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23 General Pathology > 11/9 - Hematopoetic and Lymphoid System > Flashcards

11/9 - Hematopoetic and Lymphoid System Flashcards

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1
Q

what are plasma cell tumors

A
  1. multiple myeloma
  2. plasmacytoma
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2
Q

what do B-cell proliferations in plasma cell neoplasma contain

A

neoplastic plasma cells that virtually always secrete monoclonal Ig or Ig fragments which serve as tumor markers and often have pathologic consequences

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3
Q

what is the most common and deadly of plasma cell neoplasms

A

multiple myeloma

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4
Q

difference between normal plasma and myeloma

A

normal (polyclonal) - lots of different types of whole antibodies
intact Ig myeloma (monoclonal) - whole Ab and excess light chains and too many of both

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5
Q

what makes up heavy chain of normal antibody

A

G, A, M, E, D

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6
Q

what makes up light chain of normal antibody

A

kappa, lambda

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7
Q

M proteins are also called what

A

Bence Jones

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8
Q

what is the monoconal Ig identified in the blood referred to as

A

M protieins (in reference to multiple myeloma)

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9
Q

where are M proteins restricted

A

plasma and extracellular fluid

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10
Q

when and where is bence jones/m proteins excreted

A

in urine in abscnce of glomerular damage

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11
Q

neoplastic cells synthesize excess what

A

light chains (kappa or lambda) along with complete Igs

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12
Q

light chains also excreted in urine also called what

A

bence jones proteins

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13
Q

what is plasma cell neoplasm commonly associated with lytic bone lesions, hypercalcemia,renal failure, and acquired immuneabnormalities

A

multiple myeloma

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14
Q

what is most dominated disease in multiple myeloma? where else seen

A

dominated: bone disease:
seen in lymph nodes and extranodal sites

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15
Q

who gets multiple myeloma

A

Incidence higher in men and people of African
descent
Peak age is 65-70 years

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16
Q

is multiple myeloma homo or heretrogenous

A

heterogenous

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17
Q

proliferation and survival of myseloma cells are dependent on what

A

dependent upon several cytokines, most notable IL-6, which is an important growth factor for plasma cells

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18
Q

what produces multiple myeloma

A

produced by tumor cells themselves and
by resident marrow stromal cells

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19
Q

[High OR low] serum levels of IL-6 in patients with active disease are associated with poor prognosis

A

HIGH

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20
Q

what cytokine is important in multiple myeloma

A

IL-6

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21
Q
  • Usually present as destructive plasma cell
    tumors involving the axial skeleton
  • Bones most affected are the vertebral
    column, ribs, skull pelvis, femur, clavicle,
    and scapula
A

multiple. myeloma

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22
Q

multiple myeloma bone lesions radiographically

A

Bone lesions appear radiographically as
punched-out defects, usually |-4 cm in
diameter

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23
Q

high levels of what in the blood of multiple myeloma patients

A

M protein

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24
Q

most characteristic symptom of multiple myeloma

A

Bone pain, particularly in the lumbar spine, is
the most characteristic presenting feature

