Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Chapter 13 - White Blood Cells > Flashcards

Chapter 13 - White Blood Cells Flashcards

0
Q

Neutropenia

A

Decrease in neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What is leukoerythroblastosis

A

Abnormal release if immature precursors into the peripheral blood due to disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Agranulocytosis

A

Clinically significant reduction in neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does agranulocytosis occur? (2)

A

Ineffective granulopoeisis (decreased production) or accelerated removal of neutrophils (increased destruction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Most common cause of agranulocytosis

A

Drug toxicity (alkylating agents, chloramphenicol, sulfonamides, chlorpromazine, thiouracil)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a consequence of agranulocytosis

A

Infections, especially lesions of the oral cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Leukocytosis

A

Increase in number of white cells in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a leukmoid reaction

A

In severe infections, immature granulocytes appear in the blood simulating a myeloid leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of neutrophils leukocytosis (3)

A

Infection, sterile inflammation (ie tissue necrosis like MI), drugs (agranulocytosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of eosinophilic leukocytosis (2)

A

Allergic reactions, parasitic infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes basophilic leukocytosis

A

Myeloproliferative disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What causes lymphocytosis

A

Viral infections (cmv, mono), bacterial infections (bordatella)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes monocytosis

A

Chronic infections (tb), collagen vascular diseases, inflammatory bowel diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pathophysiology of lymphadenitis

A

Activation of immune cells –> primary follicles enlarge into germinal centers –> paracortical t-cell zones undergo inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the nodes in acute nonspecific lymphadenitis like

A

Enlarged and painful, may have draining sinuses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes of acute lymphadenitis and what nodes are most likely involved

A

Systemic diseases like mono, cervical and inguinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Causes of chronic lymphadenitis

A

Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the nodes like in chronic lymphadenopathy

A

Nontender since the growth occurs slowly over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What nodes are most likely involved in chronic lymphadenitis

A

Inguinal and axillary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Most lymphoid neoplasms are of what origin

A

B-cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the most common cancer of children

A

Acute lymphoblastic leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are some positive markers for pre b-cell acute lymphoblastic leukemia. What is expressed in the more mature forms

A

Deoxynucleotidal transferase (TdT) and common ALL antigen (CALLA, CD10). CD 19 and CD 20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What translocation is for B-cell ALL and what kind of prognosis does it have

A

t(12;21) –> good prognosis

t(9;22) –> has a poor prognosis because there is mutation in the Philadelphia chromosome (seen with adults)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What positive markers are there for t-cell ALL

A

TdT and negative for CD10, CD2-8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What metastatic complications are associated with B-cell ALL

A

testicular enlargement, abrupt onset, anemic symptoms, CNS manifestations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What metastatic complications are associated with T-cell ALL

A

Mediastinal mass, abrupt onset, anemic symptoms, CNS manifestations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Does ALL in pediatric patients have a good prognosis?

A

Yes 95% complete emission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does the bone marrow look like in ALL

A

Crowded with lymphoblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What disease is ALL associated with

A

Down’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the most common leukemia in the Western World

A

Chronic lymphocytic leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

In CLL what does peripheral show

A

Smudge cells (small round lymphocytes with scant cytoplasm that get distrusted while trying to make a smear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

In CLL if you get lymph node involvement and generalized lympohadenopathy what will this be called

A

Small lymphocytic lymphoma, stays localized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Complications of CLL

A

Hypogammaglobinemia (leads to infection) , autoimmune hemolytic anemia, richter syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is Richter syndrome

A

CLL/SLL transforms into a diffuse large B-cell lymphoma with a rapidly enlarging mass within a lymph node or spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Age group for CLL

A

Greater than 60 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Follicular lymphomas arise from what ? And are associated with what gene defect

A

From germinal B cells and chromosomal translocation of IgH on chromosome 14 and Bcl2 (antagonizes apoptosis) on chromosome 18

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

A positive marker that might be seen with follicular lymphoma

A

CD20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What may a follicular lymphoma progress to?

A

Diffuse large cell B lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the most common form of non Hodgkin’s lymphoma and is it aggressive or benign?

