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Path SJSM > WBC disorders B4 > Flashcards

WBC disorders B4 Flashcards

1
Q

Growth factors:

KIT ligand & FLT3 ligand are ________ growth factors

A

Stem cell growth factors

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2
Q

Growth factors:

What are the 2 Stem cell growth factors

A

KIT & FLT3 ligands

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3
Q

List the progenitor cell line for Stem cells

A

1) Hematopoietic stem cell
2) Multipotent progenitor

Growth factors are KIT & FLT3 ligands

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4
Q

List the progenitor cell line for Myeloblasts (3 paths)

A

Basophil path:
1) Myeloid stem cell (Bone marrow)
2) Myeloblast (CD33/34 neg & CD13/15 pos)
3) Immature Basophil
4) Basophil

Eosinophil path:
1) Myeloid stem cell (Bone marrow)
2) Myeloblast (CD33/34 neg & CD13/15 pos)
3) Immature Eosinophil
4) Eosinophil

Neutrophil path:
1) Myeloid stem cell (Bone marrow)
2) Myeloblast (CD33/34 neg & CD13/15 pos)
3) N. Promyelocyte
4) N. Myelocyte
5) N. Band
6) Neutrophil

growth factor is G-CSF

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5
Q

List the progenitor cell line for Monocytes

A

1) Myeloid stem cell (Bone marrow)
2) Immature monocyte
3) Monocyte

growth factor is GM-CSF

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6
Q

List the progenitor cell line for Platelets

A

1) Myeloid stem cell (Bone marrow)
2) Megakaryocyte
3) Platelets

growth factor is thrombopoietin

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7
Q

List the progenitor cell line for RBC’s

A

1) Myeloid stem cell (Bone marrow)
2) Pro-Normoblast
3) Basophilic Normoblast
4) Polychromatic Normoblast
5) Orthochromatic Normoblast
6) Polychromatic Erythrocyte
7) Erythrocyte

growth factor is Erythropoietin

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8
Q

List the progenitor cell line for Lymphocytes

A

1) Myeloid stem cell (Bone marrow)
2) Lymphoid stem cell (Lymph nodes)
3) Lymphocyte

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9
Q

Describe how corticosteroid can cause Eosinopenia, Lymphopenia & Neutrophilia

A

1) Corticosteroids trap eosinophils in the lymph nodes
2) Corticosteroids induces apoptosis in lymphocytes
3) Corticosteroids increase neutrophil release from bone marrow & decreases neutrophil adhesion molecules, so they don’t stick to the walls of blood vessels and can’t move out of the circulation

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10
Q

What are the 3 main side effects on blood WBC counts that happen with corticosteroid use

A

Eosinopenia
Lymphopenia
Neutrophilia

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11
Q

Describe how Cushing’s can cause leukopenia & eosinopenia

A

Excessively high levels of ACTH or cortisol trigger leukopenia and eosinopenia

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12
Q

How does Cushing’s impact WBC counts?

A

Eosinopenia
Lymphopenia

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13
Q

Proliferative WBC disorder with too many leukocytes

A

Leukocytosis

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14
Q

WBC disorder with too few leukocytes

A

Leukopenia

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15
Q

Agranulocytosis means there are

A

to few neutrophils (under 500) this can cause severe infections!

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16
Q

WBC with eosinophils under 30

A

Eosinopenia

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17
Q

List the normal WBC labs for:

Leukocytes

A

4500-to-11,000

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18
Q

List the normal WBC labs for:

Segmented neutrophils

A

54-62%

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19
Q

List the normal WBC labs for:

Bands

A

3-5%

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20
Q

List the normal WBC labs for:

Eosinophils

A

1-3%

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21
Q

List the normal WBC labs for:

Basophils

A

0-0.75%

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22
Q

List the normal WBC labs for:

Lymphocytes

A

25-33%

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23
Q

List the normal WBC labs for:

Monocytes

A

3-7%

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24
Q

Blast cells in the serum likely indicate what?

A

Leukemia

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25
Q

Patient presents with:

Low grade fever
WBC count of 80,000
Chronic cough
Elevated monocyte count

It likely indicates what?

