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Hemetology > Hematology 2 > Flashcards

Hematology 2 Flashcards

1
Q

Normal Hb in Children

A

11 + 0.1(Age in years)

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2
Q

Lower Normal MCV in Children

A

70+ Age in years up to 80.

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3
Q

Ferritin below __ is highly specific for IDA

A

15

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4
Q

B Thalassemia

A

One locus on each chromosome 11. Microcytosis out of proportion to the degree of anemia.

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5
Q

A Thalassemia

A

Two loci on each chromosome 16.

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6
Q

One defective alpha thal gene

A

Asymptomatic carrier

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7
Q

Two defective alpha thal genes

A

Alpha thalassemia minor, target cells. Normal Hb electro

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8
Q

Three defective alpha thal genese

A

Hb H (Clumped chains), leads to hemolytic anemia. Tx: Splenectomy and transfusions

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9
Q

Four defective alpha thal genes

A

No functional Hb, not compatible with life.

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10
Q

Transient Erythroblastopenia of Childhood (TEC)

A

Pure red cell aplasia. Occurs in healthy young children 6mo to 6 years. Normocytic anemia with low Hb but normal non RBC cell lines. Spontaneous recovery.

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11
Q

Diamond Black Fan Anemia

A

Pure red cell aplasia. Severely low Hb, macrocytosis, low rets, otherwise normal cell lines. 30-50% congenital abnormalities.

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12
Q

HbSS

A

SCD Only HbS, severe symptoms

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13
Q

HbSBo

A

SCD No HbA, severe symptoms

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14
Q

HbSB+

A

SCD Some HbA, milder symptoms

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15
Q

HbSC

A

SCD HbS and HbC present, milder symptoms.

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16
Q

Severe SCD manifestations

A

Splenic infarction, functional asplenia, low Hb, vasooclussion.

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17
Q

Aplastic crisis

A

cessation of erythropoeisis often due to parvovirus B19. Increased anemia, decreased reticulocytes.

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18
Q

SCD Painful episodes

A

triggered by cold, dehydrations, stress, alcohol, but usually no obvious cause.

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19
Q

Acute Chest Syndrome

A

SCD most common cause of death. Peak incidence between 2 and 4 years old. Dx: New infiltrate with chest pain or fever or resp distress.

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20
Q

Hereditary Spherocytosis

A

Hemolytic anemia, spenomegaly, jaundice, normal MCV, ELEVATED MCHC, elevated retics.

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21
Q

Compared with _______ transfusion strategies, _________ strategies resulted in better patient outcomes.

A

Liberal (10hb), Restrictive (7hb)

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22
Q

Indications for Plasma transfusion

A

Correction of major bleeding, Deficiency in multiple coagulation factors, Massive transfusion protocol

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23
Q

Cryoprecipitate contains:

A

Factor VIII, Factor XIII, Fibrinogen, vwF

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24
Q

Cryoprecipitate is used for:

A

Fibrinogen replacement in bleeding, when normal treatment medications are not available for vWF disease, or factor 8/13 deficiency.

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25
Q

Recombinant Factor VIII

A

Used in Hemophilia to prevent bleeding episodes and preoperative management.

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26
Q

Prothrombin Complex Concentrate

A

Contains vitamin K dependent factors: 2, 7, 9, 10

Used in hemophilia patients experiencing hemorrhage or to control perioperative bleeding.

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27
Q

IVIG

A

SCIDS, agammaglobulinemia

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28
Q

Albumin

A

Hypoalbunemia, sometimes volume replacement.

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29
Q

Febrile TR

A

Temp increased by 1C from the pretransfusion value during or up to 4 hours post transfusion. More frequent in plasma.

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30
Q

Allergic TR

A

Allergens from the donor, more likely in plasma. Urticaria and Pruritus within 4 hours. Treat with Diphenhydramine. This is the only time of TR where treatment can be restarted.

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31
Q

Anaphylaxis TR

A

Antibodies to something in the component, usually IgA. Fast HR and low BP. Stop tranfusion and place in trendelenburg. Use washed products.

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32
Q

TACO

A

Can occur within 6 hours, but usually happens during the transfusion. Causes pulmonary edema, increased BP and HR, hypoxia. Patient will have elevated BNP and bilateral “White Out” infiltrates. Treat by stopping transfusion, reverse trendelenburg, O2, and diuretics.

