5 probe RBC in thrombosis Flashcards

1
Q

is a leading cause of death and disability worldwide.

A

Thrombosis

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2
Q

typically associated with plaque rupture that
triggers accumulation of platelets into platelet-rich (“white”) clots.

A

Arterial thrombosis

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3
Q

is associated with endothelial dysfunction
and blood stasis that result in the formation of fibrin- and red blood cell(RBC)-rich (“red”) clots.

A

Venous thromboembolism (deep vein thrombosis and/or pulmonary
embolism collectively VTE)

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4
Q

the most abundant blood cell in humans

A

Red Blood Cells

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5
Q

T/F: Epidemiologic studies have detected associations between elevatedhematocrit and arterial thrombosis.The largest of these found the riskof cardiovascular disease (CVD) is more than twofold greater in high-versus low-hematocrit groups.

A

true

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6
Q

Study observed a _____ increase in major ischemic heart disease in individuals with high hematocrit, even after adjusting for age, physical activity, cholesterol, body mass index, and smoking.

A

30% increase

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7
Q

_______ risk is also increased in apparently healthy
young children with iron-deficiency anemia.

A

ischemic stroke

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8
Q

Patients with _______ secondary to myeloproliferative neoplasia have increased risk of both arterial thrombosis and VTE, and 20% of polycythemia vera (PV) patients have ________ as the presenting symptom.

A

erythrocytosis, thrombosis

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9
Q

Diseases involving qualitative RBC defects

A

abnormal size, shape, and/or viscoelastic properties,

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10
Q

Arterial thrombi arise in vessels with ________, which promotes the rapid formation of platelet-rich thrombi During arterial thrombosis,

A

high shear rates

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11
Q

arterial thrombosis promotes platelet:

A

Margination
Adhesion
Aggregation
Activation

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12
Q

form slowly in stasis or low flow (frequently in venous valve pockets) and
are RBC and fibrin rich.

A

Venous thrombosis

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13
Q

In disease states, abnormal RBCs and RBC-derived micro vesicles may also adhere to the ___________________ , activate platelets and other cells, and enhance local thrombin generation during thrombosis.

A

endothelium or extracellular matrix

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14
Q

potential contribution of arterial thrombosis

A

Increase Blood Viscosity
Adhere to Vessel Wall
Promote Platelet: Margination Adhesion Aggregation Activation

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15
Q

potential contribution of venous thrombosis

A

Increase Blood Viscosity
Aggregate (Rouleaux)
Adhere to Vessel Wall
Promote Thrombin Generation
Increase Thrombus Size
Reduce Thrombus: Permeability Dissolution

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16
Q

Sickle Cell Disease patients have clinically apparent strokes by
age ______ , ;50% of which are ischemic.

17
Q

studies consistently show that SCD/trait patients have two to fourfold increased risk of _______

A

pulmonary embolism.

18
Q

Thrombosis is also common in patients with _____________________, a disorder marked by complement-mediated RBC hemolysis, and accounts for 40% to 67% of deaths.

A

paroxysmal nocturnal hemoglobinuria

19
Q

are the primary determinants of blood viscosity.

20
Q

elevated hematocrit is correlated with increased _________

A

blood viscosity.

21
Q

At ____ (arterial) shear rates, transient deformation of RBCs reduces
_________.

A

high , blood viscosity

22
Q

at ___ (venous) shear rates, slow movement of blood coupled with discoid RBC morphology allows electrostatic interactions to promote RBC aggregation into stacked
“rouleaux” structures, which increase ___________.

A

low , blood viscosity

23
Q

Intact RBCs can directly adhere to the _________ or ________
matrix or bind through interactions with other blood proteins and/or
cells, including neutrophils and platelets.

A

endothelium , subendothelial

24
Q

receptors of SCD in these adhesive interactions which may particularly contribute to venous occlusion.

A

erythroid Lutheran blood
group/basal cell adhesion molecule,
integrin a4Bb1,
CD36,
sulfate glycolipids
intercellular adhesion molecule-4, and phosphatidylserine

25
ligands in SCD which may particularly contribute to venous occlusion.
b3 integrins thrombospondin laminin fibronectin fibrin[ogen])
26
A subset of normal, circulating RBCs, as well as RBC-MVs, have exposed _____________ on their outer membranes, and extracellular histones can increase RBC phosphatidylserine exposure.
phosphatidylserine
27
can activate the contact pathway and support thrombin generation
RBC phosphatidylserine
28
SCD patients are high in
RBC phosphatidylserine exposure and RBC-MVs
29
this interaction is a key mediator of erythrocyte sedimentation and blood viscosity.
binding of RBC to fibrinogen
30
During platelet-mediated clot contraction, RBCs within thrombi are compressed into __________ that permit tight packing and reduce clot permeability. Thus, RBCs may delay access of thrombolytic enzymes to the clot and consequently prolong thrombus resolution.
(“polyhedrocytes”) shapes
31
blocking the interaction between RBCs and fibrin(ogen) or the endothelium may reduce VTE by preventing RBC aggregation and adhesion,
VTE (Venous thromboembolism)
32
The discovery that factor _______ mediates RBC retention in venous thrombi81 suggests that inhibiting ___________ may reduce thrombus size and accelerate VTE resolution.
XIII(a) , factor XIII(a)