A

Chronic inflammation

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26
Q

Increased Bands in the serum likely indicate what?

A

An acute infection with a leftward shift

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27
Q

List some common causes of Lymphopenia

A

1) Congenital immune deficiencies (Di George syndrome, HIV, AIDS, & SCID)
2) Post treatment with glucocorticoids or cytotoxic drugs
3) Autoimmune disorders

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28
Q

1) Congenital immune deficiencies (Di George syndrome, HIV, AIDS, & SCID)
2) Post treatment with glucocorticoids or cytotoxic drugs
3) Autoimmune disorders

Are all common causes of what disordered WBC level?

A

Lymphopenia

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29
Q

Neutropenia is described as having what level of serum neutrophils?

A

WBC disorder with an absolute neutrophil count < 1500

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30
Q

Describe the possible causes of Neutropenia

A

1) Decreased production of granulocytes (aka poor granulopoiesis)

2) More destruction or sequestration of neutrophils (aka less neutrophils are released into blood)

3) Drug reactions with either Chloramphenicol (causes aplastic anemia) or Chlorpromazine (an antipsychotic sedative) both are toxic to the bone marrow and mess with granulopoiesis

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31
Q

Describe the common causes of agranulocytosis (neutrophils <500)

A

Drugs toxicity to the bone marrow (Chloramphenicol, Chlorpromazine, Sulfonamides, Thiouracil, & Phenylbutazone)

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32
Q

Describe how drug toxicity to Sulfonamides can lead to agranulocytosis

A

The sulfonamide causes the body to make antibodies against our own neutrophils (very similar to immune hemolytic anemias)

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33
Q

Describe the signs of agranulocytosis (Neutrophils <500)

A

Ulcerating necrotic lesions in the mouth, gingivae, & pharynx that are covered by a gray-green-black necrotic membrane with lots of bacteria/fungi but little to no leukocyte response

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34
Q

Patient has the following, what is the condition?

A

agranulocytosis (Neutrophils <500)

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35
Q

Leukocytosis (increased WBC #) is primarily dependent on 4 factors

A

1) The number of myeloid and lymphoid precursors and storage pools
2) The rate of cell release from storage
3) The percentage of marginating WBCs
4) The rate of extravasation (aka leaving blood-to-tissues)

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36
Q

1) The number of myeloid and lymphoid precursors and storage pools
2) The rate of cell release from storage
3) The percentage of marginating WBCs
4) The rate of extravasation (aka leaving blood-to-tissues)

Impact what component within blood labs

A

Leukocytosis

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37
Q

Describe how increased bone marrow in response to ________________________________causes leukocytosis

A

1) Chronic infection/inflammation (dependent on GF)
2) Paraneoplastic syndromes (dependent on GF)
3) Myeloproliferative disorders (independent of GF)

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38
Q

Describe how more release of leukocytes from storage in response to ________________________________causes leukocytosis

A

1) Endotoxemia
2) Infection
3) Hypoxia

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39
Q

Describe how a decreased marginating pool of WBC’s in response to ________________________________—–causes leukocytosis

A

Exercise & catecholamines

40
Q

Describe how a decrease in extravasation of WBCs going into tissues in response to ________________________________—–causes leukocytosis

A

Glucocorticoids (aka corticosteroids)

41
Q

What can stimulate neutrophilic leukocytosis

A

It can be stimulated by any stress (both catecholamines & glucocorticoids)

42
Q

Neutrophilic leukocytosis can be caused by what conditions

A

1) Acute bacterial infections
2) Sterile inflammation
3) Tissue Necrosis

43
Q

Eosinophilic leukocytosis (eosinophilia) can be caused by what conditions

A

1) Allergic disorders
- asthma
- hay fever
- parasitic infestation
2) Certain malignancies
- Hodgkin & some non-Hodgkin lymphoma
3) Some vasculitides
4) Atheroembolic disease
5) Polyarteritis nodosa

44
Q

Basophilic leukocytosis (Basophilia) can be caused by

A

rare myeloproliferative disease (chronic myelogenous leukemia)

45
Q

Monocytosis can be caused by

A

1) Chronic infections (Tuberculosis)
2) Bacterial endocarditis
3) Rickettsiosis
4) Malaria
5) Autoimmune disorders (SLE)
6) Inflammatory Bowel Disease (Ulcerative colitis)

46
Q

Lymphocytosis is associated with what?

A

1) monocytosis in many chronic immunological stimulation (ex. 2)Tuberculosis Brucellosis)
3) Viral infections (Hep A, CMV, EBV)
4) Bordetella pertussis infection

47
Q

Describe the features highlighted in the histo slide

A

Dohle bodies (fragmented ribosome-rich endoplasmic reticulum with a “sky-blue puddle appearance”) Usually only seen in SEVERE septic or inflammatory conditions.
&
Toxic granulations

48
Q

Describe the features of sepsis & Severe inflammatory disorders (leukocytosis)

A

1) Neutrophil count is 60,000 (very high)
2) Neutrophils have Dohle bodies, Cytoplasmic vacuoles, & toxic granulations (coarse + dark granules)

49
Q

Which conditions are NOT associated with eosinophilia (aka their non-invasive)

A

Pinworms & Adult ascariasis

50
Q

IL-5 mainly stimulates what?

A

Eosinophil production

51
Q

Describe leukemoid reactions

A

Involved with severe infections & very high WBC count >50,000 it mimics myeloid leukemia (but it’s NOT)

1) Increased mature neutrophils
2) Fewer immature neutrophils
3) Neutrophils have high levels of LAP (Levels of Alkaline Phosphate)
4) Neutrophil production is normal and they show
- positive CD13/CD15
- negative CD33/CD34 & HLA-DR

52
Q

How can you tell the difference between leukemoid reactions & malignant WBC’s

A

Myeloid leukemoid has LAP

Malignant WBC’s don’t have LAP (ex. CML)

53
Q

Pancreatitis presents with what?

A

Neutrophilic leukocytosis with inflammation

54
Q

Common leukemoid reactions include what conditions?

A

1) Pancreatitis
2) Infectious pneumococcal pneumonia
3) Neoplastic carcinoma of the lung
4) Perforated appendicitis

55
Q

Describe the following features of this histo slide

A

Normal neutrophils with high levels of LAP making this a leukemoid reaction

56
Q

Describe the following features of this histo slide

A

Malignant neutrophils with absent/very low levels of LAP

57
Q

Describe the features of acute non-specific lymphadenitis

A

Antigens cause the primary follicles to enlarge & develop pale germinal centers (where B cells make Abs vs those antigens)

The paracortical T-cell zones can also enlarge

58
Q

Antigens cause the primary follicles to enlarge & develop pale germinal centers (where B cells make Abs vs those antigens)

The paracortical T-cell zones can also enlarge

A

features of acute non-specific lymphadenitis

59
Q

Describe the features of lymphadenitis

A

The lymph nodes are enlarged/painful & the overlying skin is red (soft/fluctuant if there’s an abscess)

Suppurative infections can penetrate through the capsule of the node & can track to the skin causing draining sinuses that scar after healing

60
Q

Acute lymphadenitis histology can be described as

A

1) Big reactive germinal centers with many mitotic figures
2) Macrophages have granulation from dead bacteria or necrotic cells

First the neutrophils are prominent then the follicle centers become necrotic

61
Q

Cervical lymphadenitis is usually from infected ______&________

A

Teeth & Tonsils

62
Q

Axillary or inguinal lymphadenitis is usually from infections to _________

A

infections in the extremities

63
Q

Acute lymphadenitis in the mesenteric lymph nodes drain to form _____________

A

Acute appendicitis

64
Q

Describe the features of non-specific acute lymphadenitis

A

Foci of necrosis (the arrowhead) and acute inflammatory cells (presence of neutrophils) the arrow line

65
Q

Describe the features of chronic non-specific lymphadenitis

A

In chronic reactions lymph nodes (ex. supraclavicular or inguinal nodes commonly affected) are non-tender & enlarged it happens slowly over time with no associated tissue damage

66
Q

Describe the features of follicular hyperplasia

A

1) Has discrete & well-defined separated follicles with intrafollicular tissues
2) Follicles are varied in size/shape
3) Have well-defined mantle zones
4) Heterogeneous population of follicle center cells (large cells outnumber small cells in large follicles which are mitotically active)
5) bcl-2 staining is NEGATIVE in the germinal centers

67
Q

Malignant nodules stain __________ for bcl-2 and indicate what?

A

bcl-2 positive & indicate follicular lymphoma

68
Q

What conditions are commonly associated with follicular hyperplasia

A
  • Rheumatoid arthritis
  • Toxoplasmosis
  • Early stages of infection of HIV
69
Q

Describe the histological signs of follicular hyperplasia

A

There’s large oblong germinal centers (secondary follicles) surrounded by a collar of small resting naive B cells (mantle zones)

70
Q

Describe the following features in the histological slides

A

follicular hyperplasia:
- germinal centers (secondary follicles)
- a collar of small resting naive B cells (mantle zones) that surround the follicles
- several mitotic figures
- numerous macrophages containing phagocytosed apoptotic cells (tangible bodies)

71
Q

Describe the features of paracortical hyperplasia

A

A large of number of T-cell indicates a viral infection (stims T-cell response) such as:
- Herpes simplex virus
- Epstein barr virus (infectious mononucleosis)
- Cytomegalovirus

72
Q

Describe the following features on the slide

A

Acute lymphoblastic leukemia/lymphoma
Lymphoblast’s with condensed nuclear chromatin, small nucleoli, and scant agranular cytoplasm.

73
Q

Compared with myeloblasts, lymphoblast’s have more what?

A

1) Condensed chromatin
2) Poorly visible nucleoli
3) Smaller amounts of cytoplasm that usually lacks granules.

74
Q

Hyperplasia’s:

Describe the features of follicular hyperplasia

A

The follicles are discrete, well-separated, vary in size/shape, & have well-defined mantle zones
&
BCL-2 Negative germinal centers
Tangible bodies

75
Q

Describe the condition and the visible features on the histo slide

A

Follicular hyperplasia with tangible bodies

76
Q

A condition where:
The follicles are discrete, well-separated, vary in size/shape, & have well-defined mantle zones
&
BCL-2 Negative germinal centers
Tangible bodies

A

Follicular hyperplasia

77
Q

Hyperplasia:

Describe the features of paracortical hyperplasia

A

When stimulus triggers T-cell med immune responses (high # of Tcells = VIRAL INFECTION)

ex EBV, HSV, CMV

78
Q

When stimulus triggers T-cell med immune responses (high # of Tcells = VIRAL INFECTION)

ex EBV, HSV, CMV

What’s the condition

A

Paracortical hyperplasia

79
Q

Hyperplasia:

Describe the features of Sinus histiocytosis (aka Reticular hyperplasia)

A

Hypertrophy/hyperplasia of lymphatic endothelial cells lining the lymphatic sinusoids
&
Increase in histocytes (macrophages in the lymph node)

Sinusoids are distended/expanded

80
Q

What is a common pathological finding regarding the lymphatic sinuses in breast cancer?

A

Sinuses histiocytosis (reticular hyperplasia) where there’s Hypertrophy/hyperplasia of lymphatic endothelial cells lining the lymphatic sinusoids braining the breast
&
Increase in histocytes (macrophages in the lymph node)

81
Q

Pre-cursor B-cell neoplasms:

Describe the etiology of B-cell acute lymphoblastic leukemia/lymphoma (B-ALL)

A

Tumor activity targets lymphoblasts (aka B-cell development)

Happens in kids under 15yrs old, peak incidence ~3yrs (higher risk in Hispanics)

82
Q

Pre-cursor B-cell neoplasms:

Describe the pathogenesis of B-cell acute lymphoblastic leukemia/lymphoma (B-ALL)

A

Loss-of-function mutation of genes involved in B-cell development:
- PAX5
- E2A
- EBF
&
Translocations of (12:21) involving the ETV6 & RUNX1 genes

83
Q

Pre-cursor B-cell neoplasms:

Describe the morphology of B-cell acute lymphoblastic leukemia/lymphoma (B-ALL)

A

1) Hypocellular bone marrow packed with lymphoblasts & apoptosis inducing macrophages giving it a Starry-sky appearance

2) Tumor cells have condensed/finely stippled nuclear chromatin, small nucleoli, & a scant rim of agranular cytoplasm

84
Q

1) Hypocellular bone marrow packed with lymphoblasts & apoptosis inducing macrophages giving it a Starry-sky appearance

2) Tumor cells have condensed/finely stippled nuclear chromatin, small nucleoli, & a scant rim of agranular cytoplasm

Describes the morphology of what condition?

