Pathology II Block 1



Q: What are myeloid cells?
A: Precursor cells of erythroid, granulocytic and thrombocytic series.

Q: Why is it called white cell?
A: Because it forms the white “buffy coat” when you spin it down. Platelets are also in the buffy coat.

Q: Which ones are the granulocytes?
A: neutrophils, eosinophils and basophils (BEN). But of course there are other cells like lymphocytes that have granules but are NOT designated “granulocytes.”

Q: What’ s the current definition of leukemia?
A: Increase immature myeloid/lymphoid precursors in bone marrow and blood. Patients with leukemia would have a larger buffy coat layer than normal.

Q: Compare white blood cells
A: Basophils — largest granules — pick up blue stain a lot — hard to see nucleus
Eosinophils — two lobes
segmented neutrophils — neutral color, three lobes. like monocytes, they can phagocytize.
band neutrophil — nucleus look like band rather than polymorphic
lymphocyte — sometimes see granules, but usually not
monocyte — sometimes see bacteria and other things in cytoplasm.
platelets — have granules.

Q: What are the relationships?
A: Myeloid stem cell –> Eo, Mono, PMN, Platelets, RBC, Baso
Lymphoid stem cell –> B, T, NK

Q: What is Myeloid: Erythroid ratio?
A: Ratio of white blood cells to red blood cells, although the term is a misnomer becuase erythrocytes derive from myeloid lineage.

Q: What is the most common white blood cell in the marrow?
A: Band neutrophils –> Lymphocytes

Q: What’s the most common white blood cell in the blood?
A: Segmented Neutrophils (vs. band neutrophils) –> lymphocytes –> monocyte

Q: What’s the least common white cell in the blood?
A: Basophil

Q: What does a “left shift” mean?
A: It’s when there’s a shift to more immature cells in blood.

Q: What causes “left shift”?

Q: What is hypersegmentation?
A: neutrophils with 5, 6, 7 lobes etc. or leukocytes that have 3, 4 lobes.

Q: What causes hypersegmentation?
A: Due to folate, B12 deficiencies, but also see it with infections (but doesn’t cause as many lobes)

Q: What is toxic granulation?
A: increased number of granules.

Q: What turns on toxic granulation?
A: INFECTIONS, so more granules can fight the infection.

Q: What do you see in toxic granulation?
A: Döhle bodies — which is overactivated endoplasmic reticulum. You see purple granules as well.

Q: Is percentage of white cell important?
A: no. what’s important is ABSOLUTE COUNT of white cell, not percentage!!

Q: What is the lifespan of WBCs in the blood?
A: neutrophils — 1-48 hrs
B cells — hours/days
T cells — days/years
Eosinophils — 1-48 hrs

Q: Bacterial infections cause what?
A: neutrophilia (neutrophilic leukocytosis)

Q: Viral infections cause what?
A: lymphocytosis (increase in lymphocytes vs. lymphocytopenia, which is a decrease)

Q: Allergies cause what?
A: eosinophilia

Q: Chronic infections cause what?
A: monocytosis

Q: What are the pools you can detect?
A: Precursor pool — progenitor and precursor cells in BONE MARROW
Storage pool — immature (band) and mature cells in BONE MARROW
Marginating pool — movement of cells out of the circulatory system in PERIPHERAL BLOOD
Circulating pool — in PERIPHERAL BLOOD
Tissue pool — in TISSUE

Q: If you have an infection what happens?
A: white cells leave storage pool, enter peripheral pool, then eventually tissue pool.

Q: How does exercise and epinephrine cause leukocytosis?
A: It decreases margination

Q: How does endotoxemia, acute infection, and hypoxia cause leukocytosis?
A: release from marrow is increased — left shift

Q: How does chronic infection, tumor, and myeloproliferation (bone-marrow proliferation like Chronic Myelognous Leukemia CML) cause leukocytosis?
A: increased marrow precursors

Q: Why do patients taking glucocorticoids (like cortisone) have difficulty fighting infections?
A: white cell don’t go to tissue, so accumulate in blood.


Q: What is it called when you have a transient (vs. due to malignancy) increase in WBC or immature precursors of WBCs?
A: Leukemoid reaction

Q: What can you measure to differentiate between leukemoid reaction and CML (which has similar presentation)?
A: In leukemoid reaction, the leukocyte alkaline phosphatase score is elevated, whereas in CML, the count is low.

Q: What’s the most common cause of acquired neutropenia?
A: Infection (transient leukemia)

Q: Most common cause of clinically significant neutropenia?
A: Drugs

Q: What is agranulocytosis?
A: severe neutropenia

Q: Relative vs. Absolute Eosinophilia?
A: Relative = if more than 3% of your blood is eosinophils
Absolute = if you have more than 0.7 x 10^9/L of eosinophils

Q: What eosinophil counts are mild, moderate, and marked eosinophilia?
Mild Eosinophilia = 0.35 – 0.9 x 10^9/L
Moderate Eosinophilia = 1 – 5 x 10^9/L
Marked Eosinophilia = >5 x 10^9/L

Q: Most common cause of Eosinophilia in US?
A: Unknown –> Allergy –> Asthma

Q: Most common cause of Eosinophilia in Singapore?
A: Helminthiasis –> Allergy

Q: Which immune cell antigens are primary associated with T-cells?
A: CD1,3,4,5,8

Q: Which immune cell antigens are associated with B-cells?
A: CD10,19, 20, 79a (10, 19 are on precursor Bs, and 20 and 79 are added on when they mature)

Q: Which immune cell antigens are associated with monocyte/macrophages?
A: CD11c, 14, 15

Q: Which immune cell antigens are associated with NK cells?
A: CD16, 56

Q: Which immune cell antigen is present on ALL leukocytes?
A: CD45 aka Leukocyte Common Antigen (LCA)

Q: Which immune cell antigen is also expressed by Reed-Sternberg cells and some Hodgkin lymphomas
A: CD15

Q: Which immune cell antigen do EBV bind to?
A: CD21

Q: What are the reference values of total lymphocytes for people of different ages?
Ages 6-11 = 1.5 – 6.5 x 10^9/L
Ages 12-15 = 1.2 – 5.2 x 10^9/L
Adults = 0.9 – 2.9 x 10^9/L

Q: What’s the normal ratio of CD4 to CD8?
A: 1:1 to 4:1 — so either same or more CD4.

Q: What is the normal ratio of Kappa to Lambda B cells?
A: 1:1 to 2:1 — so either same or more Kappa.

Q: What is the most common lymphocyte in circulation?
A: T cells

Q: Lymphocytosis vs. Lymphocytopenia?
A: Lymphocytosis = too much lymphocytes
Lymphocytopenia = too little lymphocytes

Q: Lymphocytosis — which diseases cause it?
A: Mono (makes Downey cells)

Q: Lymphocytopenia — which diseases cause it?
A: AIDS, Hodgkin’s Disease, Aplastic anemia, Acute bacterial infection, cancer, SLE, SOMETIMES viral infections.

Q: What are some tests you can do for Mono?
A: Monospot test — good sensitivity. tests for heterophile antibodies (IgM produced by body in response to EBV but doesn’t react to EBV, but instead to something else).
Epstein Barr Virus Antibodies against capsid antigen — use for heterophile negative cases.
Differential Heterophil Absorption test — very specific but less sensi

Some Immune Review:
Q: B cells go to what part of lymph node?
A: Primary Follicle –> Mantle Zone –> Germinal Center (Dark zone –> Light zone) –> Marginal Zone –> Bone Marrow for Plasma Cell, Lymph Node Medulla for Memory B cell
Q: T cells go to what part of lymph node?
A: Paracortex

Q: What is the most mature B cell?
A: Plasma Cells


Q: Lymphadenopathy vs. Lymphadenitis?
A: Lymphadenopathy = enlargment of lymph node (not necessarily due to infection of lymph node). PAINLESS
Lymphadenitis = enlargement of lymph node due to infection of lymph node. Acute is PAINFUL. Chronic is PAINLESS.

Q: What is the most common cause of lymphadenopathy?
A: Viral infection. Other causes include immune response, sarcoidosis, lymphomas, metastasis.

Q: If you find a lymph node that is larger than 4 cm, what is it likely to be?

Q: Most lymphadenopathies are found where?
A: Head and Neck

Q: What causes acute lymphadenitis?
A: bacterial infection

Q: What are the three reactive hyperplasias that happen with chronic nonspecific lymphadenitis?
Follicular Hyperplasia — remember B-cells in primary follicles/germinal centers. B cells and tingible body macrophages (macrophages in the germinal centers) increase. Due to RA, Toxoplasma.
Paracortical Hyperplasia — remember T-cells in paracortex of lymph nodes. T cells increase. due to mono, virus.
Sinus Histiocytosis — hyperplasia of the macrophages lining sinuses of the lymph nodes.

Q: What are tingible body macrophages?
A: they are macrophages in the germianl centers that phagocytize apoptotic cells. They are increased in follicular hyperplasia in chronic lymphadenitis, which remember is PAINLESS.

Q: Cat scratch Disease has what type of granulomas?
A: Self-limited lymphadenitis. First you get sarcoid-like granulomas, then it becomes stellate (start-shaped) necrotizing granulomas.

Q: What are the three classes of neoplastic proliferation of white cells?
A: Lymphoid Neoplasms — proliferation of llymphocytes — Leukemia, lymphoma
Myeloid Neoplasms — proliferation of erythroid, granulocytic, or thrombocytic cells
Histiocytic Neoplasms — proliferation of macrophages

Q: What are the types of lymphoid neoplasms?
A: leukemia, lymphoma

Q: What are the types of myeloid neoplasms?
A: Acute myelogenous leukemias, myelodysplastic syndromes, chronic myeloproliferative neoplasms

Q: What genetic changes cause lymphoid neoplasms vs myeloid neoplasms?
A: Lymphoid neoplasms often have gene rearrangement.
Myeloid neoplasms often have chromosomal translocation.

