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OMS II BECOM Exam 1 > Hematology of White cell disorders - Stillwell > Flashcards

Hematology of White cell disorders - Stillwell Flashcards

1
Q

bandemia

A

elevated number of band forms in the blood

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2
Q

neutropenia (aka agranulocytosis)

A

-decreased number of neutrophils in the blood

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3
Q

pancytopenia

A

-decreased WBCs, platelets, and RBCs

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4
Q

left shift**

A
  • increase # of immature neutrophils** (including band cells (horseshoe), metamyelocytes, myelocytes, promyelocytes)
  • stimulated by cytokines (TNF-alpha, IL-1)
  • myeloblasts not seen –> think leukemia if present**
  • see in inflammation/infection - bone marrow in overdrive
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5
Q

leukemoid rxn

A

-extreme leukocytosis, may see immature neutrophils present (but no blasts)

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6
Q

leukemia

A

-cancer of blood forming tissue (bone marrow and lymphatic system)

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7
Q

neutrophils aka granulocyte or PMN

A
  • # 1 WBC on a differential (40-60% of Total leukocytes)
  • 3-5 lobes common (>5 abnormal)
  • band cell (bilobe nucleus) - 0-5% of WBCs (>5% during left shift inflammatory response)
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8
Q

lymphocyte

A
  • 20-40% of all WBCs (2nd most common on differential)

- increased in viral infections

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9
Q

smudge cells**

A

-fragile B lymphocytes (atypical lymphocyte) –> seen in CLL (chronic lymphocytic leukemia)***

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10
Q

monocytes

A
  • 4-8% of all WBCs
  • larger, more cytoplasm than lymphocytes
  • can differentiate into macrophages and dendritic cells
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11
Q

basophil and eosinophil

A
  1. basophil - darker granules (0-1% of WBCs)

2. eosinophil - eosinophilic granules; peroxidases (1-3% of WBCs)

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12
Q

Wright’s stain blood smear

A
  • 1 WBC for every 500 RBCs or 40 platelets

- count # of platelets and multiply by 10k to estimate

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13
Q

differential count

A
  • not included in a CBC**
  • has to be specifically ordered**
  • info. about the types and amount of WBCs in blood sample
  • 2 types: manual and automated
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14
Q

manual differential

A
  • lab tech looks at 100 WBCs on Wright stain –> gives you specifics about WBC toxic granulations, immature WBCs (left shift and band cells), RBCs, and platelets**
  • howell jolly bodies (DNA fragments) if spleen isn’t working
  • start with this with hematologic and septic issues**
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15
Q

automated differential

A
  • machine evaluates thousands of cells, but can’t detect specifics like manual** (won’t see left shift cells)
  • typical point of care diffs –> give you % of neutrophils, lymphocytes, and mid cells (mono+eos+baso+bands)
  • auto diffs –> can differentiate b/w cells above
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16
Q

colony stimulating factors (CSFs)

A
  • glycoproteins that help with cells viability, proliferation, differentiation, maturation, function, and regeneration
  • stimulate WBC production and function –> help fight off infection
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17
Q

types of CSFs

A
  1. CSF-1 (macrophage-CSF or M-CSF)
  2. CSF-2 (granulocyte/macrophage-CSF or GM-CSF)
  3. CSF-3 (granulocyte-CSF or G-CSF)
  4. Multipotential-CSF (multiple-CSF)…..thought to be Interleukin-3 (IL-3)
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18
Q

CSFs - commercial preparations (recombinant, made in E. coli)***

A
  1. G-CSF (Filgrastim/tradename-Neupogen), short half-life
  2. G-CSF/polyethylene glycol (PEG-Filgrastim/trade name-Neulasta), longer half-life
  3. GM-CSF is (Sargramostim/tradename-Leukine)

-used to increase bone marrow recovery in chemo patients** (increased risk of sepsis with low WBCs)

no commercial preps for M-CSF or multiple-CSF

19
Q

neutrophilia causes

A
  1. increased production - due to CML, inflammation, drugs, necrosis
  2. increased bone marrow production - due to corticosteroids, inflammation/infection/endotoxin
  3. demargination - due to EPI, corticosteroids, NSAIDs, stress
  4. decreased WBC removal - someone with splenectomy** (always have a higher white count)**
20
Q

neutrophilia with leukemoid rxn**

A
  • nonmalignant; high white count due to infection, necrosis, or severe bleeding
  • elevated WBCs with neutrophilia and left shift (no dysplastic changes or blasts)
  • diagnosis: no malignancy or blasts with left shift; leukocyte alkaline phosphatase (LAP) elevated in normal inflammatory response (LAP not found in CML or AML patients)*
  • cause: C. difficile colitis and ischemic bowel/bowel infarction***
21
Q

lymphocytosis causes

A
  • count greater than 4k
    1. increased production due to lymphomas or leukemias
    2. increase bone marrow release due to many viral/bacterial/parasite infections, autoimmunity, thyrotoxicosis**
22
Q

eosinophilia causes

A
  • count >500
  • western world –> allergic/atopic dermatitis most common cause**
  • developing world –> parasite infections most common cause**
    1. allergic disorders, nephritis, drug rxns (IgE mediated induced by basophils and mast cells)
    2. parasitic infections (ex. trichinosis)
    3. malignancies (Hodgkins lymphoma    )
    4. autoimmune - SLE, eosinophilic granulomatosis** with polyangitis (churg-strauss syndrome), sarcoidosis**
    5. Hyper IgE syndrome (Job syndrome)
    6. coccidioidomycosis, HIV
23
Q

monocytosis causes

A
  • count >950
  • occur with chronic inflammation
    1. increased production
    2. increased bone marrow release - in a febrile person, TB always stimulates monocytosis***
24
Q

basophilia causes

A
  • count >200

- associated with neoplastic conditions and myeloproliferative neoplasms like CML

