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Hemotology And Oncology > Rx Test > Flashcards

Rx Test Flashcards

1
Q

Chest pain,dyspnea,splenomegaly, and mild normocytic anemia is most suggestive of an episode of …

A

sickle cell crisis (vaso-occlusive crisis), a complication ofsickle cell disease(SCD).

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2
Q

Acute chest syndrome in children

A

Pain is less frequent, and fever more common

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3
Q

Acute chest syndrome characteristics (in sicle cell disease)

A

Intense chest pain, dyspnea, coughing, normal WBC

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4
Q

Sickled RBCs …

A

Have more surface adhesion molecules than normal red cells, and they release inflammatory cytokines

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5
Q

Chloramphenicol used for?

A

Bacterial meningitis or rickettsial diseases, or used for patients who have life-threatening diseases and allergies to other antibiotics

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6
Q

Laboratory findings in aplastic anemia?

A

Normal TIBC , normal serum ferritin , normal haptoglobin , DECREASED reticulocyte count

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7
Q

Laboratory findings in B12/ folate deficiency?

A

Normal TIBC , normal serum ferritin , normal haptoglobin , INCREASED reticulocyte count

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8
Q

Basophilic stippling is observed in …

A

Lead toxicity , arsenic toxicity , sideroblastic anemia , and thalassemia

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9
Q

Burton lines?

A

Thin black-blue lines along the margin of the gums at the base of the teeth

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10
Q

Mutation type in sickle cell anemia?

A

Sickle cell anemia is an autosomal recessive disease caused by a MISSENSE MUTATION in the sixth position of the beta-chain of hemoglobin

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11
Q

Hereditary spherocytosis most commonly seen in patients of …

A

Northern European descent

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12
Q

Laboratory findings in sickle cell anemia?

A

Low hemoglobin and hematocrit, thrombocytosis and leukocytosis (due to vaso-occlusive crisis)

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13
Q

Sickling is facilitated by?

A

Increased temperature (fever), decreased pH (acidosis), and high mean corpuscular hemoglobin concentration (dehydration)

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14
Q

Pernicious anemia is associated with …

A

Other autoimmune disorders, such as thyroiditis

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15
Q

Pancytopenia

A

Low hemoglobin, hematocrit, WBC count, and platelet count

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16
Q

Cause of death in severe forms of beta-thalassemias?

A

Heart failure

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17
Q

Classic pentad of thrombotic thrombocytopenic purpura (TTP)?

A

Fever, neurological symptoms (delirium, seizure, and stroke), decreased renal function, thrombocytopenia, and microangiopathic hemolytic anemia

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18
Q

Risk factors in TTP?

A

Pregnancy, viral infections, malignancies, and autoimmune conditions.
TTP usually develops in previously healthy patients.

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19
Q

Laboratory findings in TTP?

A

Because the anemia is a microangiopathic hemolytic anemia, laboratory tests will demonstrate increased serumindirect bilirubin, decreased serumhaptoglobin, and visible schistocytes on a peripheral blood smear.

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20
Q

Target cells

A

RBCs with an outer ring of hemoglobin surrounding a central condensation of hemoglobin

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21
Q

RBC distribution width (RDW) in thalassemia and iron-deficiency anemia?

A

In thalassemia, the RBCs are fairly similar in size, meaning the RDW is either LOW or NORMAL.
While iniron-deficiency anemia, the RBCs get smaller and smaller as the iron deficiency progresses, leading to variability in RBC size and an INCREASE in the RDW.

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22
Q

Iron content in breast milk?

A

Approximately 0.35 mg/liter

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23
Q

Iron requirement in infants from 6 to 12 months old?

A

11 mg of iron per day

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24
Q

Decreased TIBC?

A

Hemochromatosis , hemosiderosis ,thalassemia ,hyperthyroidism ,nephrotic syndrome, andanemia of chronic disease.

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25
Q

Increased ferritin level?

A

Acute and chronicliverdisease,iron overload(hemochromatosis),end-stage renal disease, and chronic alcohol overuse, among others.

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26
Q

Increased reticulocyte count

A

Increasedreticulocytecounts occur afterbleeding, afterhemolysis, and in response to therapy.

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27
Q

Hemolysis indicatives?

A

Scleral icterus , increased reticulocyte count, increased lactate dehydrogenase , increased total bilirubin , and decreased serum haptoglobin

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28
Q

Oxidative stress in G6PD deficiency?