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25
symptoms of multiple myeloma
Hypercalcemia (C) Renal dysfunction (R) Anemia (A) Bone pain with lytic lesions punched out lesions"(B)
26
common cause of death of multiple myeloma patients
Renal insufficiencies and failure are a common cause of death - kidneys become overburdened with the excess circulating light chain proteins of the tumor cells
27
what do multiple myeloma cells produce
produce abnormal clonal, complete or incomplete, immunoglobulins which can be detected in the blood and in the urine
28
in multiple myeloma, abnormal immunoglobulin, usually a light chain, was previously referred to as ___
Bence-Jones protein
29
what suppress normal humoral immunity in multiple myeloma
neoplastic cells
30
oral manifestations of mulptiple myeloma
- Jaws involved in 30% of cases - Jawbone pain and paresthesia - Petechial hemorrhage of oral mucosa - Bleeding tendency - Infections - Patients often on IV bisphosphonates- results in medication related osteonecrosis of bone (MRONJ) - Prognosis depends on stage of disease
31
multiple myeloma treatment
32
what is unifocal, monoclonal, neoplastic proliferation of plasma cells that usually arise within bone?
plasmacytoma
33
are extramedullary lesions in plasmacytoma COMMON or UNCOMMON
uncommon
34
who gets plasmacytoma? where?
>. males; average age at diagnosis is 55 years > in spine
35
symptoms of plasmacytoma? what does it look like in xray
swelling or bone pain well-defined, unilocular radiolucency
36
how is plasmacytoma treated
radiation therapy
37
virtually all patients with plasmacytoma develop ___ by 15 years following their diagnosis
MM (multiple myeloma)
38
what displays a mixture of properties, which they share with macrophages such as self-maintenance and ontogeny
langerhan cells
39
what is capable of presenting antigen and actively presenting antigen and actively migrate to the draning lymph nodes, which qualifies them as DCs
langerhans cells
40
what is an umbrella term designated for variety of prolierative disorders of dendritis cells or macrophages
Histiocytosis
41
what is a clonal (genetically identical) proliferation of a special type of immature dendritic cell
langerhans cell histiocytosis
42
LBH lies between when spectrum
malignant and benign spectrum
43
in LCH, majorit have driver mutations in what genes
cancer associated genes
44
neoplastic cells in LCH express what
chemokine receptors
45
normal LC expression vs LCH cells
Normal LCs express CCR6 neoplastic express CCR6 and CCR7
46
what do LCH neoplastic cells with CCR6 and CCR7 allow
allowing the neoplastic cells to migrate into tissues that express the relevant chemokines- CCL20 in skin and bones and CCL19 and CCL21 in lymphoid organs
47
what has abundant, often vacuolated cytoplasm and vesicular nuclei containing linear grooves or folds
proliferating LC
48
characteristic morphology of LCH
Birbeck granules in cytoplasm and kidney bean shaped cells
49
who gets LCH
1. Rare; 1to 2 newborns per million per year 2. May occur at any age but is more likely to occur in those <15 years of age
50
LCH clinical features
51
what are the LCH prognostic category classifications
1. single organ involvement 2. multiorgan involvement
52
what is part of LCH single organ involvement
1. unifocal disease 2. mutifocal disease
53
what is part of LCH multiorgan involvement
1. no organ dysfunction 2. organ dysfunction (low risk and high risk) low risk - skin, LN, bone and or pit gland high risk - lung, liver, spleen and or BM
54
traditional clinical classifications of LCH
1. Monostotic or polyostotic eosinophilic granuloma 2. Chronic disseminated histiocytosis (Hand-Schuller-Christian disease) 3. Acute disseminated histiocytosis (letterer-Siwe disease)
55
what is LCH that involves solitary or multiple bone lesions without visceral involvement
Monostotic or polyostotic eosinophilic granuloma
56
what is LCH that involves skin, bone and viscera
Chronic disseminated histiocytosis (Hand-Schuller-Christian disease)
57
what is LCH that has Prominent cutaneous, visceral, and bone marrow involvement mainly in infants
Acute disseminated histiocytosis (letterer-Siwe disease)
58
in LCH, ___ is affected in 10-20% of all cases; dull pain and tenderness often accompany ___ lesions
jaw; jaw
59
what disease: Ulcerative or proliferative mucosal lesions; proliferative gingival mass develops if it breaks out of bone
LCH oral manifestation
60
what disease: Radiographically, lesions often appear as sharply ***punched-out*** radiolucencies without a corticated rim
LCH oral manifestation
61
what disease: Bone involvement in the mandible is seen in the posterior areas; ***scooped out*** appearance is evident causing the teeth to appear as if they are ***floating in air***
LCH oral manigestation
62
LCH tx
1. Accessible bone lesions, such as those in the maxilla and mandible are treated by curettage 2. Low dose of irradiation may be used for less accessible lesions 3. Multiple chemotherapeutic agents are given in high-risk situations
63
what are tests for evaluating hemostasis
1. prothrombin time (PT) 2. partial thromboplastin time (PTT) 3. test for platelet count 4. test or platelet function
64
what does prothrombin time test
this test assesses the extrinsic and common coagulation pathways (PT = Play Tennis OUTSIDE)
65
prolonged PT can result from deficiency or dysfunction of what?
V, VII, X, prothrombin and fibrinogen
66
what does partial thromboplastin time test
this test assesses the intrinsic and common pathway (PTT = Play Table Tennis INSIDE)
67
prolonged PTT can be due to deficiencies or dysfunction of what
V, VIII, IX, X, XI, XII, prothrombin or fibrinogen
68
what is reference range for testing platelet count to evaluate for hemostasis
Reference range is 150 x to 350 X 10^3/ μL
69
how to test for platelet function to evaluate for hemostasis
- At present no single test provides an adequate assessment of the complex function of platelets - In clinical setting platelet aggregation measures the ability of platelets to adhere to one another in response to thrombin
70
what can excessive bleeding result from
1. Increased fragility of vessels 2. Platelet deficiency or dysfunction 3. Derangement of coagulation
71
abnormal hemorrhage is due to what
1. increase fragility of blood vessels 2. inadequate hemostatic response due to either platelet deficiency or dysfunction 3. derangement in clotting mechanism
72
what are clinical conditions in which vessel wall abnormalities cause bleeding disorders
Hereditary hemorrhagic telangiectasia Perivascular amyloidosis Drug reactions Infections Ehlers Danlos syndrome Scurvy (Harry Potter DIES)
73
what is bleeding related to reduced platelet number called
thrombocytopenia
74
reduction in platelet number constitutes an important cause of what
generalized bleeding
75
how many counts of platelets constitute THROMBOCYTOPENIA
Count <150,000 platelets /µL constitutes thrombocytopenia
76
how many counts of platelets can aggravate POSTTRAUMATIC BLEEDING
Counts in range of 20,000 to 50,000 platelets/ µL can aggravate posttraumatic bleeding
77
how many counts of platelets is associated with SPONTANEOUS BLEEDING
Count <20,000 platelets/ µL may be associated with spontaneous bleeding
78
causes of thrombocytopenia
1. decreased platelet production 2. decreased platelet survivala 3. sequestration 4. dilution
79
what cause decreased platelet production
- Drug induced: alcohol, thiazides, cytotoxic drugs - Infections: measles, HIV - Nutritional deficiencies: B 1 2, folate, - Leukemia, disseminated cancer, granulomatous diseases
80
what causes decreased platelet survival
- Immunologic destruction - nonimune destruction
81
what diseases cause immunologic destruction that decrease platelet survival
***- Chronic immune thrombocytopenic purpura - acute immune thrombocytopenic purpura***
82
what causes nonimmune destruction that decreases platelet survival
***disseminated intravascular coagulation***
83
what is characteristic in thrombocytopenia
small vessel bleeding
84
what does thrombocytopenia produce
petechia, purpura, and ecchymosis

23 General Pathology (24 decks)

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