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BMS 460 > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

what is hemostasis and what are its 3 main components?

A
  • hemostasis: helpful blood clotting
    1. vascular wall (specifically endothelium)
    2. platelets
    3. coagulation cascade
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2
Q

what does regulation of the 3 components of hemostasis cause?

A
  • formation of blood clots to stop bleeding from injured vessels
  • activation of natural anti-coagulation and fibrinolytic systems to limit clot formation. this prevents clot from blocking blood flow
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3
Q

describe how the intrinsic and extrinsic pathways converge

A
  • both result in thrombin release, which is a serine protease
  • thrombin converts fibrinogen to fibrin, which ultimately forms the blood clot
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4
Q

what does effective circulation require?

A

a balance between ability to form clots to repair injuries and the need to maintain proper blood flow

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5
Q

what must happen with the coagulation cascade to prevent major issues?

A

it must be restricted to the site of vascular injury!!

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6
Q

what is the pathologic counterpart of hemostasis?

A

thrombosis - this is the formation of a blood clot within intact blood vessels

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7
Q

define embolus

A

when a clot gets detached

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8
Q

define embolism

A

when a detached clot (embolus) gets carried in circulation and blocks an arterial capillary bed

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9
Q

describe virchow’s triad

A
  • three points: endothelial injury (ex: atherosclerosis), hypercoagulability (like estrogen therapy), and abnormal blood flow (like atrial fibrillation)
  • in the middle, we have thrombosis
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10
Q

describe the function of plasminogen

A
  • plasminogen activators see that there is a clot that needs to be shaved down, so they convert plasminogen into plasmin (active form)
  • plasmin shaves off parts of the clot, releasing fibrin fragments
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11
Q

what are platelets?

A
  • anucleate cell fragments
  • shed from megakaryocytes in the bone marrow into the bloodstream
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12
Q

what determines platelet function?

A
  • glycoprotein surface receptors
  • contractile cytoskeleton (actin and myosin)
  • two types of cytoplasmic granules
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13
Q

describe platelet glycoprotein surface receptors

A
  • mediate adhesion to exposed subendothelial components
  • also mediate aggregation with other platelets
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14
Q

what are the specific surface receptors on platelets

A
  • ADP receptor
  • von Willebrand factor (vWF)
  • thromboxane 2 (TxA2) receptor
  • epi receptor
  • collagen receptor
  • fibrinogen receptor
  • thrombin receptor
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15
Q

describe the alpha granules in platelets

A
  • have P-selectin (adhesion molecule) on the membranes and
  • contain fibrinogen
  • fibronectin
  • factors V and VIII
  • platelet factor 4 (heparin-binding chemokine)
  • platelet-derived growth factor (PGDF)
  • transforming growth factor-beta (TGF-B)
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16
Q

describe the dense granules in platelets

A
  • ADP
  • ATP
  • ionized calcium
  • histamine
  • serotonin
  • epinephrine
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17
Q

what are the three steps of hemostasis?

A
  1. immediate response of a blood vessel to injury is vasoconstriction/vascular spasm. this decreases blood flow and possibly a platelet plug can form in small vessels (arterioles, capillaries, venules)
  2. thrombocytes (platelets) adhere to underlying tissue at the site of the injury. this can form a platelet plug in a small vessel
  3. coagulation cascade is needed for larger vessels. this is where inactive clotting factors present in circulation are activated via a sequence of rxns.
18
Q

primary vs. secondary hemostasis

A
  • primary: steps 1 and 2
  • secondary: step 3 (coagulation cascade)
19
Q

describe the origin of the immediate response of vasoconstriction

A
  • this is mostly a myogenic spasm, meaning it is initiated within muscle cells and not from the nervous system
  • it is enhanced by local secretion of factors like endothelin, which is a powerful vasoconstrictor produced by damaged endothelial cells, and only lasts a few minutes
20
Q

factor I

A

fibronogen

21
Q

factor II

A

prothrombin

22
Q

factor III

A

tissue thromboplastin (tissue factor and phospholipid)

23
Q

factor IV

A

ionized calcium

24
Q

factor V

A

occasionally called labile factor of proaccelerin

25
Q

factor VI

A

unassigned (activated factor V)

26
Q

factor VII

A

occasionally called stable factor or proconvertin

27
Q

factor VIII

A

antihemophilic factor (hemophilia A)

28
Q

factor IX

A

plasma thromboplastin component, christmas factor (hemophilia B)

29
Q

factor X

A

occasionally called stuart-prower factor

30
Q

factor XI

A

occasionally called plasma thromboplastin antecedent (hemophilia C)

31
Q

factor XII

A

hageman factor

32
Q

factor XIII

A

fibrin-stabilizing factor

33
Q

what are PAI’s?

A
  • serine protease inhibitors
  • 2 forms:
    1. plasminogen activator inhibitor 1 (PAI-1)
    2. plasminogen activator inhibitor 2 (PAI-2)
34
Q

PAI-1

A
  • aka serpin E1
  • mainly produced by endothelium
  • also made by other tissues like adipose tissue
    -is the principle of tPA and uPA (also serine proteases)
35
Q

describe the role of PAI-1 in disease

A
  • a congenital deficiency of PAI-1 leads to hemorrhagic diathesis (tendency to bleed)
  • it plays a big role in the progression to fibrosis in inflammatory conditions
  • present in increased levels in disease states such as cancer, sepsis, obesity, and metabolic syndrome –> linked to increased occurance of thrombosis in people with these conditions
35
Q

PAI-2

A
  • inhibits uPA and tPA
  • secreted by the placenta (specifically the trophoblastic epithelium)
  • only present in the plasma in specific amounts during pregnancy
36
Q

overall, what is required for effective circuation?

A

balance between ability to form clots to repair vascular injury and maintenance of proper blood flow!

37
Q

is the endothelial wall normally pro or anti thrombotic?

A

it is normally antithrombotic, but can become prothrombotic when injured

38
Q

3 ways that coagulation is normally constrained to sites of vascular injury

A
  • limiting enzymatic activation to phospholipid complexes provided by activated platelets
  • natural anticoagulants are emphasized at sites of endothelial injury or during coagulation cascade activation
  • induction of fibrinolytic pathways involving plasmin via multiple plasminogen activators
39
Q

procoagulant effects of thrombin

A
  • activates fibrinogen to fibrin to generate cross-linked fibrin
  • activates factor XIII to stabilize thrombin
  • activates factors XI, VIII, and V
40
Q

anticoagulant effects of thrombin

A
  • inactivates VIIIa and Va (clotting factors) by binding to thrombomodulin and activating protein C
  • directly induces platelet aggregation and thromboxane (TxA2) production
  • activates endothelial cells to express adhesion molecules
  • activates many mediators:
    –> fibrinolytic: tPA
    –> vasoactive: NO, PGIx
    –> cytokine mediators: PDGF (alpha granules)

BMS 460 (34 decks)

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