Chapter 12 Flashcards

1
Q

When a blood vessel is sealed to prevent blood loss or hemorrhage.

A

Hemostasis (asis- stop bleeding)

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2
Q

when inappropriate blood clotting occurs or when clotting is insufficient to stop the flow of blood from the vascular compartment.

A

Abnormal hemostasis

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3
Q

Is needed to activate factors II, VII, IX, X

A

Vitamin K

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4
Q

what happens during normal hemostasis?

A

sealing of broken blood vessel

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5
Q

what happens during abnormal hemostasis?

A

inappropriate clotting- thrombosis insufficient clotting

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6
Q

platelets live up to:

A

8-9 days in circulation

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7
Q

platelets are also called

A

thrombocytes

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8
Q

platelets are large fragments of _____ that come from ___

A

megakaryocytes, bone marrow

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9
Q

What triggers platelet production

A

thrombopoietin (hormone) that triggers new megkaryocyte formation

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10
Q

platelets are made in the :

A

liver, kidney, smooth muscle, and bone marrow

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11
Q

platelets are stored in the:

A

spleen

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12
Q

healthy people have what # of platelets

A

150,000-400,000 circulating at any given time

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13
Q

platelet structure is:

A

* a hybrid between RBC and WBC * have glycoproteins that stick out from cell to help them connect to other platelets (clot formation) * inside: glycogen, enzymes, mitochondria *A granules, and B granules

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14
Q

a granules are made of what and do what?

A

fibrinogen, coagulation factors, plasminogen * they facilitate platelet aggregation, blood clotting, and vessel repair * Return things to normal

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15
Q

B granules are made of what and do what?

A

ADP, ATP, calcium, histamine, serotonin. * they vasoconstrict and perform platelet adhesion to injured site

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16
Q

Coagualtion Factors: (2)

A

Plasma Proteins & Calcium (Favor IV)

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17
Q

Plasma proteins:

A

circulate as inactive pro-coagulation factors synthesized by liver EX: vWF made my megakaryocytes and endothelium

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18
Q

Examples of anticoagulants:

A

Antithrombin III Protein C&S Plasmnogen __> Plasmin

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19
Q

Damaged Endothelial ___ clotting while healthy endothelium ___ clotting

A

encourages prevents

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20
Q

Clot Formation and Dissolution Steps (5)

A
  1. Vessel Spasm 2. Platelet plug formation 3. blood coagulation 4. clot retraction 5. clot dissolution and lysis
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21
Q

1.) Vessel spasm

A

1st thing in clot formation * TXA2- released by Nervous System to spasm vessel

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22
Q

2.) Platelet plug formation

A

2nd step in clot formation *vWF is needed to bind to collagen and create adhesion Adhesion–> granule release–>platelet aggregation

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23
Q
  1. Blood coagulation
A

3rd step in clot formation * coagulation cascade of factors

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24
Q
  1. Clot Retraction
A

4th step in clot formation- 1st in dissolution * actin and myosin pull damaged vessel closed *exudate is squeezed out of cells in the process

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25
Q
  1. Clot dissolution and lysis
A

5th step in clot formation- 2nd in dissolution *plasminogen–> plasmin: fiber breakdown

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26
Q

Plasminogen is activated by?

A

Tissue plasminogen factor (TPa)

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27
Q

1st thing to happen when tissue gets damaged * is the spark that starts the coagulation cascade*

A

Tissue Factor gets released from the extrinsic pathway

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28
Q

prothrombin turns into thrombin with what activator?

A

calcium Ca++

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29
Q

Factor XIII 13 helps do what?

A

turn fibrin strands into the platelet plug by creating the meshwork that holds the clot together

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30
Q

What converts fibrinogen into fibrin?

A

thrombin

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31
Q

Extrinsic meets the intrinsic pathway in the coagulation cascade where?

A

Factor X and Factor V

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32
Q

the important last 3 factors in the intrinsic pathway are?

A

Factor X and V: activates prothrombin–> Factor II: thrombin –> which activates –> Factor I: Fibrinogen –> Fibrin

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33
Q

Tissue plasminogen activator (tPA) does what?

A

fast acting clot breakdown (stroke patients)

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34
Q

examples of anticoagulants made by Endothelial cells:

A

prostacyclin and Nitric Oxide

Adenosine Diphosphate- breaks down ADP

Histamine

Thrombomodulin- breakdown clots/inhibit formation

TPa- breaks down clots already formed, fast acting.

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35
Q

hypercoagulability

A

increased ability of the body to clot (abnormal)

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36
Q

hypercoagulability can be grouped into two categories:

A

increased platelet function Accelerated coagulation system activity

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37
Q

Increased platelet formation in Hypercoagulability:

A
  • increased platelet # - blood flow disturbances - endothelial damage - platelet aggregation
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38
Q

Accelerated coagulation system activity in Hypercoagulability:

A
  • Increased procoagulation factors - decreased anticoagulation factors
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39
Q

with accelerated coagulation systems activity in hypercoagulability, what are pt’s most at risk for?

A

deep vein thrombosis

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40
Q

accelerated coagulation system activity can be a result of what?

A

mutation of Factor V (5) it mutates so that Protein C can’t recognize it and break it down.

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41
Q

thrombocytopenia

A

decreased platelet levels below 100,000/uL

42
Q

Thrombocytopenia is characterized by:

A

-spontaneous bleeding in intercellular junctions of postcapillary venules - PETECHIA & PURPURA

43
Q

Petechia and Purpura

A

petechia- pinpoint hemorhages purpura- dark purple brusing of skin

44
Q

Calcium, Vitamin K, and prothrombin-

A

all needed to activate certain Factors -Without calcium, blood can’t clot.

45
Q

chelating

A

ionizing calcium so stored blood can’t clot

46
Q

cling to walls of blood vessels and bone marrow. Have appendiges that stick out into the blood vessesl so the blood rushing past sheers off pieces of it.

A

Megakaryocytes

47
Q

thrombopoetin is regulated by

A

of platelet cells circulating in blood stream

48
Q

the celll membrane has an important role in what?

A

platelet adhesion and coagulation process

49
Q

the phospholipids in the cell membrane are important for:

A

binding of calcium and coagulation factors

50
Q

where are coagulation factors synthesized and how do they work?

A

liver

they activate one another so there needs to be a stimulus (injury) in order for them to create a clot.

51
Q

promotes blood flow by blocking platlet adhesion and activation, the coagulation process, and losing blood clots.

A

normal endothelium (uninjured)

52
Q

if platelets are activated in healthy endothelium, they can’t activate why?

A

because of circulating ADP, Nitric Oxide and Prostacylcins in blood

53
Q

what two natural anticoagulants inactive thrombin (factor IIa)

A

Heparin & Thrombomodulin

54
Q

adhesion of platelets to the vessel wall occurs when?

A

when vWF binds to platelet membrane- this links platlets to exposed collagen fibers

55
Q

a granules contain ___ which is required for ____ component of hemostasis

A

calcium; coagulation

56
Q

during platlet plug formation, a granules binds with _____ allowing them to bind with ____ to form aggregates

A

ADP; Firbinogen

57
Q

___ and ___ combine and create the primary hemostatic platlet plug

(expands the platelet aggregation)

A

ADP & TXa2

58
Q

Aspirin does what?

while

Plavix and Ticlid does what?

A
  • inhibits prostaglandin synthesis including TXa2
  • inhibit ADP pathways in platlet to creat antiplatlet effects
59
Q

the intrinsic pathway of the coagulation cascade begins what what factor?

A

Factor XII (12)- Hageman Factor

60
Q

decreases prothrombin and procoagulation factors. alters vitamin K so it can’t reproduce itself in teh liver, is readily absorbed, and takes effets in 36-72 hours after taken

A

Warfarin

61
Q

the process of dissolving the fribrin strands in a clot

A

fibrinolysis

62
Q

^ platlet #

A

thrombocytosis

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