A

B-cell acute lymphoblastic leukemia/lymphoma (B-ALL)

85
Q

Loss-of-function mutation of genes involved in B-cell development:
- PAX5
- E2A
- EBF
&
Translocations of (12:21) involving the ETV6 & RUNX1 genes

Describes the pathogenesis of what condition

A

B-cell acute lymphoblastic leukemia/lymphoma (B-ALL)

86
Q

Tumor activity targets lymphoblasts (aka B-cell development)

Happens in kids under 15yrs old, peak incidence ~3yrs (higher risk in Hispanics)

Describes the etiology of what condition?

A

B-cell acute lymphoblastic leukemia/lymphoma (B-ALL)

87
Q

Pre-cursor B-cell neoplasms:

Describe the immunotype of B-cell acute lymphoblastic leukemia/lymphoma (B-ALL)

A

TdT +
CD19+
CD22+
CD10+
PAX5+

88
Q

The following immunotype indicates what condition?
TdT +
CD19+
CD22+
CD10+
PAX5+

A

B-cell acute lymphoblastic leukemia/lymphoma (B-ALL)

89
Q

Pre-cursor B-cell neoplasms:

Describe the clinical signs of B-cell acute lymphoblastic leukemia/lymphoma (B-ALL)

A

Abrupt onset (days-weeks)
1) Hypocellular bone marrow symptoms
- Fatigue
- Anemia
- Fever
- Neutropenia
- Thrombocytopenia (bleeding)
- Higher risk of infection

2) Generalized metastasis
- Bone pain (expanding marrow)
- Generalized lymphadenopathy, hepatosplenomegaly, &
testicular enlargement

3) CNS metastasis
- Headaches, vomiting, & nerve palsies (from meningeal
spread)

90
Q

Abrupt onset (days-weeks)
1) Hypocellular bone marrow symptoms
- Fatigue
- Anemia
- Fever
- Neutropenia
- Thrombocytopenia (bleeding)
- Higher risk of infection

2) Generalized metastasis
- Bone pain (expanding marrow)
- Generalized lymphadenopathy, hepatosplenomegaly, &
testicular enlargement

3) CNS metastasis
- Headaches, vomiting, & nerve palsies (from meningeal
spread)

A

clinical signs of B-cell acute lymphoblastic leukemia/lymphoma (B-ALL)

91
Q

Pre-cursor B-cell neoplasms:

Describe the signs of GOOD prognosis of B-cell acute lymphoblastic leukemia/lymphoma (B-ALL)

A

1) Onset is between 2-10yrs old
2) Low WBC #
3) Hyper diploidy (more genetic intervention opp. for medicine)
4) Translocation at (12:21)

92
Q

1) Onset is between 2-10yrs old
2) Low WBC #
3) Hyper diploidy (more genetic intervention opp. for medicine)
4) Translocation at (12:21)

Indicate a _______ prognosis for B-ALL

A

Good :)

93
Q

Pre-cursor B-cell neoplasms:

Describe the signs of POOR prognosis of B-cell acute lymphoblastic leukemia/lymphoma (B-ALL)

A

1) Onset under 2yrs old (infantile translocations involving MLL gene)
2) Presents in adolescence or adulthood
3) Peripheral blood blast levels above 100,000

94
Q

1) Onset under 2yrs old (infantile translocations involving MLL gene)
2) Presents in adolescence or adulthood
3) Peripheral blood blast levels above 100,000

Indicate a _______ prognosis for B-ALL

A

Poor :(

95
Q

Trisomy 21 (Down syndrome) has what similarity to B-ALL

A

People with XXX21 have a higher risk of developing acute lymphoblastic lymphoma which often present with enlarged testicles

96
Q
A

Path SJSM (26 decks)

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