A

Diffuse large b-cell lymphoma, highly aggressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What age group does diffuse large b-cell lymphoma typically present in

A

60 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How does diffuse large b-cell lymphoma arise?

A

Derives from a germinal center or transformation from a low grade lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How does a diffuse large b-cell lymphoma clinically present?

A

Presents as a rapidly enlarging mass at a nodal or extra nodal site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Diffuse large b-cell lymphomas can be complicated by

A

HIV either immunodeficiency related with EBV or an effusion lymphoma with malignant pleural or ascitic effusion (with HHV-8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Burkitt’s lymphoma is associated with what disease

A

EBV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What types of Burkitt’s lymphoma are there and what organs do they involve

A

African type (jaw) and American type (abdomen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What appearance of Burkitt’s lymphoma have on histology and what causes it

A

Starry sky appearance from clear cytoplasmed macrophages that ingested nuclear remnants from tumor cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the gene mutation associated with Burkitt’s lymphoma

A

c-MYC on chromosome 8 to the Ig heavy chain locus on chromosome 14

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What markers does CLL/SLL Express

A

CD 5 and 20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are plasma cell dyscrasias

A

Bcell proliferations with neoplastic plasma cells that secrete immunoglobin or a immunoglobin fragment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What do neoplastic plasma cells synthesize an excess of

A

Light or heavy chains with complete immunoglobins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What body part does multiple myeloma usually involve

A

The skeleton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Most common primary malignancy of bone

A

Multiple myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Age incidence of multiple myeloma

A

65-75 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

For the myeloma cells to survive, what do they need?

A

IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are Bence Jones proteins

A

If only light or heavy chains are produced in a plasma cell dyscrasia, the free light chains are small enough to be excreted in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the mechanism of bone pain in multiple myeloma and what is the result of it

A

Plasma cells activate RANKL on osteoclasts –> bone destruction –> punched out skeletal lesions on x-Ray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is roleux formation and what disease is it seen in

A

Seen in multiple myeloma: high level of M proteins causes reed cells in peripheral blood smear to stick together in linear formations (can also be seen in lupus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Other than the skeletal system, what other organ can multiple myeloma damage

A

Kidney –> Bence jones proteins can cause myeloma kidney by damaging tubular epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What areas will multiple myeloma primarily affect

A

Vertebra (mostly) also rib skull pelvis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is seen on bone marrow aspirate for multiple myeloma

A

Normal cells replaced by plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is found on electrophoresis for multiple myeloma

A

M spike due to IgG or IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What’s the most common plasma cell dyscrasia

A

Monoclonal gamma patchy of uncertain significance (MGUS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

MGUS is most likely seen in what age group

A

Elderly disease. 3% of those older than 50 years and 5% of those older than 70

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What signs are associated with MGUS

A

M spike on electrophoresis, other features or multiple myeloma are absent. Since it shares a chromosome mutation, it may progress to multiple myeloma so you should monitor it

66
Q

What is Waldenström macroglobinemia

A

B-cell lymphoma with IgM production in a sufficient amount to cause a hyperviscosity syndrome, no Bence jones proteins and no bone destruction

67
Q

Symptoms associated with lymphoplasmacytic lymphoma/Waldenström macroglobinemia (4)

A

Lymphadenopathy, hepatomegaly, splenomegaly, hyperviscosity syndrome

68
Q

What is hyperviscosity syndrome

A

Visual impairment (retinal hemorrhages), neurological problems, bleeding, cryoglobinemia (ie. Raynaud’s phenomenon)

69
Q

Prognosis of lymphoplasmacytic lymphoma

A

Incurable progressive disease, median survival of 4 years

70
Q

Plasma cell Neoplasm presenting as a solitary lesion of bone or soft tissue

A

Solitary myeloma/plasma chroma

71
Q

Most patients with solitary skeletal plasmacytoma progress to what

A

Multiple myeloma, if it’s extra osseous though, you can prob just resect that

72
Q

Mantle cells lymphomas commonly present in what age group and gender

A

Male 50-60 years old

73
Q

Mantle cell lymphomas over express

A

Cyclin D1

74
Q

What genetic abnormality is found in mantle cell lymphoma

A

t(11,14) translocation of cyclin D1 and the IgH locus

75
Q

Most common presenting symptom of mantle cell lymphoma and what is it’s prognosis

A

Painless lymphadenopathy, survival 3-4 years

76
Q

What diseases are marginal zone lymphomas associated with?

