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Pathology > Blood > Flashcards

Blood Flashcards

1
Q

two components of hematopoietic system

A

Myeloid tissues and lymphoid tissues

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2
Q

Myeloid tissues

A

bone marrow and the cells derived from it

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3
Q

Lymphoid tissues

A

thymus, lymph nodes and spleen

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4
Q

where does hematopoiesis first occurs

A

Yolk Sack

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5
Q

where are the first HSC (hematopoietic stem cells) produced

A

Aorta gonad mesonphros AGM

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6
Q

where is the site of adult hematopoiesis

A

bone marrow

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7
Q

pluropotency

A

ability to differentate to all blood cell lineages

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8
Q

quick description of the differentiation of blood cells

A

steam cell pluripotent cell –> multipotent cell –> committed precursor cell (either myeloid or lymphoid) –> mature blood cell

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9
Q

what dopes a blood smear show (3)

A

estimated cell count, proportion of different cells and cell morphology

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10
Q

quiescent stat of HSCs

A

protects HSCS fro genotoxic insults (sleep) part of bone marrow niche

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11
Q

interferon alpha and interferon gamma in the bone marrow niche

A

push cells out of sleep to start proliferating

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12
Q

purpose of the spleen

A

filter the blood are recycle old erythrocytes (red pulp)
major repository for platelets and lymphoscyes (white pulps)

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13
Q

function of thalamus

A

site of T cell differentiation

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14
Q

lymph nodes

A

small glands located throughout the body that drain fluid from tissue allowing antigens to be seen

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15
Q

structure of lymphoid

A

lobules surrounded by lymph filled sinuses and enclosed in capsule

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16
Q

what are red blood disorders largely classified as

A

Anemias

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17
Q

how are anemias diagnosed

A

hematocrit and hemoglobin concentration

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18
Q

hematocrit

A

ratio of packed red cells to total blood volume

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19
Q

symptoms of anemia

A

pale skin, weakness, malaise and easy fatiguability.

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20
Q

how is anemia classified

A

based on red cell size (normocytic, microcytic, marcrocytic)
colour of red cells ( normochromic,
hyperchromic or hypochromic)

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21
Q

haemoglobinpathies

A

inherited disorders of haemoglobin synthesis or structure

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22
Q

cause of sickle cell disease

A

common hemoglobinopathy caused by point mutation in 6th codon of B global

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23
Q

what does compensatory erythroid hyperplasia in sickle cell

A

bone marrow is hyper plastic (expansion of marrow and resorption of bone)

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24
Q

what does jaundice indicate

A

increased break down of hemoglobin causing hyperbilirubinemia in sickle cell

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25
Q

effect of sickle cell on the spleen

A

rapid splenic enlargement –> infarction (poor blood flow) –> fibrosis and progressive shrinkage

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26
Q

pathogenesis of white cell malignancies

A

pro growth mutation (cell division), mutations that influence self renewal and pro survival

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27
Q

what cells maintain the quiescent state of HSC

A

Stromal Cells

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28
Q

what cells push HSC out of quiescent state

A

Interferons Alpha and gamma (IFN)

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29
Q

Cumulative damage of sick cell to red cells

A

Hbs polymers poke through membrane
influx of Ca
effluck of K and H2O

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30
Q

most serious clinical feature of sickle cell

A

microvasculate occlusion cells not passing through properly causing hypoxia

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31
Q

morphology of spleen with infarction

A

fibrosis red pulp congestion and sinusoids filled with red blood cells

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32
Q

what is leukemia

A

cancer with wide spread involvement of bone marrow and peripheral blood

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33
Q

what is lymphoma

A

cancer that arises as a discreet tissue mass

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34
Q

classification of lymphoid neoplasm

A

non Hodgkins lymphomas (precursor B/T peripheral B/T)
Hodgkins lymphoma

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35
Q

____ chromocal abnormalities most commonly ____ are present in most white cell neoplasms

A

non random, Transloactions

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36
Q

what other abnormalities is lymphoid cancer associated with

A

immune

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37
Q

homing to tissue

A

tendency of B and T cells to travel and spread common in cancer associated with these cells

38
Q

how does Hodgkin lymphoma spread compared to non Hodgkin lymphoma

A

in an orderly fashion

39
Q

what does a flow cytometry describe

A

size and shape as well as complexity and granularity as well as a specific protein

40
Q

what are acute lymphoblastic leukemias/ lymphomas (ALL) composed of

A

immature B (pre B) or T (pre T) lymphoblasts

41
Q

morphology of lymphoblasts

A

condensed nuclear chromatin, small nucleoli and scant granular cytoplasm

42
Q

ETV6- RUNX1

A

most common translation in B-ALL

43
Q

RUNX1

A

transcription factor regulates hematopoietic stem cells into mature blood

44
Q

what does the mix of RUNX and ETV6 gene code for

A

Creates a fusion gene which is regulated like ETV6 but acts like RUNX

45
Q

most common gain of function mutation in T-ALL

A

NOTCH1

46
Q

What does NOTCH1 do?

