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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
what cases monocytosis?
chronic infections i.e. TB
26
what causes lymphocytosis?
accompanies monocytosis, viral infections
27
what are primary lymphoid tissues?
- bone marrow | - thymus
28
what are secondary lymphoid tissues?
- lymph nodes - spleen - tonsils - adenoids - peyer's patches- in small intestine
29
what are the lymph nodes?
first site of contact between antigen and lymphocytes
30
what is acute lymphadenitis?
- sudden inflammation of lymph nodes - painful - causes tissue damage - common in cervical region
31
what is chronic lymphadenitis?
- inflammation of lymph nodes - not painful - grows slowly - no tissue damage - common in inguinal and axillary region
32
what type of cell do most lymphoid neoplasms come from?
- majority from B cells | - some can come from T or nk cells
33
what are histiocytoses?
uncommon proliferative lesions of macrophages and dendritic cells
34
etiologic and pathogenic factors for proliferations of WBC
- acquired chromosomal translocations - inherited genetic factors - viruses - chronic immune stimulation - iatrogenic factors - smoking
35
lymphomas
enlargement of lymph nodes
36
leukemias
signs and symptoms related to suppression of normal hematopoiesis- bone marrow involvement
37
plasma cell neoplasms
- arise in marrow | - composed of terminally differentiated B cells
38
acute lymphoblastic leukemia/ lymphoma (ALL)
- 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
B cell ALL
- peak age is 3 | - due to b lymphoblast cells
40
T cell ALL
- peak age is 15 (teens) | - due to T lymphoblasts
41
symptoms of ALL
- fatigue, fever, bleeding - mass effects: bone pain, lymphadenopathy, splenomegaly, hepatomegaly - testicular enlargement - CNS manifestations: HA, vomiting, nerve palsies
42
chronic lymphocytic leukemia (CLL)
- 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
symptoms of CLL
- 40% are asymptomatic - fatigue, weight loss, anorexia - lymphadenopathy and hepatosplenomegaly - immune abnormalities
44
Hodgkin Lymphoma
- 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
why is it believed that reed-sternberg cells develop?
due to exposure to epstein barr virus
46
what is cutaneous anergy?
- chemokines released by RS cells in HL - reduces helper T cell response - cannot mount good immune response
47
stage 1 of HL
1 lymph node is enlarged above diaphragm
48
stage 2 of HL
multiple lymph nodes above diaphragm are enlarged
49
stage 3 of HL
enlargement of lymph nodes above and below diaphragm
50
stage 4 of HL
spreads to bone marrow and other tissues
51
progression of diseased tissues in HL
- lymph node - spleen - liver - bone marrow - other tissues
52
non-hodgkin lymphoma
- 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
plasma cells
- specialized type of B cell - produces antibodies - one stage of B cell maturation is plasma cell
54
multiple myeloma
- 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
clinical features of multiple myeloma
- lytic bone lesions - hypercalcemia - renal failure - acquired immune abnormalities - neuronal excitability - Bence jones proteins*
56
how does multiple myeloma progress?
- secretes IL-6 - stimulates growth of myeloma cells and makes interaction with bone marrow stromal cells - inhibits osteoblasts, stimulates osteoclasts
57
what are bence jones proteins?
- excess synthesis of light chain antibodies - excreted in urine - marker for multiple myeloma - toxic to kidneys so buildup can cause renal failure
58
myeloid neoplasms
- originate from hematopoietic progenitor cells - mostly involve bone marrow - clinical presentation related to abnormal hematopoiesis
59
categories of myeloid neoplasms
- acute myeloid leukemias - myelodysplastic syndromes - myeloproliferative disorders
60
pathogenesis of myeloid neoplasms
- 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
Acute myeloid leukemia (AML) pathogenesis
- 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
clinical features of AML
- anemia - neutropenia - thrombocytopenia - fatigue, fever - spontaneous mucosal and cutaneous bleeding - increased bleed risk - infections - CNS manifestations rare
63
what age group AML occur in?
- can occur at any age - peak age is 60 - increased risk as you age - prognosis is not good
64
myeloproliferative disorders
- caused by constitutively activated tyrosine kinase | - originate from multipotent myeloid progenitors
65
what do tyrosine kinases do
- enzyme - transfers phosphate group to tyrosine - participates in growth and survival pathways - in myeloproliferative disorders it becomes constitutively active
66
chronic myelogenous leukemia
- 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
CML clinical features
- primarily occurs in adults - fatigue - weakness - weight loss - anorexia - progresses slowly
68
stages of CML
- stage 1 chronic stage - stage 2 accelerated stage - stage 3 blast crisis
69
stage 1 CML
- chronic stage/ stable stage - 90% of pts are diagnosed in this stage - able to be contained/ managed well - blast cells <10%
70
stage 2 CML
- 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
stage 3 CML
- blast crisis - difficult to treat - blast cells > 20%
72
treatment for CML
- curable in 75% of pts with bone marrow transplant - first line of treatment is imatinib - all managements are very effective in chronic phase
73
spleen
- filters blood - site of immune response to blood born antigens - normally weighs about 150 grams
74
what are the areas for storing blood in the spleen?
- venous sinuses | - pulp
75
what is the splenic pulp?
- spleen has permeable capillaries where blood oozes through into trabecular mesh - white pulp as WBC - red pulp has RBC
76
what is the red pulp?
- reservoir with large quantities of concentrated RBCs in the spleen
77
what is the white pulp?
- 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
function of spleen
- phagocytosis of blood cells and particulate matter - antibody production - hematopoiesis - sequestration of formed blood elements
79
splenomegaly
- enlargement of spleen - causes dragging sensation in upper left quadrant - pressure on stomach, discomfort after eating
80
hypersplenism
- overactive spleen - destroys all cell types - results in anemia, leukopenia, thrombocytopenia
81
congestive splenomegaly
- 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
cor pulmonale
isolated HF due to isolated lung disease
83
splenic infarct
- emboli from the heart travels to the splenic artery | - causes occlusion
84
splenic rupture
- can occur due to infection or blunt trauma | - capsule surrounding spleen bursts open
85
thymus
- trains T cells - grows until puberty - after puberty starts to regress in size - mostly composed of thymic epithelial cells and immature T lymphocytes
86
DiGeorge syndrome
- common syndrome of thymus gland | - also has manifestations of parathyroid aplasia and congenital heart conditions

Patho 1 (12 decks)

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