White Blood cells and Platelets Pathology Flashcards

1
Q

what is leukocytosis

A

an increase in total circulating white blood cells

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2
Q

what is neutrophilia (granulocytosis) seen in

A

bacterial infections

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3
Q

what is lymphocytosis seen in

A

viral infections

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4
Q

what is eosinophilia seen in

A

parasitic infections, allergic reactions

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5
Q

what is leukemoid reaction

A

an elevated white blood cell count that is a physiologic response to stress or infection

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6
Q

what is leukopenia

A

a decrease in total circulating white blood cell count

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7
Q

what is neutropenia caused by

A

antineoplastic therapy, drugs

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8
Q

what is lymphopenia caused by

A

steroid therapy

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9
Q

what is pancytopenia

A

all cell lines are affected- anemia, thrombocytopenia, neutropenia

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10
Q

what terms are used interchaneably with granulocytopenia

A

neutropenia and agranulocytosis

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11
Q

describe neutropenia

A
  • normal adult peripheral white blood cell count - 4,500- 11,000 / mm^3
  • clinically relevant neutropenia- absoulte neutrophil count less than 500/mm^3
  • susceptibility to bacterial and fungal infections
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12
Q

what are the causes of neutropenia

A
  • decreased production
  • increased destruction- autoimmune reactions
  • in severe neutropenia the signs of infection may be absent
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13
Q

decreased production is caused by what in causes of neutropenia

A
  • drugs
  • hematologic disease- cyclic neutropenia
  • nutritional deficiency- B12, folate
  • melophthisis
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14
Q

what is the treatment of neutropenia

A

clindamycin 1200 mg/day

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15
Q

what are the clinical lab values for neutropenia

A
  • WBC: 1,600 cells/ul
  • polys: 4%
  • lymphocytes: 69%
  • monocytes: 27%
  • eosinophils: 0%
  • basophils: 0%
  • absolute neutrophil count = 64 neutrophils/ul
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16
Q

describe cyclic neutropenia- symptoms and tx

A
  • regular, periodic reductions in neutrophils
  • symtpoms greatest at nadir- fever, lymphadenopathy, malaise, pharyngitis, ulcerations, periodontitis
  • treatment- supportive care, cytokine therapy
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17
Q

what are leukemias

A

the neoplastic cells are in the bone marrow and blood

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18
Q

what are lymphoams

A

the neoplastic cells are in the lymph nodes- also extranodal sites

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19
Q

what are the neoplasms of hematopoietic cells

A

leukemia and lymphomas

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20
Q

describe leukemia

A
  • arises in bone marrow
  • spreads to peripheral blood
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21
Q

describe lymphomas

A
  • arises in peripheral lymphoid tissue, usually in lymph nodes
  • forms a discrete tissue mass
  • may eventually spread to peripheral blood and bone marrow
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22
Q

describe acute leukemia

A
  • abrupt, stormy onset
  • no maturation- precursor cells proliferate
  • kills rapidly without treatment
  • cure is possible
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23
Q

describe chronic leukemia

A
  • insidious course
  • maturation - mature cells proliferate
  • often not treated unless symptomatic
  • cannot be cured
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24
Q

describe white blood cell maturation

A
  • pluripotent stem cell -> myeloid stem cell or lymphoid stem cell
  • myeloid stem cell -> erythroblast, megakaryoblast, myeloblast, monoblast
  • lymphoid stem cell-> pre B lymphocyte or pro T lymphocytes
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25
Q

what are the classifications of leukemias by cell of origin and clinical course

A
  • acute lymphoblastic leukemia
  • acute myelogenous leukemia
  • chronic lymphoblastic leukemia
  • chronic myelogenous leeukemia
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26
Q

what are the clinical symptoms of acute leukemia and describe each

A
  • cytopenias- depression of normal bone marrow function
  • bleeding- petechiae, ecchymoses, epistaxis, gingival hemorhhage due to thrombocytopenia
  • fever- infections due to absence of mature granulocytes
  • fatigue- anemia
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27
Q

describe acute lymphoblastic leukemia

A
  • lymphoblasts - immature precursor B or T lymphocytes arrested at early stage of development
  • a disease of children
  • good prognosis with aggressive chemotherapy
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28
Q

describe acute myeloblastic leukemia

A
  • myeloblasts - immature myeloid precursors with no terminal myeloid differentiation
  • adults
  • prognosis- chemotherapy, bone marrow transplantation, more difficult to treat than ALL
  • gingival enlargment in monocytic types of AML
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29
Q

what are the types of AML

A
  • granulocytic
  • monocytic
  • erythroid
  • megakaryocytic
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30
Q

