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BLOCK POSTING 4 > LYMPHOID TISSUE INFLAMMATION > Flashcards

LYMPHOID TISSUE INFLAMMATION Flashcards

1
Q

What is the normal white blood cell (WBC) count?

A

5-10 K/μL.

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2
Q

What is leukopenia?

A

A low WBC count (<5 K/μL).

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3
Q

What is leukocytosis?

A

A high WBC count (>10 K/μL).

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4
Q

What are the main causes of neutropenia?

A

Drug toxicity (e.g., chemotherapy) and severe infection (e.g., gram-negative sepsis).

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5
Q

What pharmacological agents can boost granulocyte production?

A

GM-CSF or G-CSF.

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6
Q

What are the main causes of lymphopenia?

A

Immunodeficiency (e.g., HIV, DiGeorge syndrome), high cortisol state, autoimmune destruction, and whole-body radiation.

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7
Q

What is neutrophilic leukocytosis

A

and what causes it?

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8
Q

What is monocytosis

A

and what causes it?

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9
Q

What is eosinophilia

A

and what causes it?

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10
Q

What is basophilia

A

and when is it commonly seen?

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11
Q

What are the causes of lymphocytic leukocytosis?

A

Viral infections (e.g., EBV) and Bordetella pertussis infection.

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12
Q

What is infectious mononucleosis (IM)?

A

An EBV infection causing lymphocytic leukocytosis of reactive CD8+ T cells.

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13
Q

How is EBV transmitted?

A

Via saliva (‘kissing disease’), typically affecting teenagers.

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14
Q

What organs are primarily infected by EBV?

A

Oropharynx (pharyngitis), liver (hepatitis), and B cells.

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15
Q

What causes splenomegaly in infectious mononucleosis?

A

T-cell hyperplasia in the periarterial lymphatic sheath (PALS) of the spleen.

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16
Q

What test is used to screen for infectious mononucleosis?

A

The monospot test, detecting heterophile IgM antibodies.

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17
Q

What does a negative monospot test suggest?

A

Cytomegalovirus (CMV) as a possible cause of infectious mononucleosis.

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18
Q

What are the complications of infectious mononucleosis?

A

Splenic rupture, rash after ampicillin exposure, and increased risk of B-cell lymphoma during immunodeficiency.

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19
Q

What are the primary lymphoid organs?

A

Bone marrow and thymus.

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20
Q

What are the secondary lymphoid organs?

A

Lymph nodes, spleen, and mucosal-associated lymphoid tissues (MALT).

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21
Q

What are the two broad categories of the immune system?

A

Innate and adaptive immune systems.

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22
Q

What is leukopenia?

A

A condition marked by decreased circulating leukocytes, especially neutropenia.

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23
Q

What is the most common cause of agranulocytosis?

A

Drugs, particularly cytotoxic agents.

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24
Q

What is leukocytosis?

A

An increase in the number of WBCs in the peripheral blood.

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25
Q

What conditions can cause neutrophil leukocytosis?

A

Bacterial infections and tissue necrosis.

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26
Q

What is eosinophilia and its common causes?

A

Increased circulating eosinophils due to allergies, parasitic infections, or drug reactions.

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27
Q

What causes basophilia?

A

Chronic myeloproliferative diseases.

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28
Q

What is lymphadenitis?

A

Inflammation of lymph nodes.

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29
Q

What are the classifications of chronic nonspecific lymphadenitis?

A

Follicular hyperplasia, paracortical hyperplasia, and sinus histiocytosis.

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30
Q

What is follicular hyperplasia?

A

Activation of the humoral immune system, commonly seen in HIV and rheumatoid arthritis.

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31
Q

What is paracortical hyperplasia?

A

Activation of the cellular immune system, seen in viral infections or post-immunization.

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32
Q

What is sinus histiocytosis?

A

An increase in the size and number of cells lining lymphatic sinusoids, often seen in lymph nodes draining cancer sites.

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33
Q

What is Hodgkin lymphoma characterized by?

A

Presence of Reed-Sternberg cells and orderly spread to contiguous lymph node chains.

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34
Q

What are the five subtypes of Hodgkin lymphoma?

A

Nodular sclerosis, mixed cellularity, lymphocyte-rich, lymphocyte depletion, and nodular lymphocyte predominance.

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35
Q

What is the most common subtype of Hodgkin lymphoma?

A

Nodular sclerosis.

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36
Q

What is the typical immunophenotype of classical Hodgkin lymphoma?

A

CD15+, CD30+, negative for CD45.

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37
Q

What is the characteristic cell in nodular lymphocyte predominance Hodgkin lymphoma?

A

Popcorn cells (L&H cells).

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38
Q

What are the clinical features of Hodgkin lymphoma?

A

Painless lymphadenopathy, B symptoms (fever, weight loss, night sweats), and immune dysregulation.

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39
Q

What are the key functions of lymphoid organs?

A

Protect against pathogens and optimize antigen recognition and lymphocyte activation.

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40
Q

What cells are derived from hematopoietic stem cells?

A

Lymphocytes, neutrophils, monocytes, eosinophils, basophils, and other blood cells.

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41
Q

What are the main types of lymphocytes?

A

T-cells (helper, cytotoxic, suppressor, memory) and B-cells (plasma cells, memory B cells).

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42
Q

What are the causes of neutropenia?

A

Drug toxicity, suppression of HSCs, ineffective hematopoiesis, and increased destruction/sequestration of neutrophils.

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43
Q

What is the morphology of bone marrow in neutropenia?

A

Can show hypercellularity (compensatory) or hypocellularity (depletion of precursors).

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44
Q

What are the clinical consequences of neutropenia?

A

Increased susceptibility to bacterial and fungal infections, ulcerating lesions, and life-threatening infections.

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45
Q

What cytokines maintain WBC homeostasis?

A

Cytokines like IL-1, TNF, and growth factors such as G-CSF and IL-5.

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46
Q

What is the pathogenesis of leukocytosis in infections?

A

Cytokines induce granulocyte release from the bone marrow and proliferation of precursors.

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47
Q

What is the difference between reactive and neoplastic leukocytosis?

A

Reactive leukocytosis is due to infections or inflammation, while neoplastic leukocytosis is due to malignancy.

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48
Q

What are the key features of chronic nonspecific lymphadenitis?

A

Follicular hyperplasia, paracortical hyperplasia, and sinus histiocytosis.

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49
Q

What are the causes of follicular hyperplasia in lymphadenitis?

A

HIV, rheumatoid arthritis, and toxoplasmosis.

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50
Q

What are the morphological features of paracortical hyperplasia?

A

Expansion of T-cell zones, immunoblasts, and hypertrophy of vascular endothelium.

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51
Q

What are the causes of sinus histiocytosis?

A

Commonly associated with lymph nodes draining cancer sites.

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52
Q

What distinguishes Hodgkin lymphoma from Non-Hodgkin lymphoma?

A

Hodgkin lymphoma spreads in an orderly fashion and features Reed-Sternberg cells, while NHL spreads unpredictably.

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53
Q

What genetic mutations are commonly seen in Hodgkin lymphoma?

A

NF-κB activation by EBV or mutations in regulators like IκB or A20.

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54
Q

What is the “starry sky” appearance in histology

A

and where is it seen?

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55
Q

What are the main subtypes of peripheral T-cell and NK-cell neoplasms?

A

Peripheral T-cell lymphoma, anaplastic large cell lymphoma, adult T-cell leukemia/lymphoma, and mycosis fungoides/Sezary syndrome.

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56
Q

What is the hallmark genetic mutation in anaplastic large cell lymphoma?

A

Rearrangement of the ALK gene on chromosome 2p23.

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57
Q

What are the clinical features of adult T-cell leukemia/lymphoma?

A

Lymphadenopathy, skin lesions, hepatosplenomegaly, hypercalcemia, and leukocytosis.

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58
Q

What are the three stages of mycosis fungoides?

A

Premycotic phase, plaque phase, and tumor phase.

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59
Q

What is Sezary syndrome?

A

A variant of mycosis fungoides characterized by erythroderma, leukemic Sezary cells, and lymphadenopathy.

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60
Q

What defines acute leukemia?

A

Neoplastic proliferation of blasts with >20% in the bone marrow.

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61
Q

What causes the acute presentation in leukemia?

A

Blast crowding of normal hematopoiesis causing anemia, thrombocytopenia, and neutropenia.

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62
Q

How do blasts typically appear in acute leukemia?

A

Large, immature cells with punched-out nucleoli.

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63
Q

What are the two major types of acute leukemia?

A

Acute lymphoblastic leukemia (ALL) and acute myelogenous leukemia (AML).

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64
Q

What marker characterizes lymphoblasts in ALL?

A

Positive nuclear staining for TdT, a DNA polymerase.

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65
Q

Which demographic is most affected by ALL?

A

Children, especially those with Down syndrome (after age 5).

66
Q

What surface markers are expressed in B-ALL?

A

CD10, CD19, and CD20.

67
Q

What cytogenetic abnormality in ALL has a good prognosis?

A

t(12;21), more common in children.

68
Q

What cytogenetic abnormality in ALL has a poor prognosis?

A

t(9;22), also known as Philadelphia+ ALL, more common in adults.

69
Q

What distinguishes T-ALL from B-ALL?

A

T-ALL lacks CD10 and presents as a mediastinal mass in teenagers.

70
Q

What is the defining marker of myeloblasts in AML?

A

Positive cytoplasmic staining for myeloperoxidase (MPO).

71
Q

What are Auer rods?

A

Crystal aggregates of MPO seen in myeloblasts.

72
Q

What cytogenetic abnormality is associated with acute promyelocytic leukemia (APL)?

A

t(15;17), involving the retinoic acid receptor (RAR).

73
Q

How is APL treated?

A

All-trans-retinoic acid (ATRA), which induces blast maturation.

74
Q

What feature is characteristic of acute monocytic leukemia?

A

Infiltration of gums by monoblasts, which usually lack MPO.

75
Q

What is acute megakaryoblastic leukemia associated with?

A

Down syndrome (before age 5) and a lack of MPO.

76
Q

What is chronic leukemia?

A

Neoplastic proliferation of mature circulating lymphocytes.

77
Q

What is the most common leukemia overall?

A

Chronic lymphocytic leukemia (CLL).

78
Q

What markers are characteristic of CLL?

A

CD5 and CD20 co-expression on naïve B cells.

79
Q

What are complications of CLL?

A

Hypogammaglobulinemia, autoimmune hemolytic anemia, and transformation to diffuse large B-cell lymphoma (Richter transformation).

80
Q

What defines hairy cell leukemia?

A

Mature B cells with hairy cytoplasmic processes and positivity for TRAP.

81
Q

What is the treatment for hairy cell leukemia?

A

2-CDA (cladribine), an adenosine deaminase inhibitor.

82
Q

What is adult T-cell leukemia/lymphoma (ATLL) associated with?

A

HTLV-1 infection, seen in Japan and the Caribbean.

83
Q

What are key features of ATLL?

A

Rash, lymphadenopathy, hepatosplenomegaly, and lytic bone lesions with hypercalcemia.

84
Q

What is mycosis fungoides?

A

Neoplastic proliferation of CD4+ T cells infiltrating the skin, causing rashes, plaques, and nodules.

85
Q

What is Sezary syndrome?

A

Blood involvement in mycosis fungoides, characterized by cerebriform nuclei (Sezary cells).

86
Q

What are myeloproliferative disorders (MPDs)?

A

Neoplastic proliferation of mature myeloid cells, typically occurring in late adulthood.

87
Q

What are common complications of MPDs?

A

Hyperuricemia, gout, marrow fibrosis, and transformation to acute leukemia.

88
Q

What is chronic myeloid leukemia (CML)?

A

Neoplastic proliferation of mature myeloid cells, especially granulocytes and basophils.

89
Q

What genetic mutation drives CML?

A

t(9;22) Philadelphia chromosome, forming the BCR-ABL fusion protein.

90
Q

What is the first-line treatment for CML?

A

Imatinib, a tyrosine kinase inhibitor.

91
Q

How is CML distinguished from a leukemoid reaction?

A

CML has negative LAP stain, increased basophils, and t(9;22).

92
Q

What is polycythemia vera (PV)?

A

Neoplastic proliferation of mature myeloid cells, especially RBCs.

93
Q

What are symptoms of PV caused by hyperviscosity?

A

Blurry vision, headache, thrombosis, plethora, and post-bathing pruritus.

94
Q

What mutation is associated with PV?

A

JAK2 kinase mutation.

95
Q

How is PV treated?

A

Phlebotomy; second-line therapy is hydroxyurea.

96
Q

What distinguishes PV from reactive polycythemia?

A

PV has low EPO and normal SaO2, whereas reactive forms show increased EPO.

97
Q

What is essential thrombocythemia (ET)?

A

Neoplastic proliferation of mature myeloid cells, especially platelets.

98
Q

What symptoms are seen in ET?

A

Bleeding or thrombosis; no significant risk of hyperuricemia or gout.

99
Q

What is myelofibrosis?

A

Neoplastic proliferation of megakaryocytes, leading to marrow fibrosis.

100
Q

What causes marrow fibrosis in myelofibrosis?

A

Excess PDGF production by megakaryocytes.

101
Q

What are clinical features of myelofibrosis?

A

Splenomegaly, tear-drop RBCs, nucleated RBCs, and immature granulocytes.

102
Q

What is lymphadenopathy (LAD)?

A

Enlargement of lymph nodes.

103
Q

What causes painful LAD?

A

Acute infections (acute lymphadenitis).

104
Q

What causes painless LAD?

A

Chronic inflammation, metastatic carcinoma, or lymphoma.

105
Q

What are the regions of hyperplasia in inflammatory LAD?

A

Follicular (B-cell), paracortex (T-cell), and sinus histiocytes.

106
Q

What is follicular lymphoma?

A

Neoplastic proliferation of small B cells (CD20+) forming follicle-like nodules.

107
Q

What translocation drives follicular lymphoma?

A

t(14;18), involving overexpression of Bcl2.

108
Q

How is follicular lymphoma distinguished from reactive follicular hyperplasia?

A

Disruption of lymph node architecture, lack of tingible body macrophages, and monoclonality.

109
Q

What is mantle cell lymphoma?

A

Neoplastic proliferation of small B cells expanding the mantle zone.

110
Q

What translocation drives mantle cell lymphoma?

A

t(11;14), leading to cyclin D1 overexpression.

111
Q

What is marginal zone lymphoma associated with?

A

Chronic inflammation, such as in Sjogren syndrome, Hashimoto thyroiditis, or H. pylori gastritis.

112
Q

What is Burkitt lymphoma?

A

Neoplastic proliferation of intermediate-sized B cells (CD20+), associated with EBV.

113
Q

What translocation drives Burkitt lymphoma?

A

t(8;14), involving c-myc oncogene overexpression.

114
Q

What is the characteristic histological appearance of Burkitt lymphoma?

A

Starry-sky appearance due to high mitotic index and macrophages.

115
Q

What is diffuse large B-cell lymphoma?

A

Aggressive neoplastic proliferation of large B cells (CD20+) growing diffusely in sheets.

116
Q

What are Reed-Sternberg (RS) cells?

A

Large B cells with multilobed nuclei and prominent nucleoli, seen in Hodgkin lymphoma.

117
Q

What markers characterize RS cells?

A

CD15+ and CD30+.

118
Q

What is the most common subtype of Hodgkin lymphoma?

A

Nodular sclerosis, presenting with mediastinal or cervical lymphadenopathy.

119
Q

What cytokine is associated with eosinophilia in mixed cellularity Hodgkin lymphoma?

A

IL-5.

120
Q

What is multiple myeloma?

A

Malignant proliferation of plasma cells in the bone marrow.

121
Q

What are common features of multiple myeloma?

A

Lytic bone lesions, hypercalcemia, M spike on SPEP, Rouleaux formation, and risk of infection.

122
Q

What is Waldenstrom macroglobulinemia?

A

B-cell lymphoma with monoclonal IgM production, causing hyperviscosity symptoms.

123
Q

What are Birbeck granules?

A

Tennis racket-shaped structures seen in Langerhans cell histiocytosis.

124
Q

What are myeloproliferative disorders (MPDs)?

A

Neoplastic proliferation of mature myeloid cells, typically occurring in late adulthood.

125
Q

What are common complications of MPDs?

A

Hyperuricemia, gout, marrow fibrosis, and transformation to acute leukemia.

126
Q

What is chronic myeloid leukemia (CML)?

A

Neoplastic proliferation of mature myeloid cells, especially granulocytes and basophils.

127
Q

What genetic mutation drives CML?

A

t(9;22) Philadelphia chromosome, forming the BCR-ABL fusion protein.

128
Q

What is the first-line treatment for CML?

A

Imatinib, a tyrosine kinase inhibitor.

129
Q

How is CML distinguished from a leukemoid reaction?

A

CML has negative LAP stain, increased basophils, and t(9;22).

130
Q

What is polycythemia vera (PV)?

A

Neoplastic proliferation of mature myeloid cells, especially RBCs.

131
Q

What are symptoms of PV caused by hyperviscosity?

A

Blurry vision, headache, thrombosis, plethora, and post-bathing pruritus.

132
Q

What mutation is associated with PV?

A

JAK2 kinase mutation.

133
Q

How is PV treated?

A

Phlebotomy; second-line therapy is hydroxyurea.

134
Q

What distinguishes PV from reactive polycythemia?

A

PV has low EPO and normal SaO2, whereas reactive forms show increased EPO.

135
Q

What is essential thrombocythemia (ET)?

A

Neoplastic proliferation of mature myeloid cells, especially platelets.

136
Q

What symptoms are seen in ET?

A

Bleeding or thrombosis; no significant risk of hyperuricemia or gout.

137
Q

What is myelofibrosis?

A

Neoplastic proliferation of megakaryocytes, leading to marrow fibrosis.

138
Q

What causes marrow fibrosis in myelofibrosis?

A

Excess PDGF production by megakaryocytes.

139
Q

What are clinical features of myelofibrosis?

A

Splenomegaly, tear-drop RBCs, nucleated RBCs, and immature granulocytes.

140
Q

What is lymphadenopathy (LAD)?

A

Enlargement of lymph nodes.

141
Q

What causes painful LAD?

A

Acute infections (acute lymphadenitis).

142
Q

What causes painless LAD?

A

Chronic inflammation, metastatic carcinoma, or lymphoma.

143
Q

What are the regions of hyperplasia in inflammatory LAD?

A

Follicular (B-cell), paracortex (T-cell), and sinus histiocytes.

144
Q

What is follicular lymphoma?

A

Neoplastic proliferation of small B cells (CD20+) forming follicle-like nodules.

145
Q

What translocation drives follicular lymphoma?

A

t(14;18), involving overexpression of Bcl2.

146
Q

How is follicular lymphoma distinguished from reactive follicular hyperplasia?

A

Disruption of lymph node architecture, lack of tingible body macrophages, and monoclonality.

147
Q

What is mantle cell lymphoma?

A

Neoplastic proliferation of small B cells expanding the mantle zone.

148
Q

What translocation drives mantle cell lymphoma?

A

t(11;14), leading to cyclin D1 overexpression.

149
Q

What is marginal zone lymphoma associated with?

A

Chronic inflammation, such as in Sjogren syndrome, Hashimoto thyroiditis, or H. pylori gastritis.

150
Q

What is Burkitt lymphoma?

A

Neoplastic proliferation of intermediate-sized B cells (CD20+), associated with EBV.

151
Q

What translocation drives Burkitt lymphoma?

A

t(8;14), involving c-myc oncogene overexpression.

152
Q

What is the characteristic histological appearance of Burkitt lymphoma?

A

Starry-sky appearance due to high mitotic index and macrophages.

153
Q

What is diffuse large B-cell lymphoma?

A

Aggressive neoplastic proliferation of large B cells (CD20+) growing diffusely in sheets.

154
Q

What are Reed-Sternberg (RS) cells?

A

Large B cells with multilobed nuclei and prominent nucleoli, seen in Hodgkin lymphoma.

155
Q

What markers characterize RS cells?

A

CD15+ and CD30+.

156
Q

What is the most common subtype of Hodgkin lymphoma?

A

Nodular sclerosis, presenting with mediastinal or cervical lymphadenopathy.

157
Q

What cytokine is associated with eosinophilia in mixed cellularity Hodgkin lymphoma?

A

IL-5.

158
Q

What is multiple myeloma?

A

Malignant proliferation of plasma cells in the bone marrow.

159
Q

What are common features of multiple myeloma?

A

Lytic bone lesions, hypercalcemia, M spike on SPEP, Rouleaux formation, and risk of infection.

160
Q

What is Waldenstrom macroglobulinemia?

A

B-cell lymphoma with monoclonal IgM production, causing hyperviscosity symptoms.

161
Q

What are Birbeck granules?

A

Tennis racket-shaped structures seen in Langerhans cell histiocytosis.

BLOCK POSTING 4 (8 decks)

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