Q: Which viruses can cause white cell neoplasms?
A: HTLV-1 — cause Adult T-cell leukemia
Epstein-Barr Virus — cause Burkitts Lymphoma, Hodgkins Lymphoma, Mono and Nasopharyngeal carcinoma.
KSHV/HHV-8 (kaposi’s sarcoma-associated herpesvirus) — cause B-cell lymphoma in body cavity (Kaposi Sarcoma)

Q: Which genetic diseases can cause white cell neoplasm?
A: Down Syndrome, Hodgkin Disease

Q: What environmental agents can cause white cell neoplasm?
A: Helicobacter pylori — cause gastric B-cell lymphoma
Insecticides — can cause leukemias
HIV — cause clonal B-cell abnormalities

Q: What are Iatrogenic causes of white cell neoplasms?
A: Radiation Therapy and Chemotherapy

Q: What are the two types of malignant lymphomas?
A: Non-Hodgkin Lymphoma (which is mostly B-cell Lmphoma and some T-cell lymphomas) and Hodgkin’s Lymphoma.

Q: What is associated with activating mutations in NOTCH1?
A: Precursor T-cell leukemia/lymphoma

Q: What is Precursor B-cell/T-cell Neoplasms also known as?
A: Acute Lymphoblastic Leukemia (ALL)

Q: What is the most common type of childhood leukemia?
A: Acute Lymphoblastic Leukemia (ALL). REACTS WELL TO CHEMOTHERAPY.

Q: Who gets ALL?
A: more common in young caucasian males. DOWNS SYNDROME PATIENTS.

Q: What’s the age difference between people who get precursor B-cell vs. T-cell neoplasms (ALL)?
A: B-cell — 4 yrs old — usually present as leukemia (in circulation) with bone marrow involvement (but can occasionally be lymphoma)
T-cells — 15-20 yrs old — usually present as lymphoma (in lymph node) with thymic involvement (but can occasionally be leukemia)

Q: What is the major diagnostic cell you see in T-cell and B-cell precursor neoplasms (ALL)?
A: LYMPHOBLAST (which remember is the precursor to lymphocytes)

Q: What is aleukemic leukemia?
A: It is when you got leukemia but the leukemic cells stay in the bone marrow rather than go into the circulation, resulting in leukemia without a rise in WBCs in the bloodstream. ALL CAN SOMETIMES BE ALEUKEMIC.

Q: What do lymphoblasts (like in ALL) look like?
A: They have fewer nucleoli, more condensed chromatin than myeloblasts. There are NO CYTOPLASMIC GRANULES!

Q: What is TdT?
A: terminal deoxynucleotidyltransferase. Remember it is involved in adding N-nucleotides to VDJ exons during antibody recombination. Therefore it is found ONLY in precursor B and T cells (like in ALL)

Q: Precursor B-cells (i.e. in lymphoblastic leukemia) have what type of immune cell antigens?
A: CD19, CD20 and CD10 (CALLA+)

Q: Precursor T-cells (i.e. in lymphoblastic lymphoma) arrested at an EARLY stage have what immune cell antigens?
A: CD1,2,5,7

Q: Precursor T-cells arrested at a LATE stage have what immune cell antigens?
A: CD1,2,5,7 PLUS CD 3,4,8

Q: What is the most common chromosomal structural changes in leukemic cells?
A: HYPERDIPLOIDY (having more than the usual set of diploid chromosomes) (better prognosis) and some have PHILADELPHIA CHROMOSOME (worse prognosis)

Q: What are the clinical features of Precursor B-cell/T-cell neoplasms (ALL)?
A: Abrupt onset, Fatigue (due to anemia), Infection/Fever (due to neutropenia), Bleeding (due to thrombocytopenia), lymphadenopathy, bone pain, hepatosplenomegaly, CNS and Testicular involvement.

Q: Most patients with ALL are cured, but what are some factors that may increase chance of bad prognosis?
A: If you get ALL before 2 yrs old.
If it presents in adolescence or adulthood.
If you have a peripheral blast count of more than 100,000.
If you have Philadelphia chromosome t(9:22) or rearrangement of MLL (mixed lineage leukemia) gene.
If you have Down’s Syndrome.

Q: What is Packed Marrow Acute Lymphoblastic Leukemia?
A: When the marrow between bone trabeculae is completely filled with leukemic cells rather than the normal hematopoietic cells. Because of this you get infections (because granulocytes can’t form), hemorrhage (because platelets can’t form), and anemia (because RBCs can’t form).

Q: What is peripheral blood?
A: Blood that is flowing through the circulatory system (vs. blood in the bone marrow, liver, and other organs).



Q: What types of peripheral B-cell neoplasms are there?
Chronic Lymphocytic Leukemia (CLL)/Small Lymphocytic Lymphoma
Follicular Lymphoma
Diffuse Large B-cell Lymphoma
Burkitt Lymphoma
Plasma Cell Neoplasms (Myeloma)
Lymphoplasmacytic Lymphoma
Mantle Cell Lymphoma
Marginal zone Lymphoma
Hairy Cell Lymphoma

Q: What’s the difference between CLL and SLL?
A: They are both the same malignant cell, but if
in blood (causing leukemia), then it is CLL. If it enlarges the lymph node, then it is SLL. If over 4000 cells/mL, then called CLL.


Q: What is the most common leukemia in the western world?
A: CLL — Chronic Lymphocytic Leukemia

Q: What do you see occasionally in the lymph node in SLL?
A: You mostly see small lymphocytes (6-12 microns) but occasionally you see Prolymphocytes, which are a larger. The more prolymphocytes, the worse prognosis. They all have turtle shell appearance.

Q: What makes the leukocyte count of CLL stand out?
A: If you do a leukocyte on a CLL patient, 75-95% of the WBCs are lymphocytes (B or T cells, vs. other leukocytes).

Q: What is a Proliferation Center?
A: When you got a group of prominent and mitotically active prolymphocytes.

Q: What do the nodes often look like in SLL/CLL?
A: You see diffuse effacement of the node — basically the follicles are all gone, and you see patches of white that are the proliferation centers.

Q: What do you see in blood smear of CLL?
1. Small lymphocytes — has condensed chromatin
2. Smudge cell — disrupted tumor cells
3. Spherocytes — basically erythrocytes that are spherical in shape instead of biconcave.
4. Prolymphocytes — has more cytoplasm and therefore larger. A lot of them.

Q: What surface antigens do you see in CLL/SLL?
A: Most importantly, you see pan-B-cell markers CD19 and CD20. Distinguishing finding is you see T-cell marker CD5 as well as CD23. This distinguishes it from Mantle Cell Lymphoma, which is CD5+ but CD23-

Q: Who gets CLL?
A: Mostly male, median age 60. It’s often found incidentally because there is usually NO ABNORMAL PHYSICAL SYMPTOMS.

Q: Is CLL fast or slow growing?
A: slow growing, like follicular lymphoma. Since it’s slow growing, it doesn’t respond well to treatment (which usually requires fast growing cell), but at the same time the prognosis isn’t as bad as fast-growing tumors. The prognosis gets worse if there is Prolyphocytic Transformation (in 15-30% of cases) or Richter Transformation (in 10% of cases).

Q: Is there an autoimmune symptom of CLL?
A: Yes. Many CLL patients have autoantibodies to red cells and platelets.
It causes warm autoimmune hemolytic anemia.

Q: CLL patients with better prognosis have what mutation?
A: mutated IGVH (Immunoglobulin Variable Region Heavy Chain) and ZAP70-, CD38-

Q: CLL patients with poorer prognosis have what?
A: unmutated IGVH and ZAP70+, CD38+

Q: What is Richter Transformation Syndrome?
A: It’s a complication of CLL in which the leukemia transforms into an aggressive Diffuse Large B-cell Lymphoma.

Q: What’s the difference between CLL/SLL and ALL?
A: ALL is for both B and T cells. CLL/SLL involves only B cells (although it has a unique CD5 T cell marker). ALL is in kids and youngsters. CLL/SLL is in older folks. ALL is lymphoblastic (larger cells) while CLL/SLL is lymphocytic (small-size, mature cells).


Q: What does follicular lymphoma look like?
A: follicles (like follicular zone where B cells are) everywhere in lymph node.

Q: How can you tell it’s a follicular lymphoma rather than just follicular hyperplasia?
A: Follicular lymphomas disrupt the architecture of the lymph node, with follicles invading both cortex and medulla. You won’t see a mantle zone. In Follicular hyperplasia, there is just an enlargement of follicles. You’ll still see a normal, prominent mantle zone.

Q: What is the most common form of non-Hodgkin Lymphoma in the US?
A: Follicular Lymphoma

Q: How does the patient present?
A: Older than 55 years old, both male and female. Has a mass in cervical lymph node. Getting sick more often (because can’t fight infections as well anymore because of messed-up B-cells).

Q: What are two cell types in follicular lymphoma?
— B cell with cleaved nucleus found in follicular lymphoma
Centroblasts — larger B cells with open nuclear chromatin and increased cytoplasm.

Q: How do you grade follicular lymphomas?
A: By determining number of centroblasts it has.

Q: In follicular lymphomas, what is expressed?
A: Bcl2 protein in follicular center cells (vs. cells in mantle zone)

Q: What immunophenotype does follicular lymphoma have?
A: CD19, 20, 10 (CALLA), BCL2, BCL6, sIG.