what are clinical symptoms of chronic leukemia

A
  • often clinically silent
  • incidental leukocytosis on CBC
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31
Q

describe chronic myelogenous leukemia

A
  • adults
  • insidious onset, slow progression
  • philadelphia chromosome- t(9:22) bcr- abl fusion gene
  • splenomegaly, fever, fatigue
  • blast crisis
  • bone marrow transplantation
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32
Q

describe the philadelphia chromosome

A
  • translocation t(9:22)
  • proto- oncogene abl on long arm chromosome 9(q34)
  • transposed to bcr region (breakpoint cluster region) on chromosome 22(q11)
  • results in bcr- abl fusion gene
  • gene product is abnormal bcr- abl tyrosine kinase
  • induces cell proliferation
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33
Q

describe chronic lymphocytic leukemia

A
  • most common type of leukemia
  • adults are often asymptomatic
  • hypogammaglobulinemia- infections
  • anti red cell autoantibodies- autoimmune hemolytic anemia
  • anti platelet autoantibodies- autoimmmune thrombocytopenia
  • richter syndrome- may transform to high grade lymphoma
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34
Q

whaat are the lymphoid neoplasms

A
  • lymphocytic leukemia
  • hodgkin lymphoma
  • non-hodgkin lymphoma
  • plasma cell neoplasma
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35
Q

what is the clinical presentation of lymphoid neoplasms with lymphomas

A

non tender lymph node enlargement, extra nodal mass

36
Q

what is the clinical presentation of lymhoid neoplasms with leukemias

A

cytopenias due to suppression of hematopoiesis

37
Q

what is the clinical presentation of plasma cell neoplasms

A

bone pain, pathologic fracture

38
Q

what are the malignant lymphomas

A
  • hodgkin lymphoma
  • non hodgkin lymphoma
39
Q

what is the clinical presentation of non hodgkins lymphoma

A
  • painless lymphadenopathy with firm, enlarged, rubbery, freely movable, non tender lymph nodes
  • generally involves multiple lymph nodes in a non- contuguous pattern
  • frequently involves extranodal sites
40
Q

what is the prevalence of NHL arising in lymph nodes? extra nodally?

A
  • lymph nodes: 70%
  • extra- nodally: 30%
41
Q

oral mucosa NHL is_____

A

extra nodal

42
Q

all lymphomas are ____

A

malignant

43
Q

what are the variations of lymphomas

A
  • degree of aggressiveness varies
  • low grade- indolent, difficult to cure
  • high grade- aggressive, often curable
44
Q

describe burkitt lymphoma

A
  • high grade
  • “african jaw lymphoma”
  • B-cell NHL
  • EBV association
  • sub type of NHL
  • a high grade b cell neoplasm, most rapidly growing neoplasm
  • endemic form has predilection for jaws of children
45
Q

describe MALT lymphomas

A

-low grade
- arises from mucosal - associated lymphoid tissue - “MALT- oma” - mature B cells
- often indolent
- salivary glands, Sjogren syndrome
- may transform to high grade lymphoma

46
Q

what are the 3 clinical forms of burkitt lymphomas

A
  • endemic (african)
  • sporadic
  • HIV associated
47
Q

what is the association of epstein- barr virus with human disease

A
  • infectious mononucleosis
  • lymphomas- NHL and HL
  • nasopharyngeal carcinoma
  • oral hairy leukoplakia
48
Q

what are the cytogenetics of burkitt lymphoma

A
  • translocations t(8:14) is the most common
  • c-myc proto- oncogene on chromosome 8 has a role in cell cycle progression
  • immunoglobulin gene promoters cause overexpression of c-myc
  • overexpression of c-myc oncogene promotes inappropriate cellular proliferation
49
Q

what are the oral findings in burkitt lymphoma

A
  • rapidly growing painless swelling, producing paresthesia, loose teeth
  • rapid demise if untreated
50
Q

describe chemotherapy in burkitt lymphoma

A

-high grade lymphoma- aggressive
- cures frequent with short term, high dose chemotherapy