A

Oxidant drugs (eg,primaquineused formalaria,dapsone,rasburicase, fluoroquinolones, sulfonylureas), foods (fava beans), or infections triggers RBChemolysis, manifesting as fatigue (due to anemia), dark urine (due tourobilinogenin the urine), andjaundice(due to increasedindirect bilirubinafter hemolysis).

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29
Q

Sickle cell trait?

A

A heterozygous genetic condition in which there is one normal allele of hemoglobin beta and one of hemoglobin S (HbSA).
Patients are generally healthy ans asymptomatic, but may cause hematuria due to papillary necrosis.

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30
Q

In sickle cell trait papillary necrosis occurs …

A

Within the renal medulla, where sickling may occur because of its low partial pressure of oxygen andhypertonicand/or acidic environments. These conditions can be brought on by severepneumonia, high altitudes, or vigorous physical exercise with ensuingdehydration.

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31
Q

The papillary necrosis may cause?

A

Impaired ability to concentrate urine (isosthenuria). More uncommonly, patients may developchronic kidney disease(lowglomerular filtration rate) or increased urinary tract infections.

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32
Q

Complications in paroxysmal noctural hemoglobinuria (PNH)?

A

Chronic kidney disease,thrombosis, andpulmonary hypertension.

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33
Q

Pure RBCaplasiais characterized by?

A

Reducedhemoglobinandreticulocytecount in the presence of a normocytic,normochromic anemia.

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34
Q

Tha signs and symptoms of Fanconi anemia?

A

Pancytopenia(decreased RBCs, WBCs, and platelets) along with abnormal skin (pigmented spots), bones (wide thumbs), and facial findings (small eyes), predisposition to malignancy

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35
Q

Cause of morning hematuria in PNH?

A

Because of the concentrated nature of the morning urine (related to lack of fluid intake while sleeping) and due to increased hemolysis caused byhypoventilation, carbon dioxideretention, and decreased serum pH while asleep.

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36
Q

Bernard-Soulier syndrome is characterized by?

A

Mucocutaneous bleeding, increased bleeding times,thrombocytopenia, a lack of platelet aggregation on ristocetin and normal plasma testing, and giant platelets on peripheral blood smear.

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37
Q

vWD often presents with …

A

Epistaxis, menorrhagia, and prolonged bleeding immeadiately after an invasive procedure (ie, primary hemostasis)

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38
Q

Primary hemostasis?

A

Bleeding immediately after an invasive procedure

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39
Q

Secondary hemostasis (in hemophilia)?

A

Often exhibit appropriate hemostasis immediately after trauma or a procedure, they later exhibit hemorrhage into joints (hemarthrosis) or muscle compartments or even intracranial hemorrhage

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40
Q

Christmas disease?

A

Hemophiloa B (deficiency of factor IX ; X-linked recessive )

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41
Q

Factor XIIIa’s main function?

A

After being activated by thrombin in the presence of calcium, factor XIIIa’s main function is to covalently cross-link chains of fibrin and plasma fibronectin, reinforcing the fibrin plug (formation of covalent bonds between fibrin monomers and chains). Without factor XIII, a clot can form but is inadequate to maintain hemostasis

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42
Q

DIC noted by …

A

Multiple petechiae, ecchymoses, and active bleeding around the nose and mouth

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43
Q

Rhabdomyolysis

A

Or muscle necrosis, an acute, sometimes fatal disease in which the by-products of skeletal muscle destruction accumulate in the renal tubules and produce acute renal failure, other internal injury, and, occasionally, death

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44
Q

Classification of thrombolytics?

A

Nonfibrin-specific (streptokinase) , and fibrin-specific (alteplase - tPA)

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45
Q

Difference between nonfibrin-specific and fibrin-specific thrombolytics?

A

Evidence suggests that ribrin-specific thrombolytics work specifically on fibrin-bound plasminogen and are associated with less systemic plasmin activation and lower risk of bleeding compared with nonfibrin-specific thrombolytics

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46
Q

Chronic DIC presents with …

A

Malignancy, the more common presentation is thrombosis, which can result in depp venous thrombophlebitis (with the risk of pulmonary embolus), or superficial thrombophlebitis, and bleeding

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47
Q

Laboratory and clinical findings in chronic DIC?

