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Skin, Lymph, Blood > Dr. Singh - Hematopathology : WBC, LN, Spleen, Thymus > Flashcards

Dr. Singh - Hematopathology : WBC, LN, Spleen, Thymus Flashcards

1
Q

Leukocyte common Ag marker

A

CD45 (Basophils, N ,Eosinophil, Tcells, Bcells, NK cells, Moocytes)

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2
Q

Early myeloblast marker

A

CD34

E, N, B

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3
Q

Early Lymphblast marker

A

Tdt (T-cells, B-cells, NK cells)

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4
Q

lymphocyte markers

A

CD19, CD20, Pax-5 (T-cell, B-cell)

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5
Q

Natural Killer cell markers

A

CD56, CD16

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6
Q

Helper T cells markers

CTL cells markers

A

CD4+

CD8+

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7
Q

High myeloblast count can be a sign of

A

Acute Leukemia type

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8
Q

Leukopenia
What
Most common

A

Low WBC

Neutropenia (extreme neutropenia = agranulocytosis)

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9
Q

Absolute neutropenia is found how
WBC : 6.0x10^3
N : 4%
Bands : 2%

A

Absolute N Count = .06(6000) = 360

** anything under 500 is very serious

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10
Q

what can cause neutropenia

A
  1. Toxic drugs for chemotherapy destroying bone marrow
  2. Aplastic anemia
  3. Megaloblastic anemia
  4. Ab mediated destruction
  5. Hypersplenism (spleen sequesters and destroys blood cells)
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11
Q

What can happen when you have neutropenia

And how to TX

A
  1. Bacterial and Fungal infection

2. G-CSF (to recolonization)+ Abs

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12
Q

Leukocytosis

A

Too much N

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13
Q

Increased N marrow production caused by

A

Chronic infection or cancer

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14
Q

Increased release of N form marrow stores

A

Acute inflammation

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15
Q

Decreased Margination

A

Exercise (N unstick from vessels and enter circulation)

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16
Q

Decreased extraversion into tissues

A

Glucocorticoids

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17
Q

High N
High Lyphocytes
High E
High B

A

Acute bacterial infection, MI
Viral infection
Asthma, parasite, drug reactions
CML

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18
Q

Germinal centers + medullary sinuses expand

A

During infection

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19
Q

Acute supportive lymphadenitis

A

Painful puss filled LN usually from pyogenic infection, high neutrophils, abscess forms in LNs

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20
Q

Follicular hyperplasia

A

Lymphadenitis
Many follicular areas that swell
The lymphocytes expand in the germinal center usually viral

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21
Q

Organization in the LN

A

Germinal area or center and mantel area around it

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22
Q

Sinus histocytosis

A

M are increased in the LN sinuses and seen usually in malignancy or drainage of foreign material - tattoo ink (they are histiocytes)

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23
Q

Lymphoid neoplasia involves

A

B,T, NK, plasma cells

Hodgkin

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24
Q

Myeloid neoplasia involves

A

AML
Myelodysplasia
Myeloproliferative neoplasia

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25
Q

Histiocytic neoplasia involves

A

Langerhans Cell Histiocytosis

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26
Q

3 things usually causing WBC neoplasia

A
  • viral infection (HTLV, EBV, HHV-8)
  • Chronic infection (H Pylori)
  • Genetic mutation that’s acquired
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27
Q

Acute Lymphoblastic Leukemia/lymphoma

SX

A

Fever - no Neutrophils so easy opportunistic infection
Fatigue - anemic
Bleeding and bruising - no platelets
Pain - expansion of BM from leukemic cells
N,V,Headache - meningis in brain can also have leukemic cells pack in there

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28
Q

ALL what happens

A

The lymphoid stem cell divide excessively into blasts and dont become mature WBCs (maturation arrest)
- BM is packed with myeloblast leukemia cells and can be hard to even draws out a BM sample

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29
Q

ALL under the microscope

A

Large purple cells that are lymphoblastic ($x size of RBCs)

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30
Q

How to DX ALL on peripheral smear looking at the cell markers

A
  1. If there is TdT (prolymphocyte marker) = myeloid cells SEEN
  2. If there is CD19, 20, 10, Pax-5 = B-cells involved SEEN
  3. If there is CD 1-5, 7, 8 = T-cells are involved
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31
Q

How to TX ALL

A

Chemotherapy in CSF
Is usually very successful (age 2-10)
(12:21 transposition)