25
Q

leukopenia causes

A
  • low total WBC count
    1. acute viral infections** (can also be bacterial)
    2. pseudo-leukopenia** - sudden onset of severe infection –> WBCs migrate to site and bone marrow hasn’t had time to respond
26
Q

neutropenia causes

A
  • count <100 –> high risk for severe infection
    1. acute viral syndromes** - ex. CMV, EBV
    2. chronic viral syndromes* - ex. HIV, hepatitis B/C
    3. rickettsial diseases
    4. disseminated fungal and mycobacterial infections - wipe out bone marrow
    5. autoimmunity - ex. SLE, RA, Felty’s syndrome** (large spleen) with pancytopenia, chron’s disease
    6. folate/B12 deficiency    *
    7. EtOH* - toxic to bone marrow
    8. hepatosplenomegaly*
    9. congenital neutropenia*
    10. primary bone marrow issues*
    11. chemo and radiation
    12. drugs* - ex. methotrexate, azathioprine, cyclophosphamide
    13. toxins* - ex. arsenic**
27
Q

neutropenic fever

A
  • usually after chemo
  • medical emergency**
  • neutrophils <1k –> risk of severe sepsis**
  • bacteria gram neg. rods bad**
  • less sever by giving G-CSF prophylaxis
  • evaluation: STAT urine/blood culture**
  • treat: immediate broad spectrum antibiotics
  • give G-CSF** (monocytes come back 1st then neutrophils)
  • persistent fever for 5 days –> think fungi/virus and give anti fungal therapy**
28
Q

lymphopenia causes

A
  • count <1500
  • poor nutrition
  • T cell lymphopenia with AIDS/HIV, Idiopathic CD4 deficiency
  • B cell lymphopenia leads to humoral deficiencies (immunosuppressed patients)
29
Q

atypical lymphocytosis**

A
  • reactive CD8 cytotoxic T lymphocytes** that are activated after antigen stimulation
  • RBCs indent the cytoplasm**
  • seen in EBV/CMV mono** (downey cell)**
30
Q

toxic granulations

A
  • toxic granules containing peroxidases/hydrolases of neutrophils
  • seen in inflammatory conditions like sepsis
31
Q

hypersegmented granulocytes**

A
  • neutrophil will have 6 or more nuclear lobes (3-5 normal)***
  • B12/folate deficiency is cause***
  • sometimes Fe deficiency
32
Q

Pelger-huet anomaly

A
  • inherited (autosomal dominant) - heterozygote asymptomatic, homozygote is abnormal
  • nuclei of neutrophils/eosinophils are bilobed “dumbbell”**
  • acquired through AML/CML/myelodysplasia
33
Q

Chediak-Higashi syndrome

A
  • mutation of lysosome regulatory protein –> decreased phagocytic ability and WBCs lose migration ability**
  • large granules** in cytoplasm containing peroxidase
  • recurrent pyogenic infections and photosensitivity
34
Q

Auer rods

A
  • fused lysosomes with neutrophilic granules
  • in myeloblasts with multiple auer rods –> AML**
  • multiple auer rods in thick bundles(faggot cells) –> promyelocytic leukemia**
35
Q

Dohl body

A
  • light blue/grey inclusions in neutrophil cytoplasm**
  • remnants of RER and ribosomes
  • associated with left shifts and toxic granulations
36
Q

dohl body compared to morulae**

A
  • dohl body –> light blue/grey**

- morulae (in anaplasmosis or ehrlichiosis) –> dark purple**

37
Q

hyper IgE syndrome (Job’s syndrome)

A
  • abnormal neutrophil chemotaxis due to decreased production of interferon gamma by T cells
  • recurrent staph aureus and candida infections, pulmonary problems, scoliosis**, retention of baby teeth, broad nose, hyper extensible joints
  • very high IgE**
38
Q

Sezary syndrome

A
  • advanced stage cutaneous fungal infection with lymphadenopathy/leukemia
  • associated with HTLV-1 virus
  • sezary cells with cerebriform nuclei (convolutions)**
  • flower cells**
39
Q

smudge cells (aka basket cells)

A
  • remnants of fragile B lymphocytes –> think CLL with multiple smudge cells***
  • indented by RBCs
40
Q

hairy cell leukemia

A
  • B cell leukemia (subtype of CLL)
  • accumulate in bone marrow plus splenomegaly –> cause bone marrow failure and pancytopenia**
  • jagged edges/hairs around WBCs**
41
Q

morulae in a granulocyte**

A

human granulocytic ehrlichiosis/anaplasmosis (HGE/HGA)**

42
Q

morulae in a monocyte**

A

human monocyte ehrlichiosis (HME)**

43
Q

N. gonorrhea**

A

disseminated gram neg. diplococci**

-sexually active women

OMS II BECOM Exam 1 (30 decks)

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