A

Inflammatory/autoimmune diseases like Hashimotos, sjögren, and hpylori

77
Q

What is the spread and prognosis of marginal cell lymphomas like

A

Remains localized until really late and the tumor can regress if the inciting agent is taken away

78
Q

What does histology look like for hairy cell leukemia

A

Hairlike projections on peripheral blood smear. They cant really be aspirated (dry tap) because the cells are enmeshed in an extra cellular matrix composed of reticulin fibrils. Otherwise, biopsy is crowed with the neoplastic cells

79
Q

What is the clinical finding in hairy cell leukemia

A

Splenomegaly without lymphadenopathy

80
Q

What is the prognosis of hairy cell leukemia and what do you have an increased chance of

A

Good prognosis with chemotherapy and increased chance of infection

81
Q

Cells of hairy cell leukemia are positive for what marker? (Pathoma and rapid review)

A

Tartrate resistant acid phosphatase (TRAP)

82
Q

What infection is associated with adult t-cell leukemia

A

HTLV-1 human t-cell leukemia retrovirus type 1

83
Q

How is HTLV-1 involved in the pathogensis of adult t-cell lymphoma

A

It activates the TAX protein which activates NFKB, which enhances lymphocyte growth and survival

84
Q

Clinical findings in adult t-cell leukemia (5)

A

Hepatosplenomegaly and lymphadenopathy, skin lesions, hypercalcemia, punched out bone lesions (pathoma/rapid review)

85
Q

What kind of cells are related to Mycosis fungoides and Sézary syndrome

A

CD4+ helper T cells

86
Q

What body part does Mycosis fungoides infect?

A

The T cells infect the skin

87
Q

What is the difference between Mycosis fungoides and Sézary syndrome and what is Sézary syndrome’s characteristic histology

A

Sézary syndrome is when skin involvement manifests as a generalized exfoliative erythroderma. There is rarely progression to tumefaction and there is an associated leukemia of Sézary cells (cerebriform nuclei)

88
Q

Where does Hodgkin’s lymphoma first arise and where does it spread?

A

In a single node or chain of nodes and then to anatomically contiguous lymphoid tissues

89
Q

What are the characteristic cells seen in Hodgkin lymphoma

A

Reed-Sternberg giant cells

90
Q

What are Reed-Sternberg cells

A

Large b-cells with a bi-lobed nucleus, large inclusion like nucleoli and abundant cytoplasm surrounded by a clear halo

91
Q

What are the different types of Hodgkin lymphomas (5)

A

Nodular sclerosis, mixed cellularity, lymphocyte-rich, lymphocyte depletion, lymphocyte predominance

92
Q

Which one of the subtypes of Hodgkin lymphoma is the non classical type

A

Lymphocyte predominance

93
Q

What positive markers does reed-steinberg cells express

A

CD 15 and CD 30

94
Q

What are some variants or Reed-Sternberg cells and what do they look like on histology and in what disease are they seen?

A
  1. Mononuclear variants (single nucleus with a prominent nucleolus)
  2. lymphohistocytic variants - L&H (large pale staining multilobed cell - lymphocyte predominant type - popcorn cells)
  3. Lacunar cells (multilobed nucleus with many small nucleoli in a clear space with lots of cytoplasm - seen in nodular sclerosing)
95
Q

What do you need for the diagnosis of Hodgkin lymphoma

A

Reed-Sternberg cells in a background of non-neoplastic inflammatory cells

96
Q

What is the most common form of Hodgkin lymphoma? And who does it mostly present in

A

Nodular sclerosis type (70%), females predominance? (Only in pathoma and rapid review, book says equal)

