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Molecular and Cellular Pathology > Blood Disorders > Flashcards

Blood Disorders Flashcards

1
Q

What are the two components of the Hematopoietic System?

A
  1. The MYELOID tissue
  2. The LYMPHOID tissue
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2
Q

What does the myeloid tissue consist of?

A

bone marrow, red cells, platelets, granulocytes, monocytes

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3
Q

What does the lymphoid tissue consist of?

A

thymus, lymph nodes, spleen

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4
Q

Where do ALL hematopoietic cells derive from?

A

hematopoietic stem cells (HSCs)

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5
Q

What are hematopoietic cells capable of?

A

Self-renewal AND differentiation to all blood cell lineages

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6
Q

Where does Hematopoiesis begin?

A

in the yolk sack, initial wave of primitive erythroid progenitors

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7
Q

Where are the first Hematopoietic stem cells produced?

A

aorta-gonad-mesonephros (AGM) region of embryo

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8
Q

What occurs during TRANSIENT PROLIFERATION of the HSCs?

A

Hematopoietic stem cells leave AGM for placenta and fetal liver

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9
Q

Where do Hematopoietic cells colonize (hint: it is the site of ADULT hematopoiesis)

A

the bone marrow

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10
Q

What is the proper term for differentiation to all blood cell lineages)

A

Pluripotency

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11
Q

What is the bone marrow niche?

A

important for the maintenance of the blood cell system, protection from genotoxic insults

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12
Q

How is the quiescent state of HSCs maintained in the bone marrow niche?

A

by stromal cells and secreted factors which protect hematopoietic stem cells from genotoxic insults

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13
Q

What is the role of the SPLEEN in relation to blood?

A

acts as a filter, recycling of old lymphocytes

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14
Q

What is the major repository for platelets and lymphocytes?

A

the SPLEEN, connects adaptive immune response (white pulp)

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15
Q

What is the role of the thymus?

A

the site of a T cell differentiation, pluripotent precursors of T cells from bone marrow PROLIFERATE and DIFFERENTIATE

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16
Q

What drains fluid from the tissue?

A

lymph nodes drain fluid from tissue via LYMPH VESSELS

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17
Q

What are lymph nodes composed of?

A

Multiple lymphoid lobules, surrounded by lymph-filled sinuses, enclosed by capsule

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18
Q

What is the mechanism of ANEMIA overall?

A

reduction of total circulating red cell mass below normal limits

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19
Q

How are anemias diagnosed?

A

ratio of packed red cells to total blood volume (HEMATOCRIT) and hemoglobin concentration

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20
Q

What are the symptoms anemia?

A

pale skin, weakness, malaise, fatigability

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21
Q

What causes dyspnea when mildly exerted in those with anemia?

A

lowered oxygen content of the circulating blood

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22
Q

How is anemia classified?

A

underlying mechanisms, alterations in red cell morphology

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23
Q

How are alterations in red cell morphology assessed?

A

by completing a peripheral smear

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24
Q

What is looked at in a peripheral smear?

A

red cell size, degree of hemoglobinization, shape

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25
Q

What are haemoglobinopathies?

A

inherited disorders of haemoglobin synthesis (thalassaemia) or structure (sickle cell disorder)

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26
Q

What are haemoglobinopathies responsible for?

A

Significant morbidity and mortality worldwide.

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27
Q

What chromosomal abnormalities are present in majority of white cell neoplasms?

A

Non-random (translocations)

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28
Q

What plays a crucial role in the survival of normal counterpart of the malignant cell?

A

mutated or altered genes

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29
Q

What is required for particular diagnosis of neoplastic disorders?

A

specific mutations as they are associated with Specific tumor types

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30
Q

When are lymphoid tumors widely disseminated?

A

at time of diagnosis

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30
Q

What is the purpose of mutations in transcriptional regulators?

A

enhance self-renewal of tumor cells, giving them stem-cell like properties

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30
Q

What do transcriptional regulator mutations collaborate with to drive cell growth?

A

active tyrosine kinase mutations

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31
Q

What are lymphoid cancers associated with?

A

immune abnormalities, causing loss of protective immunity and breakdown of autoimmunity

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32
Q

How does Hodgkin lymphoma spread?

A

In an orderly fashion, where most forms of NHL spread wide early (less predictable)

33
Q

What is Acute Lymphoblastic Leukemia/Lymphoma?

A

cancer composed of immature B and T cells, AKA lymphoblasts

34
Q

What do Lymphoblasts look like?

A

condensed nuclear chromatin, small nucleoli, agranular cytoplasm

35
Q

What is the most common mutation in B-cell ALL?

A

t(12:21) ETV6-RUNX1 translocation

36
Q

What is RUNX1?

A

Transcription factor, regulating differentiation of hematopoietic stem cells to mature blood cells

37
Q

What is the most common mutation in T-cell ALL?