A

Increased PT and D-dimers (also acute DIC), and mildly decreased hemoglobin, normal-to-low platelets in the setting of malignancy, mildly elevated INR, PTT
Prolonged wound bleeding, venous cords

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48
Q

HIT should be suspected as the cause of thrombocytopenia with significant thrombosis if any of the following conditions are observed:

A
  1. New-onset thrombocytopenia
  2. Venous or arterial thrombosis
  3. Necrotic skin injections at the heparin injection site
  4. Acute systemic reaction (eg, fever) after injection of heparin
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49
Q

Vitamin K deficiency bleeding of the newborn (VKDB)?

A

Presents 2 to 7 days after birth with gastrointestinal, intracranial, umblical, mucosal, circumcision site, and/or cutaneous bleeding

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50
Q

First-line therapy for patients with a PE?

A

Low-molecular-weight heparin

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51
Q

Blue-purple granules in RBCs after Wright staining?

A

Pappenheimer bodies, which are siderosomes, or iron bodies

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52
Q

Drepenocytes?

A

Crescent-shaped RBCs (sickle cells)

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53
Q

RBCs with missing semicircular portions?

A

Bite cells (in G6PD deficiency)

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54
Q

Immune thrombocytopenic purpura (ITP)

A

An autoimmune disorder characterized by petechiae, purpura, epistaxis, a low platelet count, easy bruising or bleeding through skin or mucous membranes, and sometimes heavy menstrual, urinary, or gastrointestinal bleeding

55
Q

ITP in women and children?

A

In women: chronic ITP on reproductive age
In children: has an acute presentation

56
Q

In addition to warfarin, other first-line drugs for managing chronic AF include …

A

Direct thrombin inhibitors (eg, dabigatran and argatroban) and anti-factor Xa inhibitors (eg, rivaroxaban and apixaban)

57
Q

Common risk factors for TTP?

A

Drugs such as ticlopidine and clopidogrel, HIV, pregnancy, cancer, lupus, and infections

58
Q

When platelet glycoprotein IIb/IIIa receptor antagonists used?

A

These are intravenous drugs used immediately before some interventional angioplasty procedures in patients who have ST-elevation MI.
They are particularly used in those who have not been given P2Y12 receptor blockers, or in whom percutaneous coronary intervention must be done urgently

59
Q

When platelet P2Y12 receptor blockers used?

A

In preparation for percutaneous coronary intervention (after a few hours), patients with ST-elevation MI are given platelet P2Y12 receptor blockers such as prasugrel or ticagrelor

60
Q

The renal failure of multiple myeloma is mostly due to …

A

Obstruction of renal tubules by large, eosinophilic casts composed of immunoglobulin light chains. Tese are formed from Bence-Jones proteins.

61
Q

Bence-Jones proteins?

A

Filtered immunoglobulin light chains

62
Q

Renal changes in Waldenstrom macroglobulinemia?

A

IgM deposition can cause damage to the glomeruli in membranous nephropathy, which would cause albuminuria, resulting in a positive dipstick

63
Q

Causes of lymphadenopathy and splenomegaly CLL?

A

Due to extramedullary hematopoiesis, frequent infection, autoimmune hemolytic anemia

64
Q

Functional defect in nonneoplastic B cells in CLL result in …

A

Functional hypogammaglobulinemia, leading to increased infection risk

65
Q

Release of extracellularchromatinstrands is seen in …

A

Neutrophils and they are termed neutrophil extracellular traps due to their ability to trap and kill bacteria

66
Q

Clinical and laboratory findings in Adult T-cell lymphoma?

A

Back pain, generalized lymphadenopathy, hepatosplenomegaly, and several pruritic, plaque lesions on body

67
Q

Characteristic cell type in Adult T-cell lymphoma?

A

A peripheral blood smear shows characteristic “clover leaf” cells with hyperlobed nuclei

68
Q

In children who present with acute leukemia, the presumptive diagnosis is … until proven otherwise.

A

Acute lymphoblastic leukemia/lymphoma (ALL). To confirm the diagnosis, a bone marrow examination is essential

69
Q

Clumps of azurophilic granular material that group together to form elongated needles?

A

Auer rods in AML

70
Q

Benign paracortical hyperplasia?

