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Clinical medicine A > Lecture 10: Leukocyte Evaluation > Flashcards

Lecture 10: Leukocyte Evaluation Flashcards

1
Q

What is a cytokine?

A

Any number of substances secreted by certain cells of immune system and have an effect on other cells.

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2
Q

What is granulocytopenia?

A

Reduced # of neutrophils, eosinophils, basophils

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3
Q

What are the PMN leukocytes?

A

The granulocytes: neutrophils, basophils, eosinophils.

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4
Q

What are the mononuclear leukocytes?

A

Agranulocytes - lymphocytes and monocytes

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5
Q

What is the most common type of WBC generally?

A

Segmented neutrophils

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6
Q

Where do granulocytes come from?

A

Hematopoietic stem cell (HSC)

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7
Q

How do HSC’s replicate?

A

Self-renewal and differentiation.

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8
Q

What is the proliferation cycle of a myeloblast?

A

Myeloblast => promyelocyte => myelocyte.

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9
Q

What can myelocytes do?

A

Cell division
Differentiation

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10
Q

What happens in the differentiation stage for a metamyelocyte?

A

It becomes a metamyelocyte => band => PMN cells

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11
Q

What are the immature granulocytes?

A

Metamyelocytes and bands are immature granulocytes.

PMNs are MATURE granulocytes.

Capable of maturation and differentiation but are not capable of division

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12
Q

What can myeloblasts become?

A

Basophils
Neutrophils
Eosinophils
Monocytes

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13
Q

At what point do myeloblasts become unable to replicate?

A

Once they become metamyelocytes.

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14
Q

What is the difference between proliferation and differentiation?

A

Differentiation means no more splitting/replicating.

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15
Q

What is included in neutrophil count?

A

Mature or immature neutrophils

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16
Q

What is the difference between poly-A and poly-M?

A

Poly-A means automatic examination of PMNs neutrophils.

Poly-M means manual examination of PMNs neutrophils.

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17
Q

When do we prefer absolute values for WBC diffs?

A

Pathologic states.

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18
Q

What should you always keep in mind if the relative % of one leukocyte increases?

A

The other percentages will decrease.

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19
Q

What is a neutrophil?

A

WBC

Contains granules that digest microorganisms.

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20
Q

What do neutrophils typically protect from?

A

Bacterial and fungal infection

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21
Q

Where is the storage pool for neutrophils?

A

Bone marrow.

Cannot detect neutrophils if they are in the bone marrow.

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22
Q

What are extramedullary neutrophils?

A

Circulating neutrophils in the bloodstream. They circulate approx 24 hours prior to entering a tissue.
Also known as circulation pool. (1/2 of neutrophils)
OR
Marginal pool (1/2 neutrophils)

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23
Q

What are the 1/2 of neutrophils attached to endothelial walls called?

A

Marginal pool.

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24
Q

What are the 3 pools for neutrophils?

A

Storage pool in the bone marrow (in steady state)

Extramedullary neutrophils:
Circulation pool (50%)
Marginal pool (50%)

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25
Q

What is neutrophilia?

A

Elevated ANC, aka granulocytosis.

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26
Q

What are the two possible presentations for neutrophilia?

A

Neutrophilic shift
True neutrophilia

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27
Q

What is a neutrophilic shift?

A

Shift from marginal pool to circulating pool.

It is transient, lasting 20-30 mins with a 1-2 min onset.

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28
Q

What causes neutrophilic shifts?

A

Exercise
Seizure
Paroxysmal tachycardia
Epinephrine injection
Post-op state

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29
Q

What is true neutrophilia?

A

Release of neutrophils from storage pool.

ANC elevates 5-6x

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30
Q

What are the 3 etiologic classifications of true neutrophilia?

A

Suprious: false elevated
Primary: Inherited
Secondary: MC type, and MC cause is infection.

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31
Q

What do we call a early release of bands?

A

Left shift

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32
Q

What are some secondary causes of true neutrophilia?

