? What anemia can cause SOB and neurological issues? What from history tells you that something is not sickle cell? What other anemia-related disease can cause SOB and neurological issues?

Answer 61

Hypercellular, aplastic anemia No, even though bone marrow is hypercellular, more reticulocytes don’t make it into the blood, reticulocyte index B12 deficiency anemias, sickle cell anemia, have not been to the hospital before TTP (thrombotic thrombocytopenic purpora)

Question 62

X linked sideroblastic anemia with ataxia has what deficiency gene? What kinds of sideroblastic anemias can you get later in life? Clonal issues are due to what syndromes? This increases risk of what blood disease? Porphyrias will have elevated ________ levels, whereas sideroblastic anemias have normal ________ levels because they target different ______. A normal neutrophil has how many nuclear segments? Myelodysplastic syndromes May cause how many segments? And the cytoplasm may lack what? Normal erythroid precursor cells are what shape? What shape may be dysplastic precursors? The nuclear segments may also not be what?

Answer 62

ABCB7 Gene (cleanup in aisle B7) Acquired, myelodysplastic syndromes, acute myeloid leukemia Protoporphyrin IX, protoporphyrin IX, pathways About 3, 2, granules, perfectly round, abnormal shapes, connected

Question 63

The ferritin metric measures what? How does iron deficiency anemia affect this? Why? What is STFR? How does iron deficiency anemia affect this? Why? How does iron deficiency anemia affect hepcidin? Why?

Answer 63

The body stores of iron, decreases, less iron exists to be stored The receptor that allows the erythroid precursor to bind the iron-transferrin complex, increases, less STFR is bound to iron so it floats away from the cell and accumulates in the plasma It decreases it, no need to inhibit iron absorption if iron levels are already low

Question 64

What is the most common cause of iron deficiency anemia? Over what time period? What group of women can have this? What means hidden blood loss? Where does this occur? What two things can cause occult bleeding? You may have impaired iron _____, or even have _______, which increased what regulatory hormone? This is associated with what specific type of anemia?

Answer 64

Blood loss, long term, women who menstruate Occur bleeding, GI tract, gastric ulcer / colon cancer Absorption, inflammation, hepcidin, anemia of chronic disease

Question 65

What must you decrease in sickle cell? What condition helps protect sickle cell patients? What is the goal of emergent exchange transfusion? How do sickle cell SB+ patients perform? Why? So what level is higher? How to sickle cell SC patients perform? Why?

Answer 65

HbS Hereditary persistence of fetal hemoglobin Reduce HbS to a level of about 30 / 40% Quite well (because the B+ beta thalassemia minor allele at least makes some normal HbB instead of HbS, thus less HbA is sequestered), HbA is higher Quite well (because this HbC replaces HbS, thus less HbA is sequestered)

Question 66

Sickle cells have what clustering? What happens to them? What is the life span of a sickle cell? They also have lots of _____, which forces out _____ and _____. Sickle cells do what to vessels? This causes what crisis? What does this feel like? What drugs can help this? Name five triggers of a sickle cell crisis.

Answer 66

Band3 clustering, hemolysis, 10-20 days, calcium, potassium, water They stick to them, vaso-occlusive crisis, very painful, pain drugs Hypoxia, dehydration, acidosis, infections, pregnancy

Question 67

What kind of hormone stimulates neutrophils? What is the drug name? What can you attach to it, and why? What do you call this modified drug? Use this in patients undergoing high dose ____ or _____ chemotherapy. This also stimulates transplanted ______ to produce what? It may also treat what congenital disease? Or what type of anemia? This will all reduce the risk of what? What is another name for pegfilgrastim? What does ANC mean?

Answer 67

Granulocyte colony stimulating factor, filgrastim (GRAnulocyte STIMulate) Polyethylene glycol, extend the half life, pegfilgrastim Cancer, HIV, bone marrow, neutrophils Congenital neutropenia, aplastic anemia, infection, neulasta (NEUtrophils LAST longer), absolute neutrophil count

Question 68

What other diseases may cause ITP? Only consider a _____ if they ______ after prior treatment attempts. What anti CD20 drug helps treat ITP? What platelet count means patients can safely undergo surgery? What does HIT mean? How long after does this occur? This somehow creates what antibody? It also damages what? This leads to very severe what? Stop all what?

Answer 68

Lupus, HIV, (as anything affecting the immune system could cause IMMUNE thrombocytopenia) Splenectomy, remiss Rituxan (it TUX away the immune system) 50,000 Heparin induced thrombocytopenia, 5-10 days after dose is given, IgG, endothelial cells, clotting, heparin

Question 69

What is toxic in the free form? Why? Iron in the body may be bound to what? Where? Name two functional locations for iron. Name two storage forms of iron. Why is ferritin a better form of storage? How much iron is found in the functional state? What about the storage form?

Answer 69

Iron, it creates free radicals Transferrin, circulation Hemoglobin / myoglobin Ferritin / hemosiderin, because iron stored in hemosiderin cannot be used again 2/3, 1/3

Question 70

What two pathogens are associated with innate immune cell infection? What cell does each infect? What type of cell is infectious? What serves as a reservoir for ehrlichia? What do its symptoms feel like? Without what? What kills it very well?

Answer 70

Ehrlichia/anaplasma Ehrlichia (phagocytes), anaplasma (neutrophils) Dense core cells Deer, Rocky Mountain spotted fever (without the rash), doxycycline

Question 71

What viral pathogen can cause regional and general adenopathy? It is what type of virus? What is this infection called? What triad of symptoms does it cause? What percentage of adults are seropositive? It infects what cells in what tissue? What other severe side effect can latency cause? What do you see in a PBS? What lymph nodes are commonly associated with mono? Why? Why do we ask infected adolescents to avoid contact sports? What antibody persists for life? Which one disappears?

Answer 71

Epstein Barr Virus, herpesvirus, Infectious mononucleosis Fever / pharyngitis / cervical lymphadenopathy, 90%, B cells, lymphoid tissue Hodgkin and non-Hodgkin lymphoma, nasopharyngeal carcinoma Abnormal lymphocytes with large and irregular nuclei and tons of cytoplasm Cervical lymph nodes, transmitted by kissing, splenomegaly leads to splenic rupture, IgG, IgM

Question 72

What food contains folic acid? How long does it take to deplete folic acid stores? What about B12 stores? Who often has decreased folic acid intake? Who else has increased requirements for folic acid? What disease causes increased folic acid requirements? So supplement them with what? Name one difference between B12 deficient patients and folic acid deficient patients.

Answer 72

Green leafy vegetables, a few weeks, a few years Alcoholics (they don’t eat vegetables), pregnant women, sickle cell disease, folic acid Neuropsychiatric abnormalities for B12 deficiency

Question 73

Extravascular hemolysis means cells are destroyed where? What cells? What grows in size? Both intravascular and extravascular hemolysis can cause _______ and _______. What chain does sickle cell affect? What genotype does the normal beta chain have? What genotype do sickle cell patients have? This is what specific type of mutation? Sickle cell beta chains lack what property? When is this fine? But what causes sickle cell hemoglobins to aggregate? What kind of cell does this form?

Answer 73

Liver and spleen, phagocytes, liver and spleen (primarily the spleen) Anemia, jaundice Beta chain, BB, SS, glutamic acid to valine point mutation at position 6 (wear a GluV when using a sickle) Solubility, high oxygen concentrations, low oxygen concentrations, sickle cell

Question 74

Does whole blood have harmful effects? Risk of what two things? When do people develop an ABO blood type? By when do people make antibodies against foreign blood antigens? Where do we think they come from? What are the genotypes for each blood type? What type of RBC can be given to anyone? Does this work for plasma? Because plasma has different what? Platelets require what for survival? Thus they must be in what type of bag?

Answer 74

Yes, too much volume for the CV system can kill the patient, or risk for infection Birth, 6 months, gut microbiome OO (type O) AA / AO (type A) BB / BO (type B) AB (type AB) O type, no, antigens Oxygen, gas permeable bag

Question 75

What are the three components of the CBC? What data help you understand anemia? What tells you how many erythrocytes are in your blood? Why could this be misleading? What measurement is much more informative?

Answer 75

WBC, RBC, platelets RBC indices RBC count Anemic people may have normal RBC count How much hemoglobin is present

Question 76

What stem cell can create endless growth in the bone marrow? This causes what disease? There is no room for what cell type in the bone marrow? Causing what other symptom? What signal creates more RBCs? What signal creates more monocytes / neutrophils? What signal creates more platelets?

Answer 76

Hematopoietic stem cells, leukemia, megakaryocytes, bleeding Low oxygen Infections Blood loss / injury

Question 77

What are the two components of the RBC membrane? What is the lattice called? What two things comprise it? What does actin do? What does ankyrin do? This spectrin mesh gives the RBC what property? So what does an absence of spectrin cause to happen? What cell does the RBC become?

Answer 77

Lipid bilateral, spectrin Spectrin, alpha / beta chains Actin binds the alpha subunit to band 4.1 Ankyrin binds the beta subunit to band 4.2 Flexibility, the RBC breaks apart, spherocyte

Question 78

What is the classic histological finding of cerebral malaria? How fatal is it when treated and when untreated? What history must you obtain for malaria? What is the standard diagnostic tool for Malaria? Will Malaria always be detectable? Why? So repeat a blood smear how often? P. Falciparum will have thin _____, absence of ______, and a ______ shaped gametocyte. P vivax and P ovale have _____ rings, ______ in the blood, and ______ shaped gametocytes. What dots are also visible?

Answer 78

Sequestration of infected erythrocytes in microvessels (thua blocking your brain), 5-20% when treated, 100% when untreated, travel history Giemsa stained blood smears (to see the parasite), no, symptoms appear before high enough blood concentration of parasite, every 12 hours Rings, schizonts, banana Thicker, schizonts, spherically, schuffner’s dots (the vivacious oval shuffled dots)

Question 79

Sickle cell patients have what anemia? They have ________ due to increased RBC production. When does sickle cell first become apparent? In whom do bones expand? You may have what kind of hematopoiesis? Sickle cells cause what organ to swell? This does what to the spleen? So what happens by adulthood? The spleen helps fight what type of microorganisms? Thus what are sickle cell patients susceptible to?

Answer 79

Hemolytic anemia, reticulocytosis, 4-6 months Children, extramedullary, spleen, kills it, it goes away Encapsulated, encapsulated microorganisms,

Question 80

What means various RBC sizes and volumes? What means variations in RBC shape? What do you first look for in a peripheral blood smear? What next?

Answer 80

Anisocytosis Poikilocytosis Size of the RBCs Color and shape of the RBCs

Question 81

Sickle cell splenomegaly can cause what sudden crisis? This traps too much what where? This causes what fatal symptom? What can restore this volume? What crisis means a sudden decrease in Hb for 2 weeks? What virus must infect what tissue? Sickle cell can cause what chest complication? What symptoms does this cause? Look for what on a CXR? What specific transfusion can save them?

Answer 81

Splenic sequestration crisis, blood, in the spleen, hypovolemic shock, blood transfusion Aplastic crisis, parvovirus B19, bone marrow Acute chest syndrome, dyspnea, tachypnea, low O2, hypoxemia (vicious cycle), new pulmonary infiltrates, emergency exchange transfusion (replace all of their blood)

Question 82

What does TTP mean? It is a type of what? What is another form of thrombotic microangiopathy? These both damage RBCs and cause what? Therefore what count will be high? Low what level? What pentad of symptoms exists for TTP? What enzyme is deficient? Large ________ multimers are more what? What is the treatment? To replenish what?

Answer 82

Thrombotic thrombocytopenic purpura, thrombotic microangiopathy, HUS Microangiopathic hemolytic anemia, reticulocyte count, haptoglobin 1. Thrombocytopenia 2. Hemolytic anemia 3. Renal failure 4. Fever 5. Neurological symptoms ADAMTS13, VWF, thrombogenic Immediate plasma exchange, ADAMTS 13

Question 83

What do rapid malaria tests look for? Acquired immunity is not what? Can you get infected again? But what is better with subsequent infections? What two traits protect against Malaria? What can treat chloroquine resistant malaria? Or what else? Be careful with quinine for what reason? What is the only treatment for severe malaria in the U.S.? What is used for malarial prophylaxis?

Answer 83

Malaria specific antigens, sterilizing, yes, symptoms Sickle cells trait / thalassemias, artemisinin (Artemis fowl saves you from malaria), quinine, it will accelerate the hypoglycemia associated with malarial infection some (Quinn is probably hypoglycemic) Quinidine gluconate (of course American malaria drug would be full of glucose) Chloroquine (just like chlorox wipes prevent countertop bacteria)

Question 84

# Define hemolysis. Name two types of hemolysis. Hemolysis causes an increase in _______ bilirubin, causing what symptom? What enzyme do RBCs also release? What do you see on a PBS? What process will try to increase RBC production?

Answer 84

Destruction of a RBC before its normal lifespan Intravascular hemolysis and extravascular hemolysis Unconjugated (indirect), jaundice, lactate dehydrogenase (LDH) Polychromatic reticulocytes, RBC fragments and schistocytes, erythropoiesis

Question 85

What kind of lesion damages bone marrow? What space occupying lesion results from an infection? What results from scarring? What else can cause a space occupying lesion? Name a primary malignancy of the bone marrow? Malignancies can also do what? Cancer will often spread to the bones from what two locations?

Answer 85

Space occupying lesion Granuloma, fibrosis, cancer Lymphoma, metastasize from other organs, breasts / prostate

Question 86

What dye turns reticulocytes blue? By staining what molecule? Reticulocytes are slightly larger than what? Reticulocytes are normally what % of RBC count? What anemias destroy RBCs? What cell type reaches what % to compensate?

Answer 86

Methylene blue Ribosomal RNA RBCs 1% Hemolytic anemia Reticulocytes, 2% or higher

Question 87

How will VWD affect platelet count? What is normal in all of them? What is normal in type 1 and 2a? What is longer in type 3? What test can assess platelet aggregation? What must be present for aggregation to occur? Which type has no aggregation? What drug causes VWF release from what cells? How is it administered? Or what can give them sufficient factors?

Answer 87

Doesn’t affect it (it affects the factor but not the platelets that bind the factor), PT, PTT, PTT is longer (because intrinsic factor 8 is destabilized) Ristocetin-induced platelet aggregation, VWF, VWD type 3 Desmopressin (presses down on the granules to release VWF), endothelial cells (weibel palade bodies), nasal spray Plasma transfusion

Question 88

What is the best way to make the specific diagnosis of PNH? You search for what two proteins on these cells? What test measures for acidic serum? To check for susceptibility to what? What other lysis test can be used? What type of drug can inhibit C5 from becoming C5a? What is it called? This prevents what system from killing cells?

Answer 88

Flow cytometry, CD59, CD55 Ham’s test (acidic ham with orange juice), cell lysis, sucrose lysis test Monoclonal antibody, eculizumab, complement system

Question 89

What process restores normal blood flow after injury? What is the first step? What is the second step? What is formed here? What is the third step? What happens here? What is the fourth step? What happens here? What vessel layer contains collagen? What endothelium organelles contain VWF? What are inactive platelets shaped like? Some coagulation factors depend upon what?

Answer 89

Hemostasis Vasoconstriction, primary hemostasis (platelet plug is made) Secondary hemostasis, fibrin strengthens the platelet plug Fibrinolysis, clot resorption Subendothelium, Weibel-Palade bodies Discs Vitamin K

Question 90

How many main porphyrias are there? These are due to abnormal enzymes for what pathway? What are the major two categories? With what symptoms? What does a neurovisceral attack look like? What causes the neurotoxicity? What tuberculosis medicine can induce acute porphyria? What poisoning, with what unique cytoplasmic appearance? What technique can let you measure the amount of each porphyrin? To treat acute porphyrias, treat what? Then give them medicine for what?

Answer 90

8, heme synthesis Acute porphyrias (neurovisceral attacks), cutaneous porphyrias (photosensitive skin lesions) Abdominal pain with some neurological issue, a buildup of ALA Isoniazid, lead positioning, basophilic stippling, HPLC Underlying cause, pain

Question 91

What are the three categories of quantitative platelet disorders? What condition can trap too many platelets in the spleen? What are the two classes of qualitative platelet disorders? Name three inherited qualitative platelet disorders. What can cause non-inherited defective platelets?

Answer 91

Decreased production, increased destruction, sequestration Hypersplenism Inherited, non-inherited Bernard-Soulier, Glanzmann’s thromboasthenia, von willebrand disease Aspirin

Question 92

Pink tissue in a BMB indicates what? This may cause what? Tumor cells in a BMB will cause what? What disease causes a hypocellular BMB? What cells are very huge on a peripheral blood smear? They have very open what, and visible what? When should you see myeloblasts in a peripheral blood smear? What disease causes this?

Answer 92

Fibrosis / scar tissue, anemia Anemia Aplastic anemia Myeloblasts, chromatin, nucleoli Never, leukemia

Question 93

What two major types of thalassemia exist? What two types of beta thalassemia occur? What four types of alpha thalassemia occur?

Answer 93

Beta thalassemia / alpha thalassemia 1. Minor 2. Major 1. Silent carrier 2. Alpha-thal-trait 3. Hemoglobin H disease 4. Hydrops fetalis

Question 94

What two symptoms does Zika cause? What transmits it? What is detectable after viral infection? What percent are symptomatic? Are symptoms severe? it can cause what type of adenopathy? It can rarely trigger what neurological complication? What is the most feared complication? What kind of PCR can identify Zika?

Answer 94

Measles like rash, conjunctivitis, mosquitos, Zika viral RNA 20%, no, generalized Guilin-Barre syndrome Congenital microcephaly RT-PCR (to amplify cDNA from viral RNA)

Question 95

Which porphyria presents with brown teeth? What swells? When is it spotted? How? What protoporphyria is gain of function? What is its inheritance pattern?

Answer 95

Congenital erythropoietic porphyria, spleen, infancy, reddish urine color X-linked protoporphyria, X-linked gain of function

Question 96

What wavelength and compound are used to visualize hemoglobin? What are immature erythrocytes called? They also lack what? What do they still contain? Reticulocytes are what color? They are released to circulate for how long? Then where do they go?

Answer 96

540 nm, cyanomethemoglobin Reticulocytes Nuclei RNA Bluish 1 day (because they have to return to the bone marrow immediately) Back to bone marrow

Question 97

What stain can detect iron? What disease prevents bone marrow from staining for iron? Why? What do we call erythroid precursors storing dusty iron? What are the two major sources of iron loss?

Answer 97

Prussian blue, iron deficiency anemia, all of the iron stores have been used up already Sideroblast Sloughing off (intestinal cells) and menses (blood loss)

Question 98

What kind of anemia results from inflammation? What cytokine causes hepcidin to release? Hepcidin blocks what transporter? This causes iron to be pushed into where? What iron studies will anemia of chronic disease result in? This may somehow also reduce the response to what hormone? What type of PBS results would you see? Where are there adequate iron stores?

Answer 98

Anemia of chronic disease, IL6, ferroportin, storage Low serum iron Decreased or normal TIBC (because body is not missing iron so it doesn’t increase free transferrin) Increased ferritin EPO Normocytic / normochromic, and hyocytic / hypochromic In the bone marrow

Question 99

What chemical classically causes aplastic anemia? So always ask them what? Name some viral causes of pancytopenia. Name one inherited cause of aplastic anemia. What inheritance pattern? Or hypoplasia of what? Most patients with pancytopenia have what cause? What two options may treat pancytopenia?

Answer 99

Benzene, where they work, EBV / CMV / rubella Fanconi anemia (Batman made Falconi anemic), autosomal recessive (loss of function) Kidneys (due to less EPO being produced by failing kidneys) Idiopathic Bone marrow transplant, immunosuppression (to treat an idiopathic autoimmune etiology)

Question 100

What is recombinant interleukin 11 called (both names)? This binds what receptor? This stimulates what process, which in turn produces what? Give this to what kinds of patients? What drug interacts with the thrombopoietin receptor (both names)? What kind of molecule is it? What gives it a longer half life? You only treat what disease with this? What other drug (both names) stimulates the thrombopoietin receptor? It is a non-______ molecule.

Answer 100

Oprelvekin/neumega (new megakaryocytes) (Oprah is worth 11 billion dollars), IL-11 receptor, megakaryocytopoiesis, platelets, thrombopenic patients on chemotherapy Romiplostim (Nplate), peptibody, two Fc fragments, idiopathic thrombocytopenic purpura (ITP) that is not responsive to corticosteroids (to reduce autoimmunity) or splenectomy ***The Roman named Eltrom Bopag goes directly to the thrombopoietin receptor*** Eltrombopag (promacta), non-peptide

Question 101

Children with sickle cell develop _____ vessels in their brain, which clog with what? This can cause what stroke? The brain compensates by making new what? Why is this dangerous? What sickle cell complication causes sustained erection? How do you treat this? What specific bone infection does sickle cell cause? What should you give to help with their splenic susceptibility to capsulated pathogens? What chemical helps by increasing HbF? Thus they form what strange tetramer? These don’t what?

Answer 101

Thick, clots, ischemic stroke, vessels, weak new vessels causing hemorrhagic stroke (sickle cell can kill you from a brain hemorrhage) Priapism, exchange transfusion Salmonella osteomyelitis Prophylactic antibiotics, hydroxyurea (hydroxy gives them HIGH oxy), alpha/alpha/beta/gamma, aggregate

Question 102

An anemic patient will have reduced what level? What will increase the percentage of hematocrit without anemia? For what is RDW a mathematical representation? What value best measures hemoglobinization of RBCs? What other value can be visualized on a blood smear based on cell size?

Answer 102

Hematocrit Dehydration Anisocytosis MCHC - mean corpuscular hemoglobin concentration MCV

Question 103

Pregnant women have too much what? This diluted what layer? Therefore, what falsely appears to be too low? What is hematocrit (RBC) also called? What technique lets you visualize RBCs? What stain is added to the smear?

Answer 103

Plasma Hematocrit Hematocrit Packed cell volume Peripheral blood smear Giemsa Wright stain

Question 104

What do platelets lack? What shape do inactive platelets have? They are fragments of what? They stay away from what? What is their lifespan? What hormone triggers their synthesis? What two granules do they have? What 6 things are stored within alpha granules? What 4 things are stored within dense granules? What factor is found in the platelet cytoplasm (outside of granules)? What does it do?

Answer 104

Nuclei, disc shaped, megakaryocytes, vessel wall, 7-10 days, thrombopoeitin Alpha granules, dense granules VWF, fibrinogen, factor V, factor XI, PDGF (platelet derives growth factor), PF4 (platelet factor 4) ADP, calcium, epinephrine, serotonin Factor XIII, binds fibrin that strengthens platelet plug

Question 105

What is vitamin B12 called? It is used for the conversion of what to what? More specifically, what version of cobalamin is required? What specific version of cobalamin is used to convert homocysteine to methionine? What two things will a B12 deficiency increase? Whereas a folic acid deficiency will only increase what? It will not increase what?

Answer 105

Cobalamin, methylmalonyl Coenzyme A to succinyl coenzyme A Adenosyl cobalamin Methylcobalamin Methylmalonic acid (methylmalonyl CoA) / homocysteine Only homocysteine, methylmalonic acid (methylmalonyl CoA)

Question 106

What does DIC mean? This is activation of what? Thus what two substances deposit in the body? Which one causes a positive feedback loop? What term means the clotting uses up the platelets and factors? Thus there is low what? How does this affect PT and PTT? What is very high in the plasma? What gets cleaved to d dimers? What gets split to fibrin split products? Which metabolite is very specific to DIC? What is not specific to DIC? So what specific thing must you measure for DIC?

Answer 106

Disseminated intravascular coagulation, clotting cascade, thrombin / fibrin, thrombin Consumptive coagulopathy, platelet count, increases them, fibrin split products (d dimers) Fibrin-fibrin bands, fibrin monomers D dimers (DD for DIC), fibrin split products, d dimers

Question 107

What two reactants begin heme synthesis? They form what, with what enzyme? Two of these then condense to form what? With what enzyme? Four porphobilinogens then condense to form what? With what enzyme? This then forms what? With what enzyme? Coproporphyrinogen then forms what penultimate molecule? With what enzyme?

Answer 107

Succinyl CoA and glycine, ALA (aminolevulinic acid), ALA synthase Porphobilinogen, porphobilinogen synthase Uroporphyrinogen 3, uroporphyrinogen synthase Coproporphyrinogen 3, uroporphyrinogen decarboxylase Protoporphyrin 9, coproporphyrinogen oxidase

Question 108

What do we use antiplatelet drugs for? What is the most common antiplatelet drug? Name the four classes of antiplatelet drugs. Aspirin inhibits what enzyme? Which prevents formation of what? The P2Y purine receptors ultimately do what? Name four of the P2Y antagonists. Which two are prodrugs? They require what for activation? Thus different patients may have what?

Answer 108

Prophylactic prevention of clots, aspirin 1. Thromboxane A2 inhibitors 2. P2Y purine receptor antagonists 3. PAR (protease activates receptor) antagonists 4. GP IIb/IIIa antagonists ***You have the thromboxane, the fibrinogen binders, and the two P’s*** Cyclooxygenase I, thromboxane A2 Turn on the fibrinogen receptors, clopidogrel / prasugrel / ticagrelor / cangrelor (PURe gruel = purine grel) Clopidogrel / prasugrel, CYP2C19, different activation

Question 109

What does DAT stand for? What does it test for? It may also test for a ______ reaction, or a ______ disease of the fetus. What is the process of a DAT? What are the two possible results? What does IAT stand for? What does it look for? You do this to prevent what? What is the procedure for IAT?

Answer 109

Direct antiglobulin test, autoantibody attacking the patient’s own RBCs, transfusion reaction, hemolytic Add patient’s RBCs to tube, add anti-globulin antibody, and of the patient’s RBCs are covered in auto-antibodies, the anti-globulin antibodies will agglutinate them together, positive / negative Indirect antiglobulin test, antibodies in the plasma (hence it is indirect) that target all sorts of other potential antigens in the donor’s blood, transfusion reactions Mix ***donor*** RBCs with recipient plasma to let any plasma antibodies attack them, and then add an anti-globulin antibody to agglutinate if positive result

Question 110

What four factors are vitamin K dependent? What two anticoagulation proteins are dependent upon vitamin K? Name two drugs used for anticoagulation?

Answer 110

2, 7, 9, 10 Protein C, protein S Warfarin, heparin

Question 111

The female anopheles mosquito injects ______ into the host, which enter cells in the _____ and form a “_______”, which ruptures and enters the _______ cycle. The immature trophozoite in the RBC is called what? It then develops into a ______ trophozoite, before forming a _______ that ruptures and infects other blood cells. Or, the ring stage could form into a _______ that is indicative of plasmodium ______ if it is shaped like a what? Malaria feels like the what? What type of malaria involves the CNS? What medical condition causes black water fever?

Answer 111

Sporozoites, liver, schizont, erythrocyte Ring stage, mature, schizont Gametocyte, falciparum, banana, flu, cerebral malaria, hemoglobinuria

Question 112

Immature blasts often have a large what? And ____ or open chromatin. Mature cells have smaller what? What condenses? What word describes maturation of the cytoplasm without nuclear maturation? What are these cells called? Because they still have what? B12 or folic acid deficient anemia causes what in the bone marrow? What happens to most megaloblasts in the bone marrow? Thus causing what symptom?

Answer 112

Nucleus, lacy, nuclei, chromatin Asynchronous growth, megaloblasts, nuclei Hypercellularity (even though it causes anemia, the DNA damage makes it grow too quickly), they die, anemia

Question 113

What means you get a normal alpha chain? What means you deleted an alpha chain? What is a healthy genotype for alpha chains? What is the genotype for a silent alpha thalassemia carrier? What are the two genotypes for the “alpha thalassemia trait” presentation? How many copies must you lose for hemoglobin H disease? What about hydrops fetalis? These fetuses lack what adult chains? So what aggregates instead? What is this aggregate called?

Answer 113

A, - (A/A, A/A) (Four chains are wild-type) (A/-, A/A) (Silent misses one chain) (A/-, A/-) or (A/A, -/-) Three, four (fatal) Alpha, gamma chains, hemoglobin Bart

Question 114

What drug can cause hapten-mediated immunohemolytic anemia? The ______ only attacks the RBC if what else is bound? What drug can cause immune complex immunohemolytic anemia? In this case, what forms first? Then what happens next? The third type involves a true what? What drug causes this? This drug induces the formation of what? In which two scenarios will drug removal resolve the issue? In which scenario will removal of the drug not resolve the issue? Why?

Answer 114

Penicillin, antibody, penicillin Rifampin, immune complex of rifampin and antibody, this complex binds the RBC “True anti-RBC antibody”, methyldopa, anti-RBC antibody Hapten mediated / immune complex mediated True anti RBC antibody, the anti RBC antibodies will always be in the body

Question 115

Immature erythrocytes are called what? Describe them. Why are they blue? What is the name for a single blue dot in a RBC? What is the name for a bunch of blue dots in a RBC? Immature erythrocytes still contain the entire what?

Answer 115

Reticulocytes Anucleate, purplish / bluish cytoplasm, slightly larger than RBCs They have already lost their nuclei but they still have some RNA left over Howell Jolly body Basophilic stippling Nucleus

Question 116

What infection causes severe swelling of the legs? What infects you? What are the three pathogens? What transmits them? What lymph nodes are most commonly infected? What causes pain? Diagnosis involves testing for what? Microscopically, these look like giant what?

Answer 116

Lymphatic filariasis, roundworm Wuchereria bancrofti, brugia malaya, brugia timori, mosquitos Inguinal lymph nodes, lymphadenopathy, antigens, worms

Question 117

Name two types of dietary iron. Which one is complexed? Which one is uncomplexed? Non heme iron is in what state? What oxidation state does this mean? What must happen before it enters the enterocyte? Through what transporter? Which iron can enter immediately? What is the storage form of iron in what cell?

Answer 117

Heme iron, non heme iron Heme iron, non heme iron Ferric, plus 3, reduced to Fe2+, DMT1 Heme iron Ferritin, enterocyte

Question 118

What will a PBS of someone with iron deficiency anemia show? What will be completely missing in bone marrow? What will iron studies show for iron deficiency anemia? What hemoglobin do normal adults have? What chains does it have? What percentage? What other hemoglobin exists in adults? What chains does it have? What percentage?

Answer 118

Hypochromic microcytes, pencil shaped cells, lots of variation Iron stores Low serum iron, high TIBC, low saturation of transferrin, low ferritin HbA, two alphas and two betas, 97% BbA2, two alphas and two deltas, 3%

Question 119

What allowed for safe blood transfusions? What technology allows you to remove only the blood component you need? At first, ____ blood is taken. The potency means the _____ is of a sufficient level. They send some blood off for ____ testing. This whole blood is put into a what? What is the only reason to give whole blood? What can you give if you only want to increase pressure? Give whole blood if there is what? Or conditions that reduce what capacity?

Answer 119

ABO typing, apheresis Whole, hematocrit, viral, centrifuge, increase oxygen carrying capacity, saline Uncontrolled bleeding, oxygen carrying capacity

Question 120

Ask a patient about the _____ of the bleeding, and if it occurs ________ or if it was induced by what? Which type is more severe? Ask what to determine if it is inherited? What results from small vessel bleeding? These look like what? Larger bleeds create a what? What two terms describe this? Deep tissue bleeding can cause pain where? What is this called? Or a collection of blood called what?

Answer 120

Duration, spontaneously, trauma, spontaneous Family history, petechiae, red pin pricks on the skin Bruise, purpura / ecchymosis Joints, hemearthrosis, hematoma

Question 121

A patient who needs how much blood per week likely has hemolysis? Thus what can indicate hemolysis? What patients keep attacking blood with improper antigens? Why is this difficult to treat? What can cause basophilic stippling? What unique pattern will a thalassemia patient have? What has much lower Hb? What anemias can be acquired?

Answer 121

1 or 2 pints, transfusion requirement Sickle cell patients, hard to find enough blood products that they won’t react to Thalassemia, ***slightly*** low Hb with incredibly low MCV Iron deficiency anemia, thalassemias

Question 122

What anticoagulation protein can be bound or free? What binds the free form? It is referred to as a what? This means it is rapidly increases when? C4bBP binds to free what? This depletes what? Leading to what state? What diseases can cause this triggering inflammation? Thus what protein mediates the hyper coagulation of inflammation? What zymogen mediates fibrinolysis? What activates this? What other factor can do this? This turns plasminogen into what? Plasmin then does what? What are fibrin split products not quite the same as?

Answer 122

Protein S (may or may not be strapped), C4bBP (stick some C4 on the protein S), acute phase reactant, during inflammatory states Free protein S, depletes free protein S, hypercoagulable state, cancers, C4bBP Plasminogen, TPA (tissue plasminogen activator), factor XII, plasmin, degrades the clot, D-dimers

Question 123

Neulasta will cause what symptom? What other side effect will a CBC reveal? When cleared, increased neutrophils make what organ swell? What older granulocyte stimulating factor has been replaced? Why? What side effects does it have? What kinds of growth factors create more platelets? What two classes are there?

Answer 123

Mild to moderate bone pain, granulocytosis, spleen Sargramostim, severe side effects, flushing / hypotension / nausea / vomiting / dyspnea Thrombopoeitic growth factors, those that target the interleukin-11 receptor, those that target the thrombopoietin receptor

Question 124

Iron deficiency anemia can cause what oral symptom? So can what other two anemias? They may complain of what when eating? Due to what? What means ulcers in the corner of your mouth? What means spoon shaped nails? Anemic patients may have pallor of what? What means they eat odd things? What will their CBC show?

Answer 124

Glossitis (Beefy red tongue), B12 / folate deficiency Dysphagia, esophageal webs Angular cheilitis (keys scratching the corner of your mouth) Koilonychia (coiled up spoons), conjunctiva, pica Low RBC, low Hb, low Hct, low MCV, low RI, high RDW

Question 125

What type of hypo-proliferative anemia causes a low MCV? What type of hypo-proliferative anemia causes a normal MCV? What type of hypo-proliferative anemia causes a higher MCV?

Answer 125

Iron deficiency anemia, thalassemia, anemia of chronic disease Bone marrow damage (tumors), aplastic anemia, anemia of chronic disease, renal failure (not enough EPO) Folic acid deficiency, B12 deficiency, impaired DNA synthesis (cells don’t divide enough this they become too large)

Question 126

What causes tularemia? What often transmits it? It is in what region? How is it transmitted to humans? It grows how? What does it require to grow? It spreads to where immediately after a bite? How does it evade the immune system? What is the incubation period? What type of fever? What is the most common form? What appears at the bite? With a central what? And regional what? What is your first line treatment?

