Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > hematopoetic part 1 > Flashcards

hematopoetic part 1 Flashcards

1
Q

Leukocytosis

A

an increase in total circulating white blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

when are these seen?

individual cell forms of leukocyotsis

A

 Neutrophilia (granulocytosis) - bacterial infections
 Lymphocytosis - viral infections
 Eosinophilia - parasitic infections, allergic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

confused with? test?

leukemoid rxn

A

an elevated white blood cell count that is a physiologic response to stress or infection
can be confused with leukemia- clarified with LAP test (low in leukemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Leukopenia

A

a decrease in total circulating white blood cell count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

can be due to?

forms of leukopenia

A

Neutropenia – antineoplastic therapy, drugs
Lymphopenia – steroid therapy
Pancytopenia – all cell lines affected – anemia, thrombocytopenia,
neutropenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

interchangable terms of neutropenia

A

The terms agranulocytosis, granulocytopenia and neutropenia are
often used interchangeably

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

normal/abnormal count?

Neutropenia

A

Normal adult peripheral white blood cell count – 4,500 – 11,000 /mm3
Clinically relevant neutropenia –
Absolute Neutrophil Count (ANC) < 500 /mm3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

neutropenia can allow sus to?

A

Susceptibility to bacterial and fungal infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

causes neutropenia

A

 Decreased production due to:
* Drugs
* Hematologic disease – cyclic neutropenia
* Nutritional deficiency – B12, Folate
* Myelophthisis
 Increased destruction - autoimmune reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

severe neutropenia ana signs of infection

A

 In severe neutropenia the signs of infection may be absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

WNL WBC

A

cells/ul (4,000 – 11,000)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cyclic Neutropenia

A

 Regular, periodic reductions in neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

when are symptoms the greatest?

symptoms of cyclic neutropenia

A

 Symptoms greatest at nadir – fever, lymphadenopathy, malaise, pharyngitis, ulcerations, periodontitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

tx cyclic neutropenia

A

 Treatment - supportive care, cytokine
therapy (G-CSF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

where are the neoplastic cells

Leukemias

A

the neoplastic cells are in the bone marrow and blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

where are the neoplastic cells

Lymphomas

A

Lymphomas - the neoplastic cells are in the
lymph nodes – (also extranodal sites)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

terms? describe?

Neoplasms of
Hematopoietic Cells

A

Leukemia and Lymphoma describe the tissue distribution of disease

Leukemia
* Arises in bone marrow
* Spreads to peripheral blood

Lymphoma
* Arises in peripheral lymphoid tissue, usually in lymph nodes
* Forms a discrete tissue mass
* May eventually spread to peripheral blood and bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

onset? maturation? tx/death? cure?

Acute vs Chronic Leukemia

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Classification of Leukemias by Cell of
Origin and Clinical Course

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

cell level? bleeding? fever? energy? what is each due to?

Clinical Symptoms of Acute Leukemia

A

Cytopenias - depression of normal bone marrow function
Bleeding – petechiae, ecchymoses, epistaxis, gingival hemorrhage due to thrombocytopenia
Fever - infections due to absence of mature granulocytes
Fatigue - anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

gingiva with acute leukemia

A

Spontaneous Gingival Hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what can be on palate with AL

A

Palatal Petchiae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what oral hemmorhage can be seen (aside from petechaie) with AL?

A

Ecchymoses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

nose and AL

A

epitaxis (nose bleed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Acute Lymphoblastic Leukemia
cells invovled?
A disease of?
prognosis ?

A

Lymphoblasts - immature precursor B or T lymphocytes
arrested at early stage of development
A disease of children
Good prognosis with aggressive chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Acute Myeloblastic Leukemia
 cells?
Age?
Prognosis?
Gingiva?

A

Myeloblasts – immature myeloid precursors (granulocytic,
monocytic, erythroid, megakaryocytic) with no terminal
myeloid differentiation
Adults
Prognosis – chemotherapy, bone marrow transplantation.
More difficult to treat than ALL.
Gingival enlargement in monocytic types of AML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

which leukemia likely caused this

A

AML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Clinical Symptoms of Chronic Leukemia

A

Often clinically silent
Incidental leukocytosis on CBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Chronic Myelogenous Leukemia
Age?
 onset/progression?
 chr?
 signs?
 crisis?
 tx?

A

Adults
Insidious onset, slow progression
Philadelphia chromosome – t(9:22) bcr-abl fusion gene
Splenomegaly, fever, fatigue
Blast crisis
Bone marrow transplantation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

seen with which neoplasm?

Philadelphia Chromosome

A

SEEN WITH CML
 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Chronic Lymphocytic Leukemia
commonality?
 age? symptoms?
 infections?
autoantibodies?
Richter syndrome?

A

Most common type of leukemia
Adults, often asymptomatic
Hypogammaglobulinemia – infections
Anti red cell autoantibodies – autoimmune hemolytic anemia
Anti platelet autoantibodies – autoimmune thrombocytopenia
Richter syndrome – may transform to high grade lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

4 kinds of Lymphoid Neoplasms

A

 Lymphocytic Leukemia
 Hodgkin Lymphoma
 Non-Hodgkin Lymphoma
 Plasma cell neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Clinical Presentation of Lymphoid Neoplasms: Related to ________

A

Related to Anatomic Distribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Lymphoma presentation

A

Lymphoma - non-tender lymph node enlargement, extra-nodal mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Leukemia cytopresentation, why?

A

cytopenias due to suppression of hematopoiesis

36
Q

Plasma cell neoplasms presentation

A

bone pain, pathologic fracture

37
Q

all lymphomas are?

A

malignant

38
Q

classes of lymphomas

A

Hodgkin Lymphoma – HL
Non-Hodgkin Lymphoma - NHL

39
Q

Clinical Presentation of NHL
 lymph nodes?
 Generally involves?
 Frequently involves?

A

 Painless lymphadenopathy with firm,
enlarged, rubbery, freely movable,
non-tender lymph nodes
 Generally involves multiple lymph
nodes in a non-contiguous pattern
 Frequently involves extranodal sites

40
Q

Extra-Nodal Non-Hodgkin
Lymphoma
Most NHL arises within?
NHL may also arise?
Oral mucosa?

A

Most NHL arises within lymph nodes – 70%
NHL may also arise extra-nodally – 30%
Oral mucosal NHL is extra-nodal

41
Q

areas of mouth where extra nodal NHL may present

A

palate
alveolar ridge

42
Q

agression/ grades of lymphomas

A

All Lymphomas are Malignant
Degree of aggressiveness varies
Low grade - indolent, difficult to cure
High grade - aggressive, often curable

43
Q

Burkitt Lymphoma
Grade?
 known as
 HL or NHL?
 vrial association?

A

Burkitt Lymphoma – High Grade
“African Jaw Lymphoma”
B-Cell NHL
EBV association

44
Q

MALT Lymphoma
Grade?
Arises from?
 onset?
 what can increase risk?
 May transform into?

A

MALT Lymphoma – Low Grade
Arises from Mucosal-
Associated Lymphoid Tissue
“MALT-oma” - mature B cells
Often indolent (slow onset)
Salivary glands, Sjogren
Syndrome can increase risk
May transform to high grade
lymphoma

45
Q

Burkitt Lymphoma
A sub-type of?
 grade/growth rate/cell involved?
 endemic predilection?

A

A sub-type of non-Hodgkin lymphoma (NHL)
A high grade B cell neoplasm, most rapidly-growing human neoplasm
The endemic form has a predilection for jaws of children

46
Q

Burkitt Lymphoma
Three clinical forms

A

Endemic (African)
Sporadic
HIV-associated

47
Q

Cytogenetics of
Burkitt Lymphoma
 Translocations?
 gene?
 overexpression?
 cellular proliferation?

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

48
Q

death if untreated?

Oral Findings in Burkitt Lymphoma

A

Rapidly growing painless swelling, producing paresthesia, loose teeth
Rapid demise if untreated

49
Q

Endemic Burkitt Lymphoma radiograph

A

large luceny

50
Q
A

sporadic form of burkitt

51
Q

what histological pattern can be seen with burkitts

A
52
Q

when to use? doseage/terms?

chemo with burkitts

A

High grade lymphoma - aggressive
Cures frequent with short-term, high-dose chemotherapy

53
Q

Three Examples of
Non-Hodgkin Lymphoma

A

Burkitt Lymphoma
Diffuse large cell lymphoma
MALT-oma

54
Q

Hodgkin Lymphoma (HL) distinguished by?

A

The neoplastic cell: Reed-Sternberg cell (owl eyes)

55
Q
A

reed sternberg cells=hogdkin lymphoma

56
Q

The Reed-Sternberg Cell:
 fraction of the tumor mass?
Most are of what origin?
 appearnce?
hallmark for what dx?

A

HALLMARK CELL OF HODGKIN LYMPHOMA
A minor fraction of the tumor mass
Most are of B cell origin
Bilobate nucleus with large inclusion-like nucleoli -“owl-eye” cell

57
Q

General Characteristics of
Hodgkin Lymphoma
 age distribution?
 lymph?
Constitutional symptoms?
Fever?
Night?
Weight?
skin?
Association with?

A

Bimodal age distribution - young adults, older adults
Painless lymphadenopathy
Constitutional symptoms variable
Fever – Pel-Ebstein fever
Night sweats
Weight loss
Generalized pruritus (itchy skin)
Association with Epstein Barr virus

58
Q

Spread of Hodgkin Lymphoma

A

 Uniform, predictable pattern of spread from one lymph node region to the next

59
Q

staging of NHL

A

Characterizes extent of disease
* Stage I– Single lymph node region
* Stage II– Multiple lymph node regions
– Same side of diaphram
* Stage III– Multiple lymph node regions
– Both sides of diaphragm
* Stage IV– Disseminated disease

60
Q

“B” Symptoms for Staging of Non-Hodgkin Lymphoma

A

Recurrent, unexplained fevers
Night sweats
Unintended weight loss

61
Q

low vs high grade (local/advanced)

Treatment of Non-Hodgkin Lymphoma

A

Low-grade lymphomas - treat only if symptomatic

High-grade lymphomas
Localized stage - RT
Advanced stage – CT or combination CT/RT

62
Q

Staging of Hodgkin Lymphoma

A

Characterizes the Extent of Disease
 Stage I - single lymph node region
 Stage II - multiple lymph node regions on same side of diaphragm
 Stage III - multiple lymph node regions on both sides of diaphragm
 Stage IV - disseminated disease

63
Q

what determines treatment of Hodgkin Lymphoma

A

Stage determines treatment protocol
Localized (Stage I) - local radiation therapy=Risk of second cancers
Disseminated (Stage IV) -chemotherapy

64
Q

Prognosis of Hodgkin Lymphoma
Stage?
Histologic sub-type?
Curable?

A

Stage - most important
Histologic sub-type - least important
Curable - Stage I – 90% cure rate

65
Q

location? spread? waldeyer? extranodal?

Comparison of Hodgkin Lymphoma with
Non-Hodgkin Lymphoma

A
66
Q

Multiple Myeloma
 age?
 cells?
 signs? (bones? ca?)
 associated conditions? (cell levels? predespostion to?)

A

Older adults
Disseminated neoplasm of terminally-differentiated B
lymphocytes (plasma cells)
 Multifocal lytic bone lesions, hypercalcemia, bone pain
 Myelophthisic anemia (decreased RBC due to neoplasia in marrow), predisposition to infections

67
Q

radiographic sign of MM

A

punch out lucencies of bone

68
Q
A

punch out lucencies= MM

69
Q

Oral Findings:
Multiple Myeloma

A

Lytic lesions, loose teeth, pain, paresthesia, pathologic fracture
Macroglossia due to amyloidosis

70
Q

amyloidosis of MM can be seen where?

A

can be seen orally/facially

71
Q

Laboratory Findings:
Multiple Myeloma
 Ca, pro, Ig
 erythrocyte sedimentation rate?
Rouleaux?

A

Laboratory Findings:
Multiple Myeloma
Elevated serum calcium, protein, immunoglobulins
Elevated erythrocyte sedimentation rate (ESR)
Rouleaux formation- stacks of RBCs

72
Q

Ig lab finding of MM

A

Monoclonal gammopathy - M-spike
Bence-Jones proteinuria immunoglobulin light chains

73
Q

complications of MM

A

Renal failure- due to breece jame pro, toxic to kidneys
Infection
Anemia

74
Q

Normal Platelet Function in Vessel Wall

A

Normal Platelet Function in Vessel Wall
primary and secondary hemostatsis

75
Q

bleeding time tests
what cells are being assessed?
represents?
WNL?
abnormal when?
drugs that can cause abnormal result?
common dx?

A

 Clinical assessment for adequate number and function of platelets.
 The bleeding time test represents the time taken for a standardized skin puncture to stop bleeding
 The normal range depends on the actual method used and varies from 2 to 9 minutes
 It is abnormal when there are congenital or acquired platelet defects
 Drugs – ASA, NSAIDS
 Von Willebrand Disease

76
Q

Platelet Disorders

A

Platelet Disorders
Thrombocytopenia - decrease
Thrombocytosis - increase
Functional defects

77
Q

drugs and effects? potetnial dx?

Platelet Functional Defects -
Thrombasthenia

A

 Aspirin - inhibits aggregation for lifetime of platelet (8-10d) (irreversible)

 NSAIDs - inhibits aggregation until drug eliminated (reversible)

 Von Willebrand Disease - compound defect involving platelet function and
coagulation pathway: Normal platelet count with increased bleeding time

78
Q

Hemorrhage Terminology:
Skin and Mucosa

A

 Petechiae - pinpoint hemorrhages
 Purpura - petechiae become confluent
 Ecchymosis - purpurae become confluent
 Hematoma – cavity

79
Q
A

 Petechiae
 Purpura
 Ecchymosis

80
Q

Thrombocytopenia
Normal platelet count?
Thrombocytopenia?
gradient of symtpoms

A

Normal platelet count - 150,000 to 450,000 /mm3
Thrombocytopenia < 100,000 /mm3

81
Q

production? destruction? spleen? transfusions?

Causes of Thrombocytopenia

A

Decreased production - aplastic anemia
Increased destruction – immunologic destruction
Sequestration in spleen –splenomegaly
Dilution - massive transfusion

82
Q

tx

Immune Thrombocytopenic
Purpura/ Idiopathic Thrombocytopenic Purpura

A

Autoimmune disease– antiplatelet autoantibodies = produce thrombocytopenia
Treatment with steroids, splenectomy

83
Q

ITP plattelt count

A

<7000/ ml

84
Q

forms? due to?

Thrombocytosis
(Thrombocythemia)

A

Primary thrombocytosis (essential) - hematopoietic stem cell disorder:
Increased numbers of megakaryocytes producing dysfunctional platelets

Reactive thrombocytosis due to:
Asplenia
Inflammatory disorders

85
Q

what is the most common leukemia?

A

CLL

Pathology (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions