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MS2 Unit 2 > Pathology > Flashcards

Pathology Flashcards

1
Q

Where is vWF stored?

A

W-P bodies of endothelium

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2
Q

What is stored in W-P bodies?

A

1) vWF

2) p-selectins

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3
Q

What does vWF bind?

A

SEC and platelets

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4
Q

What receptor doe platelets use to connect to fibrinogen?

A

GpIIb/IIIa

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5
Q

Petechiae occurs with (quantitative/qualitative) platelet disorders

A

quantitative (thrombocytopenia)

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6
Q

Autoimmune production of IgG against platelet antigens is called ____

A

ITP

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7
Q

In ITP, autoimmune antibodies are made in the _____. Red cells are consumed in the _______

A

Antibodies made in spleen

Red cells consumed in the spleen

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8
Q

Dx: Child with ITP
Rx: ________

A

usually self-limiting, possible platelet transfusion

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9
Q

Dx: Adult with chronic ITP, low platelet crisis
Rx: ______

A

IVIG

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10
Q

Dx: Adult with chronic ITP, low platelet crisis

Surgical option?

A

Splenectomy

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11
Q

Pathologic platelet micro-thrombi in small vessels is called _____

A

Microangiopathic Hemolytic Anemia

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12
Q

TTP is caused by a deficient enzyme _____

A

ADAMTS13

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13
Q

ADAMTS13 normally cleaves _____ multimers into monomers

A

vWF

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14
Q

The lack of ADAMTS13 in TTP is usually due to an underlying ________

A

autoimmune Dz

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15
Q

Hemolytic Uremic Syndorme primarily affects the _______ (organ)

A

kidney

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16
Q

The usual causative agent for HUS is ______

A

E. coli O157:H7

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17
Q

E. coli O157:H7 has the virulence factor ______ that damages renal endothelial cells

A

verotoxin

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18
Q

Name 2 Microangiopathic Hemolytic Anemias:

A
  1. TTP (thrombotic thrombocytopenic purpura)

2. HUS (Hemolytic Uremic Syndrome)

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19
Q

In Microangiopathic Hemolytic Anemias, bleed time (increases/decreases) and PT/PTT is ______

A

increases

PT/PTT is normal

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20
Q

How do you treat HUS and TTP?

A
  1. plasmapheresis

2. corticosteroids

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21
Q

In Bernard-Soulier, there is a genetic deficiency in ______

A

GP1b

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22
Q

In Bernard-Soulier, what function is impaired?

A

platelet adhesion

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23
Q

Platelets without GP1b can’t bind ____

A

vWF

Bernard-Soulier Syndrome

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24
Q

Blood smear of Bernard-Soulier Syndrome patient shows _______

A

enlarged platelets

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25
Q

In Glanzmann’s Thrombasthenia there is a genetic deficiency in ________

A

GIIb/IIIa

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26
Q

ASA blocks cyclooxygenase preventing platelets from making ____

A

TXA2

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27
Q

In vWF disease (PT/PTT) is increased

A

PTT

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28
Q

Which test is abnormal in vWF disease?

A
  1. ristocetin test

2. and PTT

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29
Q

What enzyme does coumadin block?

A

epoxide reductase

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30
Q

where is vitamin K generated?

A

gut bacteria

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31
Q

You can follow the extent of liver failure by measuring (PT/PTT)

A

PT

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32
Q

The best screening test for DIC is _______

A

elevated D dimer

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33
Q

A serine protease that converts plasminogen to plasmin

A

tPA

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34
Q

Dissolves fibrin clots:

1) cleaves fibrin
2) clears serum fibrinogen
3. destroys clot factors

A

plasmin

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35
Q

Lab findings: increased PT and PTT, increased bleed time, increased fibrinogen splits, no D-dimer
Dx: ?

A

overactive plasmin

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36
Q

Lines of Zahn: their presence implies thrombosis at a site of rapid blood flow that happened with the patient (alive/dead)

A

alive!

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37
Q

Coagulation can be kicked off by either ____ or ___

A

SEC or TF

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38
Q

Blocks platelet aggregation (TXA2/ PGI2)

A

PGI2 blocks

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39
Q

Promotes platelet aggregation (TXA2/ PGI2)

A

TXA2 promotes

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40
Q

on the surface of endothelial cells, serves as a cofactor for thrombin

A

TM: thrombomodulin

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41
Q

Name 3 endothelial damages that increase clot risk

A
  1. atherosclerosis
  2. vasculitis
  3. elevated homocystine
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42
Q

Vitamin k is required for which blood protein factors to work?