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32
Q

B-cell non-Hodgkin leukemia EXs

A
  1. CLL
  2. Follicular lymphoma
  3. Diffuse large B-cell lymphoma (DLBCL)
  4. Burkitt lymphoma
  5. Mantel cell lymphoma
  6. Marginal Zone lymphoma
  7. Hairy Cell Leukemia
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33
Q

CLL/SLL

Sx and blood smear

A 
None really (usually older adults) however you can run a CBC and see some clone mature lymphocytes that are small (size of RBCs since they are mature)
They are delicate and can smudge (smudge cells seen)
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34
Q

CLL/SLL markers seen

A
  1. CD19, CD5 (B-cells)
    CD20
  2. Look at light chains that are all the same
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35
Q

CLL/SLL prognosis

A

Usually fine, however can become aggressive Richter Transformation (from MYC or TP53 mutation)

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36
Q

Follicular lymphoma DX

A

It looks the same as Follicular Hyperplasia so you look at the cells
1. 14:18 translocation (IgH next to BCL-2)

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37
Q

Follicular Lymphoma SX

A

Painless B-cell proliferation and generalized lymphadenopathy

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38
Q

How to stain and see difference in Follicular lymphoma and Follicular hyperplasia

A

Follicular Lymphoma : granular center is stained all brown (+ stain)
Follicular hyperplasia : granular center is stained brown in marginal area only granular center is white

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39
Q

Follicular lymphoma grading scale

A

Grade 1 : smaller cells (more mature cells)
Grade 2 : some larger cells
Grade 3 : all larger cells (mostly immature cells)

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40
Q

DLBCL is what

A

LARGE Masses in LN or other organ like the spleen

Aggressive and fast growing

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41
Q

DLBCL special types

A
  1. Immunodeficiency - related LCL (HIV, post-transplant, or something linked to EBV)
  2. Primary effusion lymphoma (HHV-8)
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42
Q

DLBCL DX how

A

Cells muted in BCL-6 = over expressed B cells

You see all other B- cell markers

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43
Q

Burkitt lymphoma
Looks like
And happens how

A

Starry sky pattern, 99% are dividing constantly
B-cells + MANY tingible (stainable) Ms = to eat a bunch of cells and debri
(Seen with the Ki-67 stain)

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44
Q

Burkitt lymphoma from what translocation

A

8: 14 (IgH next to MYC)

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45
Q

3 types of Burkitt Lymphomas

A
  1. EBV associated (Endemic in Africa, causing mandibular growth)
  2. Sporadic
  3. HIV-related
    = can be TX well if diagnosed early
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46
Q

Mantel Cell Lymphoma is what looks like what

A

B- cells resembling mantle cell layer

Small, mature, and fast dividing and aggressive

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47
Q

Mantel Cell Lymphoma TX

A

Aggressively and BM transplant

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48
Q

Mantel Cell Lymphoma can cause

A

GI mucosal involvement

Polyps (made of lymphocytes not intestinal mucosa = lymphomatoid polyposis)

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49
Q

Mantel Cell Lymphoma translocation

A

11: 14 (IgH next to Cyclin D1)

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50
Q

Marginal Zone Lymphoma looks like and where

A

In LN or extranodal sites (MALT-oma, GI, bronchial, thyroid) ——> chronic inflammation (H PYLORi INFECTION)

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51
Q

Marginal Zone Lymphoma can be seen in what organs

A

CHRONIC INFLAMMATION SITES :

  1. Gastric MALToma (from H- pylori) - Tx the infection and can cause it to go away
  2. Hashimoto’s thyroiditis can lead to MZL
  3. Chronic Sialadenitis can cause Salivary gland MZL
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52
Q

Hairy Cell Leukemia looks like what

A

NEoplastic B-cells that are about 2X as big as RBCs with projections that look hairy on them (very few of them)

53
Q

How to DX HCL

A

Drawing out BM you usually dont get anything due to the BM fibrosis
On blood smear you see some distance between each close packed cell due to hairy cytoplasm

54
Q

HCL can cause what SX

A

Fatigue
Splenomegaly (to start make cells BM cant)
Pancytopenia (very low number of cells and hard to see a hairy cell in the blood)
Anemic (no WBCs, due to hairy BM cells)

55
Q

HCL TX

A

Very good with chemotherapy

56
Q

HCL markers involved

A

CD 25 and CD11c

57
Q

How to DX any B -cell lymphoma

A

Run a flow cytometry

58
Q

Plasma Cell Neoplasia

3 kinds of it

A
  1. Myeloma
  2. Monoclonal gammopathy of uncertain significance (Mgus)
  3. Waldenström macroglubulinemia
59
Q

