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Patho 1 > Chap 13- diseases of WBC, lymph nodes, spleen, thymus > Flashcards

Chap 13- diseases of WBC, lymph nodes, spleen, thymus Flashcards

1
Q

hematopoietic stem cells

A

origin of blood cells

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2
Q

hematopoiesis

A

developmental process of blood cells

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3
Q

where is most active bone marrow in adults?

A

marrow of pelvis, skull, vertebrae, ribs, sternum

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4
Q

where is the most active bone marrow in kids?

A

marrow of long bones- femur and tibia

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5
Q

what to lymphoid stem cells produce

A
  • B cells
  • T cells
  • NK cells
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6
Q

what do myeloid stem cells produce?

A
  • neutrophils
  • monocytes
  • eosinophils
  • basophils
  • platelets
  • RBC
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7
Q

what is composition of blood?

A
  • 90% water
  • 10% solutes
  • 50% of blood volume is plasma
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8
Q

what is serum?

A

blood plasma without clotting factors

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9
Q

what are neutrophils main function?

A

phagocytize bacteria

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10
Q

what are eosinophils main fn?

A

phagocytize parasites

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11
Q

what are basophils main fn?

A

inflammatory mediators

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12
Q

what are monocytes main fn?

A

phagocytize bacteria, dead cells, cellular debris

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13
Q

what are lymphocytes main fn?

A

immune protection

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14
Q

what are platelets main fn?

A

blood clotting

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15
Q

what does leukopenia mean?

A

deficiency of WBC

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16
Q

what does leukocytosis mean?

A
  • increased number of wbc

- can be reactive or neoplastic

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17
Q

neutropenia

A
  • synnonymous with leukopenia, granulocytopenia, and agranulocytosis
  • reduction in neutrophils
  • normally protect us from bacterial infection
  • most common cause is drug induced
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18
Q

what are the granulocytes?

A
  • neutrophils
  • eosinophils
  • basophils
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19
Q

symptoms of neutropenia

A
  • increased risk of infection
  • malaise, chills, fever
  • ulceration in different areas of mouth
  • can cause pneumonia
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20
Q

what is reactive leukocytosis?

A
  • in response to an infection
  • release cytokines and GF that signal bone marrow to increase production
  • increase production can be of specific cells or more general
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21
Q

factors that determine circulating pool

A
  • storage pools in BM, thymus, circulation, and peripheral tissues
  • rate at which cells are released
  • how many cells are stuck to blood vessels (marginal pool)
  • rate of extravasation to tissues
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22
Q

mechanisms of leukocytosis

A
  • increased production in bone marrow:
    1. chronic infection or inflammation
    2. paraneoplastic
    3. myeloproliferative disordres
  • increased release from marrow stores
    1. infection
    2. hypoxia
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23
Q

what causes neutrophilic leukocytosis?

A

acute bacterial infections

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24
Q

what causes eosinophilc leukocytosis?

A

allergic disorders or parasitic infections

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25
Q

what cases monocytosis?

A

chronic infections i.e. TB

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26
Q

what causes lymphocytosis?

A

accompanies monocytosis, viral infections

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27
Q

what are primary lymphoid tissues?

A
  • bone marrow

- thymus

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28
Q

what are secondary lymphoid tissues?

A
  • lymph nodes
  • spleen
  • tonsils
  • adenoids
  • peyer’s patches- in small intestine
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29
Q

what are the lymph nodes?

A

first site of contact between antigen and lymphocytes

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30
Q

what is acute lymphadenitis?

A
  • sudden inflammation of lymph nodes
  • painful
  • causes tissue damage
  • common in cervical region
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31
Q

what is chronic lymphadenitis?

A
  • inflammation of lymph nodes
  • not painful
  • grows slowly
  • no tissue damage
  • common in inguinal and axillary region
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32
Q

what type of cell do most lymphoid neoplasms come from?

A
  • majority from B cells

- some can come from T or nk cells

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33
Q

what are histiocytoses?

