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Path Exam 5 > WBC Disorders > Flashcards

WBC Disorders Flashcards

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1
Q

General classes of WBC disorders

A

Leukopenias

Proliferative: 1) Reactive, 2) Neoplastic

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2
Q

Most common cause of leukopenia (which cell type is low)

A

Low WBCs is usually caused by neutropenia

Lymphopenia is less common

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3
Q

What are the common causes of lymphopenia?

A

Lymphopenia is commonly caused by HIV, glucocorticoid treatment, autoimmune disorders, malnutrition, certain acute viral infections.

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4
Q

Why do viral infections sometimes cause lymphopenia?

A

Viral infections cause release of interferon type I => lymphocyte redistribution and sequestration.
T-Lymphocytes become activated and their surface receptors change so that they stay in lymph nodes and adhere to endothelial cells.

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5
Q

Neutropenia => inc risk of what?

What are some of the assoc. signs?

A

Bacterial and fungal infections
Candida and Aspergillus fungus
Often see ulcerating and necrotizing lesions in the mouth, but can also be present on the skin, vagina, anus, and GI
Deep infections can occur in the lungs, GU, and kidneys
Can also see bacterial colonies growing as if on agar plates

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6
Q

What is pancytopenia?

A

decreased RBC’s, WBC’s and platelets

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7
Q

Morphology of the bone marrow for neutropenia

A

Hypercellular: in cases where granulocytes are destroyed in periphery, or with ineffective granulopoiesis (megaloblastic anemia, myelodysplastic syndromes)

Hypocellular: in cases that dec or destroy granulocyte precursors

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8
Q

Clinical features of neutropenia

A

malaise, fever, chills, fatigue, weakness

infections can cause death in hours to days

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9
Q

4 mechanisms causing leukocytosis

A

Increased production in marrow: infection/inflammation, Paraneoplastic, Myeloproliferative disorders
Increased release from marrow: endotoxemia, infection, hypoxia
Decreased leukocyte margination: exercise, catecholamines
Decreased extravasation: glucocorticoids

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10
Q

How does infection => increased leukocytes in the blood?

A

Acute infection causes release of mature granulocytes from the marrow from TNF and IL-1.
With time, TNF and IL-1 cause macrophages, bone marrow stromal cells, and T-cells to release growth factors that will increase production of leukocytes for a prolonged period

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11
Q

Sepsis or severe inflammatory disorders => what morphologic changes in neutrophils?

A

Toxic granules: coarse, dark cytoplasmic granules

Dohle Bodies: Sky-blue cytoplasmic “puddles” that are dilated endoplasmic reticulum

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12
Q

Type of leukocytosis commonly assoc with myeloproliferative disease

A

Basophilia

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13
Q

Type of leukocytosis commonly seen with allergic disorders like asthma, hay fever, parasitic infections, as well as drug reactions and some malignancies?

A

Eosiniphilia

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14
Q

When would you see monocytosis?

A

Chronic infections like TB, bacterial endocarditis, rickettsiosis, malaria, autoimmune disorders like SLE, and IBD like ulcerative colitis

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15
Q

When would you see Neutrophilia?

A

Acute bacterial infections (escpecially pyogenic), sterile inflammation caused by infarction or burns

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16
Q

When would you see lymphocytosis?

A

With monocytosis in chronic immune stimulation, viral infections, Berdetella pertussis

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17
Q

Name stages of Neutrophil progression/development

A

blast => promyelocytes => myolocytes => metamyelocytes => bands => segs

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18
Q

Reference ranges for WBC, Neutrophils, Lymphocytes

A

WBC: 5,000-10,000
Neutrophils: 1,500-6,500
Lymphocytes: 1,200-3,400

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19
Q

Normal Myeloid to Erythroid cell ratio in the marrow

A

2:1 to 5:1

More myelo/granulocytic cells than erythroid

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20
Q

Causes of neutropenia and also pancytopenia

A

Myelophthisis Anemia: infiltrative process of the marrow like cancer, infection, leukemic or lymphoma infiltrate

Aplastic Anemia: Precursor cells fail, hypocellular marrow

Large Granular Lymphocytic Leukemia: CD8+ T cell Leukemia, pancytopenia from marrow suppression by neoplastic cell products

Ineffective Production:
-Defective DNA => intramedullary death, marrow is hypercellular, hypersegmented neutrophils, macrocytes and other WBC/RBC abnormal morphology; caused by Vit B12 and folate deficiency and Myelodysplastic syndromes

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21
Q

Neutropenia due to accelerated removal/destruction

A

Immunological-mediated injury: SLE, reaction to drugs

Increased peripheral use: overwhelming bacterial, fungal, rickettsia infections

Splenic sequestration: 2ndary to enlarged spleen, Felty Syndrome= RA, splenomegaly

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22
Q

Drug-induced neutropenia

A

Most common cause of neutropenia
Cancer chemotherapy
Immunologic reactions to drugs like sulfonamides, thiouracil
Alcohol toxicity

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23
Q

Differential diagnosis of Pancytopenia

A 
Myelophthisis anemias including Leukemia
Aplastic anemia
Myelodysplatic syndromes
Megaloblastic anemias
Autoimmune like SLE
Splenic sequestration
Chemotherapy
Total body rediation
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24
Q

Other causes of Neutrophil Dysfunction

Study These Flashcards
A 
Diabetes, Malignancy, Dialysis, Sepsis
Myelodysplatic syndromes
Chronic granulomatous disease
Leukocyte adhesion deficiencies
MPO deficiency
Chediak-Higashi syndrome
25
What does a 'left shift' suggest?
Suggests a bacterial infection
26
What is a leukemoid reaction?
Leukemia-like reaction where the granulocyte counts are above and beyond the normal upper limits. Usually caused by severe infection or tumors
27
What is a leukoerythroblastic reaction?
Left shift in the presence of nucleated RBC's | Implies a bone marrow space-occupying lesion
28
What signaling molecule will cause an increase in Eosinophils?
IL-5
29
Types of eosinophilic pneumonias
Coccidioidomycosis Loeffler's pneumonia Chronic eosinophilic pneumonias
30
What is classic sign of eosinophilia?
Charcot-leyden chrystals left behind and in macrophages
31
Relationship between Neutrophils and Monocytes in terms of infection
Neutrophils show up first, but subside with time as monocyte numbers rise unless it is a pyogenic infection.
32
Causes of monocytosis
``` Chronic infection: TB Bacterial endocarditis Rickettsiosis Malaria IBD: ulcerative cholitis Autoimmune: RA, SLE ```
33
Causes of reactive lymphocytosis
``` Bordetella pertussis (whooping cough) Chronic infection (TB) Viral infection ```
34
Common viral causes of lymphocytosis and differences between them
Infectious mononucleosis (IM) caused by EBV: likely diagnosis if >20%reactive lymphs CMV: IM-like but w/o cervical lymph node involvement Toxoplasmosis: IM-like Viral hepatitis
35
What do reactive or atypical lymphs look like?
These are CD8+ lymphs Larger cells with large and abnormally shaped nuclei If seen, first think leukemia, but if large cytoplasm present then think virus caused
36
What to think when see nucleated RBC's in the peripheral blood
Rapidly evolving anemia=> increased release of RBC's from the marrow Post splenectomy Bone marrow replacement–think myelophthisic process (space-occupying lesion in the bone)
37
Categories of Neoplastic Proliferations of White cells
1) Lymphoid 2) Myeloid 3) Histiocytosis, Langerhans cell type
38
Risk factors for leukemia
Inherited: defects in DNA repair–Bloom Syndrome, Ataxia Telangiectasia, Fanconi Anemia; Down Syndrome; Neurofibromatosis type I Viruses, Radiation and Chemicals, Chemotherapy, Smoking, Benzene
39
Categories of Leukemia
Can be acute or chronic Can be lymphocytic or myelocytic ALL, AML, CLL, CML All acute cause death within months if not treated Chronic cause death within years, CML=>death earlier than CLL
40
Leukemia vs lymphoma
Leukemia is a lymphocytic neoplasm in the marrow | Lymphoma is a lymphocytic neoplasm in the lymph nodes or other place outside the marrow
41
WHO classification of lymphoid malignancies
Precursor B and T cells (lymphoblasts): in marrow or thymus | Peripheral lymphoid malignancies: in lymph nodes, spleen, blood
42
Pathogenesis of ALL
Accumulation of mutations (fewer than with solid tumors) T-cell: NOTCH-1 gain of function in 70% of cases B-Cell: Transcription factor PAX5, loss of development factors E2A, EBF; t(12;21) ETV6: RUNX in early precursors Chromosomes often abnormal in number
43
General epidemiology for ALL
Most common childhood malignancy | Generally
44
Epidemiology of Pre-T neoplasms
``` Lymphomas 50-70% of the time Adolescent males Mediastinal mass of Thymus Respiratory symptoms Rapidly progresses to leukemic phase Worse prognosis than pre-B type ```
45
If there are circulating blasts, think:
Acute form of leukemia
46
Lab findings for ALL
Anemia always present Thrombocytopenia almost always present Peripheral WBC count can be high, normal, or low Circulating Blasts Bone marrow: hypercellular, blasts>20% of nucleated cells
47
Significance of TdT, CD10/19/7/34, PAX 5
``` TdT indicates a precursor cell and therefore an acute disease CD10/19 are markers for B-Cells CD7 is a marker for T-cells CD34 on pre-T & B PAX 5 with pre-B ```
48
Histological presentation of ALL cells
Large, relatively uniform nuclei Increased N:C ratio Delicate chromatin Vague nucleoli
49
Symptoms of all Acute Leukemias
Think cytopenias: Anemia=> fatigue Neutropenia=> infections, fever Thrombocytopenia=> bleeding, ecchymoses, epistaxis, gum bleeding, intracerebral bleeding ``` Think Infiltrate packing: Bone pain and tenderness Generalized lymphadenopathy Hepatosplenomegaly Mediastinal mass CNS infiltrates=> meningeal spread=> headache, vomiting, nerve palsies (more common in ALL than AML) ```
50
Treatment of ALL
Chemotherapy and prophylactic CNS treatment 95% reach complete remission 75-85% are cured
51
ALL prognostic factors
``` Best: 2-10 y/o, lots of chromosomes 50-60 pre-B Low WBC counts t(12;21) trisomy of some chromosomes ``` Worst:
52
Common features of Myeloid neoplasms
Involve hematopoietic progenitor cells Involve the bone marrow May also involve the spleen, liver, lymph nodes
53
Categories of Myeloid Neoplasia?
AML Myelodysplastic syndromes Myeloproliferative diseases
54
Peak age for AML
Peak age is 60, but can happen at all ages | Incidence rises through life
55
Pathophysiology of AML
Mutation in transcription factors Blasts accumulate in bone marrow because failure to mature Causes anemia, neutropenia, thrombocytopenia
56
WHO Classification of AML
Genetic Aberrations: 11q23 (MLL gene) -poor t(8;21)-good Myelodysplasia-like: aberrations: 5q-, 7q-, 20q- all poor prognosis Therapy-related: very poor prognosis post alkylating agents; radiation > 2years Follows topoisomerase II inhibitors by 1-3 yrs
57
Auer Rods are a sign of:
AML? | They are seen in Myeloblasts
58
CD34 vs 64 in myeloid cells
CD34 expressed by immature myeloid cells | CD64 expressed by mature myeloid cells

Path Exam 5 (1 decks)

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