Plasma cells look like

A

Central dark purple nucleus, light blue cytoplasm, and dark blue Perinuclear Hoff around the cytoplasm

60
Q

Myeloma causes what things

A

Tumor in the BM

  • Lytic Ben lesions
  • Hypercalcemia
  • Renal failure
  • Immune abnormalities
61
Q

Monoclonal gammopathy + myeloma is can be seen on a graph as what and is what

A

Too much gamma seen on electrophoresis
Gamma includes many immunoglobulins
** on looking at serum levels, there is a narrow spike in gamma region and Alb region, normal results would show only a spike at Alb = M SPIKE

62
Q

In gammaopathy + myeloma which immunoglobulins are usually involved in excess

A

IgG and IgA (with K or L light chains)

63
Q

How do we know if something is myeloma or Mgus

A
  1. More then 60% plasmacytosis in BM = Multiple Myeloma DONE

2. if over 10% = you need more information (CRAB Criteria)

64
Q

CRAB criteria

A

C : Calcium elevated
R : Impaired REnal function
A : Anemia
B : Bone Lesions

65
Q

Elevated Calcium presents as and due to what

A

Due to osteolysis (from many plasma cells in the BM)

  • altered mental status
  • seizures
  • cardiac rhythmic disturbances (Short QT)
  • N,V, C
66
Q

Renal Insufficiency presents as and due to what

A
  1. From immunoglobulins that are being filtered through (Ig attach to glycoproteins Tamm Horsfall = BENCE JONES PROTEINS* in tubules) = clog tubules + damage
  2. Proteinuria + light chain in urine
  3. Amyloidosis : Congo red stain + apple green in glomerulus = AL amyloid in myeloma
67
Q

Anemia presents as and due to what

A

From plasma cells in BM not able to make WBC

  • also from IL-6 production = suppression cytokines
  • renal disease = low erythropoietin made
68
Q

Bone Lesions presents as and due to what

A

Can break bone and spontaneous fracture or holes in bone like skull

69
Q

When is hyperviscosity seen

A

Hen you have too much immunoglobulins

70
Q

Where can you see hyperviscosisty

A

Myeloma , Mgus = high IgG (monomer) or IgA (diner)= viscous

Waldenström macroglubulinemia = high IgM a pentomer = extremely viscous

71
Q

Hyperviscosity can cause what

And what does it look like

A

Thromboembolic complications due to sticky blood

Looks like Rouleaux formation (RBCs are sticking like coins)

72
Q

What is another name for Waldenström macroglubulinemia

A

Lymphoplamacytic Lymphoma , due to this disease involves mature B cells that are wanting to differentiate to plasma cells

73
Q

Waldenström macroglubulinemia an cause what

A
  1. Hyperviscosity = visual impairments, stroke, embolic conditions, Cryoglobulinemia (ischemia to fingers)
  2. High IgM
  3. Reynolds phenomenal + Reaulux formation
74
Q

Hodgkin lymphoma vs non-Hodgkin lymphoma

A

H : localized not really spreading,

NH : many different nodes, Waldeyer ring + mesenteric nodes involved, Extranodal presentation

75
Q

Classic Hodgkin Lymphoma you see and markers in it

A
  1. Reed- Sternberg cells (owl eye cells) = CD 15, CD30, Pax-5 + IgH rearrangement
76
Q

How does Classical Hodgkin lymphoma present

A

Localized in one area one LN and then later can spread to another area

  1. Nodular sclerosis : had nodules and fibrosis around it in the LN
  2. Multicellulaity : has many different cells in the LN
77
Q

Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLP HL)

SX

A

Similar to HL however histologically extremely different

78
Q

Nodular LP HL histologically looks like and markers

A

Lymphohistocytic HL cells = Popcorn cells

  • YES CD20
  • NO CD15, CD30
79
Q

NLP HL can transform to

A

DLBCL

80
Q

How to DX HL

A

You have to stain and look at the cells because the Reed- Stanberg cells are very dilute and very few in the many colonal B- cells
+ CD15 and + CD30
OR
+ Popcorn cells + CD20

81
Q

Peripheral NK/T-cell lymphomas : Anaplastic Large Cell Lymphoma

A

Aggressive T cell tumor form ALK tyrosine kinase gene translocation *

  • usually younger patients (ALK + and good prognosis)
  • some are ALK negative and older (worse prognosis)
82
Q

Peripheral NK/T-cell lymphomas : Adult T- cell leukemia/lymphoma

A

Aggressive CD4+ tumor from a HTLV-1 infection

- Cloverleaf cells in blood **, usually seen on skin as lesions and nodules

83
Q

Peripheral NK/T-cell lymphomas : Large granular lymphocytic leukemia

A

CTL T cell tumor or NK cell tumor associated with a STAT3 TF mutation + cytopenias + autoimmune phenomena

84
Q

Peripheral NK/T-cell lymphomas : Extranodal NK/T cell lymphoma

A

Aggressive tumor from NK cells and linked to EBV infection

85
Q

EBV is liked to

A
  1. Burkitt lymphoma
  2. DLBCL
  3. Extra nodular NK/T cell lymphoma
86
Q

Peripheral NK/T-cell lymphomas : Mycosis Fungoides

A

T-cell lymphoma presenting with skin plaque lesions that are saddle and if biopsied can be mistaken as inflammation, however is t-cell clones
NO HTLV-1 association

87
Q

Peripheral NK/T-cell lymphomas : Sézary Syndrome

A

T-cell lymphoma with erythroderma (Red all over body skin rash, red man syndrome) and leukemia in blood (cerebraform cells in blood)
NO HTLV-1 association

88
Q

Myeloid neoplasms 3 types

A

AML
Myelodysplastic syndromes
Myeloproliferative neoplasms

89
Q

AML

A

Leukemic stem cell which makes only a bunch of blasts and prevents maturation of cells = a bunch of myeloblasts

90
Q

AML is DX how

A
  1. Having 20% or more BLASTS (any WBC) in the BM**
  2. You can see granules in the cytoplasm at times in the blasts
  3. Fever, fatigue, bleeding, bruising, PANCYOPENIA (no blasts in peripheral blood)**
91
Q

AML with genetic aberrations

A

Translocation of 8:21 or 15:17

Good prognosis

92
Q

AML with MDS like features

A

First the patient has myeloid dysplasia and it becomes AML

Poor prognosis

93
Q

AML therapy related

A

Getting AML from therapy such as chemotherapy

Poor prognosis

94
Q

AML not otherwise specified

A

Other types of differentiated blasts like erythroid blasts, Megakaryocytic blasts, Monocytic blast

95
Q

AML 8:21

What happens

A

Usually younger patients
CBF makes mature cells however in this type of translocation a ETO protein + RUNX1-RUNX1T1 blocks the CBF and there is no maturation of the myoblasts

96
Q

AML with 15:17

A

Is also called Acute Promelocytic Leukemia ***8

YOU SEE AUER RODS

97
Q

AML with 15:17 happens how

A

Usually RAR bind to RA and = allows differentiation to N

In this RAR is bound by a PML protein and makes it not want RA, no differentiation to Ns

98
Q

AML 15:17 TX

A

Gleevec or ALL TRANS RA which overrides the PML protein bound to the RXR

99
Q

AML 15: 17 SX and Why when you dont have leukocytosis and panocytopenia sx

A
  • NO leukocytosis, panocytosis at times
  • YOU see HYPERCOAGABILITY (bruising and bleeding and coagulation of blood due to the myloblasts having Annexin = plasminogen -> plasmin AND activated and TF to make F10a)
100
Q

Other unusual AML SX not involving hypercoagability or leukemia or panocytopenia

A
  1. Extra nodular involvement of gingiva (black and red infiltration of myloblasts), and Leukemia cutis (myloblasts to skin)
  2. Soft tissue masses stained +CD34 (in any part of the body)
101
Q

Myelodysplastic Syndrome

A

Clonal disorder in many cell types (not one identical clone)
Usually from therapy
Can come before AML

102
Q

Myelodysplastic Syndrome SX

A

Cytopenia (anemia usually)

103
Q

Myelodysplastic Syndrome DX how

A
  1. Which lineages are effected
  2. Chromosomal translocation
  3. Blast count : increased a bit (are higher risk for AML transformation)
  4. You can see Dyserythropoiesis (multinucleated RBCs), Ring sideroblasts (Fe deposits), Pseudo Pelger-Huet cells (Bilobed N), Dysmegakaryopoiesis (small MK with separate lobes)
104
Q