Answer 126

Francisella tularensis, rodents, central U.S. Animal / insect bite or ingestion, very slowly, cysteine, regional lymph nodes Suppressed oxidative burst, a few days, acute onset remitting fever Ulceroglandular form, ulcer, eschar, adenopathy, aminoglycoside

Question 127

What kinds of diseases have influenced major wars? They have what gram property? What two factors make these difficult to study? What two groups are there? What kinds of organisms transmit these? What does RMSF stand for? Is it lethal? What name has its unique rash given it? Most cases are found where, and not where? What unique symptom distinguishes it from bacterial infections? It targets what cells? It can therefore lead to what? What is the drug of choice? How do they propel themselves?

Answer 127

Rickettsial diseases, negative, very small / obligate Intracellular Spotted fever group / typhus group, lice / ticks Rocky Mountain spotted fever, often lethal, Black measles, Southeastern U.S. and not the Rockies Rash on palms and soles of feet (like where you would pick up rocks), endothelial cells, hemorrhage, doxycycline, propel themselves with Intracellular actin (propelled itself from Rocky Mountains down to the south)

Question 128

What washes out coagulation factors? What else prevents coagulation? What two cells block tissue factor from escaping the subendothelium? Platelets also release what two things to dilate smooth muscle? Endothelial cells also have what molecule on their surface? This sequesters what protein? Thus activating what protein (and what cofactor) in what cascade? These inhibit what clotting factors?

Answer 128

Blood flow, healthy endothelial cells Platelets, endothelium, NO, prostaglandin Thrombomodulin, thrombin, protein C, (cofactor protein S), anticoagulation cascade, factor 5 and 8

Question 129

How does hemophilia affect PTT and PT? What assay would you use? How do you treat them? They develop what? So what must you do? What is the most common inherited platelet disorder? What are the two functions of VWF? VWF is made by what endothelial organelles? What cell also makes VWF? What therefore stores but does not make VWF? Where is it stored? What specific form is released? What enzyme chops it up?

Answer 129

Longer PTT, normal PT, factor 8 or 9 assay, give them recombinant factor 8 or 9, autoantibodies to the transfused factors, keep giving them larger doses of recombinant factor Von Willebrand disease, adhered platelet GP 1b to collagen / stabilizes factor 8 Weibel Palade body Megakaryocytes, platelets, alpha granules, ultra large von willebrand factor, ADAMTS-13

Question 130

HUS stands for what? This causes acute what? It also lowers count of what? And kills off what other cell type? What specific pathogen can cause this? What toxin does this produce? It activates what? Bernard Suolier syndrome is a deficiency of what? Thus platelets cannot bind what? So what cannot adhere? Results in severe what? What is instantly recognizable about this disease? Glanzmann Thrombasthenia is a deficiency of what? This prevents platelets from doing what? What does this receptor bind? This results in what? What will you see in a PBS? Both of these diseases are obtained how?

Answer 130

Hemolytic uremic syndrome, renal failure, platelets, RBCs E. coli 0157:H7 (e coli went to HS and can cause renal failure), Shiga-like toxin, platelet activation and aggregation GP1B, VWF, platelets, bleeding, very large PBS platelets (GP1-Bernard) GP2B-3A, aggregating, fibrinogen, severe bleeding, nothing (platelets appear to be normal) (Fibers on your glands) Genetically

Question 131

How many Heme groups are in Hb? What value tells you is anemia is destructive or proliferative? Hemoglobin A is comprised of what? What does the A stand for? What type of Hb to fetuses have? What irreversibly binds Hb?

Answer 131

Four heme groups Reticulocyte index 2 alpha chains and 2 beta chains, adult Gamma Carbon monoxide

Question 132

What is the most common cause of B12 deficiency? What surgery can cause this? What disease produces auto-antibodies that attack the stomach? What auto-antibody blocks B12 from binding intrinsic factor? What autoantibody prevents B12/intrinsic factor from binging to the ileum receptor? What autoantibody inhibits the proton pump that activates pepsin?

Answer 132

Lack of intrinsic factor, stomach surgery Pernicious anemia, autoantibody 1 Autoantibody 2 Autoantibody 3

Question 133

What percent of leukocytes are neutrophils? What about lymphocytes? What about monocytes? What about eosinophils? What about basophils?

Answer 133

70% (neutrophils) 20% (lymphocytes) 3-8% (monocytes) 2-4% (eosinophils) 0.5-1% (basophils)

Question 134

What means Co2 and acid decrease Hb oxygen binding affinity? This makes what more effective? Lower amounts of BPG will increase the fraction of what? Higher BPG will decrease the fraction of what? Why?

Answer 134

Bohr effect Oxygen delivery to the muscles Oxyhemoglobin Oxyhemoglobin, because the BPG binds to deoxyhemoglobin and prevents oxygen from ever binding

Question 135

What patients will you give epoietin alpha? What other type of chemotherapy can cause anemia? What eventually causes this to not work well? You may also give epoetin alpha to ______ patients so that you don’t require a what? What is the risk of using this drug? What EPO derivative is only used for chronic kidney disease? It is given via what two routes? Which route requires a lower dose? Why? What hematocrit level do you want to produce? What hematocrit level increases heart attack probability?

Answer 135

Chemotherapy patients, HIV chemotherapy, chemotherapy begins to damage the stem cells Surgery, transfusion, it boosts hematocrit very high and causes HTN Darbepoietin (darts thrown into your kidneys), IV or subcutaneous, subcutaneous, because much of IV administered drug is cleared out by the liver, 33-36%, over 40%

Question 136

What is the study of blood? What does CBC mean? What molecule carries oxygen? What is reduced in anemia?

Answer 136

Hematology Complete Blood Count Hemoglobin Oxygen carrying capacity

Question 137

What can people have severe transfusion reactions to? What process removes the excess plasma? You do this for patients with severe what? Or if they have what blood procedure performed? Thus washing prevents what? What testing ensures the recipient survives? You must confirm what? What does this mean? What does RH stand for? What antigen does this correspond to? What does Rh positive mean? Giving Rh+ blood to an Rh- patient will do what? Does this matter in men? Why does it matter in women?

Answer 137

Plasma, plasma washing, allergic reactions, extracorporeal membranous oxygenation (ECMO), allergic reactions Pre-transfusion testing, ABO compatibility, there are no extra antigens Rhesus, D antigen, blood contains the D antigen, make them produce anti Rh antibodies, no, giving a woman anti Rh antibodies may kill an Rh+ fetus

Question 138

What causes Lyme disease? It has what gram property? What shape is it? What is its vector? It is the leading what? Is it lethal? But it causes chronic what? Is it contagious? It triggers what in the body? Where in the US has the most cases? Why don’t ticks in the south cause many infections? What tick phase causes the most infections? These ticks are not born with what? So how do they acquire the infection? Are deer a reservoir? This organism binds to what in the body? Initial symptom is what? Some patients have a painless what? Stage 2 can involve what three systems? What neurological symptom may occur? What drugs treats it in adults? What about children?

Answer 138

Borrelia burgdorferi, gram negative, spiral shape (you can spiralize a lime), deer ticks, leading arthropod borne infectious agent in the U.S. No, arthritis, no, inflammation (hence joint pain) Northwest, they live in low grass where it’s harder to find them, nymph phase, not born with infectious agent in them, feed on infected mice, no Connective tissue (hence it reaches the joints), flu like illness, a painless lesion, CV / neuro / MSK, Bell’s palsy (that actress got lyme Bell’s palsy) Doxycycline, amoxicillin (gentler in children)

Question 139

Platelets can also convert ______ acid into ________, using what enzyme? Prostaglandin G2 then becomes what final chemical in the platelet? What drug inhibits COX-1? Thus aspirin does what? Name three receptors on platelets and what they bind.

Answer 139

Arachidonic, prostaglandin G2, COX-1 Thromboxane A2 (TXA2) Aspirin, inhibits clot formation Glycoprotein 1a-2a (binds collagen) Glycoprotein 1b-V-IX (binds VWF) Glycoprotein IIb-IIIa (binds fibrinogen and VWF) **The last two bind VWF, but the last one binds fibrinogen also

Question 140

What type of iron is the oxidized state? What is the name for ferric iron hemoglobin? What % do you normally have? Why is this dangerous? What disease makes your skin blue?

Answer 140

Ferric iron (+3 oxidation state) Methemoglobin 1.5% It binds oxygen too tightly Methemoglobinemia

Question 141

What anemia does not increase TIBC? Why? GI bleeding is the most common source of iron deficiency anemia in what two groups? If you cannot identify the source of the bleeding, what must be performed? What often causes this bleeding? What color are platelets? Where are iron stores in the body depleted first? What will iron deficient anemia look like in bone marrow?

Answer 141

Anemia of chronic disease, body is hiding iron from the infection but still has it (thus it doesn’t overcompensate by making more transferrin) Males, post-menopausal females A GI workup, colon cancer Blue Bone marrow, hypercellular (to compensate) with no Prussian blue iron (even though it is hypoproliferative thus reticulocytes don’t make it to the blood)

Question 142

Patients with G6PD deficiency only become symptomatic with what trigger? What can cause this stress? What beans? And three big classes of drugs can trigger oxidative stress? How will these patients present? What two kinds of hemolysis? Intravascular hemolysis shows up as what? What will the CBC show? What will the PBS show?

Answer 142

Something that increases oxidative stress Infections, fava beans Antimalarials (fluoroquinolone), anti-inflammatories (aspirin), sulfa drugs ***my AAS triggers oxidative stress*** Healthy until they have sudden hemolysis after exposure (1-2 days later), intravascular hemolysis and extravascular hemolysis Red brown urine, normocytic anemia, bite cells

Question 143

What is the mnemonic for the five types of white blood cells? What are the three classes of bone marrow produced cells?

Answer 143

Little Blue MEN (lymphocytes, basophils, monocytes, eosinophils, neutrophil) ***Notice that basophils are blue and lymphocytes are little*** Red blood cells / white blood cells / platelets

Question 144

How do you prevent cold agglutinin immunohemolytic anemia during a blood transfusion? What type of immunohemolytic anemia also occurs after a viral infection in children? Using what antibody? Which recognizes which antigen on the RBC? What disease causes chronic immunohemolytic anemia?

Answer 144

Use blood warmers Cold hemolysin type, IgG, P antigen Cold agglutinin disease

Question 145

What type of bacterial infection causes a red streak from the point of inoculation? What three things can cause filarial lymphangitis? What causes fish tank granulomas? These patients are often what? What means fungus spreads through lymph nodes in a chain? What do pyogenic organisms cause? This causes a very ____ node, and what two specific types of organisms cause this? What does the skin look like? Where does this often occur and why?

Answer 145

Group A strep W Bancrofti, B malayi, B timori M marinum, immunosuppressed Lymphocutaneous sporotrichosis Acute suppurative lymphadenitis, large, streptococcus pyrogenes, staphylococcus aureus, red, neck and mouth (thats where strep and staph enter the body)

Question 146

What term means the percentage of blood that is made of RBC? What does MCV mean? What does this tell you? This lets you classify what? What does MCH mean? It tells you the average what? What does MCHC mean? It tells you what? What may increase this? What is a spherical RBC called?

Answer 146

Hematocrit Mean cell volume, the volume of RBCs, anemias Mean cell hemoglobin, average hemoglobin in a cell Mean cell hemoglobin concentration, average amount of hemoglobin relative to cell size, if the RBC shrinks to a sphere Spherocyte

Question 147

All heparins are called what inhibitors? What is the core of heparin? It has much of what atom? What happens if these are missing? Does heparin itself have anticoagulant activity? What does it require? What gets reused? What gets destroyed after one use? Thus we say antithrombin is a what? What part of heparin activates antithrombin III? The rest attracts what? And brings it in proximity to what?

Answer 147

Indirect inhibitors (because they must use antithrombin III), repeating pentasaccharide, sulfur, it is inaccurate No, antithrombin III (hence it is indirect), heparin, antithrombin III, suicide substrate Core pentasaccharide, thrombin, antithrombin III

Question 148

What blast cells indicate B12 / folic acid deficient anemia? Are they healthy? What blood cells will be very big? What are these called? What other type of large RBC may you see? What abnormal WBC may be seen? This is all due to what type of growth?

Answer 148

Megaloblasts, no RBCs, macrocytes, ovalocytes, hyper-segmented neutrophil Asynchronous growth

Question 149

What kinds of diseases prevent iron from being incorporated into the heme groups? This leads to what deposits in RBCs? What do these look like? Iron is located in what organelle? This leads to what type of anemia? Name two types of congenital sideroblastic anemias. What is the most common congenital cause of sideroblastic anemia? What enzyme is missing? This requires what cofactor?

Answer 149

Sideroblastic anemias, ringed sideroblasts, blue dots encircling the nucleus, mitochondria, hypochromic microcytic anemia X-linked sideroblastic anemia, x-linked sideroblastic anemia with ataxia X-linked sideroblastic anemia, aminolevulinate synthetase 2, vitamin B6,

Question 150

What anemias cause lemon yellow complexion? Due to what condition? Because of _______ hemolysis of defective cells. A patient with microcytic hypochromic anemia may have a slight increase in what? What is this called? What will slight hemolysis increase?

Answer 150

B12 and folate deficiency anemia, jaundice, intravascular Platelets, reactive thrombocytosis LDH and reticulocyte count

Question 151

Warfarin antagonizes what? Thus it shuts down what factors? In what pathways? What test measures warfarin? Why only this one? What is the standardized measurement for PT? What test measures heparin? Heparin activates what? What does it inhibit? Why can’t you use PT to measure heparin? Endothelial cells are covered in a molecule similar to what? Like heparin, these activate what? What does Antithrombin III inhibit?

Answer 151

Vitamin K, 2, 7, 9, 10, intrinsic, extrinsic, common PT time (extrinsic factor 7 has shortest half life, so will measure extrinsic pathway even though warfarin also affects the intrinsic pathway), INR PTT, anti-thrombin III, thrombin, 9, 10, 11, 12 (in the intrinsic and common pathways), Because heparin doesn’t inhibit anything in the extrinsic pathway Heparin (thus your endothelium makes its own heparin), antithrombin III, thrombin, 9, 10, 11, 12 (which is what heparin therefore also inhibits through antithrombin III)

Question 152

Hemolytic anemia causes what to form? What treats hereditary spherocytosis? Why? What inheritance pattern is G6PD deficiency? What are the two recessive alleles called? These may arise to protect from what? Which one is more severe? Which one is the milder one from Africa? What does glucose-6-phosphate dehydrogenase maintain? This protects against what? What makes RBCs more susceptible to oxidative damage?

Answer 152

Pigmented gall stones Splenectomy, spleen is what destroys the healthy RBCs and turns them into spherocytes X linked recessive, G6PD-, G6PD Mediterranean Malaria, G6PD Mediterranean, G6PD- Intracellular store of reduced glutathione (GLUcose = GLUtathione), ROS, age

Question 153

What are the two classes of coagulation factor issues? Name three congenital coagulation factor issues. Why is von willebrand disease both a problem with coagulation factors and with platelet function? Name three acquired causes of coagulation factor issues.

Answer 153

Inherited, acquired Hemophilia A, hemophilia B, von willebrand disease Because this factor is required for normal platelet function Acquired factor inhibitor, vitamin K deficiency, DIC (disseminated intravascular coagulation)

Question 154

What parasitic infection is cat transmitted? What pathogen? What is the only animal that lets the organism complete its full life cycle? This causes symptoms similar to what disease? What are these symptoms? Congenital infection can cause deformity of the what? Growth of what? And what sequelae?

Answer 154

Toxoplasmosis, toxoplasma gondii, cats Mononucleosis, fever / malaise Eyes, liver and spleen, neurological sequelae

Question 155

What other chemical helps to aggregate platelets together? In the coagulation cascade, the goal is to generate what? Factor ____ and cofactor ______ are responsible for converting _____ into thrombin? One way to activate factor 10 is for ______ to trigger factor ______, which then activates factor 10. But factor VII has what flaw? A much faster way is for factors ____ and ____ to bind together and activate factor X.

Answer 155

Thromboxane A2 Thrombin, factor Xa, cofactor 5a, prothrombin Tissue, VII, it activates this very slowly (Faster way) VIII, IX

Question 156

What is destruction anemia also called? What duration is decreased? What index is increased? How high? what hormone is elevated to compensate? What means you are making the wrong type of hemoglobin? What type of hemoglobin is made by sickle cell? Or what part of the RBC may be weakened? What disease classically weakens the membrane? What enzyme deficiency may destroy RBCs?

Answer 156

Hemolytic anemia, RBC life span, reticulocyte index, over 2%, EPO Hemoglobinopathy, HbS, membrane, hereditary spherocytosis Glucose-6-phosphate dehydrogenase deficiency

Question 157

Sickle cell patients have what hemoglobin? Sickle cell affects what chain? The SS genotype has how much HbA? How much HbF? How much HbS? The BS genotype is called what? How much HbA? How much HbF? How much HbS?

Answer 157

HbS, beta chain (sickle chopping a beta in half) Absolutely no HbA, 2-20% HbF, 75-90% HbS The sickle cell trait (it is only a trait because it is one allele), 60% HbA, 1% HbF (because they don’t have to compensate as much), 40% HbS

Question 158

What medical condition does bartonellosis cause? What is it confused with? This is the agent of what disease? How does this differ from Kaposi sarcoma? What often swells? It has what factor? What is the first sign drug? What tick borne disease is really important to spot early?