A

it is essential for T cell development, precursor to RUNX

47
Q

what does the NOTCH ligand do

A

Cleaves NOTCH through metalloproteinases release intracellular domain, Converts CSL from repressor to activator

48
Q

two hit modle of ALL

A

1) ETV6/RUNX1 mutation
2) other mutations that increase kinase singling

49
Q

chronic lymphocytic leukemia (CLL) is a ____ __ cell cancer

A

Peripheral B cell cancer

50
Q

most common genetic deletions in

A

deletion TP53
Deletion of ATM
miR15a miR-16-1

51
Q

most chemotherapy drugs target ____ dependent pathways

A

P53

52
Q

what does ATM do

A

Bind the p53 and stabilize it

53
Q

miR-15 miR-16-1 deletion in CLL

A

deletion in this gene will block mitochondrial calcium leaving and shift cell to survival

54
Q

what does miR-15 miR-16-1 do?

A

regulates translation of proteins

55
Q

CLL blood spear

A

small lymphocytes with condensed chromatin as well as bursted cells

56
Q

where is the growth of CLL confined to

A

proliferation centres (lymph nodes bone marrow spleen and liver)

57
Q

what id coagulation

A

cells form a intravascular blood clot in response to vessel injury to prevent hemorrhage.

58
Q

steps of coagulation

A
  1. primary homestasis
  2. secondary homeostasis
  3. clot stabilization and resorption
59
Q

process of primary homestasis

A

formation of platelet plug through exposed von willebrand factor and collagen activation platelets

60
Q

process of secondary homeostasis

A

formation of hemostatic fibrin plug through Thrombin cleaves fibrinogen into insoluble fibrin which polymerizes into mesh network

61
Q

what happens when platelets are activated

A

Shift from small round discs to flat spiky plates

62
Q

permanent plug in coagulation

A

polymerized fibrin and platelet under contraction

63
Q

process of clot stabilization and resorption

A

restore normal blood flow through tissue plasminogen activator (t-PA) catalysis plasminogen to plasmin to break down the clot.

64
Q

thrombomodulin role in clot stabilization and resorption

A

converting thrombin from pro to anti coagulant enzyme

65
Q

what is thrombocytopenia

A

defects in primary hemostasis not enough platelets

66
Q

petechiae

A

small hemmorhages present in thrombocytopenia

67
Q

purpura

A

larger hemorrahges present in thrombocytopenia

68
Q

major complication of thrombocytopenia

A

brain bleeds

69
Q

secondary hemostasis defects

A

coagulating factor defects

70
Q

secondary hemostasis defects symptoms

A

bells into soft tissue and joints

71
Q

secondary hemostasis defects clinical significant

A

loss of iron anemia

72
Q

hemophilia A and B cause and effect

A

VIII and IX deficiency X linked recessive disorder stops clotting

73
Q

treatment of hemophilia A and B

A

supplement with VIII and XII

74
Q

thrombosis

A

blood clots due to too much coagulation

75
Q

three main abnormalities leading to thrombosis

A

endothelial injury
abnormal blood flow (stasis)
hypercoagulability (genetic and acquired)

76
Q

what tis turbulence in thrombosis

A

alterations in normal blood flow

77
Q

effects of turbulence

A

endothelial unjust
counter currents causing stasis
platlets in contact with endothelium

78
Q

hypercoagulatin is a predisposition to _____

A

thrombosis

79
Q

prothrombin

A

common single nucleotide changes which elevates levels of prothrombin and increases risk of thrombosis

80
Q

acquired predispositions to thrombosis

A

cardiac failure
pregnancy/ contraceptives
disseminated cancer

81
Q

where do arterial (cardiac) thrombi being

A

site of endothelia injury or turbulence

82
Q

where do venous thrombi usually occur

A

on site of stasis

83
Q

characteristic of all thrombi

A

firmly attached at the point of origin

84
Q

complication of thrombosis

A

embolus into distance site causing tissue disfunction

85
Q

embolism

A

emboli travels through blood until it reaches vessel it cannot pass causing vascular occlusion

86
Q

what is an emboil

A

peace of thrombus that breaks off

87
Q

pulmonary embolism

A

most common, deep vein thrombosis emboli to lungs

88
Q

infarction

A

areas of ischemic necrosis commonly caused bu arterial occlusion

89
Q

vast majority of occlusion are ___ and ___

A

arterial thrombosis or arterial embolism

90
Q

dominat histological characteristic of infraction

A

ischemic coagulative necrosis

91
Q

ischemic coagulative necrosis

A

dead tissue is preserved for days. swollen cells without nuclei, inflammatory cells present.

92
Q
A

Pathology (14 decks)

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