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Block 7 Week 1 Colt > Non-Neoplastic WBC Abnormalities - Usera > Flashcards

Non-Neoplastic WBC Abnormalities - Usera Flashcards

1
Q

what are the four methods to measure WBCs in the lab?

A
  1. automated hem. analyzers
  2. bone marrow aspirate and biopsy
  3. flow cytometry
  4. peripheral smear
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2
Q

what are the three general factors that affect neutrophil concn in the blood?

A
  1. bone marrow production and release
  2. rate of egress to tissue and survival time in the blood
  3. ratio of marginating to circulating neutrophils in peripheral blood
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3
Q

What is the number at which someone has neutrophilia?

A

ANC> 7.0 x 10^9/L

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4
Q

T/F: Neutrophilia can be in response to a physiologic, not just pathologic process

A

true

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5
Q

How long does it take for marginated neutrophils to return the to circulating pool?

A

20-30 minutes

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6
Q

Stress, steroids, epinephrine, and what cytokine can move neutrophils from margination into the ciruclating pool?

A

IL6

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7
Q

How long does it take for neutrophils from the marrow storage pool to be released into the blood?

A

4-5 hours; released by IL6

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8
Q

How long does it take to increase the marrow mitotic pool?

A

days

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9
Q

How does epi increase the neutrophil count?

A

causes them to demarginate

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10
Q

What are six major categories of causes of neutrophilia?

A 
DIPINN
Drugs
Inflammation
Physiologic
Infection
Neoplastic
Necrotic
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11
Q

Vascular collagen and vasculitis are (blank) causes of neutrophilia

A

inlfammatory

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12
Q

Bacteria, fungi, parasites, viruses, and spirochetes are (blank) causes of neutrophilia

A

infectiious

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13
Q

stress, exercise, and pregnancy are (blank) causes of neutrophilia

A

physiologic

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14
Q

Carcinoma, sarcomas, and MPDs are (blank) causes of neutrophilia

A

neoplastic

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15
Q

burns, ischemic necrosis, and tissue damage are (blank) causes of neutrophilia

A

necrotic

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16
Q

What is the ANC in REACTIVE neutrophilia?

A

<30

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17
Q

Reactive neutorphilia shows with a (blank) shift in myeloid maturation to band cells

A

left shift

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18
Q

Toxic granulation, Dohle bodies, and vacuolization are morphologic changes of neutrophils seen in (blank)

A

left shifting during reactive neutrophilia

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19
Q

T/F: the leukemoid reaction is benign

A

true

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20
Q

The ANC in the leukemoid reaction is usually (blank) and has many circulating (blank) leuokcyte precursos

A

> 50 with many immature leukocyte precursors

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21
Q

What type of cell is ocassionally present during a leukemoid reaction

A

blast celss

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22
Q

What disease do you need to exclude when the leukemoid reaction is on you DDx?

A

CML

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23
Q

The (leukemoid/leukoerythroblastic) rxn has the presence of nucleated RBCS

A

LEB

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24
Q

the LEB reaction has a left shift in (blank) maturation

A

granulocyte

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25
Q

The (leukemoid/LEB) rxn is associated with myelophthisic processes, severe hemorrhage, hemolytic anemia, or MDS

A

LEB; anemias and hemorrhage make you think of RBCs

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26
Q

What are the limits in whites and blacks for neutropenia?

A

whites: <1.3

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27
Q

What is the ANC to define agranulocytosis?

A

<0.5

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28
Q

Pseudoneutropenia is caused by (blank)

A

endotoxin

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29
Q

What drug that is used to treat schizophrenia can cause agranulocytosis?

A

Clozapine

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30
Q

T/F: Cachexia often leads to neutrophilia from the presence of a shock state

A

phony as a 3 dollar bill. Cachexia = neutropenia

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31
Q

What are the six general causes of neutropenia?

A 
iCHOAD
intrinsic defects
Cachexia
Hematologic disorders
OVERWHELMING infection
Autoimmune
Drugz
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32
Q

What are the 4 intrinsic defects that cause neutropenia?

A

F*CCK!!

  1. Fanconi’s
  2. Kostmann’s
  3. Cyclic neutropenia
  4. Chediak-Higashi
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33
Q

Megaloblastic anemia, myelodysplasia, marrow failure, hypersplennism are all (blank) disoders that lead to neutropenia

A

hematologic

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34
Q

Chloramphenicol, EtOH, chemo, abx, and clozapine can all cause (neutrophilia/neutropenia)

A

neutropenia

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35
Q

What are the three protozoal infections that commonly cause neutropenia?

A

Malaria, Kala-azar, Relapsing fever

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36
Q

Of the intrinisic defects leading to neutropenia, what is the only one caused by a maturation defect? What is the cause of all of the others?

A

Chediak-Higashi is caused by a maturation defect. All the others are caused by myeloid hypoplasia

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37
Q

Name this disease:
Panmeyloid hypoplasia
Heterogenous presentation due to csome instability
Presents in childhood: aplastic anemia, congenital physical deformities.
Susceptible to hematopoetic and solid organ malignancies

A

Fanconi’s Anemia– you’ll see the XRay of the weird joints

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38
Q 
Name the disease:
ANC<200/uL
Variable modes of inheritance
Early myeloid precursors in the marrow that do not mature,
ELA2 and HAX1 implicated
A

Kostmann’s Syndrome,

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39
Q

What is the medical name for Kostmann’s Syndrome?

A

Infantile genetic agranulocytosis

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40
Q 
Name the disease:
Presents in infancy or childhood
Auto. Dom with variable exrpression
21-30 DAY PERIODICITY
ANC
A

cyclic neutropenia

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41
Q

ELA (1/2) is also known as neutrophil elastase

A

ELA2

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42
Q

What are the two most common congenital neutropenias?

A

Pregnancy induced hypertension and infection

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43
Q

EDTA-dependent agglutinin, old speciments, WBC fragility and paraprotein formation can all lead to (blank) neutropenia

A

spurious

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44
Q

What is this morphology?

Azurophilic granules associated with Dohle bodies and vacuolization during septicemia and other toxic states

A

toxic granulation

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45
Q

What makes up a Dohle body?

A

remnants of free ribosomes and the rER

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46
Q

When do you see Dohle bodies?

A

During severe bacterial infections, pregnancy, burns, and toxic states

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47
Q

(Toxic granulation/Dohle bodies/Vacuolizatoin) is a precursor to sepsis

A

vacuolization

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48
Q

T/F: vacuolization may be a false finding in stored blood

A

true

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49
Q

Why do we get vacuolization in neutrophils?

A

Lots of dead and dying material around them gets phagocytosed, that’s why its an early marker of sepsis as it indicates everything is fucking dying

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50
Q

Shistocyte RBC morphology indicates the pt could be in what life threatening condition?

A

DIC

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51
Q

If you see a bacteria (such as a diplococci like S. aureus) inside a neutrophil, you are looking at what morphologic state?

A

abnormality

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52
Q

What stages of neutrophil maturation do we see toxic granulation?

A

Meta, band, and neutrophil stages

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53
Q

The Pelger-Huet Anomaly is autosomal (dom/rec)

A

dominant; has homo and heterozygous forms

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54
Q

T/F: Pelger-Huet anomaly indicates a functional defect in the neutrophil

A

false; clinically asymptomatic

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55
Q

A pince-nez nucleus indicates what morphologic state?

A

Pelger-Huet anomaly

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56
Q

The Pelger-Huet anomaly can be confused with a reactive (blank) shift

A

left

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57
Q

What are the general characteristics of a Pelger-Huet anomaly?

A

Hyposegmented neutrophils, sparse granules, single or pince-nez nucleus

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58
Q

> 5% of neutrophils with (blank) or more lobes or any single one with (blank) lobes constitutes hypersegmentation

A

5% with 5, or one with 6

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59
Q

What states are associated with hypersegmentation?

A

Megaloblastic anemia (B12 def), chronic infection, MDS

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60
Q

T/F: Hereditary hypersegmentation is associated with refractory megaloblastic anemia

A

false; associated with no disease!`

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61
Q

A loss of vibratory proprioception indicates what vitamin def?

A

B12

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62
Q

The Alder-Reilly anomaly is auto (dom/rec)

A

recessive

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63
Q

Large, purplish Granules that stain METACHROMATICALLY with TOLUIDINE BLUE lets you know you’re looking at what anomaly?

A

Alder-Reilly

64
Q

The anomaly that is associated with Hunter’s and Hurler’s Syndromes is:

A

Alder-Reilly

“Does he REILLY have Hurlers?!”

65
Q

Mucopolysaccharidoses is a disease state assoicated with what neutrophilic change?

A

Alder-Reilly anomaly

66
Q

Chediak-Higashi is autosomal (dom/rec)

A

recessive

67
Q

Name the disease:

  1. Giant gray-green peroxidase- positive bodies in cytoplasm of leukocytes and other cells.
  2. Abnormal melanosomes (skin hypopigmentation, photophobia)
  3. Lymphadenopathy and hepatosplenomegaly
A

Chediak-Higashi

68
Q

The giant peroxidase bodies in Chediak-Higashi are (blank) bodies

A

inclusion bodies

69
Q

What is the defect that causes the formation of inclusion bodies in Chediak Higashi?

A

fusion of cytoplasmic membranes, locomotion, and chemotaxis; therefore hypopigmentation because melanosomes can’t move their melanin to the skin surface!

70
Q

T/F: Chediak Highashi is both a morphological and functional defect

A

true

71
Q

What autosomal dominant trait has large Dohle-body like inclusions in granulocytes that contain RNA?

A

May-Hegglin Anomaly

72
Q

Which myosin heavy chain is fucked up in May-Hegglin anomaly?

A

myosin heavy chain 9

73
Q

T/F: the dohle-body like inclusions in May Hegglin anomaly cause a functional defect in GRANULOCYTES

A

false

74
Q

Describe the platelet morpholgoy in May Hegglin? What effect does this have on their function?

A

Giant oval platelets, associated with thrombocytopenia and bleeding disorders

75
Q

What disease can’t handle catalase organisms because of a defect in the respiratory burst oxidase (NADPH oxidase) system?

A

CGD

76
Q

What are the two methods of inheritance of CGD?

A

sex linked and auto recessive inheritance

77
Q

In CGD neutrophils form (blanks) when they phagocytize but do not kill

A

granulomas

78
Q

Defects in membrane-associated cytochrome b (subunits gp91 and p22), and cytosol-associated p47 and p67 are the molecular causes of (blank)

A

CGD

79
Q

T/F: defects in ANY portion of the NADPH oxidase system will lead to CGD

A

true

80
Q

What is the difference between CGD and myeloperoxidase deficiency?

A

MPO still has NADPH oxidase activity but can’t make bleach aka HOCl aka hypochlorite; whereas CGD has NO NAPDH activity!

81
Q

On the NBT (nitrobule tetrazolium test), MPO would be (blue/yellow-pink) while CGD would be (blue/yellow-pink)

A

MPO: blue
CGD: yellow-pink

82
Q

What is the treatment for CGD?

A

Abx prophylaxis

83
Q

T/F: MPO def can be acquired or genetic

A

true

84
Q

In what two cells do you get an MPO def?

A

neutrophils and monocytes

85
Q

T/F: infections are a common complication in both CGD and MPO

A

false; only in CGD

86
Q

How do you diagnose CGD or MPO?

A

CGD: NBT test
MPO: MPO stain

87
Q

Which LAD deficiency involves Selectins?

A

LAD II

88
Q

Which LAD deficiency involveds CD11a/CD18

A

LAD I

89
Q

Which LAD deficiency involves CD11a/CD18 activation?

A

LADIII

90
Q

Recurrent pyoderma gangrenosum or a failure of umbilical cord separation are disroders associated with which LAD deficiency?

A

LAD I

91
Q

What is the threshold for eosinophilia?

A

> 0.45

92
Q

Eosinophilia is associted with (cell mediated/humoral) immunity

A

cell mediated

93
Q

When would you see eosiniphilia in kids?

A

with allergies or GI food allergies

94
Q

What is the most common cause of eosinophilia? Be specific!

A

Tissue INVASIVE parasites

95
Q

Addison’s Disease often causes (neutrophilia/eosinophilia)

A

eosinophilia

96
Q

Collage disease often causes (eosinophilia/neutrophilia)

A

eosinophilia

97
Q

Besides parasites, what is a major general class of causes of eosinophilia?

A

idiopathic reasons; leukemias and GI disorders

98
Q

T/F: allergies and infections can both cause eosinophilia

A

true

99
Q

What is the threshold for eosinophilic leukemia?

A

> 1.5 x 10^9/L

100
Q

t/f: eosinophilic leukemia has no known cause

A

true

101
Q

Describe Loffler’s syndrome?

A

Pulmonary infiltrate with eosinophilia syndrome and tropical eosinophilia

102
Q

What parasite often causes Loffler’s?

A

strongyloids

103
Q

Charcot-Leyden crystals from eosoniophil granule fusion are seen in what disorder?

A

Loffler’s syndrome

104
Q

Charcot-Leyden crystals are particularly dangerous to what organ?

A

heart; release of granule contents

105
Q

Corticosteroids sequester Eos in the (blank) leading to (blank)

A

lymph nodes; eosinopenia

106
Q

Sequestration of eos in the lymph nodes can be caused by the release of corticosteroids from what disease processes?

A
  1. Cushing’s syndrome
  2. ACTH
  3. Acute stress/ Epi
  4. Inflammation
  5. Prostaglandins
  6. Bacterial infection
107
Q

What is the threshold for basophilia?

A

> 0.2 x 10^9/L

108
Q

What cancer often causes basohpilia?

A

CML

109
Q

Immediate hypersensitivity reactions will cause (baso/eos)ophilia

A

basophilia

110
Q

T/F: basophilopenia is a life threatening condition

A

false; clinically insignificant

111
Q

What is the threshold for monocytosis?

A

> 0.8

112
Q

monocyte counts vary with (age/gender)

A

age

113
Q

T/F: unexplained monocytosis is common in cancer

A

true

114
Q

What is the threshold for monocytopenia?

A

<0.2

115
Q

What body fluid in babies has a high monocyte count?

A

CSF

116
Q

Monocytes are a marker of (acute/chronic) disease processes

A

chronic

117
Q

Post-splenectomy pts will often shown elevated counts of what cell type?

A

monocytes

118
Q

Langerhans Cell histiocytosis, Letterer-Siwe disease are both disorders of what cell type?

A

monocytes

119
Q

(Monocytosis/penia) is a finding common in hematologic malignancy

A

monocytosis

120
Q

Aplastic anemia, hairy cell leukemia, and glucocorticoid therapy are all causes of (monocytosis/penia)

A

monocytopenia

121
Q 
Gaucher Disease
Neimann-Pick Disease
Tay-Sachs Disease
Fabry Disease
Wolman’s Disease
Tangier Disease
are all (blank) storage disorders of monocytes
A

lipid

122
Q

(blank) disease ppresents with glucocerebrosidase deficiency in macrophages in the bone marrow, lymph node, liver, and spleen

A

Gaucher disease

123
Q

In Gaucher disease, serum acid phosphatase is (up/down)

A

up

124
Q

What is the threshold for lymphocytosis in adults and children?

A

Adults: >4.0
kids: >9.0

125
Q

Most changes in lymphocyte counts are due to (T/B) cells

A

t cells

126
Q

(T/B) cells account for 60-80% of PERIPHERAL blood lymphocytes

A

T cells

127
Q

Majority of circulating lymphoid cells are CD(4/8) T cells

A

CD4

128
Q

Coxsackie A and B6, Echovirus, and Adenovirus are common causes of acute infectious (blank) in children

A

lymphocytosis

129
Q

Persistent polyclonal B cell lymphocytosis should raise your suspicion of:

A

chronic leukemia

130
Q

What two risk factors increase your chance of having a persistent polyclonal B cell lymphocytosis?

A

female smoker and post-splenectomy

131
Q

Infectious mono infects (monocytes/B cells)

A

B cells

132
Q

T/F: mono is self limiting

A

true

133
Q

Infectious mono gains entry to the cell via what receptor?

A

CD21

134
Q

What is the wBC range for someone with infectious mono?

A

12-25

135
Q

What Ab is positive in people with infectious mono?

A

Heterophile Ab

136
Q

what is the threshold for lymphocytopenia in adults and kids?

A

adults: <2.0

137
Q

What congenital immunodef can cause lymphocytopenia?

A

Wiskott-Aldritch

138
Q

T/F: abnormal lymph circulation can lead to lymphocytopenia

A

true

139
Q

T/F: AIDS or HAART can cause lymphocytopenia

A

true

140
Q

Most SCID pts are (m/f)

A

male

141
Q

Describe the difference in T and B cell counts in X linked vs. autosomal forms of SCID?

A

Xq13: absent to severely reduced T cells; thymic hypoplasia
Autosomal: severe def of both T and B cells (ADA def)

142
Q

What is the Tx for SCID?

A

bone marrow transplant

143
Q

What is the mode of inheritance of WA syndrome?

A

X linked

144
Q

What are the three hallmakrs of WA syndrome?

A

eczema, thrombocytopenia, and immunodef

145
Q

Pts with WA syndrome are at an increased risk of secondary (blank)

A

neoplasm

146
Q

Pts with WA syndrome have a progressive decrease in (blank)-dependent immunity

A

thymus

147
Q

T/F: WA syndrome patients have absent Abs to blood groups

A

true

148
Q

Describe the mitogenic response to CD43 in WA syndrome patients?

A

ABSENT

149
Q

When would a WA syndrome pt present with abnormal bleeding?

A

neonatal period

150
Q

(blank) syndrome presents with abscence/hypoplasia of thymus, hypoPTH, congenital heart defects, dysmporphic facies, HYPOCALCEMIA, and is caused by a del22(q11.2)

A

diGeorge syndrome

151
Q

X-linked Agammaglobulinema
causes a block in the B cell maturation at the (blank) phase due to a failure of variable and constant regions of IgM to connect

A

pre-B cell stage

152
Q

X-linked Agammaglobulinema

presents with absent (blank) cells

A

plasma cells and decreased B cells

153
Q

What is the Tx for X-linked Agammaglobulinema

A

gammaglobulin

154
Q

What disease is auto. rec. and presents with Progressive ataxia, immune dysfunction, increased risk of malignancy, Defect in cell-mediated immunity with thymic hypoplasia or dysplasia?

A

Hereditary Ataxia-Telangiactasia

155
Q

How do you diagnose hereditary ataxia-telangiactasia?

A

increased csome breakage at t(14;14)

Block 7 Week 1 Colt (9 decks)

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