Q: What is the hallmark genetic change that cause Follicular Lymphomas?
A: t(14:18) — translocation of BCL2 gene on chromosome 18 and IgH gene on chromosome 14. Remember Bcl2 is an anti-apoptotic gene. So if this is translocated to a stronger promoter, it inhibits apoptosis even more, and cells proliferate.

Q: Where is Bcl2 expressed in Follicular lymphomas?
A: Bcl2 is normally expressed just in the mantle zone. In Follicular Lymphoma, it is expressed in both the mantle zone and the follicular center.

Q: Follicular Lymphoma often transforms into what (50% of the time)?
A: Diffuse Large B-Cell Lymphoma — worse prognosis. It can sometimes also transform into Burkitt-like lymphoma if there is C-MYC translocation.

Q: Is follicular lymphoma fast or slow growing?
A: Slow growing, but hard to treat — so you don’t often catch it on time. Doesn’t respond well with radiotherapy because only works well with rapidly-dividing cells. It becomes fast growing if it becomes Diffuse Large B-Cell Lymphoma.

Q: How does Follicular Lymphoma look in the spleen?
A: It looks shotty, and all over the spleen. Compare with Diffuse Large B-cell lymphoma, where the tumor is one big mass.

Q: So in summary, what neoplasms have CD10 (CALLA)?
A: Pre-B ALL, Follicular Lymphoma.


Q: Happens in who?
A: More in males over 60. More common in HIV patients.

Q: Do they form follicles?
A: No.. they are diffuse.

Q: Is it fast or slow growing?
A: FAST!! very POOR prognosis (cure rate only 30%)

Q: What do the lymphocytes look like?
A: LARGE! they have large nuclei with open chromatin. prominent nucleoli.

Q: How does Diffuse Large B-cell lymphoma look in the spleen?
A: isolated large mass (vs. multifocal like in follicular lymphoma)

Q: What markers do you see?
A: CD19, 20, sIg, many have a dysregulated BCL6, which is a zinc-finger transcription regulator.

Q: What are the clinical subtypes of Diffuse Large B-Cell Lymphoma?
A: Mediastinal LBCL — in young women
Immunodeficiency-associated LBCL — in end-stage HIV infection and Epstein-Barr Virus.
Body Cavity LBCL — associated with KSHV/HHV-8 (Kaposi’s Sarcoma virus)


Q: What are the three types of Burkitts Lymphoma?
1. African (endemic)
2. Sporadic (non-endemic) — in US
3. HIV1+ individuals — very aggressive.

Q: Do you find Burkitt’s Lymphoma in the nodes?
A: usually it is extranodal.

Q: Where do Burkitt’s Lymphoma present in Endemic vs. Sporadic forms?
A: Endemic — in mandible, ovary, kidneys, adrenals — presents with enlarged parotid gland.
Sporadic — in ileocecal portion of bowel and peritoneum — presents in abdominal/pelvic lesions.

Q: What does Burkitts Lymphoma look like (morphology)?
A: “Starry Sky” Pattern. Has intermediate-sized lymphocytes. The clear-colored macrophages amongst a sky of malignant Burkitt cells make them look like stars.

Q: What is the immunophenotype of Burkitt’s Lymphoma?
A: Cd19, 20, 10. Hypermutated mature follicular center B-cells (like Follicular Lymphoma) with IgM, kappa or lambda light chains.

Q: What are the genetics of Burkitts Lymphoma?
A: t(8;14) — c-MYC on Chrom 8 translocation with IgH locus on 14
t(8;2) — c-MYC on 8 translocation with kappa on 2
t(8;22) — c-MYC on 8 translocation with lambda on 22

Q: What virus causes endemic Burkitt Lymphoma (but sometimes sporadic)?
A: Epstein-Barr Virus

Q: How is the prognosis?
A: Although aggressive (probably most aggressive of all cancers), most young children and adults can be cured with chemotherapy.


Q: What is the common feature of plasma cell neoplasms (or dyscrasia)?
A: It usually involves a single clone (rather than all B cells) that just synthesizes a single monoclonal immunoglobulin (mostly IgG, or sometimes IgA), called the “M Component” (M for Monoclonal). An overproduction of the single monoclonal immunoglobulin is called an “M Spike.”

Q: What is Bence Jones protein?
A: they are free Light chains that are secreted by the plasma cell neoplasms that can be detected in the urine.

Q: What are the types of Plasma Cell Neoplasms?
A: Multiple myeloma — plasma cell myeloma
Plasmacytoma — single mass (can develop into multiple myeloma)
Waldenstrom Macroglobulinemia — secrete lotsa IgM
Heavy/Light Chain Disease — secretees free Heavy or Light chain fragments
Primary or Immunocyte-associated Amyloidosis — free Light chains that lead to amyloidosis
Monoclonal Gammopathy of Undetermined Significance (MGUS) — M components in blood but no other signs/symptoms. Benign, but can transform into other plasma cell neoplasms.

Q: What is Rouleaux?
A: when RBCs stick together and look like trains because immunoglobulins stick to RBCs, which cause them to stick to each other in the blood.


Q: Who gets it?
A: More common in Blacks, males, 80-90. Presents to office with lower back pain.

Q: Where on the body does multiple myeloma happen the most?
A: Vertebrae (i.e. lower back) –> Ribs –> Skull

Q: What drives the proliferation of multiple myeloma?
A: IL-6

Q: What is the immunophenotype of Multiple Myeloma?
A: CD38, CD138. NO CD19!!

Q: What do the bones look like in multiple myeloma?
A: they look punched out (multifocal destructive bone tumor), hence called “multiple” myeloma. The bones are destroyed because of the osteoclastic activating factor. The bone calcium goes to the blood, causing hypercalcemia.

Q: What do you see microscopically in the bone marrow of those with multiple myeloma?
A: The marrow is nearly gone and replaced with plasma cells, much of which is atypical with multiple nuclei.

Q: What kind of plasma cell variants do you see in Plasma Cell Neoplasms (Dyscrasias)?
A: Flame cell, Mott cell, Russell bodies.

Q: What chromosomal mutation do you see in multiple myeloma?
A: translocation on 14q32

Q: What other clinical features do you see in patients with multiple myeloma?
A: Hypercalcemia, recurrent infections (because abnormal B cells –> pancytopenia or lack of normal B cells). You also see amyloidosis due to all those transformed monoclonal plasma cells and Bence Jones proteins conglomerating and depositing in renal tubules –> renal failure, protein in urine.

Q: What are the four major clinical signs of Multiple Myeloma?
A: CRAB — hyperCalcemia, Renal failure, Anemia, Bone pain.

Q: What’s the most common monoclonal gammopathy in multiple myeloma?
A: IgG most common.

Q: What’s the prognosis of multiple myeloma?
A: 6-12 months if untreated. If treated with chemotherapy, survival less than 5 yrs.

Q: What’s the staging for multiple myeloma like?
A: unlike staging all other tumors — if you have renal failure it is bad, because infection and renal failure most common cause of death in multiple myeloma.


Q: What is it commonly called?
A: Waldenstrom Macroglobulinemia (IgM — which is very sticky, very large)

Q: What’s the morphology?
A: Lymphocytes, plasma cells, immunoglobulin inclusions — Russel bodies — cytoplasm, Dutcher bodies — nucleus

Q: What is the immunophenotype?
A: Has CD19, 79a, IgM, IgD, sometimes CD20, 38

Q: Clinical Features?
A: Lymphadenopathy, hepatosplenomegaly, Half of cases have Hyperviscosity Syndrome.

Q: What causes hyperviscosity Syndrome?
A: high levels of IgM (which is the biggest immunoglobulin)

Q: What symptoms do you see in hyperviscosity Syndrome?
A: Visual impairment, Neurologic problems, NO LYTIC BONE LESIONS (like in multiple myeloma)

Q: What is the prognosis?
A: 4-5 yrs.

Q: In summary, which neoplasms have CD19, 79?
A: Waldenstrom macroglobulinemia, Marginal Zone Lymphoma


Q: Epidemiology?
A: males, onset: 50-60 yrs old.

Q: Morphology?
A: HOMOGENEOUS small lymphocytes — in mantle layer surrounding follicular center

Q: Immunophenotype?
A: overexpression of CYCLIN D1 due to the translocation!!!!!!!! You see CD19, 20 (both are your usual B cell markers) and also CD5 (normally a T-cell marker), BUT NO CD23 (unlike CLL/SLL).

Q: Cytogenetics?
A: t(11;14) — translocation of Cyclin D1 on 11 and IgH on 14.

Q: Clinical Features?
A: PAINLESS lymphadenopathy, sometimes LYMPHOMATOID POLYPOSIS (Extranodal GI involvement)

A: 3-5 yrs.


Q: What is it also known as?
A: MALTOMAS — mucosal-associated lymphoid tissue lymphomas — because initially recognized on mucosal sites, like in GI tract (i.e. stomach).

Q: Where?
A: Extranodal (GI and spleen) and lymph nodes

Q: How does it arise?
A: when you first have INCITING AGENT that causes chronic inflammation somewhere — like if you get Helicobacter pylori, campylobacter jejuni, Sjogren’s, Hashimoto’s thyroiditis.

Q: When can it regress?
A: MAINLY in gastric cases, if you remove H. pylori

Q: Immunophenotype?
A: CD19, 79a, and sometimes Bcl2 (which are usually in naive cells, even though these are not naive cells)
NO CD5, 10, 23, or cyclinD1!!!!!! (vs. mantle cell)

Q: Cytogenetics?
A: Mainly caused by inciting agent, but sometimes translocation also occurs:
t(1;14) — translocation between BCL10 on 1 and IgH on 14.
t(11;18) — translocation between MALT1 on 11 and IAP2 on 18.

Q: What’s the prognosis?
A: If caused by inciting agent, then prognosis good.
If caused by translocation, then tumors don’t regress
Can transform into diffuse large B-cell lymphoma.

Q: What is hyperspenism?
A: it traps cells to get rid of bad cells, but then u also get cytopenia because it becomes a “trap” for normal cells as well.


Q: Epidemiology?
A: RARE. middle-age white men

Q: Morphology?
A: HAIRY CELLS (transformed B cells) that look HAIRY in peripheral blood

Q: Immunophenotype?
A: CD11c, CD103, PAX, TRAP!!!!!!!!!!!!!!!!

Q: Clinical Features?
A: Infiltrates the bone marrow, liver and spleen. SPLENOMEGALY, PANCYTOPENIA.

Q: How easy is it to get a sample of hairy cell leukemia?
A: It doesn’t aspirate easily (doesn’t suck out of a needle easily) because these hairy B cells become so packed in the bone marrow (which is normally very liquidy), making it solid and hard to suck out of a needle. This is called a “dry tap” because the needle comes out “dry.”

Q: Prognosis?
A: Indolent. It’s not too bad because VERY sensitive to chemotherapy.

Q: In summary what are the translocations?
t(11;14) — Cyclin D1 is on 11. Mantle Cell Lymphoma expresses Cyclin D1
t(14;18) — Bcl2 (anti-apoptotic protein usually on mantle zone, but now found on follicular) is on 18. Follicular Lymphoma.
t(8;14) — c-myc is on 8. Burkitt Lymphoma. “c-myc 8”



Q: How does the prognosis compare with B-cell lymphomas?

Q: Is it usually in lymph nodes or outside of lymph nodes?”
A: EXTRANODAL!!! (vs. B-cell lymphoma)

Q: Where in the world do you see more T-cell neoplasms?

Q: What do T-cells like to infiltrate?
A: SKIN!!! so T-cell lymphomas cause ITCHINESS!!!

Q: What kind of T-cell lymphomas are there?
A: precursor T-lymphoblastic leukemia/lymphoma.
Peripheral T cell lymphomas can be either leukemic (T-CLL/PLL) or solid tumors.


Q: Where are they in the body?
A: Lymph nodes (which remember among T-cell neoplasms, is in the minority)!!

Q: Prognosis?
A: less than 1 year, even with treatment!!!

Q: Clinical features?
A: lymphadenopathy, pruritus (ITCHING), fever, weight loss.


Q: What gene rearrangement is associated with it?
A: ALK gene, 2p23

Q: What’s the prognosis with the gene rearrangement?
A: good prognosis (if not, then bad prognosis)

Q: What are the hallmark cells of Anaplastic large cell lymphomas?
A: Horseshoe like or embryo-like nuclei, with lotsa cytoplasm. You see a lot of ALK protein when you stain it.


Q: What causes it?
A: HTLV-1 !!!!!!!!!!!

Q: Where in the world is it endemic?
A: Southern Japan, West Africa, CARIBBEAN

Q: How’s the prognosis?
A: less than a year

Q: What’s characteristic of the cells?
A: cloverleaf nucleii

Q: immunophenotype?


Q: What are the phases?
A: Inflammatory erythrodermic pre-mycotic –> plaque –> tumor

Q: Where in body does it occur?
A: skin — lesions look like fungus but it is NOT!! NOTHING TO DO WITH FUNGUS

Q: Prognosis of mycosis fungoides without sezary syndrome?
A: 8-9 yrs

Q: What is Sezary Syndrome?
A: When Mycosis Fungoides leads to RASH ALL OVER (full skin involvement of the neoplasm)

Q: What cells do you see in Sezary Syndrome?
A: SEZARY CELLS — in leukemic phase — has cerebriform nuclei (looks like brain?)

Q: What’s the prognosis with a patient with Sezary syndrome?
A: less than 3 yrs.


Q: How common is it?
A: Rare. it’s only famous because the cells look unique.

Q: What are the two variants?
A: T-cell — INDOLENT (lazy tumor)

Q: What do you see under the microscope?
A: lymphocytes with blue cytoplasm.

Q: Clinical presentation?

Q: Associated with what other syndrome?
A: Felty Syndrome — Rheumatoid arthritis with splenomegaly and neutropenia


Q: What was it formerly known as?
A: Lethal midline granuloma — because it is lethal, and involves midline skin and testes.

Q: Where do the tumor cells invade?
A: invade small vessels

Q: Clinical presentation?
A: Sinonasal lymphoma

Q: Prognosis?
A: poor.

Q: What virus is it related to?
A: Epstein-Barr virus


Q: WHat are the four stages?
I — involves single lymph node
II — involves same side of diaphragm
III — involves both sides of diaphragm
IV — multifocal and extralymphatic involvement

Q: What are the two categories?
A — patients without symptoms of B
B — patients with unexplained weight loss, fever, and night sweats


Q: What types of Hodgkin Lymphomas are there?
Nodular Lymphocyte Predominance Hodgkin Lymphoma — CD15-/30- IMPORTANT!
Classical Hodgkin Lymphoma — Nodular Sclerosis, Mixed Cellularity, Lymphocyte-rich, Lymphocyte-depleted subtypes (backgrounds)
Anaplastic Large Cell Lymphoma-Like Hodgkin Lymphoma (NEW)

Q: What do Hodgkin Lymphoma patients present with?
A: Fever, Night sweats, weight loss, lymphadenopathy (that spreads continuously)

Q: What are the four subtypes of Classical Hodgkin Lymphoma?
A: These are all “backgrounds”
1. Nodular Sclerosis — most common HL. Mediastinum. Young adults. Most common in WOMEN. CD15+/30+/EBV-. Multilobed nuclei (lacunar cell)
2. Mixed Cellularity — most common HL in patients over 50. SEE LOTSA TYPES OF CELLS like eosinophils and plasma cells. CD15+/30+/EBV+
3. Lymphocyte-rich — uncommon HL. CD15+/30+/sometimes EBV+
4. Lymphocyte-depleted — uncommon HL. CD15+/CD30+/EBV+. WORST PROGNOSIS b/c lotsa Reed-Sternberg cells!!

Q: Hodgkin (HL) vs. Non-Hodgk
in (NHL):
A: (slide 192)
1. HL — contiguous spread. NHL — noncontiguous spread
2. HL — bi-modal age of diagnosis. NHL — usually happen in elderly.
3. HL — excellent response to treatment. NHL — poor response to treatment
4.HL — mortality rates declining. NHL — mortality rates increasing
5. HL — extranodular spread uncommon. NHL — extranodular spread common.
6. HL — involves more axial lymph nodes. NHL — involves more peripheral lymph nodes.

Q: What’s another name for CD15 and CD30 (found on all HL’s)?
A: CD15 = Leu-M1
CD30 = Ki1

Q: What’s the commonality between the four types of classical hodgkin lymphomas?
A: They all have CD30+, CD15+ (which are the markers of Reed-Sternberg Cells), and some sort of EBV involvement.

Q: Compare Nodular Lymphocyte Predominance Hodgkin Lymphoma with Classical HL:
A: NO CD30 or CD15 or EBV!!! But you see CD20+

Q: HL is mostly what kinda cell lymphoma?
A: B CELL LYMPHOMA!! but occasionally see T cell.

Q: What’s the most common form of Hodgkin Lymphoma?
A: Nodular Sclerosis subtype of Classical Hodgkin Lymphoma

Q: What’s the most common form of Hodgkin Lymphoma in patients over 50?
A: Mixed Cellularity subtype of Classical Hodgkin Lymphoma

Q: What kinda cell do you see in Hodgkin Lymphoma?
A: Reed-Sternberg Cell — They are malignant B cells with biloped nucleus. Look like “double owl eye” (vs. single owl eye cells in CMV, which are mononucleate). Their markers are CD15 (Leu-M1) and CD30 (Ki-1)

Q: How do Reed-Sternberg Cells relate to prognosis of Hodgkin Lymphoma?
A: More Reed-Sternberg Cells = Worse prognosis.

Q: What kinda cell do you see in Nodular Sclerosis type of Classical HL?
A: Lacunar Cell — multilobed nucleus

Q: What kinda cells do you see in Nodular Lymphocyte-Predominance HL?
A: Popcorn Cells — lymphocytes surrounding either pale-staining lymphocytes or histiocytes. You have predominantly lymphocytes, so less Reed-Sternberg cells, so better prognosis. Probably why it’s CD15-/30-!!!!!!


Q: What’s the prognosis of nodular sclerosis subtype of Classical HL?
A: excellent

Q: Why is it called mixed-cellularity subtype HL?
A: because you see all types of cells in there — eosinophils, lymphocytes, histiocytes.