A

Benign paracortical hyperplasia (reactive interfollicular hyperplasia) is another pattern of reactive lymphadenopathy in which abnormal cellular expansion of the interfollicular zones of the lymph nodes (containing the T cells) predominates. It is often seen as the result of viral infections—including Epstein-Barr virus, cytomegalovirus, and herpesvirus—that cause a T cell–mediated immune response. Histology of involved lymph nodes demonstrates expansion of the interfollicular T-cell zones.

71
Q

Nodal marginal zone lymphoma?

A

Nodal marginal zone lymphoma is a type of non-Hodgkin lymphoma that is proposed to occur from proliferation of neoplastic marginal zone B cells that have acquired mutations in oncogenes and tumor suppressor genes. On histology, involved lymph nodes display a proliferation of small to large B cells with indented nuclei and abundant pale cytoplasm (called monocytoid B cells) that surround and infiltrate follicles.

72
Q

Rouleaux formation in multiple myeloma (MM)?

A

There is an excessive production of positively charged, light-chain IgG immunoglobulins, which reduces the negative charge normally present on erythrocytes, thus allowing the erythrocytes to stick together and resulting in a rouleaux appearance.

73
Q

Causes of epistaxis and bleeding gums in Waldenstrom macroglobulinemia (WM)?

A

The IgM may also coat platelets and interact with clotting factors, resulting in bleeding abnormalities (eg, epistaxis, bleeding gums)

74
Q

Histopathology of the spleen in mantle cell lymphoma?

A

Would show broad, darkly staining, malignant lymphoid cells in the mantle region surrounding residual reactive germinal centers.
Histologically, mantle cell lymphoma demonstrates an abundance of small lymphocytes with scantcytoplasm, irregularly shaped nuclei, and small nucleoli.

75
Q

The prominent symptoms of CML?

A

Weight loss, night sweats, and dragging abdominal sensation (because of splenomegaly).

76
Q

Disease mechanism in acute promyelocytic leukemia (APL)?

A

This variant is strongly associated with the t(15;17) chromosomal rearrangement. The genetic abnormality in APL creates a fusion protein (PML-RARa) that makes the cell unresponsive to normal levels of retinoic acid, leading to arrested cell maturation at the promyelocyte stage. These abnormal promyelocytes release procoagulants and fibrinolytic factors, raising the risk of DIC. This condition is responsive to treatment with all-trans retinoic acid.

77
Q

T-cell acute lymphoblastic lymphoma?

A

May present with signs and symptoms of anemia, thrombocytopenia, leukocytosis, and mediastinal mass. Biopsy of the mass would show cells with light-blue, scanty, and nongranular cytoplasm, which represents lymphoblasts.

78
Q

ALL anc other malignancies treated by?

A

Methotrexate by preventing the conversion of folic acid to THF (inhibits DHF reductase)

79
Q

Adverse effects of methotrexate can be reversed by?

A

Leucovorin (folinic acid)

80
Q

Abbreviation of TdT?

A

Terminal deoxynucleotidyltransferase

81
Q

Most side effects of corticosteroids which come from chronic use?

A

Osteoporosis, immunosuppression, cataracts, atherosclerosis, acne, and Cushingoid body changes

82
Q

Most side effects of corticosteroids which come from acute use (high-dose corticosteroids)?

A

Hypertension, amenorrhea, hyperglycemia, and psychiatric, behavioral, or mood changes

83
Q

The most common presentation of Burkitt lymphoma in North America?

A

Loss of appetite (anorexia), severe constipation, and abdominal pain or distention, all of which are caused by enlarged lymph nodes in the abdomen.

84
Q

The gold standard for chemotherapy to treat Hodgkin lymphoma?

A

The ABVD protocol consisting of Adriamycin (doxorubicin), bleomycin, vinblastine, and dacarbazine.

85
Q

Prophylaxis against adverse effect of doxorubicin?

A

Dexrazoxane, an iron-chelating agent

86
Q

Patients with Hodgkin lymphoma who are unresponsive to the ABVD regimen may require advanced treatments such as …

A

Glucocorticoids and cyclophosphamide. However, these are not first-line agents.

87
Q

Symptoms of ALL may include?

A

Fever, easy bruising and bleeding, hepatosplenomegaly, anemia, enlarged lymph nodes, pale skin, fatigue, and bone pain with increased lymphoblasts on smear.

88
Q

Symptoms of ALL may include?

