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.

A

45 years

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.

A

RBC

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
Q

ligands in SCD which may particularly contribute to venous occlusion.

A

b3 integrins
thrombospondin
laminin
fibronectin
fibrin[ogen])

26
Q

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.

A

phosphatidylserine

27
Q

can activate the contact pathway and support thrombin generation

A

RBC phosphatidylserine

28
Q

SCD patients are high in

A

RBC phosphatidylserine exposure and RBC-MVs

29
Q

this interaction is a key mediator of erythrocyte sedimentation and blood viscosity.

A

binding of RBC to fibrinogen

30
Q

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.

A

(“polyhedrocytes”) shapes

31
Q

blocking the interaction between RBCs and fibrin(ogen) or the endothelium may reduce VTE by preventing RBC aggregation and adhesion,

A

VTE (Venous thromboembolism)

32
Q

The discovery that factor _______ mediates RBC retention in venous thrombi81 suggests that inhibiting ___________ may reduce thrombus size and accelerate VTE resolution.

A

XIII(a) , factor XIII(a)