A

2, 7, 9, 10, C and S

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43
Q

Which has the shortest half-life? (2, 7, 9, 10, C or S)

A

C and S! hence the need for HEP therapy along with coumadin

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44
Q

Heparin binds and activates _____

A

ATIII

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45
Q

What are the 4 types of micorcytic anemias?

A
  1. sideroblastic
  2. thalasemia
  3. iron deficient
  4. anemia of chronic Dz
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46
Q

anemia, dysphagia w/ esophageal web, red beefy tounge is ____ _____ disease

A

plummer-vinson

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47
Q

what acute phase reactant sequesters Iron?

A

hepcidin

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48
Q

what does TIBC stand for?

A

total iron binding capacity

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49
Q

Hx: bone marrow suppression w chemo and anemia

how can you treat the anemia?

A

erythropoietin

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50
Q

Protoporphyrin is attached to iron in what cell compartment?

A

mitochondria

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51
Q

iron laden mitochondria occurs in _______ anemia

A

sideroblastic

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52
Q

alcoholism can lead to a ________ anemia

A

sideroblastic

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53
Q

intracellular protein that stores iron and releases it in a controlled fashion, commonl measured in labs

A

ferritin

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54
Q

decreased synthesis of globin chains is called ______

A

thalassemia

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55
Q

which leads to a worse thalasemia, cis or trans deletion?

A

cis

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56
Q

Where is the cis deletion thalassemia more commonly seen? (asia/africa)

A

asia

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57
Q

4 beta chains in a thalassemia is called Hb__

A

HbH

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58
Q

a tetramer of gamma chains in hemoglobin is called Hb_____

A

Hb barts

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59
Q

Beta thalassemia leads to (microcytic/macrocytic) anemia

A

microcytic

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60
Q

Massive erythroid hyperplasia such as in SS and beta thal leads to what appearance on skull radiograph?

A

“crew cut”

due to massive erythroid hyperplasia

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61
Q

why is a person w/ beta thalassemia at risk for hemochromotosis?

A

frequent transfusion

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62
Q

Electrophoresis: no HbA, increased HbA2 and HbF
Dx: ________

A

beta thalassemia major

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63
Q

Macrocytic anemia is usually due to a deficiency in ______ of _______

A
  1. folate

2. vitamin B12

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64
Q

Three diseases that can lead to a macrocytic anemia are:

A
  1. alcoholism
  2. liver disease
  3. chemo drugs: 5-FU, methotrexate and folate def.
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65
Q

R binder is produced by the ______, then complexed to vit. B12 for absorption

A

salivary glads

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66
Q

intrinsic factor that binds B12 is produced by the _____ cells o the stomach

A

parietal

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67
Q

B12 is stored in large volume in the _______ (organ)

A

liver

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68
Q

Pernicious anemia is due to _________ destroying the parietal cells of the stomach

A

autoimmune disease

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69
Q

With low serum B12, serum homocystine and _______ build up, leading to spinal cord damage

A

methylmalonic acid, can damage the spinal cord

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70
Q

Hemoglobinemia with hemoglobinuria and hemosiderinuria (intravascular/extravascular) destruction of RBCs

A

intravascular destruction

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71
Q

brown urine”, with chronic intravascular hemolysis is called _________

A

hemosiderinuria

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72
Q

what 3 tethering molecules are deficient in Hereditary spherocytosis?

A
  1. spectrin
  2. ankrin
  3. band 3.1
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73
Q

what virus infects erythrocyte pre-cursors?

A

Parvovirus B19

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74
Q

Treatment for Hereditary spherocytosis is _______

A

splenectomy

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75
Q

Howell-Jolly bodies indicate _______

A

splenic dysfunction, (such as post splenectomy)

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76
Q

Three risk factors for RBC sickling are:

A
  1. acidosis
  2. dehydration
  3. hypoxemia
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77
Q

Swollen hands and feet due to vaso-occlusive infarts of bones is called _______

A

dactylitis

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78
Q

in kids with SS, there is increased risk of infection with _____ _____

A

encapsulated bacteria

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79
Q

What lab test can allow identification of HbS?

A

Metabisulfite

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80
Q

What two molecules linked by GPI prevent complement form destroying Red cells?

A
  1. DAF: decay accelerating factor

2. MIRL: Membrane inhibitor of reactive lysis

81
Q

Nightime shallow breathing and acidosis lead to activation of ______

A

complement

82
Q

Lack of CD55 indicates the disease ______

A

CD55 is DAF,

indicates PNH: paroxysmal nocturnal hemoglobinuria

83
Q

Patients with PNH, paroxysmal nocturnal hemoglobinuria have an increased risk for which caner?

A

AML, acute myeloid leukemia

84
Q

G6PD deficiency renders cells susceptible to _______ _______

A

oxidative stress

85
Q

Red cells as Bite cells are seen with _________

A

G6PD deficiency

86
Q

Warm agglutinin is seem with (IgG/IgM) mediated immune hemolytic anemia

A

IgG

87
Q

The two autoimmune disease, 1. ITP and 2. immune hemolytic anemia can be treated with ____

A

IV IG

88
Q

RBC are bound by antibodies in the colder extremities with (IgG/IgM) immune hemolytic anemia

A

IgM

89
Q

deficiency of all types of blood cells due to lack of blood cell progenitors is called _____ _____

A

aplastic anemia

90
Q

A pathologic process that replaces bone marrow with fibrosis, tumor, granuloma etc, is called a ________ proces

A

myelophthisic process

91
Q

Where is most of the marginated pool of neutrophils?

A

the lung endothelium

92
Q

A left shift with immature neutrophile means a decrease in the _____ receptor or CD ____

A

Fc receptor = CD 16

93
Q

Basophelia is associated with (ALL/APL/CML)

A

CML

94
Q

Which cells are enlarged ‘monocytes’ in Mononucleosis?

A

CD8+ T-cells

Mononucleosis is a misnomer

95
Q

Mononucleosis increases the risk for ______(organ) rupture

A

splenic

96
Q

acute leukemia is a neoplastic proliferation of ______, greater than 20% in Bone marrow

A

blasts

97
Q

You can specifically identify a Lymphoblast by the presence of (TdT/ MPO) in the nucleus

A

TDT

98
Q

You can specifically identify a myeloidblast by the presence of (TdT/ MPO) as crystals of auer rods

A

MPO: myeloperoxidase crystalizes as auer rods

99
Q

What are the two types of acute leukemia?

A

AML: Acute myeloid leukemia
ALL: Acute lymphoblastic leukemia

100
Q

ALL is common in children with ______ syndrome after the age of 5

A

downs

101
Q

The more common B-ALL usually has the translocation t(__:__)

A

t(9:22)

102
Q

T-ALL usually presents as a T_____ (organ) mass in a T___ aged person

A

Thymic mass in a Teenaged

103
Q

Hairy Cell Leukemia is a proliferation of (B cells/ T cells)

A

B cells

104
Q

In CML, the predominant cell is the (RBC/ basophil/ neutrophil/ eosinophil/ monocyte/ megakaryocyte)

A

Basophil

105
Q

CML is driven by the translocation t(__:__)

A

t(9:22)

106
Q

A patient with CML can transform to (AML/ ALL)

A

ALL or AML! the mutation is in the Hematopoietic stem cell

107
Q
  1. Polycythemia Vera,
  2. Essential Thrombocythemia and
  3. Myelofibrosis are driven by a mutation in ______
A

JAK2 kinase

108
Q

Budd-Chiari syndrome with thrombosis in the portal vein can be cause by this blood cell proliferation _______

A

Polycythemia vera

109
Q

In Polycythemia vera there are increased red cells AND ____ cells, which can degranulate in heat causing itching after bathing

A

mast cells

110
Q

low SaO2, increased EPO, high red count (lung Dz/ Renal cell carcinoma/ polycythemia vera)

A

lung Dz

111
Q

normal SaO2, increased EPO, high red count (lung Dz/ Renal cell carcinoma/ polycythemia vera)

A

Renal cell carcinoma

112
Q

normal SaO2, low EPO, high red count (lung Dz/ Renal cell carcinoma/ polycythemia vera)

A

polycythemia vera

113
Q

In myelofibrosis, megakaryocytes overproduce _____ resulting in fibrosis of the marrow space

A

PDGF

114
Q

follicular lymphoma is characterized by the translocation [ t(14:18)/ t(11:14)/ t(8:14) ]

A

t(14:18)
Ig heavy chain: 14
Bcl-2: 18

115
Q

over-expression of Bcl-2 will (promote/ inhibit) apoptosis

A

inhibit

116
Q

Tingible body macrophages that eat up apoptotic B cells are (present/ absent) in follicular lymphona

A

absent! lack of B- cell apoptosis

117
Q

mantle cell lymphoma is drive by translocation [ t(14:18)/ t(11:14)/ t(8:14) ]

A

t(11:14)
Ig heavy chain: 14
Cyclin D1: 11

118
Q

Which B cell proliferation is associated with chronic inflammatory states like hashimotos and sjogrens (Follicular/ Mantle cell/ Marginal zone) Lymphome

A

Marginal zone lymphoma

119
Q

Burkitt lymphoma is driven by [ t(14:18)/ t(11:14)/ t(8:14) ]

A

t(8:14)
Ig heavy chain: 14
c-myc: 8

120
Q

Reed–Sternberg cells are CD__ and CD__ positive and not CD20+

A

CD15+ and CD30+

121
Q

In Multiple myeloma, neoplastic plasma cells can activate the RANK receptor leading to ____-___ lesions on x-ray

A

punched out lesions

122
Q

An M-spike on Serum protein electrophoresis may indicate the neoplastic proliferative disorder ______ _______

A

Multiple myeloma

123
Q

Free light chain excreted in the urine with multiple myeloma is called ____-_____ protiens

A

Bence-Jones

124
Q

Lytic bone lesions, hypercalcemia, M-spike, AL-amyloid and Bence-Jones protiens all indicate ______ _____

A

Multiple myeloma

125
Q

An M-spike with IgM, absent lytic bone lesions, generalized LAD and increased bleeding are all characterisitcs of _____ _____

A

Waldenstrom macroglobulinemia

126
Q

A Neoplastic proliferation with Birckeck, tennis racket granules and CD1a+ and S100+ cells is _______ _______

A

Langerhans Histiocytosis

127
Q

Benign proliferation of langerhans cells, presents with pathologic fracture, skin not involved.

A

Eosinophilic granuloma, will have inflammatory eosinophils

128
Q

What are the 3 Langerhans cell histiocytosis?

A
  1. Eosinophilic Granuloma (benign)
  2. Letter Siwe disease (malignant, >2y.o.)
  3. Hand-Schuller-Christian disease (malignant >3y.o.)
129
Q

Are there blood vessels in the epidermis?

A

no, they stop at the dermis

130
Q

Which layer of the epidermis has desmosoms that look like spinous processes?

A

the stratum spinosum

131
Q

vitamin A derivatives are used to treat acne by (killing P. acnes/ reducing keratin production)

A

reducing keratin production

132
Q

Benzoyl peroxidase is used to treat acne by (killing P. acnes/ reducing keratin production)

A

antimicrobial, kill P. acnes

133
Q

Caused by excessive keratinocyte proliferation (psoriasis/ eczema)

A

psoriasis

134
Q

usually on flexor surfaces (psoriasis/ eczema)

A

eczema = atopic dermatitis

135
Q

usually on extensor surfaces (psoriasis/ eczema)

A

psoriasis

136
Q

A type I hypersensitivity rxn associated with asthma and rhinitis (psoriasis/ eczema)

A

eczema = atopic dermatitis

137
Q

Associated with HLA-C, lesions arise more frequently with trauma (psoriasis/ eczema)

A

psoriasis

138
Q

diffuse epidermal hyperplasia is called ________

A

Acanthosis

139
Q

perakeratosis, with excess keratin and retention of nucleii is (psoriasis/ eczema)

A

psoriasis

140
Q

pinpoint bleeds with elongated dermal papilla (psoriasis/ eczema)

A

psoriasis

141
Q

What are the p’s of lichen Planus?

A 
pruritic
planar
polygonal
purple 
papules
142
Q

Autoimmune destruction of desmosomes leading to blisters (Pemphigus Vulgaris/ Bullous Pemphigoid/ Dermatitis Herpetiformis)

A

Pemphigus Vulgaris

143
Q

Autoimmune destruction of hemi-desmosomes at basement membrane (Pemphigus Vulgaris/ Bullous Pemphigoid/ Dermatitis Herpetiformis)

A

Bullous Pemphigoid

144
Q

IgG mediated (Pemphigus Vulgaris/ Bullous Pemphigoid/ Dermatitis Herpetiformis)

A

Bullous Pemphigoid and Pemphigus Vulgaris

145
Q

Bullae or blisters rupture more easily (Pemphigus Vulgaris/ Bullous Pemphigoid/ Dermatitis Herpetiformis)

A

Pemphigus Vulgaris, blisters in stratum spinosum, not at basal layer

146
Q

Mediated by IgA at tips of dermal papillae (Pemphigus Vulgaris/ Bullous Pemphigoid/ Dermatitis Herpetiformis)

A

Dermatitis Herpetiformis

147
Q

Strong association with celiac disease (Bullous Pemphigoid/ Dermatitis Herpetiformis/ Erythema Multiforme)

A

Dermatitis Herpetiformis

148
Q

Resolves with a gluten free diet(Bullous Pemphigoid/ Dermatitis Herpetiformis/ Erythema Multiforme)

A

Dermatitis Herpetiformis

149
Q

Most commonly seen with HSV infection (Bullous Pemphigoid/ Dermatitis Herpetiformis/ Erythema Multiforme)

A

Erythema Multiforme

150
Q

Multiple erythmentaous rashes with white middle targetoid appearance (Bullous Pemphigoid/ Dermatitis Herpetiformis/ Erythema Multiforme)

A

Erythema Multiforme

151
Q

Rank from least severe to most severe (Steven Johnson syndrome/ Erythema Multiforme/ Toxic epidermal necrolysis )

A

Erythema Multiforme, Steven Johnson syndrome, TEN. the are all the same, just different levels of involvement

152
Q

A benign proliferation of squamous cells with a “ stuck on appearance” (Acanthosis Nigricans/ Seborrheic keratosis)

A

seborrheic keratosis

153
Q

The Lesser-Trelat sign is when multiple of these arise sugesting an underlying GI carcinoma (Acanthosis Nigricans/ Seborrheic Keratosis/ Basal cell carcinoma)

A

seborrheic keratosis

154
Q

Epidermal hyperplasia with darkening of the skin and a “velvet-like” appearance (Acanthosis Nigricans/ Seborrheic Dermatosis/ Basal cell carcinoma)

A

Acanthosis Nigricans

155
Q

Associated with insulin resistance, diabetes, or underlying malignancy
(Acanthosis Nigricans/ Seborrheic Dermatosis/ Basal cell carcinoma)

A

Acanthosis Nigricans

156
Q

Risk factors include prolonged exposure to sunlight, albinism and xeroderma pigmentosum (Acanthosis Nigricans/ Squamous cell carcinoma/ Basal cell carcinoma)

A

Basal cell carcinoma

157
Q

appears as a nodule with a central area of ulceration and surrounded by telangectasia, especially on the upper lip. (Acanthosis Nigricans/ Squamous cell carcinoma/ Basal cell carcinoma)

A

Basal cell carcinoma

158
Q

Risk factors include sunlight exposure, immunosupressive thereapy, arsnic poisoning and chronic inflammation. (Melanoma/ Squamous cell carcinoma/ Basal cell carcinoma)

A

Squamous cell carcinoma

159
Q

Usually presents on the lower lip (Melanoma/ Squamous cell carcinoma/ Basal cell carcinoma)

A

Squamous cell carcinoma

160
Q

Actinic keratosis is a precursor to (Melanoma/ Squamous cell carcinoma/ Basal cell carcinoma)

A

squamous cell carcinoma

161
Q

Melanocytes are derived from which neural layer (ecterderm/ mesoder/ endoderm/ neural crest)

A

neural creast

162
Q

vitiligo is (autoimmune/congenital)

A

autoimmune

163
Q

Albinism is (autoimmune/congenital)

A

congenital

164
Q

Due to defect in the enzyme tyrosinase (vitiligo/ albinism)

A

albinism

165
Q

A freckle is darker than the surrounding sking due to a localized increase in (melanocytes/ melanosomes)

A

melanosomes, the number of melanocytes remains the same

166
Q

A mask like hyperpigmentation of the cheeks is called _____

A

melasma

167
Q

Which will have hair growing from it? (melanoma/ nevus)

A

Nevus, benign

168
Q

Which has the worst prognosis? (Melanoma/ Squamous cell carcinoma/ Basal cell carcinoma)

A

melanoma

Squamous cell and basal are very fixable

169
Q

Melanomas: Which two have a good prognosis (Lentigo Maligna Melanoma/ Superficial Spreading Melaona/ Nodular Melanoma/ Acral Lentiginous melanoma)

A

Lentigo Maligna Melanoma and

Superficial Spreading Melaona

170
Q

Melanomas: which has an early vertical phase, therefore a poor prognosis?
(Lentigo Maligna Melanoma/ Superficial Spreading Melaona/ Nodular Melanoma/ Acral Lentiginous melanoma)

A

Nodular Melanoma

171
Q

Melanomas: Which arises on palms and soles?