Q: What’s the mortality rate of the years with HL vs. NHL?
A: HL — decreasing. NHL — increasing


Q: What are the three categories of myeloid neoplasia?
1. Acute Myelogenous Leukemia — more than 20% immature myelogenous precursor cells accumulated in bone marrow
2. Myelodysplastic Syndromes — peripheral blood cytopenia because defective hematopoiesis.
3. Chronic Myeloproliferative Disorders — increased production of one or more myeloid cell (i.e. RBC, BEN, platelet)

Q: How do you classify Acute Myelogenous Leukemias according to French and British (FAB) Classification?
M0 — minimally differentiated AML — myeloblasts have no Auer rods or myeloperoxidase, but have myeloid lineage surface markers.
M1 — AML without differentiation — more than 3% of myeloblasts are myeloperoxidase positive.
M2 — AML with maturation — greater than 20% of bone marrow cells are myeloblasts, but many are in later stages.
M3 — ACUTE PROMYELOCYTIC LEUKEMIA — HIGH INCIDENCE OF DIC, epistaxis. Associated with t(15;17). Lotsa Auer rods. JUST KNOW THIS ONE!!
M4 — Acute Myelomonocytic Leukemia — monoblasts are positive for nonspecific esterase. Everything positive.
M5 — Acute Monocytic Leukemia — myeloperoxidase negative, nonspecific esterase positive.
M6 — Acute erythroleukemia
M7 — Acute Megakaryocytic Leukemia

Q: What are the symptoms of AML?
A: Since you have leukemic cells in the bone marrow, it pushes out all the normal leukocytes (myelocytes and lymphocytes) that can develop. So you develop pancytopenia (causing bleeding problems, problems with infection, and anemia).

Q: What are Auer Rods made of?
A: fused lysosomes of granules (and remember AML is all about granulocytes!)

Q: How do you classify Acute Myeloid Leukemias according to WHO Classification?
A: The WHO added two more categories on top of the FAB classification:
1. Acute Myeloid Leukemia with recurrent genetic abnormalities
2. General Acute Myeloid leukemia — FAB + more.
3. Myeloid proliferation related to Down Syndrome

Q: Compare AML and ALL in terms of age of diagnosis:
A: AML — older folks (once named “Adult Myelogenous Leukemia”). ALL — younger folks.

Q: What do myeloblasts look like?
A: they have delicate nuclear chromatin, prominent nucleoli, and azurophilic granules (which lymphoblasts dont have). Can have many nucleoli and Auer rods. LARGE.

Q:What are the important stains for AML?
A: Myeloperoxidase (MPO) and Sudan-Black.

Q: What is the marker for multipotent stem cells (which myeloid blasts have a lot)?
A: CD34, 33

Q: What is the marker for mature myeloid cells?
A: CD64, 15

Q: What are Auer rods?
A: needle-like structures found in M3 AML leukocytes.

Q: Is it common for AML patients to have chromosomal abnormalities?
A: YES!! 90%.

Q: What chromosomal abnormalities will actually IMPROVE prognosis of AML patients?
A: t(8;21)

Q: What chromosomal abnormality is in acute promyelocytic leukemia?
A: t(15; 17) — retinoic acid receptor alpha (RARA) on 17 translocate with PML on 15 –> abnormal Retinoic acid receptor –> block differentiation of promyelocyte.

Q: How do you overcome a PML/RARA block in the differentiation of promyelocytes?
A: give doses of all-trans retinoic acid!

Q: How does the prognosis of AML compare with ALL?
A: AML worse than ALL. only 15-30% remain disease-free after 5 yrs. Most die within a year or two of diagnosis.

Q: What’s the prognosis of someone who already had myelodysplastic syndrome and then has AML?

Q: What kinda AML is increased in Down Syndrome patients?
A: Acute Megakaryoblastic Leukemia


Q: What are the types of myelodysplastic syndromes (MDS)?
A: Chronic Myeloproliferative disorders
Langerhans Cell Histiocytosis

Q: What is MDS?
A: Defect in maturation due to ineffective hematopoiesis. There is an increased risk of transformation to AML.

Q: What are two causes?
A: Idiopathic (Primary MDS) or Therapy-related from drug or radiation therapy (t-MDS).

Q: How do you classify Myelodysplasia?
1. RA — Refractory Anemia
2. RARS — Refractory Anemia with Ringed Sideroblasts
3. RCMD — Refractory Cytopenia with Multilineage Dysplasia
4. RAEB — Refractory Anemia with Excess Blasts
5. 5q Syndrome
6. t-MDS

Q: Who gets MDS?
A: people older than 50.

Q: What are the symptoms of MDS?
A: weakness, infection, hemorrhage (because of bone marrow failure), pancytopenia

Q: What are Pelger-Huet cells?
A: neutrophils that have 2 lobes instead of the normal 3. You see them sometimes in myelodysplastic/myeloproliferative syndromes.

Q: What are ringed sideroblasts?
A: They are nucleated RBCs (which remember aren’t normally nucleated) with iron granules surrounding the nucleus, making it look like a ring. You can also find this in my
elodysplastic/myeloproliferative syndromes.


Q: From what is the primary neoplastic cell derived?
A: stem cells that give rise to ERYTHROCYTES, PLATELETS, GRANULOCYTES

Q: From what is the neoplastic cell derived in CML?
A: stem cells that give rise to MYELOID CELLS and LYMPHOCYTES (so an earlier form of stem cell than other CMDs)

Q: Are there a lot of immature cells in the blood?
A: NO! Unlike AML or Myelodysplastic Syndromes (which is really pre-AML), the neoplastic cells in CMDs differentiate into mature cells (since it’s chronic, giving them enough time to mature). So instead of seeing lots of blast cells and little mature RBCs/WBCs like you would in AML, you see increased PMNs, RBCs, and Platelets in the blood in CMDs!!! Therefore you don’t experience bleeding, pancytopenia, or immunity problems like you normally would in AML (although you see some anemia sometimes for some reason). But since you have lots more of these cells, your spleen will try to get rid of it, causing splenomegaly. You also get hypercellular bone marrow, since you got so many cells and all of the fat is pushed out.

Q: What is Chronic Myeloproliferative disorders associated with?
A: increased activity of mutated tyrosine kinases (i.e. JAK2 kinase)… hence increased proliferation.

Q: What are the Myeloproliferative neoplasms (MPN)?
1. Chronic Myelogenous Leukemia (CML) — BCR-ABL1
2. Chronic Neutrophilic Leukemia (CNL)
3. Polycythemia vera
4. Primary Myelofibrosis
5. Essential Thrombocythemia
6. Chronic Eosinophilic Leukemia
7. Mastocytosis

Q: How can you distinguish between the chronic myeloproliferative disorders histologically?
A: You can’t. You just see lots of PMNs, RBCs, Platelets in all of them.


Q: What’s the unique translocation in CML?
A: t(9;22) — BCR on 9 translocates with ABL on 22. (PHILADELPHIA CHROMOSOME). This causes a constitutively active tyrosine kinase (JAK/STAT) that doesn’t need stimulation to be active, leading to cell over-proliferation.

Q: What do you see in the blood of a CML patient?
A: leukocytosis, mature PMNs, metamyelocytes, myelocytes, +/-BASOPHILIA (like in all myeloproliferative disorders)!!

Q: What is a myelocyte?
A: a young granulocyte (BEN) that is still in the bone marrow.

Q: What is a metamyelocyte?
A: the next stage up from myelocyte. It is undergoing granulopoiesis to become a full granulocyte.

Q: Symptoms?
A: splenomegaly, anemia, hypermetabolism, weakness, etc.

Q: Treatment?
A: Imatinib aka Gleevac (BCR-ABL kinase inhibitor!)

Q: So if you get an infection, your body normally releases band neutrophils early from the bone marrow to fight off the infection. This is called Leukemoid reaction and looks a lot like CML. But how do you distinguish it from CML?
A: Leukemoid reaction will test postive for leukocyte alkaline phosphatase (which is in all normal white blood cells), however, since CML white blood cells are neoplastic (although mature for the most part), they don’t produce leukocyte alkaline phosphatase, hence they will test negative.

Q: What’s the progression for CML?
A: Slow progression. But half of patients eventually enter an ACCELERATED PHASE followed by a BLAST CRISIS and develop AML!!


Q: What is Polycythemia Vera?
A: Like CML except this is a primary disorder. panmyelosis (so ERYTHROCYTOSIS (primary), granulocytosis, thrombocytosis) +/- basophilia (like in all myeloproliferative disorders). Your bone marrow produces too much RBCs, causing too high of a hematocrit, and hyperviscocity of the blood. However, erythropoietin is suppressed, because you got too much blood already. Eventually, your bone marrow will get tired making all these cells, and so it will go into a “spent stage” where it gets myelofibrosis. You gotta continue making blood somewhere, so your stem cells travel to the spleen, and make a lot of myelocytes as well (extramedullary hematopoiesis), causing splenomegaly. The increased basophils also releases more histamine, causing pruritus and peptic ulcers.

Q: What special disease do some PV patients develop?

Q: What symptoms?
A: hypercellular marrow, splenomegaly, major bleeding, and thrombosis (increase in platelets). Pruritus, peptic ulcer (because of increased histamine release from basophils)

Q: So PV and CML both cause overproliferation of predominantly mature blood cells. But what’s the difference?
A: PV is more RBC dominant. CML is more evenly spread between the three cell lines. They both are due to tyrosine kinase (JAK/STAT) mutation causing them to constitutively proliferate cells, but they are due to different reasons. CML is due to t(9;22) BCR-ABL Philadelphia Chromosome. PV is due to some other mutation. They can both lead to AML.


Q: What is it?
A: proliferation of MEGAKARYOCYTES in bone marrow which lead to a PLATELET count greater than 450,000. Also see some GIANT PLATELETS (same size as RBC, but non-functional). Your bone marrow eventually gets tired and leads to scarring –> myelofibrosis.

Q: How do you diagnose it?
A: Diagnosis of EXCLUSION, because all Chronic Myeloproliferative Disorders have thrombocytosis.


Q: What’s special?
A: extensive collagen deposition in bone marrow by non-neoplastic fibroblasts –> obliterates the marrow, fibrosis in bone marrow. Occupies much of the marrow space. Eventually dysplastic precursor cells show up.