97
Q

What lymph nodes does the nodular sclerosis type of Hodgkin lymphoma usually involve

A

Anterior mediastinal, and cervical and supraclavicular

98
Q

What is the histology associated with the nodular sclerosis type of Hodgkin lymphoma

A

Lacunar variant of Reed-Sternberg and the deposit of collagen in bands that divide the lymph nodes into circumscribed nodules

99
Q

Which type of Hodgkin lymphoma has a strong association with EBV and what group of people does it commonly involve

A

Mixed-cellularity type (70%), older men

100
Q

What does histology appear as on the mixed cellular it type of Hodgkin lymphoma

A

Classic Reed-Sternberg cells and mononuclear variants, eosinophils

101
Q

Which type of Hodgkin lymphoma has the best prognosis

A

Lymphocyte-rich type

102
Q

Which is Hodgkin lymphoma is the most aggressive type and what population does it most likely involve

A

Lymphocyte depletion, elderly and HIV+

103
Q

What does the non classical form of Hodgkin lymphoma look like on histology and what markers does it express

A

LandH variants of Reed-Sternberg cell, typical of germinal center B cells (CD20)

104
Q

What population doe the lymphocyte predominant form of hodgkin lymphoma present in

A

Young male with cervical or axillary nodal enlargement

105
Q

What do Reed-Sternberg cells secrete

A

Cytokines

106
Q

Symptoms seen in Hodgkin lymphoma

A

Fever, chills, night sweats, painless lymphadenopathy

107
Q

What age group does acute myeloid leukemia usually present in

A

15-59, likelihood increases as you go older and peaks at 60

108
Q

What do you need to see in the bone marrow to diagnose AML

A

20% myeloid blasts

109
Q

What are auer rods

A

Seen in AML, they are fused azurophilic granules that are splinter-shaped rod structures present in the myeloblasts, they are peroxide se positive

110
Q

What are the classifications of AML

A

M0-7 French American British classification system

111
Q

What is seen in M0 AML and are Auer rods present?

A

Minimally differentiated, no Auer rods

112
Q

M1 AML? Are Auer rods present?

A

AML without maturation, rare Auer rods

113
Q

M2 AML? Auer rods?

A

AML with maturation, Auer rods present, most common type

114
Q

M3 AML? Auer rods?

A

Numerous Auer rods, possible DIC, t(15;17) translocation, abnormal retinoids acid metabolism, high doses of all trans retinoids acid may induce remission by maturing cells

115
Q

M4 AML? Auer rods?

A

Acute myelomonocytic, Auer rods uncommon

116
Q

M5 AML? Auer rods?

A

Acute monocytic, no Auer rods, gum infiltration, usually lack myeloperoxidase

117
Q

M6 AML?

A

Acute erythroleukemia, Multinucleated erythroblastosis, myeloboasts present

118
Q

M7 AML?

A

Acute megakaryocytic AML, myelofibrosis in bone marrow, increased incidence in of own syndrome in children less than 3 years old

119
Q

What is the genetic defect seen in M3 of AML?

A

t(15;17) translocation of the retinoic acid receptor (RAR) on 17 to 15

120
Q

Which form of AML is associated with Down’s syndrome

A

M7 acute megakaryocytic

121
Q

What disease has a very high risk of transforming to AML

A

Myelodysplastic syndrome

122
Q

What age group does myelodysplastic disorders typically effect?

A

Elderly 70 years old

123
Q

What is the defect common in all myelodysplastic syndromes

A

Ineffective hematopoesis and maturation defects

124
Q

The bone marrow in myelodysplastic syndromes is most commonly..

A

Hyper cellular

125
Q

In myelodysplastic syndromes a common abnormalities seen in the erythroid cells is _____ and what are they composed of

A

Ringed sideroblasts, erythroblasts with iron laden mitochondria

126
Q

What is seen on CBC for myelodysplastic syndromes

A

Pancytopenia

127
Q

What age group is CML most seen in

A

50-60 years old

128
Q

What is the gene defect seen in CML

A

t(9;22) translocation on ABL proto oncogene, proto oncogene fuses with the break cluster region (bcr) on chromosome 22 –> Philadelphia chromosome

129
Q

Symptoms associated with CML

A

Splenomegaly, accelerated phase after 3 years (increasing anemia and thrombocytopenia, sometimes with basophil rise) –> 6-12 months = blast crisis (like acute leukemia)

130
Q

The same type of mutations seen in CML are seen in what other disease?

A

ALL

131
Q

Polycythemia Vera is a proliferation of _____, and what is the most likely cause of symptoms

A

Red cells, granulocytes, and platelets. Red cell proliferation causes the symptoms

132
Q

What mutation is polycythemia associated with

A

Tyrosine kinase JAK2

133
Q

Symptoms of polycythemia Vera

A

Due to hyperviscosity of blood: blurry vision, headache, increased venous thrombosis, flushed face, itching, minor hemorrhages

134
Q

Treatment for polycythemia Vera

A

Phlebotomy

135
Q

What is the spent phase of polycythemia Vera

A

Clinical and anatomical features of myelofibrosis develop –> splenomegaly, fibrosis in bone marrow

136
Q

Mutation associated with essential thrombocytosis

A

JAK2 or MPL (receptor tyrosine kinase that’s normally activated by thrombopoietin)

137
Q

What does peripheral smear reveal for essential thrombocytosis

A

Abnormally large platelets

138
Q

Symptoms associated with essential thrombocytosis

A

Thrombois, erythromyalgia (throbbing and burning of hands and feet by occlusion of small arterioles by platelet aggregates) –> all similar to polycythemia Vera

139
Q

How can you distinguish essential thrombocytosis from polycythemia Vera and marrow fibrosis

A

The absence of polycythemia and marrow fibrosis

140
Q

What is the hallmark of primary myelofibrosis

A

Development of obliterative marrow fibrosis

141
Q

What mutations are present in primary myelofibrosis

A

JAK2 or MPL

142
Q

What causes the marrow fibrosis seen in primary myelofibrosis

A

Megakaryocytes produce excess PGDF causing marrow fibrosis

143
Q

Clinical features of primary myelofbrosis (3)

A

Splenomegaly (extrameduallary hematopoiesis), leukoerythroblastic smear (tear drop RBC), and immature granulocytes

144
Q

What is the characteristic sign seen in langerhans cell histiocytosis

A

Birbeck granules in the cytoplasm, look like tennis rackets

145
Q

What is letterer siwe disease

A

Malignant proliferation of langerhans cells

146
Q

What population would you see letterer-siwe test in? And what clinical signs would be present

A

Skin rash and cystic skeletal defects in an infant of less than 2 years

147
Q

What is the prognosis of letterer-siwe disease

A

Rapidly fatal because it involves many organs, 5 year survival

148
Q

What is eosinophilic granuloma

A

A benign proliferation of langerhans cells in bone

149
Q

What is the common population that eosinophilic granuloma appears in

A

Adolescent with a pathologic fracture

150
Q

What is Hand-Schüller-Christian Disease

A

Malignant proliferation of Langerhans cells

151
Q

What is the classic presentation of Hand-Schüller-Christian disease

A

Calvrial bone defects, diabetes insipidus, exophthalmos

152
Q

What kind of sensation will a patient with an enlarged spleen experience

A

Dragging sensation in hype left upper quadrant

153
Q

What is hypersplenism

A

Anemia, leukopenia, thrombocytopenia, alone or in combination

154
Q

DiGeorges syndrome results in defects of what organs

A

Thymic hypoplasia and hypoparathyroidism

155
Q

A thymoma is a tumor of what type of cells

A

Thymic epithelial cells

156
Q

What location will a thymoma most likely arise in

A

Anterior mediastinum

157
Q

What is seen on histology with an invasive thymoma

A

They penetrate through the capsule into surrounding structures

158
Q

Most common variant of a Thymic carcinoma

A

Squamous cell carcinoma

159
Q

What disease is a thymoma associated with

A

Myasthenia gravis

160
Q

What are symptoms of a thymoma related to?

A

Impingement on mediastinal structures

Pathology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions