IVMS-Hematology-Oncology Terminology Summary Table
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7/28/2019 IVMS-Hematology-Oncology Terminology Summary Table
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HEMATOLOGY/ONCOLOGY TRMINOLOGYSUMMARY TABLE
Terms Definitions
Platelet - contains dense granules (ADP, calcium) and -granules (vWF,fibrinogen)
- approximately 1/3 of the body's platelet pool is stored in spleen
- life span of 8-10 days
- vWF receptor: GpIb- Fibrinogen receptor: GpIIb/IIIb
Macrophage - Phagocytoses bacteria, cell debris, and senescent red cells and
scavenges damaged cells and tissues- long life in tissues
- activated by -interferon
- can function as APC via MHC II- CD14 surface marker
Eosinophils - bilobate nucleus
- packed with large eosinophilic granules of uniform size
- highly phagocytic for Ag-Ab complexes- produces histamine and arylsulfatase (help limit reaction
following mast cell degranulation)
- causes of eosinophilia: neoplasia, asthma, allergic processes,
collagen vascular diseases, parasites
Basophils - mediates allergic reactions
- bilobated nucleus
- densely basophilic granules contain: heparin (anticoagulant),histamine (vasodilator), and other vasoactive amines, and
leukotrienes (LTD4)
- found in blood
Mast cell - mediates allergic reaction
- degranulation - histamine, heparin, and eosinophil chemotatic
factors
- can bind the Fc portion of IgE to membrane- structurally and functionally similar to basophils
- involved in type I hypersensitivity reactions
- found in tissue
Factor XII - first step of the intrinsic pathway- activated by collagen, basement membrane, activated platelets,
and HMWK (bradykinin precursor)
- activates factor XI and converts prokallikrein to kallikrein
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Kallikrein - activated by factor XII
- converts HMWK to bradykinin (kinin cascade)
- converts plasminogen to plasmin (degrades fibrin)
Bradykinin - part of Kinin cascade, activated by intrinsic coagulation
pathway
- vasodilation- permeability
- pain
Common coagulation
pathway
- X (+V) II (aka thrombin) Fibrin aggregation (by XIII
and Ca2+)
- both extrinsic and intrinsic pathways convert on factor X
Factors effected by VitaminK deficiency Factor II (thrombin, common pathway) Factor VII (extrinsic pathway)
Factor IX (intrinsic pathway) Factor X (common pathway
protein C
protein S- vit K activated by epoxide reducatase cofactor in maturation
of II, VII, IX, X, C, and S from precusors
Antithrombin - activated by heparin
- inhibits thrombin and: factor VII (extrinsic)
factor IX (intrinsic) factor X (common) factor XI (intrinsic)
factor XII (intrinsic)
Protein C - Protein C is activated by thrombomodulin from endothelial cells
- protein S assist activated protein C in the cleavage and
inactivation of Va and VIIIa
tPA - activates plasmin, which degrades fibrin- used as a thrombolytic
platelet plug formation - injury: vWF binds to exposed collagen
- adhesion: platelets bind vWF via GpIb receptor and releaseADP and Ca2+ (necessary for coagulation cascade) - ADP: helps platelets adhere to endothelium, ADP binding to
receptor induces GpIIb/IIIa expression at platelet surface
aggregation: fibrinogen binds GpIIb/IIIa receptors and links
platelets
Aggregation balance - Pro-aggregation factors: TXA2 (released by platelets) blood
flow and platelet aggregation
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- Anti-aggregation factors: PGI2 and NO (released by endothelial
cells) blood flow and platelet aggregation
Drugs that disrupt
thrombogenesis
- aspirin: cyclooxygenase ( TXA2 synthesis)- Ticlopidine and clopidogrel: inhibits ADP-induced expression
of GpIIb/IIIa (platelets can't cross link)
- Abciximab: inhibits GpIIb/IIIa directly
Erythrocyte sedimentation
rate
- acute-phase reactants in plasma can cause RBC aggregation,thereby RBC sedimentation rate
- ESR: infections, inflammatory diseases, malignany
neoplasms, GI disease, pregnancy
- ESR: polycythemia, sickle cell anemia, CHF, microcytosis,hypofibrinogenemia
Pathologic RBC forms:
acanthocyte
(AKA: spur cell)
- liver disease- abetalipoproteinemia
Pathologic RBC forms:
basophilic stippling
- Thalassemia
- Anemia of chronic disease- Iron deficiency
- Lead poisoning
Pathologic RBC forms:
Elliptocyte
- hereditary elliptocytosis
Pathologic RBC forms:
macro-ovalocyte
- megaloblastic anemia (also hypersegmented PMNs)
- marrow failurePathologic RBC forms:
ringed sideroblasts
- sideroblastic anemia
Pathologic RBC forms:
schistocyte
- DIC
- TTP/HUS
- traumatic hemolysis
Pathologic RBC forms:
spherocyte
- hereditary spherocytosis
- autoimmune hemolysis
Pathologic RBC forms:
teardrop cell
- bone marrow infiltration
Pathologic RBC forms:
target cells
- HbC disease
- Asplenia- Liver disease
- Thalassemia
Pathologic RBC forms:
Heinz bodies
- oxidation of iron from ferrous to ferric form leads to
**denatured hemoglobin precipitation and damage to RBC
membrane- -thalassemia
- G6PD deficiency
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Pathologic RBC forms:
Howell-Jolly bodies
- basophilic nuclear remnants found in RBCs
- due to functional hyposplenia or asplenia
Microcytic anemias - Iron deficiency- Anemia of chronic disease (may initially present as normocytic
anemia)
- Thalassemias- Lead poisoning
- Sideroblastic anemia
Normocytic, nonhemolytic
anemias
- Anemia of chronic disease (progresses to microcytic)
- Aplastic anemia
- Kidney disease
Hemolytic anemias -intrinsic - RBC membrane defect: hereditary spherocytosis- RBC enzyme deficiency: G6PD, pyruvate kinase deficiency
- HcC- Sickle cell anemia
- Paroxysmal nocturnal hemoglobinuria
Hemolytic anemias -
extrinsic
- Autoimmune- Microangiopathic hemolytic anemia (MIHA)
- Macroangiopathic hemolytic anemia (MAHA)
- Infections
Megaloblastic anemias - Folate deficiency- B12 deficiency
Macrocytic,nonmegaloblastic anemias - DNA synthesis is impaired-caused by liver disease, alcoholism, reticulocytosis MCV,
metabolic disorders, congenital deficiencies of purine andpyrimidine synthesis and drugs (5-FU, zidovudine, hydroxyurea)
Iron deficiency anemia - microcytic, hypochromic
- iron heme synthesis- Plummer-Vinson: iron deficiency anemia, esophageal web,
atrophic glossitis
- Labs: serum iron
transferrin or TIBC
ferritin % transferrin saturation
-thalassemia - microcytic, hypochromic- defect in -globin gene mutation -globin synthesis
- prevalent in Asian and African populations
- peripheral blood smear: basophilic stippling, target cells, Heinzbodies
- 4 gene deletion = hydrops fetalis, (Hb Barts, 4)
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- 3 gene deletion = HbH disease (4)
- 1-2 gene deletion = no significant anemia
-thalassemia minor - microcytic, hypochromic- point mutations in splice sites and promoter sequences -
globin synthesis
- HbF (22)- peripheral smear: anisocytosis, poikilocytosis, target cells,
schistocytes
- seen in Mediterranean populations
- minor = heterozygote- chain is underproduced
- usually asymptomatic
- Diagnosis confirmed by HbA2 (22) on electrophoresis
-thalassemia major - microcytic, hypochromic-point mutations in splice sites and promoter sequences -
globin synthesis
- HbF (22)- seen in Mediterranean populations
- major = homozygote
- chain is absent severe anemia requiring blood transfusions
-presents with marrow expansion skeletal deformities,Chipmunk facies
HbS/-thalassemia
heterozygotes
- mild to moderat sickle cell disease depending on amount of -
globin production
Lead poisoning anemia - microcytic, hypochromic
- lead inhibits ferrochelatase and ALA dehydratase heme
synthesis, protoporphyrin in blood
- also inhibits rRNA degredation- presents with lead lining the epiphyses of long bones on x-ray,
encephalopathy, erythrocyte basophilic stippling, abdominal
colic, wrist/foot drop and sideroblastic anemia- adults: headache, memory loss, demyelination
- treatment: Dimercaprol, EDTA, and succimer (for kids)
Sideroblastic anemia - microcytic, hypochromic- defect in heme synthesis- Hereditary: x-linked defect in -aminolevulinic acid synthase
gene
- reversible etiologies: alcohol, lead
- peripheral smear: ringed sideroblasts (from iron-ladenmitochondria)
- Labs: iron, normal TIBC, ferritin
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- extravascular hemolysis
- defects in ankyrin, band 3, protein 4.2, or spectrin which are
involved in cytoskeleton and membrane integrity- less membrane spherocytes premature removal by spleen
- labs: MCHC, RDW
- presents with splenomegaly, aplastic crisis (B19 infections),positive osmotic fragility test
- treat with splenectomy
Mean Cell Volume (MCV) - Average **size of red blood cells
- Normal range: 80-100 fL (1 fL = 10-15 L)- Differentiates between
microcytic (MCV < 80)
normocytic (MCV 80-100)
macrocytic (MCV >100) anemias
Mean cell hemoglobin
concentration (MCHC)
- Concentration of Hgb RBC - expresses coloration**
- Normal range: 32-36 g/dL
- Differentiates between hypochromic (MCHC < 32) andnormochromic (MCHC 32-36) anemias
- normochromic cells have a "zone of central pallor" (that white
dot in the middle of the cell) that is no more than 1/3 the diameter
of the red cell.- Hypochromic red cells have just a thin rim of hemoglobin.
Red cell distribution width
(RDW)
- Standard deviation of the MCV
- Tells you how much the RBC differ from each other in size.Anisocytosis
- If they are all pretty similar in size, the RDW is low.
- If some are little and some are big, the RDW is high.- Normal range = 12-13.5%
G6PD deficiency - intrinsic hemolytic, normocytic anemia
- intravascular and extravascular hemolysis
- x-linked- hemolytic anemia follows oxidative stress
- presents with back pain and hemoglobinuria a few days later
Pyruvate kinase deficiency - intrinsic hemolytic, normocytic anemia- extravascular hemolysis- autosomal recessive
- defect in pyruvate kinase ATP rigid RBCs
pyruvate kinase catalyzes pyruvate to lactate
- hemolytic anemia in newborns
HbC defect - intrinsic hemolytic, normocytic anemia
- glutamic acid-to-lysine mutation at position 6 in chain mutation
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- patients with HbSC (1 of each mutated gene) have milder
disease than do HbSS patients
Paroxysmal nocturnal
hemoglobinuria
- intrinsic hemolytic, normocytic anemia- intravascular hemolysis
- complement-mediated RBC lysis
- impaired synthesis of GPI anchor/decay-accelerating factor inRBC membrane
- urine hemosiderin
- complication: thrombosis
Sickle cell anemia -point mutation on -chain (glutamic acid valine at position 6)
- sickling from low O2 or dehydration- complications: aplastic crisis (Parvovirus B19),
autosplenectomy, splenic sequestration crisis, salmonella
osteomyelitis, painful crisis (dactylitis [painful hand swelling],acute chest syndrome), renal papillary necrosis, microhematuria
- treatment: hydroxuria (HbF), bone marrow transplant
autoimmune hemolytic
anemia
- extrinsic hemolytic, normocytic anemia- warm agglutination (IgG) - chronic anemia seen in SLE, CLL,
or with certain drugs
- cold agglutination (IgM) - acute anemia triggered by cold, seen
in CLL, Mycoplasma pneumonia infections, or mononucleosis- usually Coomb's test positive
Erythroblastosis fetalis - seen in newborns due to Rh or other blood antigenincompatibility- mother's Ab attack fetal RBCs
Direct Coomb's test - anti-Ig antibody added to patient's RBCs agglutinate if RBCs
are coated with Ig
Indirect Coomb's test - normal RBCs added to a patient's serum agglutinate if serumhas anti-RBC surface Ig
Microangiopathic anemia - extrinsic hemolytic, normocytic anemia
- intravascular hemolysis- RBCs are damaged when passing through obstructed or narrow
vessel lumina
- seen in DIC, TTP-HUS, SLE, and malignant hypertension- schistocytes on blood smear
Macroangiopathic anemia - extrinsic hemolytic, normocytic anemia- intravascular hemolysis
- prosthetic heart valves and aortic stenosis may also cause
hemolytic anemia, mechanical destruction- schistocyte on peripheral smear
Hemochromatosis - labs:
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serum iron
transferrin
ferritin % transferrin saturation
Acute intermittent
porphyria
- defective heme synthesis that leads to accumulation of heme
precursors- affected enzyme: porphobilinogen deaminase
- accumulation of porphobilinogen, - ALA, uroporphyrin
- presents with painful abdomen, red wine colored urine,
polyneuropathy, psychological disturbance, precipitated by drugs- treat with glucose and heme
Porphyria cutanea tarda - defective heme synthesis that leads to accumulation of heme
precursors
- affected enzyme: Uroporphyrinogen decarboxylase- accumulation of uroporphyrin
- blistering cutaneous photosensitivity
- most common porphyria
PT (prothrombin time) - tests the extrinsic pathway
- factor VII (also I, II, V, and X)
- defect leads to increased time
aPTT (Partial
Thromboplastin Time)
- tests the intrinsic pathway- all factors except VII and XIII
- defect leads to increased timeHemophilia - aPTT
- A: deficiency in VIII- B: deficiency in IX
- macrohemorrhage, hemarthroses, easy bruising
Platelet disorders - defect in platelet plug formation bleeding time-platelet abnormalities microhemorrhages, mucous membrane
bleeding, epitaxis, petechiae, purpura, bleeding time, possible
platelet count- Bernard-Soulier disease, Glanzmann's thrombathenia, idiopathic
thrombocytopenic purpura (ITP), Thrombotic thrombocytopenic
purpura (TTP)Bernard-Soulier disease - defect in platelet plug formation- GpIb defect in platelet to collagen adhesion
- platelet count
- Bleeding time
Glanzmann's
thrombasthenia
- defect in platelet plug formation- GpIIb/IIIa defect in platelet to platelet aggregation
- bleeding time, blood smearshows no platelet clumping
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Idiopathic
thrombocytopenic purpura
(ITP)
- platelet survival
- anti- GpIIb/IIIa antibodies peripheral platelet destruction
- megakaryocytes- bleeding time
- platelet count
Thrombotic
thrombocytopenic purpura
(TTP)
- platelet survival- deficiency of ADAMTS 13 degradation of vWF multimers
platelet aggregation and thrombosis
- Labs: schistocytes, LDH
- presents with pentad of neurologic and renal symptoms, fever,thrombocytopenia, and microangiopathic hemolytic anemia
- platelet count
- bleeding time
von Willebrand's disease - vWF carries and protects factor VIII, connects GpIb of plateletto collagen
- defect of intrinsic pathway, vWF may see aPTT
- defect of platelet adhesion to collagen bleeding time- mild, but most common bleeding disorder
- treatment: desmopressin (releases vWF stored in epithelial cells)
DIC - wide spread activation of clotting leads to a deficiency in
clotting factors bleeding state- caused by sepsis (G (-)), trauma, obstetric complications, acute
pancreatitis, Malignancy, Nephrotic syndrome, Transfusion
- Labs: schistocytes, fibrin split product (D-dimer), fibrinogen, factors V and VII
Factor V Leiden - production of mutant factor V that cannot be degraded by
protein C
- most common cause of inherited hyprcoagulability
Prothrombin gene mutation - leads to hypercoagulable state
- mutation in 3' untranslated region associated with venous clots
Antithrombin deficiency - leads to hypercoagulable state- inherited deficiency of antithrombin
- reduced in PTT after administration of heparin
Protein C or S deficiency - leads to hypercoagulable state- ability to inactivate factors V and VIII- risk of thrombotic skin necrosis with hemorrhage following
administration of warfarin
Blood transfusion therapy:
packed RBCs
- Hb and O2 carrying capacity
- acute blood loss and severe anemia
Blood transfusion therapy:
platelets
- platelet count
- usually given in 6 platelet units for therapeutic effect
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- stop significant bleeding (thrombocytopenia, qualitative platelet
defects)
Blood transfusion therapy:
Fresh frozen plasma
- coagulation factor levels by about 20%- treats DIC, cirrhosis, warfarin over-anticoagulation
Blood transfusion therapy:
cryoprecipitate
- contains fibrinogen, factor VIII, factor XIII
- treats coagulation factor deficiencies involving fibrinogen and
factor VIII
Blood transfusion risks - infection
- reactions
- iron overload
- hypocalcemia - citrate is a calcium chelator
- hyperkalemia - RBCs may lyse in older blood unitsHodgkin's lymphoma - Reed-Sternberg cells (CD30+/CD15+)
- localized to single group of nodes- contiguous spread
- constitutional signs/symptoms - low-grade fever, night sweats,
weight loss- mediastinal lymphadenopathy
- 50% of cases associated with EBV
- bimodal age distribution
- more common in men except the nodular sclerosing type(lacunar variant of RS cells)
- good prognosis = lymphocytes, RS cellsNon-Hodgkin's lymphoma - may be associated with HIV and immunosuppression
- multiple peripheral nodes- extranodal involvement common
- noncontiguous spread
- majority involve B cells (except for those of lymphoblastic Tcell origin)
- fewer constitutional signs/symptoms
- peak incidence for certain subtypes at 20-40 years
Nodular sclerosing
Hodgkin's lymphoma
- most common type (65-75%)
- variant type RS cells
- increased # of lymphocytes- excellent prognosis- collagen banding, women >men, primarily young adults
Mixed cellularity Hodgkin's
lymphoma
- lots of RS cells
- increased lymphocytes
- intermediate prognosis- 25% of Hodgkin's lymphoma cases
Lymphocyte predominant - seen in males under 35
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Hodgkin's lymphoma - some RS cells, lymphocytes
- excellent prognosis
- 6% of Hodgkin's lymphoma cases
Lymphocyte depleted
Hodgkin's lymphoma
- slight increase in lymphocytes
- RS high relative to lymphocytes
- seen in older males with disseminated disease- poor prognosis
Burkitt's lymphoma - non-Hodgkin's lymphoma
- seen in young adults
- genetics: t(8;14) c-myc gene moves next to heavy-chain Ig gene
- "starry-sky" appearance - sheets of lymphocytes withinterspersed macrophages
- EBV
- Jaw lesion most common, pelvis or abdomen in sporadic form
Diffuse large B-cell
lymphoma
- non-Hodgkin's lymphoma
- usually seen in older adults, 20% in kids
- most common NHL- may be of mature T cell origin (20%)
Mantle cell lymphoma - non-Hodgkin's lymphoma, B cell
- seen in older males
- genetics: t(11;14) overexpression of cyclin D regulatory gene- CD5+
- poor prognosisFollicular lymphoma - non-Hodgkin's lymphoma, B cell
- seen in adults- genetics: t(14;18) bcl-2 expression inhibits apoptosis
- difficult to cure, indolent course
Adult T cell lymphoma - non-Hodgkin's lymphoma, T cell- seen in adults
- caused by HTLV-1
- adults present with cutaneous lesions- especially effects populations in Japan, West Africa, and the
Caribbean
- aggressiveMycosis fungoides/Sezary
syndrome
- non-Hodgkin's lymphoma, T cell- seen in adults
- adults present with cutaneous patches/nodules
- indolent CD4+
Multiple myeloma - monoclonal plasma cell (fried egg appearance) cancer that arisesfrom the marrow and produces large amounts of IgG (55%) or
IgA (25%)
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- most common 1 tumor arising within bone in the elderly
- intracytoplasmic inclusions containing Ig
- CRAB: hyperCalcemia
Renal insufficiency
Anemia Bone lytic lesions Back pain
(distinguish from Waldenstrom's macroglobulinemia M spike
= IgM, and no lytic bone lesions)
MGUS - monoclonal gammopathy of undetermined significance- monoclonal plasma cell expansion without symptoms of
multiple myeloma
Leukemias - unregulated growth of leukocytes in bone marrow
- or number of circulating leukocytes in blood and marrowfailure
- anemia, infections, & hemorrhage
- leukemic cell infiltrates in liver, spleen, and lymph nodes arepossible
ALL - Acute lymphoblastic
leukemia/lymphoma
- usually seen < 15 y/o
- may present with BM involvement in children or mediastinal
mass in adolescent males- BM replaced by lymphoblasts
- TdT+ (marker of pre-T/B cells)
- CALLA+- most responsive to therapy
- may spread to CNS or testes
- genetics: t(12;21)
SLL - small lymphocytic
lymphoma/CLL - chronic
lymphocytic leukemia
- usually seen > 60 y/o- often asymptomatic
- smudge cells in peripheral smear
- warm antibody autoimmune hemolytic anemia- SLL is same as CLL except CLL has peripheral blood
lymphocytes
Hairy cell leukemia - seen in adults- Mature B cell tumor in elderly- cells have filamentous hairlike projections
- stain TRAP (tartrate-resistant acid phosphatase) positive
AML - Acute myelogenous
leukemia
- seen in 60 y/o
- Histo: Auer rods in cytoplasm- circulating myeloblasts on peripheral smear
- genetics: t(15;17) M3 AML (acute promyelocytic leukemia)
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responds to all-trans retinoic acid (vitamin A), which induces
differentiation of myeloblasts
- DIC is common presentation
CML - Chronic
myelogenous leukemia
- 30-60 y/o
- Philadelphia chromosome - t(9;22), bcr-abl
- JAK2 mutation?- myeloid stem cell proliferation
-presents with RBC, neutrophils, metamyelocytes, basophils,
platelets; splenomegaly
- may accelerate and transform to AML or ALL (blast crisis)- very low leukocyte alkaline phosphatase due to immature
granulocytes
- treat with imatinib
Auer bodies - peroxidase-positive cytoplasmic inclusions in granulocytes andmyeloblasts
- commonly seen in acute promyelocytic leukemia (M3)
- treatment of AML M3 can release Auer rods DIC
Langerhans cell
histiocytosis (LCH)
- proliferative disorder of dendritic (langerhans) cells from
monocyte lineage
- etiology unknown
- cells are functionally immature and do not efficiently stimulateT lymphocytes
- cells express S-100 and CD1a
- Birbeck granules (look like tennis rackets on EM)
Polycythemia vera - chronic myeloproliferative disorders
- abnormal clone of hematopoietic stem cells are increasingly
sensitive to growth factor
- RBCs ( plasma volume, RBC mass)- WBCs
- platelets
- genetics: JAK2+
Essential thrombocytosis - chronic myeloproliferative disorders
- similar to polycythemia vera, but specific for megakaryocytes
- platelets- genetics: JAK2+ (30-50%)
Myelofibrosis - chronic myeloproliferative disorders
- fibrotic obliteration of BM
- teardrop cells in blood smear
- RBCs- variable amounts of WBCs
- variable amounts of platelets
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- presents with achlorhydria (lack of gastric acid) due to parietal
cell destruction, chronic gastritis, increased risk of gastric
carcinoma, elevated serum gastrin, and signs of vitamin B12deficiency