A

gain of function mutation in NOTCH1, gene essential for T-cell development

38
Q

What is the greatest success story of oncology?

A

Pediatric ALL

39
Q

What percentage of children with ALL obtain a complete remission?

A

95% of children when treated with aggressive chemotherapy

40
Q

What is the percentage of adults with ALL that are cured?

A

35% to 40%

41
Q

What is Chronic Lymphocytic Leukemia?

A

example of peripheral B-cell cancer, with cytogenic abnormalities like trisomies and deletions

42
Q

What are the most common genetic deletions for CLL?

A

deletion of TP53, deletion of ATM, miR-15a and miR-16-1

43
Q

What are smudge cells?

A

disrupted tumor cells, found in a CLL blood smear

44
Q

Where is the growth of CLL cells confined to?

A

proliferation centers

45
Q

What is a Coagulation?

A

a protective mechanism in response to a vessel injury, seals injury to prevent hemorrhage

46
Q

What is the process of blood coagulation?

A

cells and soluble proteins interact to form a intravascular blood clot

47
Q

What is Blood coagulation also known as?

A

Hemostasis

48
Q

What occurs in pathological situations with Blood coagulation?

A

triggered without vessel injury, formation of a thrombus which obstructs blood flow to embolize a distant organ (thrombosis)

49
Q

What are the three steps of coagulation?

A

Primary hemostasis, secondary hemostasis, and clot stabilization/resorption

50
Q

What occurs in primary hemostasis?

A

interactions between platelets and injured vessel wall, formation of platelet plug

51
Q

What occurs in secondary hemostasis?

A

enzymatic reactions, formation of hemostatic fibrin plug

52
Q

What occurs during clot stabilization?

A

restore normal blood flow and integrity of vessel

53
Q

What are clotting factor disorders?

A

defects of primary hemostasis, focus on defective platelets > thrombocytopenia

54
Q

What does thrombocytopenia entail?

A

small bleeds in skin or mucosal membrane

55
Q

What is signified by small 1-2 mm hemorrhages in the skin?

A

Petechiae

56
Q

What is slightly larger than petechiae but still the same?

A

purpura

57
Q

How do clotting factors disorders manifest in secondary hemostasis?

A

defects of secondary hemostasis which are present bleeds into soft tissue or joints

58
Q

What is the clinical significance of clotting factor disorders?

A

depends on blood volume, location, rate of bleeding > iron deficiency anemia

59
Q

What is Hemophilia A and B?

A

Both X-linked recessive disorders, more > 1000 mutations leading to range of severity

60
Q

What is thrombosis?

A

formation of blood clot inside a blood vessel

61
Q

What does thrombosis result from?

A

excessive activation of coagulation or impaired endogenous regulation

62
Q

What are the three main abnormalities leading to thrombosis?

A

Endothelial injury, abnormal blood flow, hypercoagulability

63
Q

What counts as alterations to normal blood flow?

A

turbulence and endothelial injury

64
Q
A
65
Q

What occurs during turbulence?

A

turbulence leads to endothelial injury, preventing dilution and inflow of inhibitors

66
Q

What occurs during endothelial injury?

A

leads to platelet activation; injury exposes von Williebrand factor

67
Q

What contributes to endothelial injury?

A

inflammation, metabolic abnormalities, infection, toxins

68
Q

What is Hypercoagulability?

A

Predisposition to thrombosis > can be genetic or acquired

68
Q

What is prothrombin?

A

common mutation (2% of population)

69
Q

Where may thrombi develop in the body?

A

Anywhere in the Cardiovascular system

70
Q

Where does arterial (cardiac) thrombi begin in the body?

A

Begins at the site of endothelial injury or turbulence

71
Q

Where does venous thrombi usually occur?

A

Usually in sites of stasis

72
Q

What is a characteristic of all thrombi?

A

firmly attached at the point of origin > then grow and become more occlusive

73
Q

What direction do thrombus grow in?

A

can grow in either direction > but propagating portion poorly attached

74
Q

What’s a complication with thrombus?

A

embolus into distant site > causes tissue dysfunction/infarction

75
Q

What is embolism?

A

travels through the blood until they encounter vessels too small

76
Q

What does embolism cause?

A

partial/complete vascular occlusion

77
Q

Where do emboli lodge?

A

anywhere in vascular tree

78
Q

What is the most common form of embolism?

A

Pulmonary Embolism

79
Q

Where do pulmonary emboli originate from?

A

deep venous thrombosis (DVT)

80
Q

What are infarcts?

A

Areas of ischemic necrosis > commonly caused by arterial occlusion

81
Q

What is the dominant histologic characteristic of infarction?

A

ischemic coagulative necrosis > dead tissues preserved for a span of some days

Molecular and Cellular Pathology (4 decks)

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