A

Infection (MC)
Stress
Cigarette smoking (constant inflammation)
Glucocorticoids
Recombinant G-CSF or GM-CSF

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33
Q

What are some primary causes of true neutrophilia?

A

Myeloproliferative disorders

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34
Q

What are some spurious causes of true neutrophilia?

A

Platelet clumping
Mixed cryoglobulinemia

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35
Q

What are the 3 types of neutropenia?

A

Mild: ANC 1000-1800
Moderate: ANC 500-1000
Severe: ANC < 500

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36
Q

What PE finding in a wound can suggest neutropenia?

A

Lack of pus in a wound.

Increased risk of sepsis from open wound.

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37
Q

What are the 3 main pathophysiologic processes responsible for neutropenia?

A

Insufficient or injured bone marrow stem cells.

Shift in neutrophils from the circulating pool to the marginal pool or tissue pool

Increased destruction in the circulation.

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38
Q

What is pseudoneutropenia?

A

Fake neutropenia as a result of medications OR

CBC being taken in the morning. Neutrophils might be resting in the marrow in the morning.

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39
Q

What is the name of the medication SE we will see for causing neutropenia?

A

Agranulocytosis.

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40
Q

What disorder category would cause increased destruction of neutrophils?

A

Autoimmune disorders.

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41
Q

What is the most common demographic for neutropenia?

A

Elderly

Asians and African-Americans may have low NORMAL neutrophil counts.

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42
Q

What is the main complication we are worried about in neutropenia?

A

Bacterial infections.

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43
Q

Why can bacterial infections be so dangerous in neutropenia?

A

Initial presenting s/s may not occur.

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44
Q

At what point are serious infections a real threat in regards to ANC?

A

ANC <500

Severe neutropenia.

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45
Q

What are some medications that are known to cause neutropenia?

A

Sulfonamides
PCN
Cephalosporins
Methimazole
Phenytoin

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46
Q

At what ANC level do we refer to heme/onc?

A

ANC <1000

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47
Q

What additional workup will heme/onc generally order for moderate-severe neutropenia?

A

Bone marrow biopsy

Serum antineutrophil antibodies

Rh factor and splenomegaly

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48
Q

What does + serum antineutrophils antibodies indicate?

A

Autoimmune neutropenia in the absence of bone marrow disorders.

49
Q

What is the standard therapy for neutropenia?

A

Myeloid growth factors

Myeloblasts are the precursor to all granulocytes.

50
Q

What are the two types of myeloid growth factors?

A

G-CSF (Granulocyte colony stimulating factor):
Filgrastim/neupogen
pegfilgrastim/neulasta

GM-CSF (Granulocyte-macrophage colony stimulating factor):
Sargramostim (Leukine)

51
Q

When can we treat neutropenia OP vs IP?

A

ANC > 1000 (mild) = OP if no other complications.

ANC < 500 (Severe) = IP with IV ABX.

ANC 500-1000 (moderate) = case dependent.

52
Q

What is the difference between filgrastim and sargramostim?

A

Filgrastim is just granulocytes. (G-CSF)

Sargramostim is granulocytes AND macrophages. (GM-CSF)

Sar Gra Mostim (GM)

53
Q

How is autoimmune neutropenia (AIN) treated?

A

Pulse steroid + intermittent myeloid growth factor

54
Q

How is myelosuppresive chemotherapy induced neutropenia treated?

A

Myeloid growth factor +/- prophylactic antimicrobials in intense therapy.

55
Q

What is a granulocyte transfusion? What is the indication for it?

A

A donor receives growth factors so that they can have their leukocytes drawn and transfused into a recipient.

Indicated for bacterial infections WITHOUT a clinical response to ABX within 24-48 hrs.

56
Q

What is a eosinophil and how do I recognize it?

A

Granules are stained by eosin. (red)

Bilobed nucleus.

57
Q

Where are eosinophils typically found and what is their role?

A

Tissue dwellers.

Assist in fighting parasites, allergies, and asthma.

58
Q

What are the MC target organs for eosinophils?

A

Skin
Airway
GI Tract

59
Q

What 3 cytokines are responsible for eosinophil development and differentiation?

A

IL-5
IL-3
GM-CSF

60
Q

How long do eosinophils circulate? How long do they live?

A

Circulate for 8-12 hours before entering a tissue.

Remain in tissue for 1-2 weeks.
Lifespan is 2-5 days normally, but increased to 2 weeks with cytokine aid.

61
Q

What are the types of eosinophilia?

A

Mild: 500-1500
Moderate: 1500-5000
Severe: >5000

62
Q

What are the causes of eosinophilia?

A

Primary clonal: genetic mutation or malignancy

Primary idiopathic: When all other causes have been ruled out. (HES)

Secondary: Reactive etiology

63
Q

What is hypereosinophilic syndrome?

A

HES is a rare disease. Not testable. It is a rule out disease.

64
Q

What is the general pathophysiology behind eosinophilia?

A

Dysregulation/overproduction of the cytokines (IL 3, IL 5, GM-CSF)

Results in either increased eosinophil production or longevity.

65
Q

What is the main complication of eosinophilia?

A

Tissue damage, occurring most commonly at AEC > 1500.

66
Q

How does organ damage occur because of eosinophilia?

A

Release of toxic granules
Production of lipid mediators that recruit inflammatory cells.
Release of cytokines involved in tissue remodeling and fibrosis.

67
Q

What are the MC target organs for eosinophils?

A

Skin
Airway
GI Tract

68
Q

What is a basophil?

A

Least-prominent WBC.

Dark-blue granules.

69
Q

What do basophils contain?

A

Histamine

Heparin

70
Q

What is the overall function of a basophil?

A

IgE antibody formation and activation.

71
Q

What is the primary cause of basophilia?

A

CML

72
Q

What are the secondary causes of basophilia?

A

Myeloproliferative disorders
Hypersensitivity/inflammation
Hypothyroidism

73
Q

What are agranulocytes?

A

WBCs with ONE-lobed nucleus and NO granules.

74
Q

What falls under agranulocytes?

A

Monocytes
Lymphocytes

75
Q

What is a lymphocyte?

A

Small leukocyte with single round nucleus and receptor molecules on surface.

Can bind to antigens AND remove them.

76
Q

Who has the greatest range of lymphocytes naturally?

A

Neonates < 28 days

77
Q

What is the more common lymphocyte?

A

T-cells: 60-80%

78
Q

Which mature lymphocyte CANNOT divide?

A

NK cells

79
Q

Where do T-cells mature and differentiate?

A

Thymus

80
Q

What is the function of a T-cell?

A

Destroy HUMAN cells that have been attacked by viruses or have become cancerous

81
Q

What are the 3 types of T-cells?

A

Helper/CD4+ T-cell
Cytotoxic/CD8+ T-cell
Regulatory T-cell

82
Q

What is the function of a helper/cd4+ t cell?

A

Recognize foreign antigens
Stimulate antibody production
Produce cytokines to activate other T cells.

83
Q

What is the function of a cytotoxic/CD8+ T-cell?

A

Attack and destroy foreign cells.

84
Q

What is the function of a regulatory T cell?

A

Dampen/turn off immune response of other T cells.

Lack of regulatory T cells leads to autoimmune diseases.

85
Q

Where do B-cells mature?

A

Bone marrow

86
Q

What is the function of a B-cell?

A

Present antigens to initiate T-cell response.
Express surface Ig receptors to specific antigens.
Become memory B-cells to provide long-lasting immunity.
Become plasma cells.

87
Q

What is the function of a plasma cell?

A

Produces large numbers of immunoglobulins (Ig) until infection is gone.

88
Q

What are the functions of NK cells?

A

Cytotoxic granule release to attack cancerous or VIRALLY infected cells. (no immune system activation required)

Maintain control of immune response. (Can differentiate between foreign and self)

89
Q

What are the two kinds of lymphocytosis?

A

Monoclonal lymphocytosis: benign or lymphoproliferative disorder.

Polyclonal lymphocytosis: Infectious, transient, reactive, benign.

90
Q

What is monoclonal lymphocytosis?

A

Expanded clonal B-cell population in blood.

No sign of any infection, autoimmune, or lymphoproliferative process.

91
Q

What does a monoclonal lymphocytosis suggest?

A

Premalignant or malignant lymphoproliferative syndrome.

92
Q

What is the MC premalignant etiology of a monoclonal lymphocytosis?

A

Monoclonal B cell lymphocytosis.

93
Q

What are the malignant etiologies of a monoclonal lymphocytosis?

A

CLL
NHL w/ circulating disease
Hairy cell leukemia (HCL)
Large granular lymphocytic leukemia (LGL)

94
Q

Why is polyclonal lymphocytosis not always a big concern?

A

Symptom of an underlying condition caused it, expected to normalize in 2 months if underlying cause is resolved.

95
Q

What is the MC infectious etiology of polyclonal lymphocytosis?

A

Mono

Other causes:
Pertussis
Cat-scratch
Toxoplasmosis

96
Q

What are the 4 etiology types for polyclonal lymphocytosis?

A

Infectious
Transient
Reactive
Benign persistent

97
Q

How do we workup lymphocytosis?

A

CBC
Smear
Flow cytometry (if high suspicion it is bacterial)

98
Q

What is flow cytometry used for in lymphocytosis?

A

Detects surface antigens specific to B or T cells.
Can detect clonal lymphocyte proliferation.

No use in viral infection.

99
Q

What are the 3 pathophysiologies behind lymphocytopenia?

A

Decreased production
Increased destruction
Splenic or lymph sequestration

Note:
Just like RBCs.

100
Q

What are the main complications we are worried about in lymphocytopenia?

A

Opportunistic infections

Malignancy and autoimmune disorder risk.

101
Q

What are the two types of lymphocytopenia?

A

Inherited
Acquired

102
Q

What are the types of acquired lymphocytopenia?

A

Infectious disease (HIV MC)
Iatrogenic (Radio/chemo)
Autoimmune
Nutritional def (ZINC, alcoholic)

103
Q

What is a monocyte?

A

Large phagocyte with oval nucleus and clear, grayish cytoplasm.

104
Q

Where do monocytes differentiate?

A

Within tissues, into macrophages or dendritic cells.

105
Q

Where are most monocytes stored?

A

Spleen (50%)

106
Q

What are the functions of monocytes?

A

Phagocytosis
Antigen presentation
Inflammatory cytokine production

107
Q

How is monocytosis described as in terms of duration?

A

Transient if no hematopoietic suppression.

108
Q

What are the etiologies of monocytosis?

A

(bacterial infections MC)
Acute/chronic leukemia/lymphomas
Aspenia
Inflammatory/autoimmune
Corticosteroids
CSF (increasing granulocytes only)

109
Q

What are the primary treatment options for leukopenia?

A

Broad spectrum ABX
G-CSF-GM-CSF

Corticosteroids
Nutritional deficiency correction
Splenectomy if chronic.

110
Q

What kind of PE exam should you never do on someone immunocompromised?

A

Rectal exams, because skin breaks and inflammatory responses will ensue.

111
Q

What is a possible source of error for a peripheral blood smear?

A

Mechanical trauma to cells.

112
Q

When do we commonly seen hypersegmentation of neutrophils?

A

Megaloblastic anemias
Myeloproliferative disorders
Chemo

113
Q

When do we commonly see granulation of leukocytes?

A

Bacterial infections

114
Q

When do we commonly see Dohle bodies?

A

Infection in general.

It is an irregular blue stain in the cytoplasm.

115
Q

When do we commonly see smudge or basket cells?

A

Fragile lymphocytes in CLL.

116
Q

When do we commonly see platelet satellitosis?

A

Artifact of EDTA anticoagulation.
EDTA is an AC used in tubes for CBC.

117
Q

What tissue type does flow cytometry assess?

A

Blood
Bone Marrow
Lymph Node

118
Q

What is the main function of flow cytometry?

A

Differentiating between normal and malignant cells.

It can detect antigens/markers via lasers.

Clinical medicine A (32 decks)

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