Q: Half of primary myelofibrosis cases have what mutation?
A: JAK2 kinase mutation (like chronic myeloproliferative disorders). This causes you to make so much blood cells that your bone marrow burns out and you get scarring of the bone marrow (and therefore dry tap, just like hairy cell leukemia). RBCs that are made have to squeeze out of the bone past these scar tissues, causing them to become “tear drop” shaped.

Q: What is a myelophthisic process?
A: something is replacing the bone marrow.

Q: What causes the splenomegaly in primary myelofibrosis?
A: extramedullary hematopoiesis, because your bone marrow gets scarred, and so your spleen makes up for it by making RBCs, causing splenomegaly.

Q: What could primary myelofibrosis develop into?
A: HYPERURICEMIA AND GOUT, or AML-LIKE BLAST CRISIS (remember AML has immature myeloid cells in the bone marrow).

Q: What do you see in blood smear of patient with primary myelofibrosis?
A: LEUKOERYTHROBLASTOSIS — basically lotsa erythroid and myeloid precursors in blood. The erythroid cells are shaped like tear-drops and they are called DACROCYTES!

Q: What’s the prognosis of primary myelofibrosis?
A: 4-5 yrs

So in Summary:
Polycythemia Vera, Essential Thrombocytopenia, and Primary Myelofibrosis –> Myelofibrosis (and therefore splenomegaly) and/or acute leukemia.
CML –> acute leukemia.


Q: What is it?
A: proliferation of dendritic cells or macrophages

Q: What do you see in the langerhans cell under the microscope?
A: Birbeck granules (HX bodies) — look like microscopes

Q: Immuno markers?
A: S100+, CD1+

Q: What are the three types of Langerhans Cell Histiocytosis?
1. Multifocal Multisystem (Letterer-Siwe Disease)
2. Unifocal
3. Multifocal Unisystem

Q: Which one is the worst?
A: Multifocal Multisystem.

Q: What do you see in Multifocal Multisystem LCH?
A: Cutaneous lesions that LOOKS LIKE seborrheic eruption, hepatosplenomegaly

Q: Who gets multifocal multis
ystem LCH?
A: babies under 2

Q: What do you see under the microscope?
A: Langerhans cell, eosinophils, lymphocytes, plasma cells, and neutrophils. EOSINOPHILIC GRANULOMAS + Langerhans Cells.

Q: What do you see in Multifocal Unisystem?
A: many places of bone erosion

Q: Half of multifocal unisystem LCH patients develop what?
A: diabetes insipidus, because affect the posterior pituitary.

Q: What triad defines the multifocal unisystem langerhans cell histiocytosis?
A: Hand-Schuller-Christan Triad — calvarial bone defect, diabetes insipidus, and exophthalmos.

Q: How do you treat multifocal vs. unifocal?
A: multifocal — chemotherapy
unifocal — excision, irradiation


Q: What behavior is it strongly associated with?
A: smoking

Q: How can it regress?
A: quit smoking!

Q: Where are the cysts for PLCH?
A: Middle and upper lung zones


Q: What are the functions of the spleen?
1. removal of waste
2. immune system — Dendritic cells, T and B cells are in spleen.
3. extramedullary hematopoiesis — hematopoiesis outside of the bone marrow
4. spleen stores about 30-40% of our platelets.

Q: What causes MASSIVE splenomegaly (>1000 gm)?
1. Chronic Myeloproliferative disorders
2. Chronic Lymphocytic Leukemia
3. Hairy Cell Leukemia
4. Lymphomas
5. Malaria
6. Gaucher Disease
7. Primary Splenic Neoplasms

Q: What causes MILD splenomegaly (<500 gm)?
1. Acute Splenitis
2. Acute Congestion
3. Infectious Mononucleosis
4. Acute Febrile Disorders

Q: What causes MODERATE (500-1000 gm)?
1. Chronic Congestion
2. Acute Leukemia
3. Hereditary Spherocytosis
4. Thalassemia major
5. Autoimmune hemolytic anemia
6. Amyloidosis
7. Niemann-Pick Disease
8. Langerhans Cell Histiocytosis
9. Chronic Splenitis
10. Tuberculosis
11. Sarcoidosis
12. Typhoid
13. Metastatic Carcinoma/Sarcoma

Q: What is Hypersplenism?
A: Splenomegaly — can cause thrombocytopenia, anemia, or leukopenia, because it can chew up the blood.

Q: How can you correct cytopenia?
A: do a splenectomy.

Q: What causes congestive splenomegaly?
A: Systemic venous congestion, cirrhosis of liver (like due to schistosomiasis), obstruction of extrahepatic portal vein or splenic vein (like due to thrombosis)

Q: What does the spleen look like in congestive splenomegaly?
A: red pulp congested –> fibrous –> Gandy-Gamma nodules — fibrosis with iron and calcium salts secondary to hemorrhages.

Q: What causes splenic infarct?
A: emboli, infectious endocarditis, sickle cell disease that causes occlusion to splenic arteries.

Q: What kind of infections can splenic infarcts lead to?
A: Infections with encapsulated bacteria (pneumococcus, H. influenza, meningococcus)


Q: What is Hepatosplenic gamma delta T-cell lymphoma?
A: neoplasm of immature CTLs — involved in spleen and liver. RARE, and poor prognosis.


Q: Where is the thymus derived from?
A: Medulla from 3rd pharyngeal pouch (ENDODERM).
Cortex from Pharyngeal cleft (ECTODERM).

Q: When is the thymus largest? When is it the smallest?
A: Largest — during puberty. Smallest — during elderly.

Q: What do you see in the thymus?
A: Hassall’s Corpuscles (which are thymic epithelial cells) and immature T-cells.

Q: What is DiGeorge Syndrome?
A: Thymic hypoplasia + parathyroid development failures — so you’ll have deficits in cell-mediated immunity.

Q: What genetic defect is in DiGeorge Syndrome?
A: 22q11 deletion.


Q: What kind of lymphocytes do you see in thymic hyperplasia?
A: B-cells, which remember should not be in the thymus.

Q: In what disease do you see thymic hyperplasia a lot?


Q: What are Thymomas?

Q: What kind of lymphocytes are in thymomas?
A: non-neoplastic T-cells.

Q: What causes Thymomas?
A: tumors of anterosuperior mediastinum, myasthenia gravis, and autoimmune diseases.

Q: What are some symptoms of Thymomas?
A: impingement on mediastinal structures.
hypogammaglobulinemia, RBC aplasia, Graves Disease, Pernicious anemia, Cushing Syndrome)

Q: What type of cells are in Benign Thymomas?
A: Medullary-Type Cells. The tumors are ENCAPSULATED.

Q: What are two types of Malignant Thymomas?
1. Type I — Invasive Thymoma — cytologically bland but acts aggressively. Most commonly Cortical-Type.
2. Type II — Thymic Carcinoma — cytologically malignant — either presents as squamous cell carcinomas or lymphoepithelioma-like carcinomas (caused by EBV).



Q: How can you tell something is a spherocyte (abnormally spherical RBC)?
A: When they have no central pallor.

Q: How long do RBCs survive?
A: 100-120 days

Q: How do RBCs change when they get older?
A: they get smaller and less elastic. they get more spherical.

Q: If we get hypoxemia, how long does the bone marrow take to increase RBC production?
A: It takes at least 7 days for erythropoietin (EPO) to kick in and increase RBC by 4-5 times.

Q: Where does hematopoiesis take place?
A: Red marrow.. found in flat bones — skull, sternum, pelvis, hands, feet. NOT in long bones like arms and legs, where marrow is mainly yellow.

Q: If worse comes to worst, and bone marrow can’t make anymore blood, what does it do to compensate?
A: liver, spleen, or lymph nodes start making blood… this is called extramedullary hematopoiesis.

Q: What regulates RBC production?
A: Erythropoiein (EPO), made by kidneys. EPO is regulated by pO2 in kidney. So basically, hemoglobin falls –> O2 level in kidney falls –> more EPO made –> more RBCs made –> more O2.

Q: What is hematocrit?
A: % of RBCs in blood. RBC/volume

Q: How do you calculate hemoglobin?
A: Hematocrit/3 = hemoglobin (total hemoglobin per volume of blood)

Q: What’s the normal levels of hematocrit in male and females? Newborn?
A: Male: 38.8 – 50
Females: 34.9 – 44.5 — slightly lower than males.
Newborn: 42-60 — very high.

Q: What are some measurements for RBCs?
RBC Count = #RBC/volume
Mean Corpuscular Volume (MCV) = average RBC size
Hemoglobin (Hgb) = Hgb/volume
Red Cell Distribution Width (RDW) = MCB standard deviation — measures anisoytosis (when RBCs vary in size)

Q: What is MCH vs. MCHC?
MCH = Hemoglobin/RBC
MCHC = Hemoglobin/hematocrit

Q: Hypo vs. Normo vs. Hyperchromic:
Hypochromic = Low MCHC
Normochromic = Normal MCHC
Hyperchromic = High MCHC

Q: Micro vs. Normo vs. Macrocytic:
Microcytic = low MCV (small RBC)
Normocytic = normal MCV (normal size RBC)
Macrocytic = high MCV (big RBC)

Q: Definitions:
Anisocytosis — variation in RBC size
Poikilocytosis — variation in shape
Reticulocyte — young RBC — a measurement of how well bone marrow is functioning) — LARGE.
Polychromasia — blue RBC — due to remnants of RNA in young RBC.

Q: What is Howell Jolly body?
A: clusters of DNA that’s left in the RBC (which remember normally has no nucleus or DNA). You see it in ppl that have no spleen (because can’t clear it away).

Q: What is Basophilic stippling?
A: precipitated RNA in RBC. You see it in thalassemias, lead poisonings, and other anemias, or anything that cause Fe to get stored in the cell, which damages enzymes that break down RNA in a reticulocyte.