A

uncommon proliferative lesions of macrophages and dendritic cells

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34
Q

etiologic and pathogenic factors for proliferations of WBC

A
  • acquired chromosomal translocations
  • inherited genetic factors
  • viruses
  • chronic immune stimulation
  • iatrogenic factors
  • smoking
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35
Q

lymphomas

A

enlargement of lymph nodes

36
Q

leukemias

A

signs and symptoms related to suppression of normal hematopoiesis- bone marrow involvement

37
Q

plasma cell neoplasms

A
  • arise in marrow

- composed of terminally differentiated B cells

38
Q

acute lymphoblastic leukemia/ lymphoma (ALL)

A
  • neoplasms of B cells or T cells
  • majority are due to B cells
  • due to accumulation of many mutations
  • abrupt onset
  • responds very well to tx and can be cured
39
Q

B cell ALL

A
  • peak age is 3

- due to b lymphoblast cells

40
Q

T cell ALL

A
  • peak age is 15 (teens)

- due to T lymphoblasts

41
Q

symptoms of ALL

A
  • fatigue, fever, bleeding
  • mass effects: bone pain, lymphadenopathy, splenomegaly, hepatomegaly
  • testicular enlargement
  • CNS manifestations: HA, vomiting, nerve palsies
42
Q

chronic lymphocytic leukemia (CLL)

A
  • excess of naive B cells
  • common in adults
  • cannot be cured but can be treated and live a long life
  • chromosomal translocations are rare
  • progresses slowly
43
Q

symptoms of CLL

A
  • 40% are asymptomatic
  • fatigue, weight loss, anorexia
  • lymphadenopathy and hepatosplenomegaly
  • immune abnormalities
44
Q

Hodgkin Lymphoma

A
  • group of lymphoid neoplasms
  • have reed-sternberg cells
  • easy to predict clinical course
  • one of most common cancers in young adults, has bimodal distribution
  • was first cancer to successfully be treated and cured
45
Q

why is it believed that reed-sternberg cells develop?

A

due to exposure to epstein barr virus

46
Q

what is cutaneous anergy?

A
  • chemokines released by RS cells in HL
  • reduces helper T cell response
  • cannot mount good immune response
47
Q

stage 1 of HL

A

1 lymph node is enlarged above diaphragm

48
Q

stage 2 of HL

A

multiple lymph nodes above diaphragm are enlarged

49
Q

stage 3 of HL

A

enlargement of lymph nodes above and below diaphragm

50
Q

stage 4 of HL

A

spreads to bone marrow and other tissues

51
Q

progression of diseased tissues in HL

A
  • lymph node
  • spleen
  • liver
  • bone marrow
  • other tissues
52
Q

non-hodgkin lymphoma

A
  • doesnt follow HL rules and doesnt have RS cells
  • usually effects people above 60
  • happens due to multiple mutations
  • very aggressive and hard to predict
53
Q

plasma cells

A
  • specialized type of B cell
  • produces antibodies
  • one stage of B cell maturation is plasma cell
54
Q

multiple myeloma

A
  • most common plasma cell neoplasm
  • usually occurs in elderly
  • very aggressive
  • due to multiple reasons
  • myeloma cells produce abnormal antibodies with light chains being produced in excess
55
Q

clinical features of multiple myeloma

A
  • lytic bone lesions
  • hypercalcemia
  • renal failure
  • acquired immune abnormalities
  • neuronal excitability
  • Bence jones proteins*
56
Q

how does multiple myeloma progress?

A
  • secretes IL-6
  • stimulates growth of myeloma cells and makes interaction with bone marrow stromal cells
  • inhibits osteoblasts, stimulates osteoclasts
57
Q

what are bence jones proteins?

A
  • excess synthesis of light chain antibodies
  • excreted in urine
  • marker for multiple myeloma
  • toxic to kidneys so buildup can cause renal failure
58
Q

myeloid neoplasms

A
  • originate from hematopoietic progenitor cells
  • mostly involve bone marrow
  • clinical presentation related to abnormal hematopoiesis
59
Q

categories of myeloid neoplasms

A
  • acute myeloid leukemias
  • myelodysplastic syndromes
  • myeloproliferative disorders
60
Q

pathogenesis of myeloid neoplasms

A
  • loss of feedback inhibition
  • normally mature cells cause negative feedback to stop hematopoiesis
  • signal doesn’t go from mature cells to bone marrow to stop
  • results in RBC, WBC, and platelet overproduction
61
Q

Acute myeloid leukemia (AML) pathogenesis

A
  • blast cells predominate
  • problem due to mutation in transcription factors and GF signaling pathways
  • differentiation capacity is reduced
  • proliferation capacity is increased
  • myeloid blasts accumulate in bone marrow
62
Q

clinical features of AML

A
  • anemia
  • neutropenia
  • thrombocytopenia
  • fatigue, fever
  • spontaneous mucosal and cutaneous bleeding
  • increased bleed risk
  • infections
  • CNS manifestations rare
63
Q

what age group AML occur in?