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33
Q

TRALI

A

Reaction requiring neutrophils to be primed and present in large numbers in the lungs. The neutrophils then react to the tranfusion and cause damage to lung tissue. Difficulty breathing, fever, chills.

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34
Q

TRALI Diagnosis Criteria

A
  • No evidence of previous acute lung injury
  • Acute lung injury within 6 hours of tranfusion
  • Hypoxemia
  • Bilateral infiltrates
  • No evidence of TACO
  • No risk factors for ALI/ARDS
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35
Q

Acute Hemolytic TR

A

RBC lysis by antibodies. Usually an ABO discrepancy. Almost always a clerical error. Triad: Fever, flank pain, red or brown urine. Tx: stop transfusion, IV saline, support.

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36
Q

Delayed Hemolytic TR

A

Development of new antibodies to RBCs. Occurs 3 to 30 days post transfusion. Should inform the patient for future transfusions.

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37
Q

Posttransfusional Purpura

A

Extremely rare, antiplatelet antibodies destroys tranfused platelets as well as host platelets. Tx: IVIg

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38
Q

Endothelin

A

Following injury, this triggers localized vasoconstriction.

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39
Q

_______ on the platelet binds to ________ on the subendothelium allowing for initial platelet adhesion and activation.

A

GpIb, vWF

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40
Q

vWF will bind to ________ in addition to GpIb.

A

Factor VIII, allows for accumulation at site of injury

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41
Q

______ On the platelet membrane binds to collagen

A

integrin alpha2beta1

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42
Q

Platelet activation causes these changes

A

Spiny shape, negatively charged phospholipids migrate to the platelet surface, release of dense and alpha granules, production and release of thromboxane A2.

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43
Q

Contents of alpha granules

A

Coagulation proteins (vWF, and Factor V) Wound healing proteins (fibronectin, PDGF)

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44
Q

Contents of dense granules

A

ADP, ATP, Ca2+, 5HT, Epi

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45
Q

______ Triggers change in conformation of GpIIb-GpIIIa receptor in platelet membrane which allows fibrinogen.

A

ADP

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46
Q

von Willebrand Disease

A

lowered vWF levels and function, reduced factor VIII. Managed with desmopressin. Type 1: most common, reduced vWF amount. Type 2: qualitative deficiency if vWF. Type 3: complete deficiency of vWF.

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47
Q

Desmopressin

A

induces release of vWF and factor VIII

48
Q

Bernard-Soulier syndrome

A

Failure of platelets to aggregate in response to stimuli. Defective interaction between vWF and GpIb. Giant platelets in PBS.

49
Q

Glanzmann thrombasthenia

A

Quantitative or qualitative defect in GpIIb/GpIIIa. Platelets won’t aggregate.

50
Q

These clotting factors contain y-carboxyglutamate (Calcium chelator)

A

Prothrombin, VII, IX, X

51
Q

The enzyme that converts glutamate to y-carboxyglutamate requires ________ as a cofactor.

A

Vitamin K

52
Q

Warfarin

A

Blocks Vitamin K epoxide reductase, preventing the recycling of Vitamin K and production of y-carboyxglutamate.

53
Q

Tissue Factor (Factor III)

A

Part of the initiation complex for the clotting cascade. Membrane bound, in the presence of Ca2+ will bind and activate factor VII.

54
Q

Factor VII

A

Part of the initiation complex foe the clotting cascade. Activated by tissue factor in the presence of calcium. Once activated, will cleave factor X into factor Xa.

55
Q

Factor X

A

Part of the initiation complex for the clotting cascade. Activated by VIIa. Once active, it slowly cleaves prothrombin to thrombin. Complexes with Va and Ca2+ to rapidly cleave prothrombin to thrombin.

56
Q

Thrombin

A

Activated from prothrombin by factor Xa. Activates factors V, VIII, and IX. Converts Fibrinogen to fibrin. Converts factor XIII to XIIIa.

57
Q

Factor V

A

Activated by thrombin. Complexes with Xa and calcium to rapidly cleave prothrombin to thrombin.

58
Q

Factor VIII

A

Activated by thrombin. Forms a complex with IXa and calcium which quickly activates factor X.

59
Q

Factor IX

A

Activated by thrombin and XIa. Forms a complex with VIIIa and calcium which quickly activates factor X.

60
Q

aPPT

A

Intrinsic pathway. assess function of factors IX, XI, VIII, X, V, prothrombin, fibrinogen.

61
Q

Factor XI

A

Activated by thrombin, cleaves IX to IXa.

62
Q

PT

A

Extrinsic pathway. Assesses function of VII, X, V, prothrombin, and fibrinogen.

63
Q

Hemophilia A

A

Factor VIII deficiency

64
Q

Hemophilia B

A

Factor IX deficiency

65
Q

Factor XIII

A

Activated by thrombin. cross links the fibrin clot to form a hard clot.

66
Q

Thrombomodulin

A

Alters the activity of Thrombin to activate protein C.

67
Q

Protein C

A

activates and binds protein S. Stimulates t-PA release.

68
Q

Protein C/S Complex

A

degrates factor Va, and VIIIa

69
Q

Factor V Leiden

A

Factor V that is resistant to cleavage by protein C/S. R506G mutation. Increased risk of hypercoagulation. 50% of inherited thrombophilia.

70
Q

Antithrombin III

A

Serpin. Binds Heparin and inhbits thrombin. Heparin-ATIII complex inhibits IXa, Xa, XIa, and XIIIa.

71
Q

Tissue Factor Pathway Inhibitor

A

Produced by endothelial cells, inhibits factor VIIa and Xa.

72
Q

Tissue Plasminogen Activator

A

Activates plasminogen to plasmin, secreted by endothelial cells, binds to fibrin clots. Inhibited by alpha 2 antiplasmin and alpha2 macroglobulin.

73
Q

Clopidogrel (Plavix)

A

Prevents ADP binding the platelets

74
Q

GpIIb-GpIIIa Inhibitors

A

Abciximab (Reopro), Eptifibatide (Integrellin), Tirofiban (Aggrastat)

75
Q

ITP

A

Immune Thrombocytopenic Purpura. Platelet destruction by autoantibodies. Associated with a viral prodrome. Low platelets in the absence of other defined causes. Tx: IgG, Steroids

76
Q

TTP

A

Thrombotic Thrombocytopenic Purpura. Huge monomers of vWF that attract platelets due to ADAMTS-13 deficiency. Causes narrowing of vessels that shear RBCs into “Helmet Cells”. Consumption coagulopathy. 90% fatal if untreated.

77
Q

TTP Triad

A

Thrombocytopenia, Microangiopathic Hemolytic Anemia, Neurological Findings, Renal Insuficiency, Fever.

78
Q

Hemolytic Uremic Syndrome

A

Most common cause of acute renal failure in children. Secondary to Shiga toxin. Toxin adheres to neutrophils and platelets, carried to golmerulus, stimulates formation of huge vWF monomers which cause microangiopathic hemolytic anemia. Tx: treat infection, tranfusion, fluids.

79
Q

Heparin Induced Thrombocytopenia

A

Autoantibodies against heparin antigen complex. Type I is transient, type II is bad. Can cause thrombosis.

80
Q

Heparin

A

Increases antithrombin activity by 1000 fold. Antithrombin inactivates thrombin and Xa.

81
Q

Hemophilia C

A

Factor XI deficiency, autosomal recessive

82
Q

Virchow Triad

A

Factors predisposing thrombosis. Endothelial injury, blood stasis or turbulence, blood hypercoagulability.

83
Q

___________ and __ are produced by the endothelium and prevent platelet adhesion.

A

PGI2 and NO

84
Q

Cardiac and Arterial Thrombi

A

Possible emoblism to brain, kidneys, spleen.

85
Q

When to further investigate thrombosis

A

Young patients, family history of thrombosis, thrombosis in absence of known risk, recurrent miscarriages, warfarin-induced skin necrosis, neonatal purpura fulminans.

86
Q

Common inherited thromophilias

A

Antithrombin deficiency, Protein C and S deficiencies, Factor V leiden, and prothrombin G20210A mutation.

87
Q

Antithrombin Deficiency

A

Autosomeal dominant, Q/Q defects, thrombotic phenomena at an early age, PE is often first manifestation.

88
Q

Protein C deficiency

A

Autosomal dominant/recessive. QQ defects. Homozygotes die in infancy, skin necrosis with warfarin.

89
Q

Protein S deficiency

A

Autosomal dominant, QQ defects, homozygotes die in utero or in early infancy from NPF. Skin necrosis with warfarin.

90
Q

Neonatal Purpura Fulminans

A

Manifestation of homozygous protein C/S deficiencies. Lethal syndrome of DIC. Skin lesions progress to full thickness necrosis that is irreversible.

91
Q

Prothrombin G2021A mutation

A

Noncoding mutation, results in 5-10% high levels of prothrombin. 2-3x risk of venous thromboembolism. 5-7% of young patients with DVT/PE.

92
Q

Acute Leukemias

A

ALL and AML. Both present with pancytopenia. Tumor cells displace healthy cells in bone marrow.

93
Q

Acute Myeloblastic Leukemia

A

Most common leukemia in adults.

94
Q

ALL

A

B-ALL and T-ALL. B-ALL is 85% of cases. Most common in children, tumors are aggressive.

95
Q

Polycythemia Vera

A

Jak2 mutation. High levels of functional RBCs. 1 year survival without treatment. Tx; Blood removal and chemotherapy.

96
Q

Essential Thrombocythemia

A

Jak2 or MPL mutations. Too many megakaryocytes. Usually asymptomatic until after 50 years old.

97
Q

Primary Myelofibrosis

A

Jak2 or MPL mutations. Fibrosis and atypical megakaryocytes. Median survival from 1 to 8 years.

98
Q

Chronic Myelogenous Leukemia

A

CML. Fusion of BCR-ABL gene. Overgrowth of granulocytic and megakaryocytic precursors in bone marrow. No treatment will result in acute leukemia within 5 years. Tx: drugs that target BCR-ABL gene (Imatinib) or stem cell transplant.

99
Q

Myelodysplastic syndrome

A

Cancer in which bone marrow does not make enough healthy blood cells and there are abnormal cells in blood or bone marrow. Can convert to AML.

100
Q

Hodgkin Lymphoma

A

Reed-Sternberg cells present. Usually arises from a single lymph node and spreads in a predictable way. Radiation and chem have a 60 to 90% cure rate.

101
Q

Non Hodgkin Lymphoma

A

Over 50 types. Range from slow growing to very aggressive.

102
Q

Chronic Lymphocytic Leukemia

A

Not associated with chromosomal translocaiton. Median age of diagnosis is 70. Increased number of small round lymphocytes. Smudge cells. Common to be asymptomatic at diagnosis. 5-11 year median survival.

103
Q

Multiple Myeloma

A

Median onset 50-60 years. Mature B cells. Rouleaux formation on the blood smear. Tumors produce partial antibodies which can be detected. Lytic Bone lesions.

104
Q

Solitary Plasmacytoma

A

Solitary mass consisting of a clonal plasma cell tumor. Does not usually produces antibodies. Can progress to multiple myeloma.

105
Q

Primary Amyloidosis

A

Clonal expansion of plasma cells in the bone marrow that secrete monoclonal light chains. These chains misfold and from deposits in tissue.

106
Q

Monocolonal gammopathy of uncertain significance

A

Detection of monocolonal immunoglobulin protein in the serum without evidence for malignancy of B cells. Risk of progression to multiple myeloma.

107
Q

Auer Rods

A

Morphology of Acute Myelogenous Leukemia

108
Q

Induction Therapy

A

Initial chemo dose, goal is to induce remission by killing cells to an undetectable level.

109
Q

Consolidation Therapy

A

Follow up dose to kill off undetectable cancer cells.

110
Q

Maintenance Therapy

A

Therapy given after patient as achieved remission. Prevents relapse.

111
Q

Oncologic Emergency

A

Pathologic spinal cord compression, superior vena cava syndrome, gynecologic bleeding

112
Q

Normal tissues at risk from acute radiation side effects

A

Bone marrow, GI mucousa, skin

113
Q

3 types of external beam radiation

A

Photons (Xrays), Electrons, and Heavy charged particles (protons and carbon)

114
Q

Linear Accelerator (LINAC)

A

Accelerates electrons to collide with heavy metals to produce Xrays.

115
Q

Applications of proton therapy

A

Pediatric tumors, CNS tumors, Skull base and paraspinal tumors, lung, head and neck, prostate.

116
Q

Radiosensitive tumors

A

lymphoma, seminoma

117
Q

Radioresistant tumors

A

head, neck, prostate, glioblastoma

Hemetology (8 decks)

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