51
Q

what are the three examples of NHL

A
  • burkitt lymphoma
  • diffuse large cell lymphoma
  • MALT-oma
52
Q

what is the neoplastic cell in HL

A

Reed- Sternberg cell

53
Q

describe the Reed- Sternberg cell

A
  • a minor fraction of the tumor mass
  • most are of B cell origin
  • bilobate nucleus with large inclusion like nucleoli- “owl eye” cell
54
Q

what are the general characteristics of hodgkin lymphoma

A
  • bimodal age distribution- young adults and older adults
  • painless lymphadenopathy
  • constitutional symptoms variable- fever - Pel- Ebstein fever, night sweats, weight loss, generalized pruritus
  • association with EBV
55
Q

describe the spread of hodgkin lymphoma

A
  • uniform, predictable pattern of spread from one lymph node region to the next
56
Q

what is the staging of NHL

A
  • stage I: single lymph node region
  • stage II: multiple lymph node regions, same side of diaphragm
  • stage III: multiple lymph node regions, both sides of diaphragm
  • stage IV: disseminated disease
57
Q

what are the “B” symptoms for staging of NHL

A
  • recurrent, unexplained fevers
  • night sweats
  • unintended weight loss
58
Q

what is the treatment of NHL

A
  • low grade lymphomas- treat only if symptomatic
  • high grade lymphomas: localized stage - RT. advanced stage- CT or combination CT/RT
59
Q

what is the tx of HL

A
  • stage determines tx protocol
  • localized (stage I) - local radiation therapy
  • disseminated (Stage IV) - chemotherapy
  • risk of second cancers
60
Q

what is the prognosis of HL

A
  • stage- most important
  • histologic sub type- least important
  • curable- stage I- 90% cure rate
61
Q

what is the location of HL? NHL

A

-HL: single axial group of nodes
- NHL: multiple peripheral nodes

62
Q

what is the spread of HL? NHL?

A
  • HL: predictable- orderly contiguous spread
  • NHL: unpredictable- con contiguous spread
63
Q

does HL involve Waldeyer ring? NHL?

A
  • HL: rarely
  • NHL: commonly
64
Q

what is the prevalence of extra nodal in HL? NHL?

A
  • HL: rare
  • NHL: common
65
Q

describe multiple myeloma

A
  • older adults
  • disseminated neoplasm of terminally differentiated B lymphocytes
  • multifocal lytic bone lesions, hypercalcemia, bone pain
  • myelophthisic anemia, predisposition to infections
66
Q

what are the oral findings of multiple myeloma

A
  • lytic lesions, loose teeth, pain, paresthesia, pathologic fracture
  • macroglossia- amyloidosis
67
Q

what are the lab findings for multiple myeloma

A
  • elevated serum calcium, protein, immunoglobulins
  • elevated erythrocyte sedimentation rate (ESR)
  • rouleaux formation
  • monoclonal gammopathy - M- spike
  • Bence- Jones proteinuria- immunoglobulin light chains
68
Q

what are the complications with multiple myeloma

A
  • renal failure
  • infection
  • anemia
69
Q

what is primary hemostasis

A

platelet plug

70
Q

what is secondary hemostasis

A

fibrin clot

71
Q

what is the bleeding time test

A
  • clinical assessment for adequate number and function of platelets
  • represents the time taken for a standardized skin puncture to stop bleeding
72
Q

what does the normal range of the bleeding time test depend on

A

the actual method used and varies from 2-9 minutes

73
Q

when is the bleeding time test abnormal

A
  • when there are congenital or acquired plateley defects
  • drugs- ASA, NSAIDS
  • VW disease
74
Q

what are the platelet disorders

A
  • thrombocytopenia- decrease
  • thrombocytosis- increase
  • functional defects
75
Q

what is thrombasthenia caused by

A
  • aspirin- inhibits aggregation for lifetime of platelet - 8-10 days - irreversible
  • NSAIDs- inhibit aggregation until drug eliminated - reversible
  • von willebrand disease - compound defect involving platelet function and coagulation pathway
  • normal platelet count with increased bleeding time
76
Q

what are petechiae

A

pinpoint hemorrhages

77
Q

what are purpura

A

petechiae become confluent

78
Q

what are ecchymosis

A
  • purpurae become confluent
79
Q

what is a hematoma

A

cavity

80
Q

what are the lab values for thrombocytopenia

A
  • normal platelet count -150,000 - 450,000 / mm^3
  • thrombocytopenia less than 100,000 / mm^3
81
Q

what are the causes of thrombocytopenia

A
  • decreased production - aplastic anemia
  • increased destruction - immunologic destruction
  • sequestration in spleen - splenomegaly
  • dilution - massive transfusion
82
Q

describe immune thrombocytopenic purpura and tx

A
  • autoimmune disease- antiplatelet autoantibodies produce thrombocytopenia
  • treatment with steroids, splenectomy
83
Q

what is the platelet count with immune thrombocytopenic purpura

A

7,000/ ml

84
Q

describe primary thrombocytosis

A
  • essential
  • hematopoietic stem cell disorder
  • increased number ofs of megakaryocytes producing dysfunctional platelets
85
Q

what is reactive thrombocytosis

A
  • asplenia
  • inflammatory disorders