A

Fever, easy bruising and bleeding, hepatosplenomegaly, anemia, enlarged lymph nodes, pale skin, fatigue, and bone pain with increased lymphoblasts on smear.

89
Q

Differences between chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL)?

A

CLL and SLL represent different clinical manifestations of the same disease: CLL is seen in the blood, while SLL is seen in the lymph nodes. They both usually occur in elderly patients, are frequently asymptomatic, have identical immunophenotypes, and involve the production of high numbers of abnormal B cells. CLL shows significant bone marrow involvement resulting in peripheral blood lymphocytosis (with absolute lymphocyte count >5000/mm3) and/or cytopenias. SLL is a type of non-Hodgkin lymphoma that causes lymphadenopathy and/or splenomegaly and show a normal or mildly reduced absolute lymphocyte count of <5000/mm3. Patients will also have anemia and thrombocytopenia.

90
Q

EBV infection is associated with …

A

Heterophile-positive mononucleosis, nasopharyngeal carcinoma, oral hairy leukoplakia in patients infected with HIV, and lymphoproliferative disorders in immunocompromised hosts (including those with Hodgkin and non-Hodgkin lymphoma) and Burkitt lymphoma.

91
Q

Plasmacytoid lymphocytes

A

Unregulated proliferation of plasmacytoid lymphocytes describes Waldenström macroglobulinemia.

92
Q

Cause of bone pain in ALL/LBL?

A

Due to rapid expansion of the marrow

93
Q

Risk factors for developing ALL/LBL?

A

Children with chromosomal anomalies such as trisomy 21 (Down syndrome) and Klinefelter syndrome or with diseases of chromosomal fragility such as Fanconi anemia, Bloom syndrome, and ataxia-telangiectasia are at increased risk for developing ALL/LBL.

94
Q

In Burkitt lymphoma biopsy will show …

A

Sheets of lymphocytes staining positive for CD20

95
Q

Cell surface markers of diffuse large B-cell lymphoma?

A

The CD19, CD20 and CD79a

96
Q

Russell bodies?

A

Russell bodies are seen in multiple myeloma. They are large, eosinophilic, cytoplasmic inclusions thought to represent distended endoplasmic reticulum.

97
Q

Large multinucleated cells with prominent eosinophilic inclusion-like nucleoli?

A

Reed-Sternberg cells which have the appearance of “owls’ eyes”.

98
Q

Hairy cell leukemia (HCL)

A

HCL is a type of chronic B-cell lymphoproliferative disorder where small, mature B cells accumulate in the spleen, bone marrow, and blood, causing cytopenias and their associated symptoms: fatigue (anemia), recurrent infections (leukopenia), and easy bruising (thrombocytopenia). Splenomegaly often occurs secondary to accumulation of abnormal cells in the spleen and can cause abdominal discomfort.

99
Q

Multiple granules that are striated and rodlike, with single-sided outpouchings?

A

Birbeck granules

100
Q

Langerhans cell histiocytosis (LCH) derived from (1) … cells, which differentiate into (2) … and perform (3) … ?

A
  1. Immature myeloid precursor cells
  2. Monocytes, macrophages, and dendritic cells
  3. Phagocytosis of foreign antigens in addition to antigen presentation and secretion of inflammatory cytokines.
101
Q

Aquagenic pruritis in polycythemia vera?

A

Which is itchiness after a warm shower secondary to increased release of histamine by mast cells.

102
Q

Three diagnostic criteria in Sézary syndrome?

A
  1. Erythroderma over >80% of the body
  2. T-cell receptor rearrangement in the blood that matches skin lymphocytes
  3. CD4+ cell count > 1000 cells/uL.
103
Q

Sézary syndrome?

A

Is a subtype of cutaneous T-cell lymphoma with leukemic and skin malignant T-cell involvement that often presents with lymphadenopathy, erythroderma, and pruritus.

104
Q

Clinical characteristics of multiple myeloma (MM)

A

Multiple lytic bone lesions, which can lead to pathologic fractures due to production of osteoclastic-activating cytokines; acute renal failure due to tubular injury; anemia, neutropenia, and thrombocytopenia due to plasma cell infiltration of the bone marrow; and symptoms of hypercalcemia (confusion, constipation) due to osteoclast activation.

105
Q

Leukocyte alkaline phosphatase is an enzyme within …

A

Mature WBCs

106
Q

In primary myelofibrosis there is typically abnormal deposition of … in the bone marrow

A

Reticulin and collagen

107
Q

Treatment for children with ALL/LBL?