Q: What is Pappenheimer body?
A: precipitated iron in RBC, caused by impaired hemoglobin synthesis or accelerated RBC division. See in sideroblastic anemia.

Q: What is Heinz Body?
A: precipitated hemoglobin from G6PD deficiency. Remember from biochem that G6PD is part of the pentose phosphote pathway, one function of which is to mop up free radicals from oxygen. RBCs carry oxygen,and so oxidative stress can cause damage to RBCs that aren’t protected because of G6PD deficiency. This causes the Heinz Body.

Q: What is Burr cell?
A: spiky RBC in renal disease patients.

Q: How can you tell a patient has anemia?
A: They are tired, have trouble breathing, have angina, and are about to faint. They have TACHYCARDIA (to compensate for low O2), and their skin, nail beds and buccal mucosa are pale.

Q: How much blood loss can cause symptoms?
A: 10-15% loss in less than 1 hr. You increase pulse and respiration. You feel lightheaded. These symptoms are all due to defect in VASCULAR VOLUME rather than lack of O2 carrying capacity.

Q: What amount of blood loss causes shock?
A: More than 20% blood loss in less than 1 hr = vascular shock. More than 30% = profound shock with confusion/air hunger. Again, symptoms due to change in vascular volume, NOT O2. In acute hemorrhage, hgb/hct (MCHC) is often NORMAL, because the CONCENTRATION of RBC in the blood is still the same (despite having decreased volume).

Q: What is chronic anemia?
A: When you decrease RBC slowly, but your body has enough time to adjust (i.e. increase 2,3-DPG).

Q: At what hemoglobin level do you become symptomatic?
A: Hgb less than 7


Q: What is Hemolytic Anemia?
A: Anemia caused by destruction of RBCs.

Q: What are the intrinsic and extrinsic causes of hemolytic anemia?
Intrinsic — hereditary (G6PD deficiency), acquired (i.e. Paroxysmal nocturnal hematuria)
Extrinsic — immune, trauma, chemical, ARTIFICIAL HEART VALVES

Q: Intravascular vs. Extravascular:
= destruction of RBCs inside the vessels — acute, catastrophic. You see hemoglobinemia/hemoglobinuria beacause you pee out the lysed stuff.
Extravascular = destruction of RBCs outside of vessels (like in SPLEEN) — increased physiological removal of RBCs. chronic, non-catastrophic. You see anemia, bone marrow hyperplasia and elevated erythropoietin (because has time to compensate).

Q: What us haptoglobin?
A: Haptoglobin is a protein that binds to free hemoglobin so it can get excreeted. In intravascular hemolysis, RBCs lyse, releasing lots of free hemoglobin, to which your haptoglobins bind. These leaves less free unbound haptoglobin in your blood. INTRAVASCULAR HEMOLYSIS –> DECREASED SERUM HAPTOGLOBIN.

Q: Intrinsic and Extravascular hemolytic anemia — how old are the RBCs?
A: shortened RBC life span due to increased SPLENIC SEQUESTRATION

Q: Why do RBC’s need deformabiliity?
A: So it can squeeze through red pulp cords in spleen into the sinus lumen to get recycled. So in Hereditary spherocytosis, RBCs become round and lose this deformablity, causing it to get trapped int he splenic cords –> splenomegaly.


Q: Heredity?
A: Autosomal dominant

Q: mutation?
A: Ankyrin and Spectrin — which are structural proteins in RBC.

Q: what happens?
A: no ankyrin/spectrin –> unstable membrane –> stress during circulation causes it to lose membrane fragments –> forms spherical shape –> gets trapped in spleen, eaten up by macrophages –> splenomegaly –> body compensates by making more reticulocytes and increasing MCHC.

Q: What test do yo do to diagnose HS?
A: Osmotic fragility test — put the RBCs in hypotonic solution and see how easy they lyse.

Q: What do you see in blood smear?
A: anisocytosis (different sizes of RBCs), no central pallor in blood (because not biconcave), and if patient is asplenic, you can see howell-jolly bodies (because no spleen to destroy RBCs with these).

Q: how old are spherocytes?
A: 10-20 days (remember normal is 120 days)

Q: How do you treat?
A: splenectomy — nearly corrects the anemia. You still have spherocytes but they can still carry oxygen. They just won’t get cleared.


Q: Mutation?
A: PIGA mutation –> decrease GPI anchors –> CD59 (which protects cells against complement) can’t bind to GPI –> can’t protect RBC against complement –> lots of complement –> damage to RBCs –> Paroxysmal Nocturnal Hemoglobinuria.

Q: Why does PNH often happen NOCTURNALLY?
A: decreased pH during sleep –> complement activation

Q: What complication can PNH lead to?
A: PNH can lead to Deep vein Thrombosis (hepatic and cerebral veins) because platelets are lysed by complement (because they don’t have GPI anchors anymore) –> released platelet factors clot RBCs together.

Q: Flow cytometry finding?
A: DECREASED CD55 and CD59 on surface of cell!!! remember these can’t protect cells against complement anymore because they can’t bind to nonexistant GPI.


Q: genetics?
A: X-linked recessive.

Q: Remember what G6PD is used for?
A: part of pentose phosphate pathway, needed to protect cells against oxidative (free radical) damage.

Q: What are the two types?
A: GDPD A- (blacks) and G6PD Mediterranean (favism — induced from eating fava beans if u got the mutation). Protective against malaria.

Q: What are the three genetic diseases that can protect u from malaria?
A: G6PD deficiency, Sickle cell, and beta thalassemia minor.

Q: Remember what “body” do u find in G6PD deficiency RBCs?
A: Heinz bodies – comglomeration of hemoglobin, from oxidatively damaged RBC. When macrophages try to remove them, they “bite” pieces off them –> “BITE CELLS.”

Q: Is G6PD Deficiency intravascular (acute) or extravascular (chronic) hemolysis?
A: BOTH. First, your RBCs are lysed because of oxidative stress (acute, intravascular), but then those cells that survive and have Heinz bodies will stay but get removed by body’s natural mechanisms via macrophages (chronic, extravascular) –> bite cells.


Q: where’s the mutation?
A: In 6th position of Beta-globin gene. Glutamic Acid –> Valine (Semantics: “Glu replaced by Valine”, or “substitution of valine for glutamic aid”)

Q: inheritance?
A: Autosomal recessive. protects against malaria falciparum.

Q: Heterozygous S?
A: 40% of Hgb is S — called “sickle cell trait.” only sickles under severe hypoxia.

Q: Homozygous S?
A: all Hgb is S — called “sickle cell disease”

Q: Can you reverse the sickling?
A: If the RBC is young, it’s still very compliant, and so it can de-sickle. But remember older cells lose elasticity –> irreversibly sickles –> cleared in spleen (extravascular hemolysis)

Q: Are sickled cells sticky?
A: Yes. They tstill to endothelial cell and to each other –> form MICROTHROMBI.

Q: Clinical finding?
A: you see symptoms after 5-6 months old when HbF diminishes. You get microvascular occlusions (from microthrombi), and ischemic tissue damage due to this –> severe pain (hand foot syndrome). You also get AUTOSPLENECTOMY because clogs up the spleen. This increases infection by encapsulated bacteria (Strep pneumo, H. influenza, Salmonella). Bone marrow expansion due to compensation. Hyperbilirubinemia + gallstones. SICKLE CRISIS

Q: What is Sickle Crisis?
A: that severe pain i was talking about due to ischemic tissue damage from microthrombi. pain in bones, lungs (from lung infarct due to microthrombi), liver, kidney, etc. ACUTE CHEST SYNDROME. Slow blood flow in lungs.

Q: Treatment?
A: Hydroxyurea therapy — erythroblasts produce more RBCs with HbF.

Q: In Sickle Cell Trait, how much hemoglobin S do u have?
A: 40%. SICKLING ONLY UNDER EXTREME STRESS so usually no hemolysis or microthrombi.

Q: Diagnostic testing?

Q: WHat is Hemoglobin C Trait?
A: another abnormal hemoglobin, called Hemoglobin C. ASYMPTOMATIC, usually in blacks.

Q: What is Hemoglobin SC disease?
A: having both HbC and HbS — milder than sickle cell disease. Also in blacks.


Q: What kinds are there?
A: Alpha and Beta thalassemias — respectively, decreased synthesis of alpha and beta globins.

Q: Where?
A: Alpha thal — SE Asia, china and blacks. A for ASIA.
Beta thal — Italy, greece. B for BYZANTIUM.

Q: What are the components of a normal hemoglobin?
A: 2 beta globins (b1, b2) from Chromosome 11 + 4 alpha globins (a1,2,3,4) from Chrom 16.

Q: Number of alpha globin defects and their diseases:
1 = silent carrier — asymptomatic
2 = alpha-thal trait — mild
3 = Hb H disease. to compensate for lack of alpha globins, your beta globins form tetramers (B Tetramers). H for Hemolytic Anemia.
4 = Hb Bart’s disease (u see hydrops fetalis, basically dead fetus)

Q: Number of beta globin defects and their diseases:
1 = B+
2 = B0
Beta thal minor = B/B+ or B/Bo
Beta thal major = Bo/Bo or Bo/B+
Beta thal intermedia = B+/B+

Q: What happens to the alpha globins that are unparied in B thalassemias?
A: they precipitate.

Q: Clinical presentation?
A: bone marrow die –> decrease erythropoiesis –> compensate by increase iron absorption –> systemic iron overload. spleen destroys defective RBCs –> extravascular anemia –> tissue anoxia –> compensate by increasing erythropoiesis –> marrow expansion –> new bone formation causing big forehead, skull, etc.

Q: Treatment?
A: red cell transfusion, oral iron chelation (so can sequester extra iron), bone marrow transplant.


Q: What are indicators of lead poisoning?
A: ELEVATED Zinc Protoporphyrins or free Erythrocyte protoporphyrins.

Q: Why is lead poisoning bad?
A: it denatures ferrochelatase (which chelates the Fe to protoporphyrin ring to form heme) –> can’t synthesize heme.

Q: What do you see clinically in lead poisoning?
A: Adults — peripheral neuropathy. Kids — low IQ, hyperactivity, from eating peeling lead paint.

Q: What “body” do you see in lead poisoning?
A: Basophilic stipping. Lead inhibits ALA synthase/dehydratase, ribonuclease and ferrochelatase –> Fe can’t bind protoporphyrin ring –> no heme and therefore no hemoglobin. Basophilic stippling is due to inhibited ribonuclease not able to degrade RNA/ribosomes –> remannts form bodies.


Q: How is ring sideroblasts formed?
A: too much Fe in bone marrow –> Fe stuck in mitochondria, so it can’t be used to make heme.


Q: DIC vs. TTP and HUS:
A: DIC — NO FEVER or Neuro symptoms!! PT/PTT ELEVATED! Normal in TTP/HUS.


Q: What is it?
A: Hemolytic anemia caused by IgG anti-RBC autoantibody. Reacts at 37 degrees C.

Q: Cause?
A: Can be primary and idiopathic, or secondary to CLL and other lymphomas.


Q: What is it?
A: Pathologic autoimmune IgM. bind to RBC at cold temperatures (i.e. peripheral circulation) –> agglutination and hemolysis –> Cryocyanosis (blue) at EXTREMITIES

Q: Cause?
A: Can be primary/idiopathic, or secondary to Waldenstrom’s Macroglobulinemia, EBV, CLL, Diffuse Large B-Cell Lymphoma, etc.


Q: What is it?
A: Pathologic autoimmune IgG autoantibodies –> bind to P blood group at low temps –> when go to warm areas, complement lysis cell –> PAROXYSMAL COLD HEMOGLOBINURIA. VERY ACUTE!!!

Q: Cause?
A: syphilis, mycoplasma, measles, mumps, flu. RARE.


Q: How do we define erythrocytosis? anemia?
A: Erythrocytosis — hematocrit greater than 97.5% of normal.
Anemia — hematocrit less than 2.5% of normal.

Q: What’s the consequence?
A: increased blood viscocity –> neuro symptoms, thrombosis.

Q: Treat?
A: Phlebotomy to decrease RBC maass if hematocrit over 54. Remember Hemoglobin below 7 you start feeling the effects.

Q: What’s the most common cause of Erythrocytosis?


Q: What are the three types?
Normochromic (normal size) — Aplastic anemia, Pure Red Cell Aplasia
Microcytic (small size) — Iron deficiency, anemia of chronic disease
Macrocytic (big size) — B12 deficiency, Folate deficiency (which remember also causes hypersegmentation in neutrophils)


Q: What is it?
A: myeloid stem cells disorder –> decreased synthesis of all RBC, WBC, platelets.

Q: Cause?
A: autoreactive CD8 T cells (autoimmune), genes, CHLORAMPHENICOL, radiation, virus.

Q: What’s the most common cause of aplastic anemia?

Q: symptoms?
A: fatigue (due to anemia), infections (due to leukopenia), PETECHIAE (due to thrombocytopenia!!).. so symptoms due to decrease in all three cell lines.

Q: What do you see in bone marrow of aplastic anemia?
A: HYPOCELLULAR. mainly fat. (vs. myeloproliferative disorders)

Q: Treat?
A: depends on the cause. You could use immunosuppressive drug, stem cell transplant, or supportive treatment. poor prognosis.


Q: What is it?
A: like aplastic anemia except ONLY WITH RBC PROGENITOR!!! decreased RBC production.

Q: cause?
A: Thymomas (which cause autoimmunity), Parvovirus B19 (which only infects young RBCs)!!

Q: How can you tell Pure Red Cell Aplasia is caused by Parvovirus?
A: In the immature RBC in the bone marrow, you see nuclear inclusions.


Q: What do you see?
A: Pancytopenia, teardrop RBC, nucleated RBC.

Q: Cause?
A: fibrosis/tumor in bone marrow –> pushes progenitor cells out of central locations (bone marrow) to peripheral locations (vessels) –> RBC squeeze through fibrosis –> warps and become tear shaped, like in primary myelofibrosis.

Q: What would you see on a question stem?
A: 60 year old patient with cancer comes in with anemia. They find tear-shaped RBCs in peripheral blood.


Q: What’s the most common cause of anemia worldwide?
A: Iron Deficiency Anemia.

Q: Cause?
A: not enough iron intake (i.e. diet, malabsorption, GI disease), too much iron loss (i.e. hemodialysis, blood loss), increased iron use by body (i.e. during pregnancy)

Q: symptoms?
A: Pica (eat dirt), fatigue, Koilonichia (spoon nails), PLUMMER VINSON SYNDROME.

Q: What is Plummer vinson syndrome (Triad)?
A: Iron Deficiency, Glossitis, Esophageal webs.

Q: What do you see microscopically?
A: microcytic (small), hypochromic (very light colored) RBCs –> anisocytosis, increased RDW. ANISOCYTOSIS (especially if you also got a blood transfusion with normal colored and normal size blood cells).


Q: What Hb is it?
A: Hb is between 9-12. Remember normally you start feeling the
effects at Hb 7.

Q: cause?
A: secondary to Chronic disease — impaired RBC production. This is a general term, so the chronic disease can be due to infection, autoimmunity, or malignancy. It causes decreased Erythropoietin levels or inability to get the iron into the RBC precursors –> less blood, but blood is NORMAL SIZE and often NORMAL COLOR. NO ANISOCYTOSIS (vs. Iron deficiency anemia).

Q: What’s the most common cause of anemia among hospitalized patients?
A: Anemia of Chronic Disease (Because a lot of patients in the hospitals have chronic disease, so anemia is secondary to this!)

Q: Compare Iron deficiency vs. Anemia of Chronic Disease:
A: Iron Deficiency: Anisocytosis, Increased RDW, Decreased Ferritin.
Anemia of Chronic: NO Anisocytosis, NORMAL RDW, INCREASED Ferritin.
THEY BOTH HAVE DECREASED RETICULOCYTES, because both don’t have enough Fe to make Hb.


Q: What is it?
A: Anemia due to impaired DNA synthesis.

Q: Why is it called megaloblastic?
A: they are RBC precursors, and they keep growing bigger without replicating (because no new DNA can be made).

Q: Cause?
A: B12 and Folate deficiency (like hypersegmentation in neutrophils or other macrocytic disorders)

Q: What makes intrinsic factor?
A: Gastric parietal cells (make IF along with HCl)


Q: Causes?
A: Vegetarianism. Pernicious Anemia (autoimmunity against intrinsic factor), increased use (i.e. pregnancy, hyperthyroidism).

Q: What does it cause?
A: hypersegmented PMNs (probably also because can’t synthesize DNA so can’t replicate but instead just grow bigger and bigger), hypercellular bone marrow, thrombocytopenia (can’t do DNA synthesis)

Q: How do you detect it?
A: Decreased Serum Cobalamin (basically B12), elevated methylmalonic acid and HOMOCYSTEINE (which needs B12 to be recycled) in blood –> Deep vein thombosis.

Q: Clinical symptoms?
A: Glossitis (“beefy tongue”), pernicious anemia, neurologic changes (due to demyelination)


Q: B12 deficiency and folic acid deficiency both cause megaloblastic anemia. However, there’s one big difference. What is it?
A: Folic Acid Deficiency does NOT cause neurologic changes!!!!!!!! B12 deficiency does!!!


Q: Why can Rh antibodies cross placenta but ABO doesn’t?
A: Because Rh is IgG (small) and ABO is IgM (doesn’t cross placenta).

Q: What’s the main cause of mortality in blood transfusion?
A: Clerical error.

Q: What infectious agents does the FDA require before collecting prepared human RBC products?
A: Hep B, Hep C, HIV, HTLV, Syphilis.

Q: What’s considered a “massive transfusion”?
A: Transfusing 10 units whole blood/RBC.

Q: Why would you give terminal patients transfusions?
A: So they feel better. You don’t want them to die while feeling the symptoms of anemia.

Q: When would you use a blood warmer?
A: in patients with cryoglobulinemia, cold-reacting antibodies, when the large dose of blood is rapidly infused, or in elderly and infants.

Q: How long after transfusion should you continue to monitor the patient?
A: 24 hrs — you’re looking for hemolytic reactions. Look for pain at infusion site, sudden onset of lower back pain, red urine, dyspnea, or sudden increase in anxiety. These are all signs of hemolytic reaction.

Q: What is TRALI?
A: Transfusion-associated Acute Lung Injury. Due to endothelial cell damage in lungs –> ARDS. you get hypoxemia, tachycardia, hypotension, cyanosis. #1 CAUSE OF DEATH FROM TRANSFUSION!!

Q: What is TACO?
A: Transfusion-associated Circulatory Overload. You put in more volume than what the heart can handle. You’re especially at risk if you have heart disease. To prevent, give blood slowly!!

Q: What is TRIM?
A: Transfusion-related Immunomodulation. Basically if you give transfusion, it could cause reduction in cellular immunity. NK and macrophage activity is decreased. Increase in INFECTIONS, and even CANCER.

Q: Should you give transfusions to critically ill patients?
A: NO! increases mortality rate.

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