Looking for excess blasts in Myelodysplastic Syndrome

A

More then 20% = AML

If above 10% : RAEB 2 (refractory anemia excess blast 2) , higher RAEB are more likely to become AML

105
Q

Myelodysplastic Syndrome happen from what mutations

A
  1. Epigenetic mutations
  2. RNA splicing factor mutation
  3. TF mutation
106
Q

Myeloproliferative neoplasms mutation is what

A

Any kinase = proliferation

107
Q

Myeloproliferative neoplasms SX

A

BM proliferated with something
The cells travel to extramedullary areas
AML or ALL can happen

108
Q

CML SX

A
  1. peripheral leukocytosis of mature myeloid cells high number of cells in BM
  2. Splenomegaly (extrameduallary hematopoiesis)
  3. Higher Buffy coat
    4.
109
Q

CML translocation

A

Philadelphia chr (9:22) = activated a kinase BCR-ABL

110
Q

What can you see when testing for CML

A

** Increased buff coat in blood that is centrifuged (higher WBCs)

111
Q

Higher Buffy coat in blood means

A

Leukemia

112
Q

Wha happens to CML over time

A

If there is a lot of leukocytosis then viscosity can increase and mutations can happen and cause increased blasts = AML or ALL

113
Q

4 types of Myeloproliferative neoplasms

A
  1. CML : WBCs
  2. Polycythemia Vera : RBCs
  3. Essential thrombocythemia : platelets
  4. Primary myelofibrosis : stroma fibroblasts
    2-4 are increased in JAK2 Kinase**
114
Q

What happens during myelofibrosis

A

Can happen as the end stage of Myeloproliferative neoplasms 2-4
- low BM elements due to fibrosis
= SPLENOMEGALY (JAKofy)

115
Q

Langerhans cell histocytosis 3 types

A

Multi focal multisystem
Unisystem
Pulmonary (smokers

116
Q

Langerhans cell histocytosis SX

A

The Langerhans cells (dendritic cells) eat away the bone = lytic lesions

  1. Cleaved nuclei many of them
  2. ** electronmicroscopy showed Birbeck granules (tennis-racket shaped)
  3. ** many E like being there in the blood smears
117
Q

Birbeck granules are found when

A

For Langerhans cell histocytosis (tennis racket shaped)

When looking at electronmicroscopy

118
Q

How to stain for Langerhans cell histocytosis

A
  1. CD1a and S100 (Langerhans cells)

2. Many eosinophils as well

119
Q

Important anatomy of spleen

A
  1. Splenic A goes to it and 1 single splenic vein drains it
  2. Blood opens up to the open circulation pockets
  3. Germinal center (white pulp) = lymphocytes
120
Q

Spleen function

A
  1. Phagocytosis
  2. Sequester RBCs
  3. Ab production
  4. Fetal and adult (if condition) hematopoiesis
121
Q

Splenomegally what and how

A
  1. Follicular hyperplasia in the germinal center = expands Spleen
    - usually from viral infection
  2. Congestive Splenomegaly from hepatic dysfunction (the 1 splenic V is blocked as it goes to the liver)
122
Q

Hypersplenism what and how

A

Enlargement of spleen due to cytopenia
(Blood or spleen problem)
- Hereditary spherocytosis (stiff RBCs)
- Sickle Cell
- Idiopathic thrombocytopenia purpura : platelets are covered by opsonizing Abs
- splenomegally can cause that type of spleen dysfunction to take more RBCs

123
Q

Splenic rupture from what and how

A

ABD trauma
Rapid splenomegaly (Infections Mononucleosis)
- causes Hypotension

124
Q

Splenic Neoplasia

A

Usually vessel neoplasm

Other leukemia’s can involve the spleen make nodules

125
Q

Splenic infarcts

A

It grows so fast it outgrows its vascular supple it needs

Clogged Spenic A (Sickle Cell)

126
Q

Thymus

A

Very cellular in babies

Adults is mostly fat (some squamous Hassle Corpuscle cells)

127
Q

Thymus Hyperplasia

A

Increased cells start to proliferate in the thymus as an adult
Can cause MG

128
Q

Thymoma

A

A tumor is in the thymus as a clonal neoplasm

  • obstruct airway or esophagus is possible
  • MYASTHERNIA GRAVIS
129
Q

Myasthenia Gravis (MG)

A

AutoAbs from thymine hyperplasia or thyoma

AB——> post-synaptic R for ACH = progressive weakness especially as the day goes on , SOB

Skin, Lymph, Blood (9 decks)

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