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Chapter 55 Flashcards

1
Q

cessation of bleeding from a cut or severed vessel

A

Hemostasis

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2
Q

occurs when the endothelium lining blood vessels is damaged or removed

A

Thrombosis

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3
Q

Cause of thrombosis

A

rupture of an atherosclerotic plaque

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4
Q

Homeostasis and thrombosis involve 3 components/process

A

Blood vessels, platelet aggregation, plasma proteins

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5
Q

_____________ cause formation or dissolution of platelet aggregates and fibrin

A

Plasma Proteins

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6
Q

Diminished blood flow distal to injury is caused by which process during hemostasis

A

Initial vasoconstriction

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7
Q

Three phases in hemostasis and thrombosis

A
  1. Formation of loose and temporary platelet aggregate at the site of injury
  2. Formation of a fibrin mesh
  3. Partial or complete dissolution of the hemostatic plug or thrombus by plasmin.
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8
Q

At what structure does platelet bind to at the site of vessel wall injury

A

Collagen

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9
Q

Collagen-bound platelets release these factors that activate platelets at the vicinity of injury

A

Thromboxane A2 (TxA2), ADP

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10
Q

This is produce during coagulation at the same site, causing further platelet activation

A

Thrombin

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11
Q

True or False. Activated platelets, change shape, and in the presence of fibrinogen and/or von Willebrand factor, aggregate to form, hemostatic, plug or thrombus.

A

True

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12
Q

Function of the fibrin mesh

A

Binds the platelet aggregate forming a more stable, hemostatic, plug or thrombus

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13
Q
A
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14
Q

Three types of thrombi

A
  1. White thrombus
    2.Red thrombus
    3.Fibrin deposits
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15
Q

True or False. All types of thrombi contain fibrin in equal amounts.

A

False
(Equal - various)

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16
Q

Type of thrombi.
Composed of platelets and fibrin, poor in RBC

A

White thrombus

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17
Q

Type of thrombi.
found in very small blood vessels or capillaries

A

Fibrin deposits

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18
Q

Type of thrombi.

Forms at the site of an injury or abnormal vessel wall, particularly in areas where blood flow is rapid (arteries)

A

White thrombus

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19
Q

Type of thrombi.

Primarily RBC and fibrin. Resembles clot formed in test tube may form in vivo in areas of retarded, blood flow or stasis (veins) with or without vascular injury.

A

Red thrombus

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20
Q

Type of Thrombi.
they also form at the site of injury or in abnormal vessel in conjunction with an initiating platelet plug.

A

Red Thrombus

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21
Q

Platelets are found in the circulation in this form

A

Unstimulated disk-shape

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22
Q

Activated platelets help form

A

Hemostatic plugs or thrombi

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23
Q

Three major steps involved in formation of hemostatic plug or thrombi

A
  1. Adhesion to exposed collagen in blood vessels
  2. Release (exocytosis) of contents
  3. Aggregation
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24
Q

Platelets adhere to collagen via this receptors on the platelet surface

A

Glycoprotein complexes (GPIa-IIa, GPIb-IX-V, GPVI)

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25
Von Willebrand factor mediates binding of
GPIb-IX-V to collagen
26
binding of GPIb-IX-V to collagen is important in
platelet adherence to the subendothelium under conditions of high shear stress (small vessels or stenosed arteries)
27
What happens to platelets bound to collagen?
Change shape and spread out on the subendothelium
28
True or false. Adherent platelets would not be able to release the contents of their storage granules
False (would not - would)
29
What type of granules are released in the storage granules during platelet adherence?
Dense granules, alpha granules
30
True or False. Molecules released amplify the responses to vessel wall injury
True
31
What hormone stimulates granule release
Thrombin
32
Hormone that is the most potent activator of platelets.
Thrombin
33
Thrombin initiates activation by interacting with what receptors
Protease-activated receptor-1 (PAR-1), PAR-4, and GPIb-IX-V on platelet PM
34
Binding to PAR-1 and PAR-4 are example of
outside-in transmembrane signaling
35
Type of signaling where in chemical messenger outside the cell generates effector molecules inside the cell
outside-in transmembrane signaling
36
The interaction of thrombin with its G-proteincoupled receptors PAR-1 and PAR-4 stimulates the activity of
phospholipase Cβ (PLCβ)
37
Function of phospholipase Cβ (PLCβ)
hydrolyzes the membrane phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2)
38
Product of reaction catalyzed by phospholipase Cβ (PLCβ)
two internal effector molecules 1,2-diacylglycerol [DAG] 1,4,5-inositol trisphosphate [IP]
39
True or False. Hydrolysis of PIP 2 is also involved in the action of many hormones and drugs.
True
40
What stimulates protein kinase C, which ultimately leads to phosphorylation of pleckstrin
DAG (1,2-diacylglycerol)
41
What protein is responsible for aggregation and release of the contents of the storage granules
pleckstrin
42
From what type of granules are ADP released from
ADP
43
How does ADP activate platelets
via its specific G-protein–coupled receptors resulting in aggregation of additional platelets
44
What causes the release of calcium ions into the cytosol from dense tubular system of smooth ER
IP3 (1,4,5-inositol trisphosphate)
45
How does calcium cause changes in platelet shape
1. release of Ca into the cytosol 2. Calcium interacts with calmodulin and myosin light-chain kinase 3. phosphorylation of the light chains of myosin 4. chains then interact with actin 5. Shape change
46
Collagen-induced activation of a platelet cytosolic phospholipase A 2 (cPLA2 ) by increased levels of intracellular Ca 2+ results in
Release of arachidonic acid from platelet membrane phospholipids
47
Arachidonic acid forms
TxA2
48
How does TxA2 activate PLCβ
Binding to its s cific G-protein–coupled receptor
49
Activation of PLCβ promotes
platelet aggregation
50
Aggregating agents, including thrombin, collagen, ADP, and others such as platelet-activating factor, occur via what type of signaling
inside-out signaling pathway
51
True or False. Inside-out signaling pathway, modify the platelet surface glycoprotein complex GPIIb-IIIa
True
52
Modification of glycoprotein complex GPIIb-IIIa by inside-out signaling pathway leads to
Receptor with higher affinity for fibrinogen or von Willebrand factor
53
Function of fibrinogen and von Willebrand factor
link adjacent activated platelets to each other, forming a platelet aggregate
54
True or False. von Willebrand factor–mediated platelet aggregation occurs under conditions of high shear stress
True
55
True or false. Epinephrine, serotonin, and vasopressin acts as inhibitors of other aggregating agents.
False. (Inhibitors - synergistic)
56
Other than aggregation, activated platelets also
accelerate the activation of the coagulation factor X and prothrombin
57
How does activated platelets activate coagulation factor X and prothrombin
It exposes anionic phospholipid phosphotidylserine on their membrane surface
58
This is released from the dense granules and helps accelerates factor V activation and factor XI activation by thrombin.
Polyphosphate
59
Contributes to overall regulation of hemostasis and thrombosis.
60
This hormone is synthesized by endothelial cells, acting as a potent inhibitor of platelet aggregation
Prostacyclin
61
Prostacyclin stimulates the activity of ________ in surface membrane of cells via ____________
Adenyl cyclase G protein-coupled receptor
62
Stimulation of adenyl cyclase leads to
increase of intraplatelet cAMP, opposing the increase in the level of intracellular Ca2+ produced by IP3 and thus inhibits platelet activation
63
How does endothelial cella regulates thrombosis
1. ADPase hydrolyzes ADP (opposes its aggregating effect) 2. Expression of proteoglycans (heparan sulfate - anticoagulant) 3. Release plasminogen activators (dissolve thrombi) 4. Nitric oxide (endothelium-derived relaxing factor), potent platelet inhibitor
64
Drugs that inhibit platelet response
Antiplatelet drugs (Aspiin - acetylsalicylic acid)
65
How does aspirin inhibit platelet response
1. irreversibly acetylates 2. inhibits the platelet cycloxygenase (COX-1) involved in formation of TxA2 3. inhibits production of PGI2 by endothelial cells
66
67
True or False. Endothelial cells can regenerate cyclooxyrgenase. This shifts the balance toward PGI2 formation, opposing platelet aggregation.
True
68
Indications for treatment with aspirin
1. management of acute coronary syndromes (angina, myocardial infarction) 2. Acute stroke syndromes (transient ischemic attacks, acute stroke) 3. Severe carotid artery stenosis 4. Atherothrombotic diseases
69
Antiplatelet drugs that include specific inhibitors of the P2Y 12receptor for ADP
clopidogrel, prasugrel, and ticagrelor
70
Antiplatelet drugs that acts as antagonists of ligand binding to GPIIb-IIIa
abciximab, eptifibatide, and tirofiban
71
Effect of antiplatelet drugs abciximab, eptifibatide, and tirofiban
interfere with fibrinogen and von Willebrand factor binding and thus platelet aggregation
72
True or False. Both Extrinsic & Intrinsic Pathways Result in the Formation of Fibrin
True
73

Biochemistry (1 decks)

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