A
  • can occur at any age
  • peak age is 60
  • increased risk as you age
  • prognosis is not good
64
Q

myeloproliferative disorders

A
  • caused by constitutively activated tyrosine kinase

- originate from multipotent myeloid progenitors

65
Q

what do tyrosine kinases do

A
  • enzyme
  • transfers phosphate group to tyrosine
  • participates in growth and survival pathways
  • in myeloproliferative disorders it becomes constitutively active
66
Q

chronic myelogenous leukemia

A
  • cell origin is pluripotent hematopoietic stem cell
  • has chimeric BCR-ABL gene
  • comes from chromosomes 22 and 9
  • usually due to reciprocal translocation called the philadelphia chromosome
67
Q

CML clinical features

A
  • primarily occurs in adults
  • fatigue
  • weakness
  • weight loss
  • anorexia
  • progresses slowly
68
Q

stages of CML

A
  • stage 1 chronic stage
  • stage 2 accelerated stage
  • stage 3 blast crisis
69
Q

stage 1 CML

A
  • chronic stage/ stable stage
  • 90% of pts are diagnosed in this stage
  • able to be contained/ managed well
  • blast cells <10%
70
Q

stage 2 CML

A
  • accelerated stage
  • more difficult to treat
  • will progress to stage 3 within 6-12 months
  • blast cells 10-20%
  • worsening sx
  • basophilia- more production of basophils
71
Q

stage 3 CML

A
  • blast crisis
  • difficult to treat
  • blast cells > 20%
72
Q

treatment for CML

A
  • curable in 75% of pts with bone marrow transplant
  • first line of treatment is imatinib
  • all managements are very effective in chronic phase
73
Q

spleen

A
  • filters blood
  • site of immune response to blood born antigens
  • normally weighs about 150 grams
74
Q

what are the areas for storing blood in the spleen?

A
  • venous sinuses

- pulp

75
Q

what is the splenic pulp?

A
  • spleen has permeable capillaries where blood oozes through into trabecular mesh
  • white pulp as WBC
  • red pulp has RBC
76
Q

what is the red pulp?

A
  • reservoir with large quantities of concentrated RBCs in the spleen
77
Q

what is the white pulp?

A
  • made up of three zones
  • periarteriolar lymphoid sheaths (PALS)- contains T lymphocytes
  • marginal zone- contains antigen presenting cells
  • between PALS and MZ have B cells with antibody production
78
Q

function of spleen

A
  • phagocytosis of blood cells and particulate matter
  • antibody production
  • hematopoiesis
  • sequestration of formed blood elements
79
Q

splenomegaly

A
  • enlargement of spleen
  • causes dragging sensation in upper left quadrant
  • pressure on stomach, discomfort after eating
80
Q

hypersplenism

A
  • overactive spleen
  • destroys all cell types
  • results in anemia, leukopenia, thrombocytopenia
81
Q

congestive splenomegaly

A
  • caused by chronic venous outflow obstruction
  • can lead to left sided heart failure and cor pulmonale
  • causes cirrhosis of the liver
  • can cause obstruction of extrahepatic portal vein or splenic vein
82
Q

cor pulmonale

A

isolated HF due to isolated lung disease

83
Q

splenic infarct

A
  • emboli from the heart travels to the splenic artery

- causes occlusion

84
Q

splenic rupture

A
  • can occur due to infection or blunt trauma

- capsule surrounding spleen bursts open

85
Q

thymus

A
  • trains T cells
  • grows until puberty
  • after puberty starts to regress in size
  • mostly composed of thymic epithelial cells and immature T lymphocytes
86
Q

DiGeorge syndrome

A
  • common syndrome of thymus gland

- also has manifestations of parathyroid aplasia and congenital heart conditions

Patho 1 (12 decks)

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