Answer 158

Bacillary angiomatosis, Kaposi sarcoma (Cat Scratch confused for Kaposi by making vessels), cat scratch disease Painful lesions and bleeding, lymph nodes Angiogenic factor, erythromycin Rocky Mountain spotted fever

Question 159

What are the four types of acute porphyria? What enzyme is deficient in acute intermittent porphyria? They have severe what? It rarely presents before when? Thus what may we infer? What drug may inhibit ALA synthetase in the liver? What blood level will be low? What enzyme is deficient in variegate porphyria? Relatively common in whom? They may have _____ issues and lesions where?

Answer 159

Acute intermittent porphyria (AIP), variegate porphyria (VP), hereditary coproporphyria (HCP), delta aminolevulinic acid dehydrators deficiency porphyria (ADP) Hydroxymethylbilane synthase (HMBS), abdominal pain, puberty, hormonal influence, hemin, sodium Protoporphyrinogen oxidase (PPOX), South Africans with Dutch ancestry, psychiatric, skin

Question 160

What is a normal myeloid to erythroid ratio? A higher erythroid component may cause what ratio? This is due to compensation for what? How do you estimate bone marrow cellularity in a certain age group? What is the cellularity of a 25 year olds bone marrow? Hemolysis causes what types of cells? They have what shape?

Answer 160

3: 1 (3 for ME) 1: 1, anemia 100% minus the age of the patient 75% Schistocytes, helmet (SS helmets)

Question 161

How long do RBCs live? How long do platelets live? How long do granulocytes live? How long do lymphocytes live? What unique feature do hematopoietic stem cells have? They also have what capacity?

Answer 161

120 days 10 days (platelets) 9 hours (granulocytes) Variable (lymphocytes) Pluripotency Capacity for self renewal

Question 162

What technique scatters light to tell you what kind of cell there is? What means low hemoglobin and hematocrit? What means low WBC count? What means low platelet count? What two terms describe increased hemoglobin / hematocrit?

Answer 162

Flow cytometry Anemia Leukopenia Thrombocytopenia Erythrocytosis / polycythemia

Question 163

Issues with what three things can cause bleeding disorders? What vitamin deficiency can damage the vessel wall? What purpura damages the vessel wall? Platelet issues can be ______ or ______. What term describes a quantitative platelet issue? This could mean decreased what? due to damage of what tissue? Or HIV can infect what cells directly? Or what type of drugs? Perhaps there is decreased _____ of platelets. What three diseases classically destroy platelets?

Answer 163

Vessel, platelets, clotting factors Vitamin C, senile purpura Quantitative, qualitative Thrombocytopenia, production, bone marrow, megakaryocytes, chemotherapy drugs Survival, ITP (immuno thrombocytopenic purpura), TTP (thrombotic thrombocytopenic purpura), HUS (hemolytic uria syndrome)

Question 164

PNH causes what hemolysis? What word means occasional? But they may also have what hemolysis? Why is it often nocturnal? This causes what two urine issues? So what symptom may they have in the morning? What does PNH significantly increase the risk of? They may also have what blood disorder? Or even what type of severe anemia? Because what stem cell is being killed off by the MAC? This will increase what two blood levels? Decrease what blood level?

Answer 164

Intravascular, paroxysmal, chronic, pH drop in blood when sleeping Hemoglobinuria, hemosiderinuria (which can cause iron deficiency), red urine Venous thrombosis, leukemia, aplastic anemia, hematopoietic stem cell LDH and indirect bilirubin, decrease haptoglobin

Question 165

What makes older people’s skin bruise? Due to issues with what protein? What therapy can also harm collagen? What vitamin deficiency impairs procollagen? Or what syndrome? What means vessel inflammation? What purpura results from immune complex deposition?

Answer 165

Senile purpura, collagen, steroid therapy Vitamin C, Ehler’s Danilo’s syndrome, vasculitis Henoch-Schonlein purpura (vessels are SCHtuffed with immune complexes)

Question 166

What is the most important aspect of RBCs? What shape do they have? What filters out most deformed RBCs? What size must they be? What is the concavity called? Why is it called this? What is its ideal size? What is the ideal RBC life span?

Answer 166

Their shape Biconcave Spleen 7-8 micrometers Central pallor, it looks clear, 1/3 of the total diameter of the cell 120 days

Question 167

How many lymph nodes do you have? What is presented in lymph nodes? To maturate what? What lymph node are usually most palpable? What surrounds a lymph node? Who are they more prominent in? What lymph nodes indicate leg infection? What are the three lymph node layers? There is also a lymphatic _____ and _____. What two cells are in the cortex? What two cells are in the paracortex? What cells are in the medulla? What do they secrete?

Answer 167

Over 600, antigens, lymphocytes Those draining head and neck, capsule, children Groin nodes, cortex, paracortex, medulla, artery, vein B lymphocytes and macrophages T lymphocytes and dendritic cells Plasma cells, antibodies ***Big Mac, ToDay, PA***

Question 168

What means too little hematocrit? What means too much hematocrit? What results in normal hematocrit but little plasma? However, dehydration may trick you into thinking what percentage is too high? Who has increased CO and increased blood volume?

Answer 168

Anemia Polycythemia Dehydration Hematocrit Second and third trimester pregnant women

Question 169

What state impairs the effectiveness of ESAs? Why? Or deficiencies in what? Too much ESA can cause what deficiency? Why? This will decrease what two iron parameters? So what do you give with the ESA? Use the _____ dose of ESAs to prevent the need for what? ESAs can kill patients with what disease? Thus what is contraindicated in a cancer patient?

Answer 169

Inflammation, stem cells used up to make lymphocytes, B12, folic acid, iron Iron deficiency, all of the iron is being used by erythrocytes, ferritin, transferrin saturation, iron Lowest, transfusion, cancer, ESAs (don’t give ESAs to people with PSAs)

Question 170

What are the two forms of dietary iron intake? Where are they found? What is their absorption rate? What vitamin enhances absorption? What states increase absorption? What two things decrease iron absorption?

Answer 170

1. Heme iron, meat, 20% 2. Non-heme iron, vegetables, 2% Vitamin C Pregnancy / blood loss Calcium, tannins (found in tea)

Question 171

What means the central pallor is too large? What means a group of RBCs has two different types of RBCs according to color? What means RBCs have much more varied color? What cells look this way? What are these cells? Because they retain what molecule? What means the distribution of RBC volumes? What does this stand for?

Answer 171

Hypochromia Dichromia Polychromasia, reticulocutes, immature RBCs, ribosomal RNA RDW, RBC distribution width

Question 172

What triggers vasoconstriction? What hormone enhances this? In primary hemostasis, platelets bind _____ by using their ______ receptor, and bind ____ using their _____ receptor. The platelet then does what? What two granule secretions help to change its shape? What is also released from the subendothelium? It triggers what by binding what? This eventually generates what? This does what? What molecule aggregates platelets together by binding what receptor? This forms a what? Thrombin then converts _____ into ______ which factor ______ covalently links together, to strengthen what?

Answer 172

Neuronal reflexes, endothelin Collagen, GP Ia-IIa, VWF, GP 1b Change shape, ADP, Ca2+ Tissue factor, coagulation cascade, factor VII, thrombin, recruits more platelets Fibrinogen, GP IIb-IIIa, platelet plug Fibrinogen, fibrin, XIIIa, platelet plug

Question 173

Thalassemias will always have what kinds of PBS cells? What other unique cell will be present? Why do they look this way? Increased hematopoiesis may also make what cells visible? Lysis will make what cells appear? This variation will increase what two parameters? What stain reveals hemoglobin H tetramers? What does HbH make these cells look like?

Answer 173

Hypochromic microcytic cells, target cells, hemoglobin clumps in the middle Nucleated RBCs, schistocytes, anisocytosis / poikilocytosis Methylene blue, golf balls

Question 174

After RBC degradation, what enzyme converts heme into what product? What enzyme then turns this into what product? What type is this? This means it is not what? So what must move it through the blood? Where does it then travel? It becomes what form? What physical property does it have? It moves through what organ and gets dumped into where? Bacteria then turn it into what substance? What is unconjugated bilirubin also called? What is conjugated bilirubin also called?

Answer 174

Heme oxygenase, biliverdin Biliverdin reductase, bilirubin, unconjugated, not water soluble, albumin To the liver, conjugated bilirubin, water soluble, gall bladder, small intestine, urobilinogen Indirect bilirubin, direct bilirubin

Question 175

What two cells are seen in a sickle cell PBS? What bodies? Why do these Howell Jolly bodies persist? What is another term for this condition?

Answer 175

Sickle cells, target cells, Howell-Jolly bodies (condensed remnants of DNA) Functional asplenia means the spleen cannot filter them out Autosplenectomy (because their own body destroyed the spleen)

Question 176

Bivalirudin is a what? It binds what directly? Blocks what activity? Use this in patients allergic to what? Rivaroxaban and apixaban are what? They can cause what symptom? What route? Dabigatran can cause what symptom on discontinuation? What drug is this? What route? Desirudin and fondaparinux can cause what symptoms?

Answer 176

Direct thrombin inhibitor, thrombin, protease activity, heparin (Rivaroxaban / apixaban) Direct factor X inhibitors, stroke, oral (Dabigatran) Stroke, direct 2a inhibitor, oral Spinal and epidural hematoma

Question 177

What is the name for Hb bound to oxygen? What is the name for Hb bound to carbon monoxide? What affinity does CO have? What is the name for Hb bound to carbon dioxide? What iron state is used in the heme group?

Answer 177

Oxyhemoglobin Carboxyhemoglobin, 210 times more than oxygen Carbaminohemoglobin Ferrous (+2 oxidation state)

Question 178

Name one PAR-1 cleavage inhibitor. This prevents what from aggregating? Name one GPIIb/IIIa inhibitor? Why is it an antibody? Why does it cause thrombocytopenia?

Answer 178

Vorapaxar, platelets (vora-PAR) Abciximab, so it can bind to and inhibit GPIIb/IIIa, body removes platelets with antibodies stuck to them (blocking fibrinogen is a pretty ABC thing to do)

Question 179

Why will an infection make anemia more likely? What does ESA mean? These are all derived from what? What releases it? What specific cells? In response to what? Name recombinant human EPO. Name three commercial preparations of it. What does NESP stand for? What is the commercial name? What is the benefit of NESP over epoietin alpha? Thus a lower what will work?

Answer 179

So many lymphocytes are made that there are fewer precursor cells left over to form erythrocytes and other cells. Erythropoiesis stimulating agent, erythropoietin, the kidney, interstitial cells, low oxygen Epoetin alpha, epogen / procrit / eprex Novel erythropoiesis stimulating protein, aranesp, longer half life, dose

Question 180

What three quantities describe reticulocyte quantity? Which quantity must be corrected? Why? What is the equation for the absolute reticulocyte percentage? How do you calculate the reticulocyte index?

Answer 180

Reticulocyte percentage, absolute reticulocyte percentage, reticulocyte index, the first two Anemia may have decreased blood volume and therefore skew a higher percentage Absolute % = reticulocyte % X (sick Hct/normal Hct) Divide the absolute % by 2

Question 181

What means patients are failing to produce only RBCs? What tumor of the mediastinum can cause this? What type of leukemia can cause this? What specific infection causes pure red blood cell aplasia? Can you recover from this? Who might not recover?

Answer 181

Pure red blood cell aplasia, thymoma, large granular lymphocytic leukemia Parvovirus B19 (small because it only affects RBCs), yes, immunosuppressed patients

Question 182

What resection can prevent B12 absorption? What disease classically results in this resection? What two things can compete for B12? What other toxin can destroy B12? What disease can affect pancreatic enzymes? What people may not consume enough B12?

Answer 182

Small bowel resection, Crohn’s disease Bacterial overgrowth / parasites Nitrous oxide (NO B12) Pancreatitis Very strict vegans

Question 183

What two things can kill a RBC by binding the surface? What test can identify an antibody? What is this test also called? What are the two forms of an anti globulin test? What specific immunoglobulin often binds to a RBC? It binds maximally at what temperature? This describes what major class of immunohemolytic anemia? What disease can result in this?

Answer 183

Antibody / complement Anti-globulin test, Coomb’s test Direct anti-globulin test (DAT), indirect anti-globulin test (IAT) IgG, 37 degrees, warm-antibody-type immunohemolytic anemia, lupus

Question 184

What is the main pathogen for cat scratch disease? How does it grow? These patients have exposure to what? A small _____ will last for several weeks at what location? When does the lymphadenitis begin? What lymph nodes are most common and why? What is a papule? What can loosely diagnose catscratch disease? What other technique has high sensitivity and specificity? Is this disease bad? Why?

Answer 184

Bartonella henslae, slowly, cat, papule, site of scratch, 1-2 weeks later, axillary, because cat scratched your arm Raised red bump, serology, bacteria PCR, no, self-limiting

Question 185

What type of RBC is long and condensed? What RBC has little spikes on it? Hemolysis creates what cells? What cells look like ovals? What two hematopoietic lineages are there?

Answer 185

Sickle cell Spur cell Schistocytes Elliptocytes Myeloid and lymphoid

Question 186

What RBC intrinsic hemolytic anemia is classically acquired (not inherited)? What anemia targets RBCs with antibodies? What means vessels destroy RBCs? What parasite causes hemolytic anemia?

Answer 186

Paroxysmal nocturnal hemoglobinuria Immunohemolytic anemia Microangiopathic hemolytic anemia Malaria

Question 187

What does B12 deficiency swell? What does this result in? What symptoms of the hands and feet? Decreased senses of what? They may have loss of what? How do you normally administer cobalamin? In what two preparations? Why? How long can full recovery take? What do you give to treat folate deficiency? What if folate reductase is deficient and therefore folate won’t work?

Answer 187

Myelinated neurons, demyelination, parestesias, vibration and position, memory Parenterally, cyanocobalamin and hydroxocobalamin, these are more stable, several months Folic acid, give them folinic acid instead

Question 188

What type of hemolytic anemia results from small vessels? What happens to the RBC? This could be _____ aggregates or what device? Who may have damaged vessels in their feet? Name five types of conditions associated with microangiopathic hemolytic anemia? Most of these cause what to aggregate? Except for what disease, where what aggregates?

Answer 188

Microangiopathic hemolytic anemia, damage, fibrin, artificial heart valve Long distance runners DIC (disseminated intravascular coagulation), TTP (thrombotic thrombocytopenic purpura), HUS (hemolytic uremic syndrome), SLE, malignant hypertension Fibrin, lupus, immune complexes / antibodies

Question 189

DIC destroys RBCs via what mechanism? How does DIC harm organs? By blocking what? What can trigger DIC? Because a toxin triggers what pathway? What two specific cancers can cause DIC? What specific injury can trigger this? Consumptive coagulopathy makes them do what? What must you treat? Give drugs for what? And give them what?

Answer 189

Microangiopathic hemolytic anemia, hypoxia, microvasculature Sepsis, intrinsic pathway Adenocarcinoma, APL (acute promyelocytic leukemia) Burns, bleed everywhere Underlying cause, infection, plasma (to restore clotting factors in consumptive coagulopathy)

Question 190

What specific type of Hb do adults need? It is what kind of protein? Made of what chains? What is heme made of? What kinds of diseases result from an incorrect type of Hb? What means not having enough of each chain? What element is needed for heme? What two toxins can block heme production? What diseases can prevent heme formation?

Answer 190

Hemoglobin a, tetramer, two alphas and two betas, iron core with porphyrin ring Hemoglobinopathies (quality is wrong), thalassemia (quantity is wrong) Iron Lead, alcohol, porphyrias

Question 191

What are the subunits of hemoglobin? What effect decreases the binding affinity of O2? What chemicals compete with binding for O2? This is important in what tissue? High what will release oxygen? And what other chemical? What effect decreases the binding affinity of CO2? This means what can displace CO2? This is useful for offloading CO2 where?

Answer 191

Two alphas / two betas Bohr effect, CO2 / H+, muscle, temperature, BPG Haldane effect, oxygen, lungs

Question 192

What carries plague? What pathogen causes it? What is the most common form of the plague? What rare version has 100% untreated mortality? What does Y pestis look like on a gram stain? What region of the country? Does it have a zoonite reservoir? Is it only in fleas? What form can be transmitted between people? What is the most common form of transmission? Where do the bacteria replicate? What causes bumps? What region of body is most infected, why? What unique procedure can identify this? What antibiotics can treat y pestis?

Answer 192

Fleas, yersinia pestis, bubonic form, pneumonic form, safety pin, desert Southwest Yes, no, pneumonic, flea and tick bites Macrophages, regional lymphadenitis, inguinal region, bites to legs, lymph node aspiration Aminoglycosides, fluoroquinolones, doxycycline / tetracycline

Question 193

What marker produces more RBCs? What organ produces it? What causes its secretion? Kidney failure will therefore cause what disease? Due to a shortage of what? What does BMB mean? What does it tell you? What does BMA mean? What does it give you? Which one tells you about the context of the cells? Which one is good for analyzing individual cell types?

Answer 193

Erythropoietin (EPO), kidneys, hypoxia Anemia, EPO Bone marrow biopsy, structure of the bone marrow as it exists in the body Bone marrow aspirate, just the cells from the bone marrow BMB, BMA

Question 194

Name the classic peripheral blood smear findings of a bone marrow malignancy? Name this constellation of findings. Why do teardrop cells form? Failure of what organ can cause anemia? By decreasing what hormone? What do you treat them with? What anemia reflects bone marrow failure? Patients present with what? What is a big cause?

Answer 194

Tear drop RBCs, immature RBCs (nucleated), immature granulocytes Leukoerythroblastosis, fibrosis squeezes RBCs Kidneys, EPO, erythropoietin Aplastic anemia, pancytopenia, drug toxicity (anti-malarial drugs, chloramphenicol, tricyclics, chemotherapy, whole body irradiation)

Question 195

What helps blood clot? What % is RBC? What percent is leukocytes and platelets? What percent is plasma? What is the leukocuye layer called?

Answer 195

Clotting factors 45% 1% 55% Buffy coat

Question 196

What hemoglobin do fetuses have? What chains? Why is it unique? What two chains develop early in development? Why? What other chain is an embryonic analogue to alpha? When does it go away? When do beta chains take off? When do gamma chains disappear? Therefore what gradually replaces what? When do adult delta chains gradually begin their formation?

Answer 196

HbF, two alpha and two gamma, very high affinity Alpha chains and gamma chains, to make fetal hemoglobin, zeta, before birth when more alpha is starting to be produced After birth, 3-6 months after birth, beta chains replace gamma chains Birth (but they stay at a low level)

Question 197

What does not bind cooperatively to hemoglobin? So it has what curve? What effect indicates that lower oxygen increases CO2 binding? This lets CO2 bind better where? What mnemonic describes the 5 things that can shift the oxygen binding curve to the right (lower affinity?)

Answer 197

CO2 Linear Haldane effect Low oxygen tissues (where CO2 must be removed) CADET (Co2, Acid, DPG, exercise, temperature)

Question 198

Which 3 anemias are macrocytic? Which 3 anemias are microcytic hypochromic? Which 3 anemias are normocytic normochromic? What anemia is the most common? What is the second most common?

Answer 198

Pernicious anemia (B12), folate deficiency, liver disease Sideroblastic, iron deficiency, thalassemia (micro-SIT-ic) Aplastic, blood loss, chronic disease (ABC is pretty normal) Iron deficiency, chronic disease

Question 199

Fatigue without chest pain can rule out what? Severe anemia of any sort presents as what? What can rule out a GI bleed? What can give women iron deficiency anemia? What heart sound can indicate anemia? Why? What type of anemia causes koilonychia and esophageal webbing? What causes abnormal gait?

Answer 199

CV issues, chest pain No occult blood Heavy menstrual periods Soft systolic murmur, heart tries to compensate by pumping more blood Iron deficient anemia B12 deficient anemia

Question 200

A deficiency in what metal can cause sideroblastic anemia? Excess ____ can bind all of the copper. Or some people just lack ______ in their diet. What drug can cause sideroblastic anemia? By interfering with what cofactor? What type of anemia will you see? What will you see in the bone marrow? Why? But why will you see fewer reticulocytes?

Answer 200

Copper (copper siding), zinc, copper Isoniazid, B6 (Iso–sideroblastic) Microcytic hypochromic anemia, erythroid hyperplasia, to compensate for loss of RBCs, they don’t make it into the blood

Question 201

What does PNH mean? What pattern of mutation causes it? What specific mutation name causes it? This mutation impairs the normal membrane binding of what three proteins? What is CD59 called? It inhibits what complex? This prevents what from binding and doing what to the cell? PNH means you lack _____, this you cannot anchor ___, ____, and _____. Thus what complex forms? What type of hemolysis is there?

Answer 201

Paroxysmal nocturnal hemoglobinuria Acquired mutation, PIG-A mutation CD59, CD55, C8 binding protein Membrane inhibitor of reactive lysis, membrane attack complex, C9, lysing it GPI, CD59, CD55, C8, membrane attack complex, intravascular hemolysis

Question 202

What type of immunohemolytic occurs anemia after an infection? This creates what antibody? This binds RBCs at what temperature? What two viruses classically cause this? EBV adds the ____ antigen to the RBC, whereas mycoplasma adds the ____ antigen to the RBC. What antibody can bind to these at cold temperatures? Where in the body may these cold temperatures be found? This activates what system? This kills RBCs by the time what happens?

Answer 202

Cold agglutinin type (a cold is a type of infection), IgM (Moldova is cold), 0-4 degrees, mycoplasma, Epstein Barr virus (Myco for M) i (little i), I (m-III-coplasma), IgM Nose, ears, toes, complement system, by the time IgM falls off

Question 203

Why are there so many hematologic malignancies? What patient characteristics can sort these malignancies? Why is immunohistochemistry limited? What technique looks at multiple surface antigens at a time? Different tumors may also have what unique differences? Genetic differences affect the _____ of the patient and the _______ agent that works.

Answer 203

Many tissues involve blood Age, gender, location, exam results, cytology, only looks at one antigen at a time, flow cytometry Genetic, prognosis, therapeutic

Question 204

What shape are lymph nodes? What system contains them? What is a high pressure system? What is a low pressure system? What kinds of things can leak out if the circulatory system? How much water is lost to the tissues per day?

Answer 204

Bean, lymphatic system, CV system, lymphatic system, water and proteins, 3L

Question 205

What are the three parts of the lymph node? These different zones contain different what? What arrangement exists in the medulla? Why is it called this? Where does lymph collect before the efferent lymphatic vessel? What wraps around the whole lymph node? What area exists just beneath the capsule? What also enters and exits the lymph node? These lead to unique structures in what layer?

Answer 205

Cortex, paracortex, medulla, different cell types Medullary cords, cords of cells in the medulla, medullary sinus, capsule, subcapsular space Blood vessels, paracortex

Question 206

What is the lymph node cortex mainly made of? These clump together into what two ways? Which one contains a germinal center? What mainly fills the paracortex? These surround the what? What other specific cells exist in the paracortex? And what small vein exists in the paracortex? What enters through the HEV? What structure exists in the medulla? What cell type? What spaces?

Answer 206

B cells, primary follicle, secondary follicle, secondary follicle T cells, follicles, interdigitating dendritic cells, high endothelial venule (HEV), B and T lymphocytes (if they come from the blood stream instead of lymph) Medullary cords, plasma cells, medullary sinuses

Question 207

Where do B cells begin development? From what stem cell? What type of immature B cell forms? This undergoes gene rearrangement of what? Thus becoming a ______ B cell. Then what gene arrangement occurs? Thus it can finally make what receptor, and be called a what? Next it exits what? What does it try to encounter? In what location? By entering through what? When it binds the antigen, it differentiates into what two other cells? Which one releases soluble immunoglobulin? If a B cell enters a lymph node and doesn’t find an antigen, where does it go? Does it mature? What are primary follicles made of? If it encounters an antigen, where does it go? What therefore forms the germinal center? What do we call the outer layer of mature but naive B cells that got pushed out by the germinal center?

Answer 207

Bone marrow, hematopoietic stem cell with lymphoid potential, progenitor B cell, immunoglobulin heavy chain, precursor, immunoglobulin light chain, B-Cell receptor, immature B cell Bone marrow, a specific antigen, lymph node, high endothelial venule (HEV), memory B cell / plasma cell, plasma cell Primary follicle, yes, mature B cells (which have NOT been activated) Secondary follicle, plasma cells and memory B cells, mantle cells

Question 208

In the germinal center, a B-_________ undergoes what two processes to give rise to a B-_________, which differentiates into what two things? Why do somatic hypermutation and isotype switching occur? Why do some centroblasts die? By what process? What eats these dead cells in the germinal centers?

Answer 208

B-centroblast, somatic hypermutation and isotype switching, B-centrocyte, plasma cells and memory cells ***(Blasts exist before cytes)*** To make a receptor that binds even better, they randomly make a worse receptor, apoptosis

Question 209

What quadrant contains the spleen? How big can it get? 80% of it is made of what tissue? What makes up the other 20%? In the white pulp, what cells are seen surrounding the central arteriole? What do we call this location? B cells also form what two structures in the white pulp? What contains a germinal center? Where do the memory B cells move to? Thus what are they called?

Answer 209

Left upper quadrant, reaches the pubis, red pulp, white pulp CD4 T helper cells, peri-arteriolar lymphoid sheaths (PALS have the helpers), primary follicles, secondary follicles, secondary follicles, marginal zone, marginal zone cells

Question 210

What are the two main compartments of the splenic red pulp? What feeds into the sinuses? By exiting what part of the spleen? This is called what type of circulation? Other central arteriole dump into where?

Answer 210

Sinuses, cords, central arteriole, white pulp, closed circulation, cords

Question 211

In the splenic cords, ______ RBCs can squeeze into the sinuses, whereas non_______ RBCs get trapped and eaten by what? What type of circulation is this called? The spleen filters out ___ and ____ red blood cells. This does what to the spleen? It also removes what from RBCs? Such as ____ bodies to make _____ cells, or ________ bodies. What may indicate that the spleen is not working? What is another function of the spleen?

Answer 211

Flexible, non-flexible, macrophages, open circulation Old, damaged, enlarges, inclusions, Heinz, bite, Howell Jolly, RBC inclusions on the peripheral blood smear Hematopoiesis

Question 212

What does the spleen create? When is this normal? When is this abnormal? What is this process called then? You see this with very severe what? What duration? What does the spleen store? What condition can trap too much? What means WBC are too low? What means platelets are too low? What % of platelets are normally in the spleen? What does the spleen use to target encapsulated bacteria? Asplenia makes you susceptible to what? Name the three bacteria that classically cause sepsis in asplenia.

Answer 212

Blood, gestation, after birth, extramedullary hematopoiesis, anemia, chronic WBC / RBC / platelets, hypersplenism, leukopenia, thrombocytopenia 40%, opsonins, encapsulated organisms Pneumococci / meningococci / H influenza

Question 213

What can heart failure cause in the spleen? Or hypertension of what system can enlarge the spleen? Why? Thus what two things often swell together? Name a life threatening splenic issue? When what bursts? What classically causes this? How do you treat this? Why is this not preferred? What cancers often enlarge the white pulp? What cancers often enlarge the red pulp?

Answer 213

Congestive splenomegaly Hepatic portal hypertension, the portal vein connects to the spleen Liver and spleen Splenic rupture, capsule, infectious mononucleosis, remove the spleen, patient becomes vulnerable to encapsulated microorganisms, lymphomas, leukemia

Question 214

What does MALT stand for? Name some places you can find it? In the small intestine, name the two layers of the mucosa? What divides the mucosa from the submucosa? A bunch of _____ cells may exist in what layer? These are what cells with what functions? Where may lymphocytes exist? What do we call them? What receptor do they have? Where may follicles exist? What cells fill them? These follicles are unique in what way? These organs may also be surrounded by what? Name the unique epithelial cells that communicate with these other lymphoid areas?

Answer 214

Mucosal associated lymph tissue, tonsils / small intestines / colorectal region / appendix Epithelium and lamina propria, muscularis mucosa Lymphoid cells, lamina propria, plasma cells secrete antibodies into lumen, macrophages consume pathogens, lymphocytes trigger adaptive response Epithelium layer, intraepithelial lymphocytes, CD8 Submucosa layer, B cells, well defined marginal zone Regional lymph nodes M cells

Question 215

Where does MALT have a unique name? What is this name? Where d T cells develop? From the _______, a ___________ with the unique marker ______ will migrate to the _______. It will then express _______ and a receptor for ______ to help commit to being a T cell. What occurs to make it an immature T cell? Give some names for these immature T cells? T lymphoblasts lack what markers? So we say they are double what? Then the ____ gene and the ______ gene create either a beta _________ or a gamma-delta ________, which are only _____ receptors. Then these thymocytes / t lymphoblasts gain both ____ and ____, and this we call them double what? Then the ______ gene adds what partial receptor? Thus creating what two types of complete receptors?

Answer 215

Distal ileum, Peyer’s patches Thymus, bone marrow, hematopoietic stem cell, CD34, thymus, NOTCH1, IL7 TCR Gene rearrangement, thymocyte / T lymphoblast, CD34, CD4, CD8, double negative Beta, gamma-delta, pre-t-cell receptor, pre-t-cell receptor, partial CD4, CD8, double positive Alpha, alpha receptor, alpha-beta / alpha-gamma-delta,

Question 216

The last step of T cell maturation tests what? This involves what kind of cell in the thymus? With what receptor for foreign antigens? The MHCII binds what T cell receptor? What receptor binds a self antigen? What does it present? What T cell receptor does it bind? What two conditions may kill the cell? Good binding is called what? Abnormal binding that kills t lymphoblasts is called what? Positive and negative selection finally creates what?

Answer 216

TCRs, antigen presenting cell, MHCII (foreign antigens), CD4 MHCI, self antigens, CD8 Binding too tightly, binding too loosely, positive selection, negative selection Mature T lymphocyte

Question 217

The thymus has what shape? It sits near what? The capsule points inwards to form what? These divide what? What layer is darker? What layer is lighter? What cells are in the dark cortex? What do cortical epithelial cells secrete? These also present what? They also lay down what structure for cellular movement? Where are the mature t lymphocytes located? Why does it look pale? What unique structure exists at the very center of a lobule? What fills it? This is extremely indicative of what organ? It stains how? What disease means the thymus gland is not developing well? What means it is completely absent? This causes what syndrome? Which is a complete lack of what?

Answer 217

Bilobed, mediastinum, septa, lobules, cortex, medulla T lymphoblasts (thymocytes) and epithelial cells, IL7, antigens, reticulum Medulla, mature T cells less packed together, Hassall’s corpuscle, keratin, thymus, eosinophilic (red) Thymic hypoplasia, thymic aplasia, DiGeorge syndrome, lack of T-cell mediated immunity

Question 218

What means Hassal’s corpuscles become hollow? Is this serious? What means the epithelial cells form a thyroid mass? This is considered what? What if it is malignant? Immature T cell lymphoma is called what? Mature T cells can simply form what?

Answer 218

Thymic crypts, no (typically benign) Thymoma, benign, thymic carcinoma Acute t-lymphoblastic leukemia / lymphoma T cell lymphoma

Question 219

Name one hematologic malignancy classification scheme? What two lineages? What two ways can you classify leukemias? Each of these could belong to what two lineages? Lymphoid neoplasms may be what? Name two classification subsets? Name two other classification subsets? What classification scheme is purely morphological? What myeloid levels are there? What lymphoid levels are there?

Answer 219

WHO (World Health Organization), myeloid and lymphoid Acute / chronic, myeloid / lymphoid Lymphomas, indolent / aggressive, Hodgkin / non-Hodgkin FAB group (French American British), M0 - M7, L1-L3

Question 220

What is the difference between leukemia versus lymphoma? Can there be overlap? How? Leukemia affects what tissues? Lymphoma looks like a what? Where? Seeing blasts in a PBS tells you what? What means rapid onset? What means slow onset? What does molecular remission mean? Remission could lead to what? What means you won’t have the cancer return? What are B symptoms? What means the lymph node architecture was destroyed by the cancer? Immature cells are the same as _____ cells which are the same as ______ cells.

Answer 220

Leukemia is widespread, lymphoma is localized, yes, a local mass may also have widespread effects Bone marrow / peripheral blood, localized mass, anywhere At least 20% of the bone marrow is involved, acute, chronic, the cells lack the harmful mutation, relapse Cure, fever / sweat / weight loss Effacement of lymph node architecture, precursor, blast

Question 221

What means lymphoblasts suddenly became cancerous and spread through the blood? What cell is involved in a follicular lymphoma? The hematopoietic stem cell has what two developmental directions? What are the two main subsets of the lymphoid arm? Thus you may have _____ B cells and _____ B cells, as well as ______ T cells and _______ T cells. These are all called what neoplasms? These cells give rise to ____ B cells and _____ T cells. These are call what neoplasms? Specifically for B cells, there may be what three categories?

Answer 221

Acute lymphoblastic leukemia B cell Myeloid / lymphoid, B cells and T cells, progenitor / precursor, progenitor / precursor, precursor neoplasms Mature, mature, mature neoplasms Pre-germinal center / germinal center / post-germinal center

Question 222

What nuclear marker to progenitor and precursor B cells express? What nuclear marker and what three CD markers do all B cells express? What do hematopoietic stem cells express? What receptor do immature B cells (later than precursor) express? What BCRs do circulating B lymphocytes express? Name an anti-apoptosis marker in mature pre-germinal B cells? Along with what two other markers at the same stage? Germans center B cells have what two unique markers? Memory B cells migrate to where? These just express our ____ markers CD 19, CD 20, and CD 79a Plasma cells are unique because they only express what pan marker? And what two new markers?

Answer 222

TdT Pax5 (Pac-Man nucleus), CD19, CD20, CD79a CD34, IgM, IgM and IgD Bcl2, CD 5, CD 23 CD10 / bcl6 (six for center, 10 for center) Mantle, pan CD 79a, CD138 (plasma is high temperature of 138 degrees) and 38

Question 223

What disease arises from a precursor B cell neoplasm? What are the two cells of origin? They will have what nuclear marker? As well as what common markers? Mature B cell neoplasms can be divided into what three categories? Name a pre-germinal center lymphoma? What two unique CD markers? What unique bcl marker? As well as what common markers? Germinal center tumors include ______, ________, ________, and __________. These will have what unique bcl marker? What unique CD marker? As well as what common markers? What B cell produces post germinal center tumors? These include ______, ______, ______, and plasma cell neoplasms. What is the prototypical plasma cell neoplasm?

Answer 223

B acute lymphoblastic leukemia (B-ALL) (young cells play with a ball), progenitor B cells, precursor B cells, TdT, pan-b-cell markers (CD19, 20, 79a) Pre-germinal center, germinal center, post-germinal center Mantle cell lymphoma (pre-germinal center), CD5, CD23, bcl2, pan-b-cell markers Follicular lymphoma, Burkett lymphoma, Hodgkin lymphoma, diffuse large B cell lymphoma (the follicle, names, and large cell are at the center), bcl 6 and CD 10 (6 for center and 10 for center), pan-b-cell markers (CD19, 20, 79a) Memory B cell, chronic lymphocytic leukemia (small lymphocytic lymphoma), hairy cell leukemia, extranidal marginal zone lymphoma, multiple myeloma

Question 224

B-ALL stand for what? What two cells can it come from? It affects who how often? What age? What are the remission rates? What are the cure rates? What environmental effect can cause it? What chromosome abnormality? What type of anemia are at risk? Due to what instability? This leukemia involves what two tissues? Can easily spread to what system? Or what other location? Bone marrow involvement may cause what symptom? They therefore have symptoms of what? Susceptible to what? Why? Bleeding due to what? What is this leukemia called when it affects the skin? Pain occurs where? What histologically will you see everywhere? These are what size? Very lacy what? Visible what? Describe it’s immunophenotype?

Answer 224

B-acute lymphoblastic leukemia, progenitor B cell or precursor B cell, children, 80% of the time (children play with the ball), 2-5 years, 95%, 85% Ionizing radiation, trisomy 21, Fanconi’s anemia, chromosomal instability (Falconi was unstable in Arkham) Bone marrow, peripheral blood, lymphatic system, brain, pancytopenia, anemia, infections, leukocytopenia, thrombocytopenia, leukemia cutis Bones, lots of B lymphoblasts, huge (2-3 times a RBC), lacy nucleus, nucleoli, TdT / CD 19, CD 20, CD 79a, possibly still some CD34 (left over from the preceding hematopoietic stem cell stage

Question 225

Describe B-ALL molecular characteristics (4 translocations, diploidy) What age group has favorable prognosis? Why? What two age groups have poor prognosis? Why?

Answer 225

Translocation 12;21 (balls are symmetrical like 12-21 which is favorable prognosis), translocation 9;22 (unfavorable prognosis), translocation variable;11q23 (unfavorable prognosis), translocation 5;14 (affects IL3 and Ig heavy chain thus increased eosinophils), hyperdiploidy (over 50 chromosomes which is a good prognosis), hypodiploidy (under 46 chromosomes which is a bad prognosis) 2-10 years, they have hyperdiploidy or translocation 12;21, under two or over ten, hypodiploidy / translocation 9;22 / translocation variable;11q23

Question 226

What cell results in mantle cell lymphoma? This is pre what? These are located where? Is it common? But it is what? What sex? In what age group? This initially affects what structure? Can travel to what blood connected areas? And what unique location? This creates what under the mucosa? What is this condition called? There are not true what? Patients present at a high what? What very specific translocation is involved? This does what? What immunological markers? What does not typically appear? (Mantle cloak does not typically shown 5)

Answer 226

Mature naive B cell (Mature Mantle), pre-germinal center, mantle zone surrounding the follicle, no, aggressive, males (mantle for males), 60s Lymph nodes, bone marrow / spleen / liver, gut, nodules, lymphomatoid polyposis, polyps Stage, translocation 11;14 (clock on my mantle says 11;14), over-expresses cyclin D1, CD19 / CD20 / CD 79a, CD5, sometimes surface immunoglobulins M and D CD5

Question 227

Mantle cell lymphoma cells are described as what? Thus they look what? They take over the whole what? Or the ______ is maintained but what layer is thickened? It looks like a bunch of _____ little cells. What immunohistochemical stain can find them? What specific variant has larger uglier cells? Why? What activity may predict prognosis?

Answer 227

Monotonous, all the same, (mantle clocks all look the same), lymph node, architecture, mantle, small, cyclin D1 Blastoid variant, looks like more like blast cells (larger nucleus and cytoplasm), mitotic activity

Question 228

Follicular lymphoma arises from what cell? What two types of cells could this be? In a follicular germinal center, _______ in the darker half migrate to become ________ in the lighter half. What marker is not expressed in the germinal center? This lymphoma is the most common what? What sex? Usually what age? What does it affect first? Can also spread to what blood related areas? Higher stage patients have widespread what? But what do they feel like? What is the most common translocation? This does what? What results from this?

Answer 228

Germinal center B cell, cebtroblast and centrocyte Centroblasts, centrocytes, bcl 2, most common indolent non-Hodgkin lymphoma, makes and females equally, 50 (fifty follicle), lymph nodes, bone marrow and spleen Lymphadenopathy, surprisingly not much (asymptomatic), translocation 14;18 (four and eight look like they contain follicles), overexpresses bcl2, inhibition of apoptosis

Question 229

Follicular lymphoma has what immunophenotype? What pattern does it morphologically have? With or without some ______ areas. What do centrocytes look like? What cebtroblasts look like? What three stages are there? 1 is what? 3 is what? Lower grade has what morphology? Higher grade has what morphology? More _______ is better, whereas more _______ is worse. Follicular lymphoma may look similar to what normal process? The presence of what cell is normal? What do these look like? What does it indicate if these are missing? What could you stain for in follicular lymphoma? If benign, what do you see? If cancerous, what do you see? Up to 50% of patients will transform into what? And rarely transform into what?

Answer 229

CD19 / CD20 / CD 79a, CD10 / bcl6 (normally found in germinal center cells because 6 and 10 are center), bcl2 Follicular pattern, diffuse, look like lymphocytes with a cleaved appearance, big cells with several large nucleoli 1 / 2 / 3, indolent, aggressive, follicular, diffuse, centrocytes, centroblasts Reactive follicular hyperplasia, tingible body macrophages, little clear dots, follicular lymphoma, bcl2, none in the germinal center, whole thing is stained Diffuse large B cell lymphoma (aggressive), Burkitt like lymphoma

Question 230

Describe diffuse large B cell lymphoma. What is the cell of origin? What two specific types of cells? What markers? This cancer may be due to aberrant what? What mutation affects bcl6? What translocation affects bcl2? Others have translocations that affect what gene? All of these mutations prevent what from happening? This is the most common what? Is it aggressive? But what is unique? It can uniquely spread to where? It can affect what cavity? Thus it is a type of what? What type of patient can get this? After what two things?

Answer 230

Diffuse growth of large B cells, germinal center B cell, centroblast / centrocyte CD19, CD20, CD79a, and germinal center markers CD10 and bcl6, somatic hypermutation 3q27, translocation (14;18), MYC gene, apoptosis, most common non-Hodgkin lymphoma (thus large occurrence) Yes, treatment has high cure rates, any site in the body, pleural cavity, primary effusion lymphoma, immunocompromised patient, HIV / post transplant

Question 231

Diffuse large B cell lymphoma patients have what symptom? What is the growth pattern? Some cells look like what? Describe them? Or they may look ______, which gives them a crazy shape. Other lymphomas can transform into what?

Answer 231

Rapid lymph node enlargement, diffuse sheets of tumor cells, centroblasts, big cell with prominent nucleoli, anaplastic Diffuse large B cell lymphoma

Question 232

From what cell does Burkitt lymphoma arise from? What two specific types? It characteristically has a translocation of the ______ gene in chromosome ____. So what accumulates? This increases what two things? All three translocations involve what chromosome and what gene? Name all three translocations? What makes this tumor unique? Very what? Gives them ______ disease due to growth. But paradoxically responds well to what? Thus what cure rate? How many clinical variants are there? What three? Describe its germinal center immunophenotype?

Answer 232

Germinal center cell, centroblast / centrocyte, MyC, 8, MYC protein, high proliferation and high cell death, 8, MYC, translocation (8;14), translocation (8;22), translocation (2;8) Fastest growing in humans, aggressive, bulky, chemotherapy, 90% 3, endemic BL, sporadic BL, immunodeficiency associated BL, CD19, CD20, CD79a, bcl6, CD10

Question 233

Endemic Burkitt lymphoma is seen in what area? In what age group? Strongly associated with what virus? Like all Burkitt lymphoma, it tends to escape the what? Sporadic Burkitt lymphoma does not have a what? Seen in what two age groups? This is still slightly associated with what virus? This tumor often appears in what system? What specific part? Immunodeficiency associated BL is associated with patients with what two viruses? Often affects what location?

Answer 233

Africa, children, EBV, lymph nodes Geographical prevalence, children / young adults (children and young adults are sporadic), EBV, GI tract, ileocecal junction HIV / EBV, CNS

Question 234

What is the unique growth pattern of Burkitts lymphoma? A bunch of monotonous _____ cells with clear _______ doing what? Why? What proliferation marker can be stained in BL? Which cells will not stain? Although it has a high _____ rate, dying tumor cells do what? They release what chemicals? This is called what syndrome? Hyperkalemia can do what? These metabolites can kill what?

Answer 234

Starry sky (stars will burn you), tumor, macrophages, eating apoptotic remnants, high growth and high apoptosis KI67, macrophages Cure, lyse, potassium / phosphorous / uric acid, tumor lysis syndrome, stop the heart, kidneys

Question 235

Name the two subgroups of Hodgkin lymphoma? What unique name do the tumor cells have? These are what size? What makes them look so unique? Or just one what? Or what cell shape? They don’t stain with ____ or ____ markers, although they are a type of ___ cell. What marker are they positive for? What is also unique about Hodgkin lymphoma? What two types of cells make up most of the tumor mass? Name some? Typically affects what age group?

Answer 235

Classical Hodgkin Lymphoma, nodular lymphocyte predominant HDL, Hodgkin and Reed Sternberg cells, giant, two or more nuclei, nucleus, irregular shape, B, T, B cell Pax5, very few tumor cells in the tumor mass, reactive and non-neoplastic cells, eosinophils / plasma cells / neutrophils / fibroblasts, young adults

Question 236

Hodgkin lymphoma has good what? It has predilection to what area? It is associated with what virus? Prognosis depends upon what? What is the staging system called? What cell variant looks like a nucleus in a big empty space? Nodular lymphocyte predominant Hodgkin’s has what unique cell type? Why does it look this way? What is the official name for this cell? Or what? Which type of Hodgkin lymphoma makes up 95% of it?

Answer 236

Cure rate (up to 85%), lymph node chains, EBV, tumor stage, Ann Arbor staging classification, lacunar variant Popcorn cell, nucleus is irregular and folded, lymphocyte histiocyte cell (LH), lymphocyte predominant cell (LP) Classical Hodgkin lymphoma

Question 237

Classical Hodgkin Lymphoma has a high association with what virus? What is the unique classical Hodgkin’s lymphoma immunoprofile? What is the unique nodular lymphocyte predominant Hodgkin’s lymphoma immunoprofile? Why do we also think these come from the germinal center? Classic Hodgkin’s is seen in what age group? With a second peak when? Nodular lymohocyte predominant Hodgkin lymphoma is seen in what age group?

Answer 237

EBV, CD 15+, CD30+, lacking CD45 CD15 minus, CD30 minus, CD45 positive (the exact opposite), because they are CD20+ / CD 79+ / bcl6+ 15-30, later in life 30-50

Question 238

What are the four subtypes of classical Hodgkin lymphoma? What is the most common subtype?

Answer 238

Nodular sclerosis / mixed cellularity / lymphocyte rich / lymphocyte depleted Nodular sclerosis

Question 239

What does CLL stand for? What is the lymphoma counterpart referred to as? What is the origin cell postulated to be? This this is what major lymphoma category? CLL is the most common what? What is the age group? The CBC must have what? Higher than what? This number is not the same as the _____ count. If the WBC is 10,000, and the % lymphs is 60%, when is the ALC? They have what? Most patients are what? This is many times an ______ finding on a routine _____.

Answer 239

Chronic lymphocytic leukemia, (SLL) small lymphocytic lymphoma, memory B cell Post-germinal B cell lymphoma, adult leukemia in the U.S., 60s, absolute lymphocytosis, 5,000 lymphocytes per cubic millimeter, WBC 6,000, chronic lymphocytic leukemia, asymptomatic, incidental, CBC

Question 240

CLL can also cause what two autoimmune issues? What does not cause this? But what does? What specific protein deficiency may also make them infection prone? PBS will show what? These look like _____ cells when crushed on the slide. What two things does CLL do to the lymph nodes? Instead it is replaced by small ______ and pale areas called what? These are filled with what two types of cancerous cells? This looks like a bunch of _______, in what type of pattern?

Answer 240

Autoimmune hemolytic anemia, autoimmune thrombocytopenia, tumor cells, tumor cells triggering normal cells to make antibodies against platelets and RBCs, hypogamma-globulinemia Many small mature lymphocytes, smudge (look smashed on the PBS), swells them and effaces their architecture, lymphocytes, proliferation centers, prolymphocytes / paraimmunoblasts Nodules, pseudo follicular pattern

Question 241

CLL has what classic nodular pattern? Looks like what? What is the classic immunophenotype for CLL? What deletion gives CLL a good prognosis? What two types of CLL are there? Which one is worse? Which is better? What process does this word refer to? So somatic _______ does what to their prognosis? What are two markers for unmutated cells?

Answer 241

Pseudo follicular pattern, bunch of pale regions CD19, CD20, CD23, CD5 (CLL can count -19,20- and add -2+3=5) Del 13q14.3 Mutated, unmutated, unmutated is worse, mutated is better, somatic hypermutation, hypermutation, makes it better Zap-70, Cd38 (in 1938 Zap away the mutation)

Question 242

What trisomy has a bad CLL prognosis? Patients under what age do worse? They tend to have what variant? They may also have presence of what two blood conditions? What can swell? They may have what swollen all over the body? What does LAD mean? All of these symptoms are part of what staging system? What happens in 5-10% of CLL patients? What is the most common on? What is this syndrome called? What just doubles in size? Now every part of the lymph node looks what?

Answer 242

Trisomy 12q, under 55, unmutated CLL, anemia / thrombocytopenia, liver and spleen, lymph nodes, lymphadenopathy Binet and Rai clinical staging system, transformation to more aggressive lymphoma, diffuse large B cell lymphoma, Richler’s syndrome, lymph nodes, pale (the Reich doubled in size and made the British pale)

Question 243

Name a rare leukemia? Seen in what population? It arises from what post germinal B cell? What three main tissues does it involve? Bone marrow involvement may result in what condition? Leukopenia can result in what? Thrombocytopenia results in what? Why do we call them hairy cells? Hairy cells may also have what appearance? What fills up the bone marrow? A bone marrow ________ may not get any cells, which is called what? So what would you have to do?

Answer 243

Hairy cell leukemia, elderly White makes (who are hairy), late activated memory B cell, bone marrow / peripheral blood / spleen Pancytopenia (hairs kill all of the cells), infections, bleeding, lots of spiky cytoplasmic projections on PBS, fried egg appearance Reticular fibers (black hairs in the bone), aspirate, dry tap, bone marrow aspirate

Question 244

Hairy cell leukemia involves what part of the spleen? It causes what to accumulate? What is the hairy cell leukemia immunophenotype? What does TRAP stand for? It looks what color? What is the prognosis for hairy cell leukemia? They respond well to what?

Answer 244

Red pulp, lakes of RBCs CD19, CD20, CD11c, CD25, CD103, annexin A1, TRAP (hairy old men trapped and annexed the 103rd battalion at 11:25) Tartrate resistant acid phosphatase, maroon (trapped in maroon county) Good, chemotherapy

Question 245

What is MALT lymphoma also called? They arise outside what? What is their postgerminal cell of origin? What does MALT stand for? What is the most common site of MALToma? What two glands? What place near the eyes? What do we call it when they take over the skin? The ______ get very large and the ______ zone cells just take off. This is due to ongoing _____ stimulation leading to what chronic state? Thus causing what?

Answer 245

Extranodal marginal zone lymphoma, lymph node, memory B cell, mucosa associated lymphoid tissue Stomach, thyroid gland, salivary gland, ocular adnexa, lymphoepithelial lesions Follicles, marginal, antigenic, inflammation, MALToma

Question 246

What infection can cause stomach MALToma? What infection can cause ocular adnexa MALTomas? What autoimmune disease causes MALToma in the thyroid? What disease for the salivary glands? How do you often cause tumor regression? What is the nonspecific MALToma immunophenotype? What three translocations are MALToma associated? What kind of prognosis does a MALToma have? But which specific translocation is the dangerous exception?

Answer 246

H pylori, Chlamydia Hashimoto’s thyroiditis, Sjogren’s disease Treat underlying cause, CD20, CD79a T(11;18), T(14;18), T(1;14) (First and last have a 1, first two have 18, last two have 14 and you need malted milk balls to figure it out), very good, T(11;18) (the first one is bad)

Question 247

What are plasma cell neoplasms also called? They come from what cell? Which secrete what? Where can you detect this? What two names describe this? What is the only part you can detect in the urine? What two types of light chains? What are these urine proteins called? What do we call a monoclonal antibody secretion disorder? Name two common forms of plasma cell neoplasms?

Answer 247

Plasma cell dyscrasias, plasma cells, monoclonal immunoglobulin, in the serum, M protein / paraprotein, free light chains, kappa / lambda, Bence-Jones proteins Monoclonal gammopathy, MGUS / multiple myeloma

Question 248

Multiple myeloma (plasma cell neoplasm) is seen in whom? What race? What three parts of the Skelton does it often affect? Creating what lesions? Look like what? What bone symptom do they have? What else? By activating ______ and inhibiting ______. Thus casing bone ________. Hypercalcemia then damages what organ? And bone marrow involvement can also cause what? What secretory product can also damage the renal tubules? What mnemonic for symptoms?

Answer 248

Older patients, African Americans, vertebral column / ribs / skull, lytic lesions, punches out spaces Bone pain, hypercalcemia, osteoclasts, osteoblasts, resorption, kidney, anemia Light chains, CRAB (calcemia, renal problems, anemia, bone pain)

Question 249

To diagnose multiple myeloma get what? Detect what protein? With what test? Of what two fluids? You then must identify what? With what test? What PBS formation appears? Because antibodies do what? You will also see the proliferation of ____ cells and _____ cells with tons of cytoplasmic __________ inclusions called what? Why does the electrophoresis show a single antibody spike? What is this spike called? Do these MM patients have a good prognosis? Why? What does MGUS this stand for? They don’t have any what? And have a much better what? They may eventually progress to what?

Answer 249

BMB, M protein, protein electrophoresis (PEP), serum / urine (SPEP / UPEP) The type of M protein, serum / urine immunofixation Rouleaux formation, make RBCs stick together, plasma, Mott, immunoglobulin, Russell bodies Because a monoclonal antibody was created, M spike No, so many symptoms, monoclonal gammopathy of undetermined significance, symptoms, prognosis, actually having Multiple Myeloma

Question 250

What does Cd stand for? T cells originally come from what cell? With what marker? It gets what receptor once it commits to the T cell lineage? And what else? This all occurs in what organ? What marker does the immature t lymphoblast have? what four other markers tell us it’s a T cell? Early t lymphoblast lacks what two things? But gains what two things after what process? What two types of mature T lymphocytes are there? What are the markers of a mature CD4 cell? What about a mature CD8 cell?

Answer 250

Cluster of differentiation, hematopoietic stem cell, CD34, IL7, NOTCH1, thymus TdT (3 syllables like immature), CD 2, CD 3, CD 5, CD 7, lacks both CD4 and CD8, gains CD4 and CD 8 after T cell rearrangement CD4 and CD8, mature CD4 cell (CD2, CD3, CD5, CD7 with the CD4 added), mature CD8 cell (CD2, CD3, CD5, CD7 with CD8 added)

Question 251

What types of T cells leave the thymic medulla? Where do 75% end up? Some go to what layer of lymph nodes? Some go to what structures in the spleen? Some go to what tissue? What three types of cells can CD4 cells become? What two types of CD8 cells can form? All of these mature CD4 and CD8 cells still express what?

Answer 251

CD4 and CD8 mature T lymphocytes, peripheral blood, paracortex, PALS, MALT CD4 regulator cells, CD4 helper cells, CD4 memory cells CD8 cytotoxic, CD8 memory cell CD2, CD3, CD 5, CD7

Question 252

What are the two broad T cell neoplasm categories? And what do they mean? What else may we call mature T cell neoplasms? What two places are called the primary lymphoid organs? Also called what? What areas are called secondary lymphoid organs, also known as what?

Answer 252

Precursor T cell neoplasms (those from the T lymphoblast), mature T cell neoplasms (those from the T lymphocyte) Peripheral T cell neoplasms Thymus and BM, central lymphoid organs MALT, spleen, lymph nodes, peripheral lymphoid organs

Question 253

Name one tumor in the precursor T cell neoplasm category? T-ALL classically presents as a what? It forms a mass in what organ? In what compartment? In what age group? But it could also prevent in any other ____ tissue like what? As a leukemia, where will is appear? How does this mass grow? They may have symptoms of what? What is highly elevated in the PBS? What do these T lymphoblasts look like? You’ll see this in the _______ or the _______. In other organs, these may have what two tumor architectures?

Answer 253

T-ALL (T acute lymphoblastic leukemia) (immature people play with B-ALL and T-ALL) Lymphoma, thymus, mediastinum, teenager (T-ALL teenagers), lymphoid, MALT, spleen, lymph nodes Peripheral blood, rapidly, pleural effusion, white blood cells, large cells with large nuclei with clear nucleoli, blood, marrow, sheets or follicle like appearance

Question 254

What marker tells you T-ALL is a lymphoblast? What markers tell you it’s a T cell? Mutations in what can be seen?

Answer 254

TdT (tells you it’s a lymphoblast), CD2, CD3, Cd5, CD7, CD4 or CD8 (if it’s late enough), NOTCH 1

Question 255

Mature T cell neoplasms are more common where? Not common where? These are very what? These may also have a predilection for what? These also have what property? What does this mean? What tells you that something is probably an NK cell?

Answer 255

Asia / Africa, not the US, aggressive, the skin, aberrant T phenotype, they don’t have all of the markers of their associated primary cell CD56 / CD57 (North Korea war in 1956/1957)

Question 256

Adult T cell leukemia / lymphoma is what category of T cell neoplasm? What particular virus is implicated? It encodes _____ which stimulates ______. This causes uncontrolled what? What three regions are associated with this virus? Both ____ and ______ may get the virus, but when do they develop it? Has a predilection to what organ? This has what unique PBS cells? Why are they called this?

Answer 256

Mature T cell neoplasm, HTLv-1 (human T cell leukemia virus type 1), TAX, nuclear factor kappa-B, cell growth, Japan / Caribbean / West Africa (two islands and Africa), children, adults, adulthood, skin, flower cells (clover leaf cells), nuclei look like flowers

Question 257

What mature T cell lymphoplasm very often has a skin rash? What appears on the skin? These tumor cells are given what term, why? Diagnosis is made with what, but not what else? These tumor cells like to stay where in the skin? Where do they move? What unique nuclei do they have? Why is it called this? These cells fuse to form what unique structure? What syndrome describes the leukemia type counterpart to this lymphoma type disease? This means cells are located where? Also causes what else? What else is super characteristic? What does it mean?

Answer 257

Mycosis fungoides, patches, epidermotrophic, like the skin, skin biopsy, not thymus / marrow / lymph node biopsy Junction of dermis and epidermis, migrate upwards into the epidermis, cerebriform nuclei, looks like a brain, pautrier’s microabscess Sezary syndrome, peripheral blood, generalized lymphadenopathy, erythroderma, red scaly rash all over body

Question 258

What type of mature T cell neoplasm occurs in children and young adults? What extremely characteristic protein is found in these tumors? This is due to what translocation? They may have lymphomas in the ____ tissues and in the _____. What other extremely diagnostic CD? What very unique type of cell appears? With what unique characteristic? What is their prognosis?

Answer 258

Anaplastic large cell lymphoma, ALK protein, t(2;5) (shot 25 ALKs), soft, skin, CD30 Hallmark cells, horseshoe nuclei (Ana’s hallmark horse shoe card), up to 80% cure with therapy (hallmark from the 1980s)

Question 259

Extranodal NK / T cell lymphoma presents as a destructive what? Obstructs what? Tumor invades what? Creates a lot of what? It is very what? It does not respond to what? What can effectively treat it?

Answer 259

Nasal mass, nasal passageway, small blood vessels, necrotic tissue, aggressive (it NK naturally kills your nose) Chemotherapy, radiation

Question 260

T cell granular lymphocytic leukemia has a mutation in what? And these patients have non-reactive _______, which means a high what? What virus may give you lymphocytosis on its own? This infections can give you a type of ______ lymphocytosis. How can you differentiate between T cell granular lymphocytic leukemia and regular reactive lymphocytosis? These patients have enlarged what? And lack what two blood cells? These cells have an enlarged ____ with lots of what in the cytoplasm? This may have _____ triad. What three things?

Answer 260

STAT-3, lymphocytosis (granular because of all the new WBCs), WBC count, EBV, reactive, more than 6 months Spleen (grains filling your spleen), RBC (anemia), neutrophils (neutropenia), nucleus, granules Felty’s triad (felty’s gRANS), Rheumatoid arthritis / neutropenia / splenomegaly

Question 261

What is the waste basket of classifying mature T cell lymphomas? Why? Thus this makes up what? These patients often have _________ of some sort, and what triad of symptoms? What are they?

Answer 261

Peripheral T cell lymphoma, you categorize unidentifiable T cell lymphomas as this, the majority of T cell lymphomas, lymphadenopathy, B symptoms (which is a triad), drenching night sweats / fever / weight loss

Question 262

What factors change breast structure? The breast is full of many what? What kind of ducts breach the surface? What wider area also holds milk? What is the deeper duct called before it ends inside the breast? It gives rise to what? The lobules are filled with _____ which are also called ______. What term describes the stroma within a lobule? What describes the stroma between a lobule? What unit is made of the terminal duct and lobule? What is secreted here? What disease can start here?

Answer 262

Sex, age, menstrual cycle phase, pregnancy, menopause Ducts, lactiferous duct, lactiferous sinus, terminal duct, lobules, acini / ductules Introbular, interlobular, terminal duct lobular unit (TDLU), milk, breast cancer

Question 263

All breast ducts are lined by what two cells? What surrounds the myoepithelial cells? Invasive carcinoma will lead to the destruction and loss of what two things? What cell causes breast carcinoma? What two types of breast cancer? Which one is most common? Invasive / ______ ductal carcinoma will break through what two things? This staining will not reveal a single what? DCIS stand for what? This means it has not done what? And some retained what? This DCIS means the cancer is not what? What may occur in the center of the lobule of DCIS?

Answer 263

Inner epithelial cells, myoepithelial cells, basement membrane, myoepithelial cells and basement membrane Inner epithelial cell, invasive ductal carcinoma, invasive lobular carcinoma, invasive ductal carcinoma (ducks are common), infiltrative, basement membrane and myoepithelial cell, myoepithelial cells Ductal carcinoma in situ, breached the basement membrane, myoepithelial cells, invasive, necrosis

Question 264

Colon has what shape? The wall has the _____, the _______ mucosa, the _______, and then the _________. There are no what in the colon? The submucosa is full of what cells, and what structures? What do we call colon epithelial cells? Where are their nuclei? Cancer doesn’t have this nice what? There are also some ____ cells secreting mucous. What lines outside of the muscularis propria? Made of what cells?

Answer 264

Tube, mucosa, muscularis, submucosa, muscularis propria Villi, adipocytes, blood vessels and lymph vessels, colonocytes, basal surface, polarity, goblet, serosa, mesothelial cells

Question 265

Colonic adenocarcinoma breaks through what and enters what? The glands do what? The cells lack what characteristic? What lets you rank how invasive the tumor is? What often limits what chemotherapy drugs you can use? You may switch to a different _____ of drugs, not the same _____ of drugs. What is important for multi-drug cocktails? Part of what therapy? Early anti cancer drugs targeted what? And they therefore affected what parts of your body? Or they damaged what molecule? This also harmed what unintentionally?

Answer 265

Muscularis mucosa, submucosa, fuse together, polarity, the deeper the tumor goes Adverse effects, class, class Drug-drug interactions, chemotherapy, rapidly dividing cells, skin, hair, DNA, your own cells

Question 266

Modern chemotherapeutic drugs target specific what? Or are antibodies against what? Name the four categories of non-specific cytotoxic agents? Name three sub components of the natural products class? What kind of drugs act in S phase? Name two. Name two self-limiting s phase specific drugs? Why are these self-limiting?

Answer 266

Specific pathways unique to the transformed cell, tumor antigens Alkykating agents, antimetabolites, natural products, non-categorized Microtubule inhibitors, topoisonerase inhibitors, RNA polymerase inhibitors Nucleotide analogues, cysteine arabinoside, hydroxyurea (cysteine and hydroxy sound like parts of DNA) 6-mercaptopurine, methotrexate, they decrease the product pool needed to make DNA (merchants on meth lost the shipment of nucleotides)

Question 267

M-phase specific drugs may mess up what? Name a few? A bunch of drugs then are not _____ and just mess up what overall? What mnemonic for them? Name a few? What specific drug blocks purine synthesis? Other drugs may block _____ synthesis. What two drugs block the conversion of these ribonucleotides to deoxyribonueotides? A bunch of drugs may block the synthesis of what? Once DNA is made, drugs can inhibit what enzyme necessary for replication?

Answer 267

Microtubules, vincristine / vinblastine / paclitaxel (axel shaped like microtubule) Specific, cell cycle, NAPCAD (nitrosoureas, alkykating drugs, procarbazine, cisplatin, anti tumor antibiotics, diacarbazine) 6-mercaptopurine, pyrimidine, 5-fluorouracil / hydroxyurea DNA, topoisomerases

Question 268

Various drugs may form ____ with DNA to indicate that it is defective. If DNA is made and RNA gets through, what drug depleted the asparagine pool? If proteins are made, what can target them? You may then try to block _______ to prevent cell division. Or drugs may trick the cell into entering what state?

Answer 268

Adducts L-asparaginase, antibodies Microtubules, terminally differentiated state

Question 269

Alkylating agents do what? What are the three major categories? What is the core molecule in all alkylating agents? The chlorine creates an ______ region that attacks its own ______ atom, creating an unstable _____ ring. This desperately attacks what on a purine? Does it only attack this? Why? The cell will do what if it has damaged DNA? Nitrogen mustards do what? This is very hard to what?

Answer 269

Modify DNA so that cell thinks it is damaged, nitrogen mustards / nitrosoureas / platinum coordination complexes Chlorethamine, electropositive, nitrogen, tricyclic, nitrogen 7, no, because it is highly unstable, apoptosis Cross link nitrogenous bases (mustard sticking stuff together), fix,

Question 270

What type of nitrogen mustard is safer? It is a _____ chloroethamine, which is less toxic than the ________ chloroethamines. For instance, cyclophosphamide is first activated by ______ in the ______, creating a product that rapidly interconverts with what other molecule? The aldophosphomide releases what therapeutic compound? What enzyme lessens the toxicity of aldophosphamide in normal cells? By doing what? They can also couple what molecule to detoxify phosphoramide mustards?

Answer 270

Cyclophosphamide, cyclic, non-cyclic, cytochrome P450, liver, aldophosphamide (Aldo the Apache interconverts with mustard), phosphoramide mustard Because normal cells have aldehyde dehydrogenase which converts aldophosphamide to inactive carboxyphosphamide, glutathione

Question 271

However, one of the cyclophosphamide (safer nitrogen mustard) breakdown products is what? Which concentrates where? It causes hemorrhage where? So what drug can we give to counteract acrolein toxicity? Thus what drug reduces the bladder toxicity of cyclophosphamide nitrogen mustards?

Answer 271

Acrolein, bladder, bladder, MESNA (takes a genius to save your bladder from the mustard), MESNA

Question 272

Name a newer type of nitrogen mustard? It has been stuck on what? Why do we use it? Its _________ is sufficient unique that even if you are resistant to other _______, you won’t be resistant to this. This therefore has significant effect against what leukemia, which resists standard ______ agents.

Answer 272

Bendamustine (new because new phones bend), a purine, lower cross resistance with other alkykating agents (iphone signals have lower overlap) Structure, nitrogen mustards, chronic lymphocytic leukemia, alkykating

Question 273

Nitrosoureas are also a type of what? What is the most important aspect of these? Thus they treat what? Name two of these drugs? Resistance may decrease what, increase the amount of what chemical, or increase what pathways? For instance, more of what enzyme can fix methylguanosine?

Answer 273

Alkykating agents, they cross the BBB (ureas can cross), brain cancer, carmustine / lomustine (must alkylate the DNA) Drug entry into cell, glutathione, DNA repair pathways, MGMT (methylguanosine-DNA methyltransferase)

Question 274

What other compounds are alkykating agents? Name three of them. These form what bonds with DNA? They also cross link what with DNA? In general, alkykating agents target what kinds of normal cells? In what kinds of tissues? Thus they suppress what, cause what, and make you lose your what? Why do they cause nausea and emesis? Why do these cause other cancers? What type of injury occurs when the drug leaks out of a vein?

Answer 274

Platinum coordination complexes, cisplatin / carboplatin / oxaplatin, covalent, proteins Rapidly dividing, intestine / bone marrow / hair follicle, immune system, anemia, hair They irritate the intestinal mucosa, because they modify DNA, extravasation injury,

Question 275

Name two categories of antimetabolites? They affect what phase? What process must move them into a cell? They must be activated where? They inhibit target what? Folate analogs have _____ higher affinity for folate related enzymes, thus they act as what inhibitors? Name the most common anti folate drug? What process generally activates them?

Answer 275

Folic acid analogs, pyrimidine and purine analogs, S phase, active transport, inside of the cell, enzymes 1,000 times, competitive inhibitors, methotrexate, polyglutamination

Question 276

Their first mechanism of folate analogs may inhibit what enzyme? Thus preventing conversion of what to what? Thus depleting TMP used to synthesize what? Methotrexate may also inhibit what enzyme that replenishes tetrahydrofolate? The second mechanism blocks production of what precursor to adenosine and guanosine?

Answer 276

Thymidylate synthase, deoxyuridine monophosphate to thymidinemonophosphate, DNA, dihydrofolate reductase (replenishes tetrahydrofolate before making methyltetrahydrofolate) Inosine monophosphate

Question 277

What carrier brings folate analogs into the cell? Once in the cell, what happens to activate it? What is the main mechanism of antifolate (methotrexate) resistance? Or what can be downregulated? Or you can prevent the _______ of the antifolate drugs. Or what enzyme is altered to have reduced antifolate binding affinity? Or how do you overwhelm the antifolate that is present? By ______ amplification or increased ______ of a given gene.

Answer 277

Reduced folate carrier (RFC), polyglutamination, ABC transporters, reduced folate carrier (RFC), polyglutamination, dihydrofolate reductase, upregulate dihydrofolate reductase, gene, transcription

Question 278

What two analogs may be incorporated into DNA? Via what pathway? What targets them? Name one?

Answer 278

Purine and pyrimidine analogs, salvage pathway, DNA repair enzymes, 5-fluorouracil

Question 279

The prostate does what specific function? It also causes what action? Thus what two components must it have? What part of the urethra passes through the prostate? What pair of vesicles and ducts join the urethra? What are the three prostatic zones? Which zone is the peri urethral zone? What condition can occlude the urethra? What zone makes up the bulk of the prostate? What zone surrounds the ejaculatory ducts?

Answer 279

Adds nutritious secretions to the sperm, ejaculation, glandular component, fibromuscular stroma (for ejaculation) Prostatic urethra, seminal vesicles, ejaculatory ducts, central zone, transition zone, peripheral zone, transitional zone (like how transitional epithelium in the bladder), benign prostatic hyperplasia (BPH), peripheral zone, central zone

Question 280

Prostatic glands are very what in shape? Whereas cancer makes the glands look what? How many cell layers are there? What layer faces the lumen? What cell is on the outside? What wraps around the basal layer? Cancer has how many cell layers? What is it? Basal cdll staining will reveal what? How big are the cancer cells? They also have very prominent what? If you see some glands with basal cell staining and others without it, what can you infer?

Answer 280

Irregular, much more like simple tubes, two, secretory cell, basal cell, basement membrane (basal for basement) One, secretory cell (of course the secretory cell becomes cancer because it is so active), no basal cells at all, much bigger, nucleoli (dark dot in the center), some of the glands are cancerous

Question 281

Name a purine analog? Name a thymine analog? This gets incorporated into ______ and ______. Modified RNA may not be what? Modified DNA may do what? Triggers the cdll to do what? 5-FU may also inhibit what enzyme? Thus ____ cannot get converted into what? So it also depleted the pool of what? What additional substance enhances 5-FU inhibition of thymidylate synthase? 5-FU causes what neurological side effect? What enzyme metabolizes 5-FU? DPD deficiency is dangerous how?

Answer 281

6-mercaptopurine, 5-fluorouracil (fluorine looks like a methyl), RNA, DNA, translated, break apart, apoptosis Thymidylate synthase, dUMP, dTMP, dTMP, folinic acid, ’chemo-brain’, DPD (dihydropyrimidine dehydrogenase), 5-FU overdose is much easier

Question 282

What is the most common cause of lymph node enlargement? Called what? What leads you to suspect infection? What leads you to suspect lymphoma? Name some benign diseases that can cause single node enlargement? Name some benign diseases that can cause generalized painful lymphadenopathy? What neoplastic diseases can cause generalized painless lymphadenopathy?

Answer 282

Infection, lymphadenitis, under 30 years old / bilateral / red / painful Long course / painless / no recent infection / unilateral Rheumatoid arthritis / toxoplasmosis / early HIV / cat scratch disease (Bartonella henslae), tularemia, plague SLE / infectious mononucleosis / HIV Leukemia / follicular B cell lymphoma

Question 283

What neoplasticism disease can cause single lymph node adenopathy? Name two differentials for “nodular pattern with large germinal centers”? Describe the presentation of reactive follicular hyperplasia? Describe presentation of follicular lymphoma? What is the progression of follicular lymphoma? 50% can become what?

Answer 283

Metastatic carcinoma / lymphoma that hasn’t spread yet Follicular hyperplasia and follicular lymphoma Painful / enlarged / red / acute Widespread lymphadenopathy / slower course Incurable / slow / waxing waning course / 7-9 year survival, large B cell lymphoma

Question 284

What kind of CBC does follicular lymphoma often have? What unique marker tells you something is a follicular lymphoma? Due to what translocation? BCL2 is not expressed on normal _____ center B cells or in benign _________. Which translocation is most often seen with follicular lymphoma? Leads to over expression of what? Which prevents what? What two cells can cause follicular lymphoma? It is a _______ center B cell. Name the follicular lymphoma immunophenotype?

Answer 284

Normal / no anemia / no leukopenia / no thrombocytopenia BCL2 (B cell lymphoma), t(14;18), follicular, follicular hyperplasia T(14;18), BCL2, apoptosis Centroblast / centrocyte, germinal (hence it germinates the follicle), CD19 / CD20 (because it’s a B cell)/ CD10 / BCL6 (germinal center)/ BCL2

Question 285

In benign follicular hyperplasia, the germinal centers are _____ and have ______ cells. Follicular lymphoma lacks ______ body macrophages and loses what characteristic. What lymphoma can involve the abdominal viscera? Advanced stages may cause what types of symptoms? What two kinds of lymphomas can aggressively involve the viscera? Name three clinical variants of Burkitt lymphoma?

Answer 285

Polarized, tingible Tingible, polarization Burkitt lymphoma, B symptoms Burkitt lymphoma / DLBCL (diffuse large B cell lymphoma) Endemic / sporadic / immunodeficiency

Question 286

Which type of Burkitt lymphoma has mandible lesions? What type involves the peritoneum and ileocecum? Name 3 B symptoms? Why are they important? What markers will be positive for Burkitt lymphoma? Is BCL2 expressed? What gene and translocation is needed for definitive diagnosis of Burkitt lymphoma? What three translocations are associated with Burkitt lymphoma? What virus infects Burkitt lymphoma cells?

Answer 286

Endemic, sporadic, fever / weight loss / drenching sweats, affect the staging of the cancer Surface IgM / CD19 / CD20 (because it’s a B cell)/ CD10 / BCL6 (germinal center), no MYC, t(8:14) 8 looks like a B T(8;14), t(2;8), t(8,22), EBV

Question 287

What two cells can cause Burkitt lymphoma? It is a __________ B cell. What other cancer can these cells also cause? Which cancer is the fastest growing human tumor? What can they release when they die? What syndrome does this cause? Prevent by adding agents that bind to what? Burkitt lymphoma has what characteristic pattern? What are these clear cells and what are they doing? What proliferation marker do you expect to see?

Answer 287

Centroblast/ centrocyte, germinal center, follicular lymphoma Burkitt lymphoma, potassium / phosphorous / uric acid, tumor lysis syndrome Uric acid Starry sky pattern (tumor expands like the universe), benign macrophages, eating dead tumor debris, Ki67

Question 288

Name four aspects of Hodgkin lymphoma? Name four aspects of Non-Hodgkin lymphoma? What is recommended for getting tissue if you suspect lymphoma? Why? What are the two types of nodular lymphoma? What are the four subtypes of classical Hodgkin lymphoma?

Answer 288

Localized to single node groups / orderly spread by contiguity / mesenteric nodes rarely involves / extranodal presentation rate Often involves many nodes / non-contiguous spread / mesenteric nodes often involved / extranodal presentation common Remove the entire lymph node, look at architecture and get enough tissue Classical predominant and nodular lymphocyte predominant Modular sclerosis / mixed cellularity / lymphocyte rich / lymphocyte depleted

Question 289

What is the cell of origin for Hodgkin lymphoma? It is a _______ center B cell. What transcription factor is activated in classical Hodgkin lymphoma? Multiple myeloma causes what pain? Lesions in the what? Hyper what? What blood issue? What makes you suspect leukemia instead of lymphoma? What cancer increases Auer rods? Acute promyelocytic leukemia can cause what severe complication? What chemical can avoid this?

Answer 289

Centroblast, germinal NF-kB Bone pain, bone, hypercalcemia, aplastic anemia Absence of lymph node growth, acute myeloid leukemia DIC, all trans retinoic acid

Question 290

CML has what unique chromosome? Due to what translocation? 6 Mercaptopurine is made how? One mechanism creates what molecule to inhibit what process? The second mechanism creates what other molecule? These get incorporated into what? Leading to what process? Do you directly administer 6-MP? What precursor do you give? 6-MP is very toxic to what?

Answer 290

Philadelphia chromosome, t(9;22) Adenine with a sulfur added to it, 6-thioguanosine monophosphate, de novo purine synthesis 6-thioguanosine triphosphate, DNA and RNA, apoptosis No, azathioprine, liver,

Question 291

6-MP can be metabolized by ________, which creates what very hepatotoxic molecule? What other enzyme breaks down 6-MP in a different pathway? This is not toxic to what? But what gout medicine inhibits XO? Thus all of the 6-MP must be converted into what? Thus damaging what organ? So you cannot take 6-MP with what drug? What is the mnemonic for the 6 natural anti cancer compounds?

Answer 291

TPMT (thiopurine-S-methyltransferase), 6-Methylmercaptopurine Xanthine oxidase, liver, allopurinol, 6-methylmercaptopurine, liver, allopurinol VECATE (vinca alkaloids / epothilones / camotothecin derivatives / antibiotics / taxanes / epipodophylotoxins)

Question 292

Where can you isolate vinca alkaloids? Name two of them? These act in what phase? Are effective against a broad range of what? They bind what subunit? They inhibit what process? But what process still works? Thus cells arrest in what phase? You can have what type of vinca alkaloids resistance? This resistance mediated by what thing?

Answer 292

Madagascar periwinkle, vinblastine / vincristine, M phase, cancers, beta tubulin, polymerization of microtubules, depolymerization, M phase Cross-resistance, p-glycoprotein,

Question 293

Where can you isolate taxanes? Name two? How are these different than vinca alkaloids? You get very long what? These arrest the cell when? What kind of adverse effects can they have? Why? What class of drug, and specific name, initiate uncontrolled microtubule synthesis? This also arrests in what phase? Thus all drugs affecting microtubules arrest in what phase?

Answer 293

Yew tree, paclitaxel / docetaxel (has tax in it), block microtubule disassembly, microtubules, M phase, neuropathy (taxes get on my nerves), neurons require long microtubules for transport Epothilones (ixabepilone), M phase, M phase

Question 294

What class inhibits topoisomerase I? Name two? Normally, topoisomerase I induces a what? This prevents what? But irinotecan and topotecan do what? Leaving a _____ strand. Then what comes through and cleaves the remaining strand? Thus making the cell do what? Topotecan is used for what cancers? Why is it limited? Irinotecan is used for what cancer?

Answer 294

Camptothecin derivatives, irinotecan, topotecan (Tecans and their top hats) Single strand nick, supercoiling, prevents topoisomerases from religating the strands, nicked, replication fork, apoptosis Ovarian cancer, small cell lung cancers, hematotoxicity (blood toxicity) (To for two cancers and toxic) Colorectal cancer

Question 295

Name the three anti-cancer antibiotics classes? Anthracyclines affect what enzyme? Thus what break forms? Making cells do what? They have what unique side effect? And also what? What two types? What mortality rate for chronic CHF due to anthracyclines?

Answer 295

Dactinomycin / anthracyclines / bleomycin (DAB) Topoisomerase II, double strand, apoptosis, myelosuppression, cardiomyopathy, acute / chronic, 50%

Question 296

Epipodophylotoxins come from what plant? Name them both? These also inhibit what? Dactinomycin is what agent? Binds to what grooves? Thus blocking what enzyme? What else is a DNA intercalator? Once in, it generates what? This directly what? What enzyme metabolizes this? What two tissues is it very uncommon in? 10% of patients can have _____ toxicity. What will you see on an X Ray? Also causes what in the skin?

Answer 296

Mandrake plant, etoposide / teniposide, topoisomerase II Intercalating agent, minor grooves (like a dactyl binding), RNA polymerase Bleomycin, free radicals, breaks DNA, bleomycin hydrolase, skin and lungs, lung, pulmonary infiltrates (bleo-ding into lungs), hyperpigmentation

Question 297

What enzyme makes asparagine in some cells? What drug cleaves asparagine? Most cells make sufficient what? But what cells lack lots of asparagine synthetase? These cells must take asparagine from the what? What drug digests asparagine in the serum? It therefore fights what cancer?

Answer 297

Asparagine synthetase, L-asparaginase, asparagine, lymphocytes, serum, L-asparaginase Acute lymohocytic leukemia

Question 298

Hydroxyurea inhibits what enzyme? This normally turns ______ to _______. Thus hydroxyurea affects what phase by preventing what? What is hydroxyurea synergistic with? Why? It is also synergistic with anything that _____ DNA. Why? Why are glucocorticoids useful in chemotherapy? Thus suppressing what? So they are used for what two kinds of cancers?

Answer 298

Ribonucleotide reductase, ribonucleotides to deoxyribonueotides, S phase, DNA synthesis Irradiation, cells are most radiation sensitive at S phase, damages, fewer deoxynucleotides around to repair the DNA Induces apoptosis of lymphocyte, immune system, leukemia and lymphomas

Question 299

Many cancers are due to incomplete what? Such as what cancer? Due to mutation in what receptor? So what can you administer that will force terminal differentiation of promyelocytes? What do you give to patients who become resistant to ATRA? This also differentiates what cells? What kind of drug will recognize a single epitope?

Answer 299

Differentiation, acute promyelocytic leukemia, retinoic acid receptor (doesn’t differentiate because it is a PRO-myelocyte), all-trans retinoic acid (ATRA) Arsenic trioxide, promyelocytes Monoclonal antibody,

Question 300

Cancer cells have a higher what ratio? And what shape? What general size? A cancer cell may have abnormal what figures? What classification system is used most often for breast cancer? What classification system is used most often for prostatic adenocarcinoma? As it gets worse, what visually occurs in the prostate?

Answer 300

N/C ratio, abnormal shape, larger, abnormal mitotic figures Nottingham histologic grading Gleason grading score, tubules fuse together

Question 301

What is the primary staging criterion for the breast? What about the colon? What about prostate? How long does a biopsy often take? But it may take how long? What means they ask someone to check for cancer on borders of a cut during surgery? So how do you quickly make the tissue so you can see it? Why is this visually limited?

Answer 301

Size of tumor Involvement of more wall layers Whether or not it’s confined to just the prostate 2 days, week Intraoperative consultation, freeze it, freezing it adds lots of artifacts

Question 302

What does TNM staging stand for? Tumor may be what staging? Node depends upon what? What means no node involvement? What can metastasis be staged as? What means no metastasis? The staging is different for different what? Name the four components of the breast panel? What color on FISH indicates overamplification?

Answer 302

Tumor / node / metastasis, 1-4, number of nodes, 0, M1-M2, M0 Organs Estrogen receptor / progesterone receptor / ki-67 / HER2 Red

Question 303

What sex has higher colon cancer? Incidence rates have done what? Colon cancer has what symptoms most often? Many patients present with what stage, despite what? What cancer is diagnosed and treated independently of colon cancer? What can reduce incidence and mortality? What procedure? Who do you refer to if you suspect anal cancer? The presence of what differentiates an anal cancer from a colon cancer? Why? How do you completely treat anal cancer? Do you need surgery?

Answer 303

Decreasing, none, early, lack of symptoms Rectal cancer, screening, colonoscopy Colorectal surgeon, keratin pearl, because the anus is keratinized squamous versus glandular (in the colon), completely cure with chemotherapy and radiation, no

Question 304

What do you do if you want a diagnosis of cancer? But what if you already have a diagnosis? Name an important test for colon cancer? Name a congenital colon cancer predisposition syndrome? If untreated, how many get colon cancer? What do you treat it with? This condition is due to a mutation in what gene?

Answer 304

Refer to a specialist, CT scan (to get staging) MSI (microsatellite status) Familial adenomatous polyposis (FAP), 100%, total proctocolectomy, APC gene

Question 305

Who has the highest incidence of prostate cancer? Why? Name some risk factors for prostate cancer? What is the precursor to prostate cancer? It’s incidence begins to rise in what age group? What chromosome has many risk factors for prostate cancer? Increasing estrogen increases risk for what? Increasing testosterone increases what? Most prostate cancer is picked up through what screening?

Answer 305

African Americans, African American men have higher testosterone levels Age / male / African America PIN (prostatic intraepithelial neoplasia), young people Chromosome 1 (you have one prostate), breast cancer, prostate cancer, PSA screening

Question 306

What are the two most common sites of prostate cancer metastasis? Thus affected patients live for how long? But it causes pain where? What three things help you determine low or high risk prostate cancer?

Answer 306

Bone / lymph nodes, a long time, bone PSA / Gleason score / clinical stage

Question 307

Neoplasia means what? Triggered by a series of what? What is desmoplasia? Dysplasia means what? These cells may have some _____ morphological features. But they may not be ______ nonetheless. What type of cancer means the basement membrane is intact? What means replacing one epithelium with another one?

Answer 307

New growth, mutations, dense connective tissue seen with tumors (fancy name for fibrosis made by tumor cells) Disordered growth (Dysordered), malignant, malignant Invasive carcinoma in situ Metaplasia (not the same as dysplasia)

Question 308

What types of cancers come from blood? What type of cancer comes from mesenchymal cell? What type of specific cancer mimics other types? Carcinoma originates from what cell type?

Answer 308

Leukemia / lymphoma Sarcoma Melanoma (mimics) Epithelium

Question 309

What is a partial mastectomy called?

Answer 309

Lumpectomy,