Lentigo Maligna Melanoma/ Superficial Spreading Melaona/ Nodular Melanoma/ Acral Lentiginous melanoma

A

Acral Lentiginous Melanoma

172
Q

Which is only along the dermal + epidermal junction with no invasion? (Lentigo Maligna Melanoma/ Superficial Spreading Melaona/ Nodular Melanoma/ Acral Lentiginous melanoma)

A

Lentigo Maligna Melanoma

173
Q

Which only invades the dermis superficially and has a good prognosis? (Lentigo Maligna Melanoma/ Superficial Spreading Melaona/ Nodular Melanoma/ Acral Lentiginous melanoma)

A

Superficial spreading melanoma

174
Q

Painless separation of the nail from the nailbed is called _______

A

onycholysis

175
Q

Do petechia blanch with pressure? (yes/no)

A

no. They are bleeding into the skin

176
Q

When RBC’s are of unequal size it is called _______

A

anisocytosis

177
Q

the luebering rapoport pathway is used to make ______

A

2,3, BPG

178
Q

which has HLA on their membrane (RBCs/ platelets)

A

Platelets have HLA

179
Q

Decreased serum ferritin is diagnostic of ______ deficiency

A

iron deficiency

180
Q

Increase in ferritin during inflammation is due to increased IL-__

A

IL-6

181
Q

Ferritin is primarily in (serum/macrophages) while transferrin is in (serum/macrophages)

A

ferritin is in macrophages

transferrin is in serum

182
Q

TIBC correlates with (ferritin/ serum transferrin)

A

serum transferin

183
Q

decreased ferritin stores leads to (increased/decreased) transferrin synthesis

A

increased, therefore TIBC increases

184
Q

The master iron regulator protein is called (hepcidin/ haptoglobin)

A

hepcidin

185
Q

Which is directly absorbed in the duodenum? (Fe3+/Fe2+)

Which is transported by transferrin in the blood? (Fe3+/Fe2+)

A

Absorbed: Fe2+
Transported: Fe3+

186
Q

In iron deficiency anemia, serum ferritin is (down/up)

In ACD serum ferritin is (down/up)

A

Iron deficiency, ferritin down

ACD, ferritin is up

187
Q

An acute phase reactant that complexes with Hb to be degraded by macrophages is (hepcidin/ haptoglobin)

A

haptoglobin

188
Q

Which indicates loss of function of splenic macrophages? (Heinz bodies/ Howell-Jolly bodies)

A

Howell-Jolly bodies

189
Q

Which is caused by oxidative stress that damages hemoglobin? (Heinz bodies/ Howell-Jolly bodies)

A

Heinz bodies

190
Q

Which is associated with SS disease? (Heinz bodies/ Howell-Jolly bodies)

A

Howell-Jolly bodies

191
Q

Which is associated with G6PD deficiency? (Heinz bodies/ Howell-Jolly bodies)

A

Heinz bodies

192
Q

Hereditary spherocytosis is inherited by (AD/AR/XR) pattern

A

AD

193
Q

Sickle cell anemia is inherited by (AD/AR/XR) pattern

A

AR

194
Q

G6PD deficiency is inherited by (AD/AR/XR) pattern

A

XR

195
Q

“smudge cells” appear in (ALL/CLL/AML/CML/APL/HCL)

A

CLL: chronic lymphocytic leukemia

196
Q

TRAP stain is positive in (ALL/CLL/AML/CML/APL/HCL)

A

HCL: Hairy cell leukemia

197
Q

Auer rods are present in (ALL/CLL/AML/CML/APL/HCL)

A

APL: Acute promyelocytic anemia

198
Q

The most common type of Hodgkin’s lymphoma is (Nodular sclerosis/ Mixed cellularity/ Lymphocyte depleted/ Lymphocyte rich)

A

Nodular sclerosis

199
Q

The hodgkin’s lymphone most associated with EBV is (Nodular sclerosis/ Mixed cellularity/ Lymphocyte depleted/ Lymphocyte rich)

A
  1. mixed cellularity: 60-70%
  2. Lymphocyte rich: 40%
  3. Lymphocyte depleted: many

MS2 Unit 2 (9 decks)

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