A

Treatment for children with ALL/LBL involves several phases, including induction, consolidation, maintenance, and central nervous system prophylaxis. Induction therapy is accomplished by a four-drug regimen that includes 1) a steroid (commonly prednisone or dexamethasone), 2) asparaginase, 3) doxorubicin/daunorubicin, and 4) vincristine, which binds and inhibits tubulin and causes cell cycle arrest in the M phase.

108
Q

Functions of doxorubicin?

A

Doxorubicin is an anthracycline commonly used in the initial stages of acute lymphoblastic leukemia treatment. It has many functions, including: 1) inhibition of DNA synthesis through the generation of free radicals that cause strand breaks, 2) intercalation (insertion) between DNA base pairs, 3) inhibition of topoisomerase II, and 4) iron chelation. As a result, doxorubicin acts during multiple phases of the cell cycle, but not during the M phase.

109
Q

Diffuse large B-cell lymphoma (DLBCL) typically manifests with …

A

A painless, rapidly growing mass, most often involving abdominal or cervical nodes, that contains many large lymphocytes. Systemic “B” symptoms (fever, weight loss >10% over 6 months, drenching night sweats) are observed in approximately 30% of patients with DLBCL. Histology shows large, malignant B cells that are typically at least twice the size of normal lymphocytes. They have large nuclei, often with multiple, small nucleoli.

110
Q

Risk factors for diffuse large B-cell lymphoma (DLBCL)?

A

One risk factor for DLBCL is immunosuppression. This can occur in disease states (eg, HIV) or result from immunosuppressive medications, such as those used for inflammatory bowel disease (eg, 6-mercaptopurine). Increasing age also boosts the risk for the development of DLBCL. In addition to occurring de novo, DLBCL can arise through the transformation of many different types of low-grade B-cell lymphomas, including B-cell chronic lymphocytic leukemia (eg, Richter transformation), lymphoplasmacytic lymphoma, follicular lymphoma, marginal zone (MALT) lymphoma, and splenic marginal zone lymphoma.

111
Q

In follicular B-cell lymphoma on histology seen …

A

Abnormal germinal centers and increased expression of B-cell markers (CD20) and bcl-2

112
Q

Histologic findings in mantle cell lymphoma?

A

Involved lymph nodes contain small- to medium-sized lymphocytes with irregular and notched nuclei.

113
Q

Myeloperoxidase-positive cytoplasmic inclusion?

A

Auer rod

114
Q

Richter syndrome (transformation)?

A

Is the development of diffuse large B-cell lymphoma in patients with other leukemias. Patients usually have a sudden decline in health, weight loss, fevers, bulky lymphadenopathy, and night sweats.

115
Q

Bome marrow biopsy in myelodysplastic syndrome (“preleukemia”)?

A

Hypercellularity (from clonal proliferation), dysplasia (from poor differentiation and maturation), and myeloblasts <20% in this patient.

116
Q

Three different clinical variants of Burkitt lymphoma?

A
  1. Endemic.mThe endemic form presents as a jaw or facial bone tumor.
    1. Sporadic. The sporadic form usually causes ascites or abdominal masses (eg, stomach, distal ileum, cecum) and/or masses in the kidney, testis, ovary, breast, bone marrow, or central nervous system (CNS).
    2. Immunodeficiency-related. The immunodeficiency-related form generally presents with signs or symptoms related to the underlying immunodeficiency with disease often seen in lymph nodes, CNS, and bone.
117
Q

The drug which is directly interact with mast cells?

A

Cromolyn sodium directly binds to mast cells, thereby preventing their degranulation and release of histamine and leukotrienes. Stabilizing mast cells treats the airway inflammation and bronchoconstriction seen in mild persistent asthma.

118
Q

Thrombopoietin function?

A

Thrombopoietin (TPO) is the primary hormone responsible for stimulating platelet production. TPO also stimulates differentiation of precursor stem cells into megakaryocytes and increased pseudopodia formation and extension into bone marrow sinusoids. These pseudopodia are capable of shedding proplatelet cells into the bone marrow.

119
Q

Thrombopoietin is produced by …

A

Parenchymal cells in the liver

120
Q

Where do platelets mature?

A

Within the bone marrow and lung vasculature

121
Q

Signs of an ischemic stroke include?

A

Acute onset of weakness and facial drooping

122
Q

Tissue plasminogen activator (tPA) administration in ischemic stroke?

A

If a patient who has had an ischemic stroke presents within 3 hours and has no contraindications such as a brain tumor, recent surgery, or recent acute bleeding, the standard treatment is tissue plasminogen activator (tPA).

123
Q

In ischemic stroke patients with blood pressure >185/110 mm Hg should be treated with …

A

Antihypertensive agents such as intravenous (IV) labetalol or nicardipine prior to starting thrombolytic therapy (tPA).

124
Q

Red and yellow marrow?

A

Hematopoietically active bone marrow is red marrow, typically found in the axial skeleton of adults (pelvis, spine, ribs, skull).
Yellow marrow is not hematopoietically active and is made up of mostly fat cells. At birth, red marrow is found throughout all bones. By age 1 year, the red marrow in the epiphyses and apophyses has converted to yellow marrow. With age, the red marrow in long bones also converts to yellow marrow. By the age of 25, most red marrow is focused in the axial skeleton.

125
Q

Clinical findings in erythroblastosis fetalis (hemolytic disease of the newborn)?

A

Edema, hepatosplenomegaly, anemia (increased bilirubin and reticulocytes), and a positive Coombs test

126
Q

Difference between first and second pregnancy in erythroblastosis fetalis?

A

The initial anti-Rh antibodies made by the mother during the first pregnancy wereIgMand thus could not cross theplacentaand harm the fetus. However, the maternal anti-Rh antibodies are eventually replaced with IgG antibodies, which can freely cross the placenta and bind to fetal RBCs. Any subsequent Rh-positive fetus is at risk for hemolytic disease of the newborn, in which the antibody-coated RBCs are phagocytized and destroyed in thespleen(extravascularhemolysis).

127
Q

Function of CD19?

A

CD19 is a cell surface protein found on B cells. CD19 has an important role in the differentiation of B cells.

128
Q

CD33 cell surface protein?

A

CD33 is a cell surface protein found on myeloid cells and plays a role in inhibiting phagocytosis.

129
Q

Absolute contraindications to alteplase or the alternatives include …

A

Prior intracranial hemorrhage, structural cerebral vascular lesion, ischemic stroke within the previous 3 months, aortic dissection, active bleeding, malignant intracranial neoplasm presence, or significant facial or closed-head trauma within the previous 3 months.

130
Q

Thrombolytic drugs are used in …

A

Acute settings where immediate fibrinolysis is needed to allow reperfusion of the myocardium or brain matter. Alteplase should be given within 30 minutes of patient presentation to an emergency department with an ST-segment elevation myocardial infarction if percutaneous coronary intervention is not possible.

131
Q

Enzyme that functions similarly to tissue plasminogen activator?

A

Urokinase

132
Q

Disease mechanism in antiphospholipid syndrome (APS)?

A

APS is caused byIgMorIgGantibodies that bindplateletphospholipids. Platelet phospholipids are required for both the intrinsic and extrinsic clotting pathways.Antiphospholipid antibodies bind to platelet phospholipids,thereby making them accessible to clotting factors and leading to recurrent venous and arterial thrombosis. Note that despite the name, the lupus anticoagulant actually causes increasedcoagulation. This is because thepartial thromboplastin time(PTT) assays use exogenous phospholipids; thephospholipidantibodies inhibit their function and paradoxically show an increase in coagulation time, hence the name lupus anticoagulant.

133
Q

Disease mechanism in paroxysmal nocturnal hemoglobinuria (PNH)?

A

PNH is caused bycomplement-mediatedlysis of RBCs. This is due to an acquiredmutationof thePIGAgene within myeloid stem cells, required to make functioning glycosylphosphatidylinositol anchors for CD55 (decay accelerating factor) and CD59 (MAC inhibitory protein). These proteins, when attached to the cell membrane, protect cells against complement-mediated attack, so the absence of the anchoring protein makes RBCs subject to complement-mediated attack. In PNH, hemolysis of RBCs occurs at night as the carbon dioxide level rises during sleep, lowering pH levels (mildrespiratory acidosis) and facilitating complement-mediated lysis of RBCs. As a result, the first morning void reveals dark urine with progressive clearing during the day.

Hemotology And Oncology (3 decks)

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