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BSNC 3000 > Module 8 - Clotting > Flashcards

Module 8 - Clotting Flashcards

1
Q

Hemostasis

A

series of events that result in formation of a blood clot that seals a site of vascular injury

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2
Q

Stages of hemostasis

A 
vascular spasm
platelet plug
coagulation
clot retraction
clot dissolution
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3
Q

Stages of platelet plug formation

A

adhesion/activation
degranulation
aggregation

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4
Q

Platelet Adhesion

A

platelets are exposed to subendothelial collagen –> attach via vWF & become activated

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5
Q

von Willebrand Factor

A

glycoprotein located in the subendothelial matrix

binds platelets to collagen by attaching to platelet receptors

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6
Q

Platelet Degranulation

A

release of substances from alpha/dense granules that activate circulating proteins and increase aggregation

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7
Q

ADP & Platelets

A

ADP binds to platelet membrane –> causes a conformational change in platelet receptors gpIIA/IIb
platelets can now bind with fibrinogen –> catch circulating proteins

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8
Q

TXA2

A

prostaglandin involved in platelet aggregation

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9
Q

Platelet aggregation

A

ADP & TXA2 promote platelet aggregation –> act on circulating platelets to activate them & begin to build the clot by binding with fibrinogen

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10
Q

Types of thrombi

A

venous
arterial
mural

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11
Q

Mural Thrombi

A

attaches to the wall of the heart

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12
Q

Composition of venous arterial thrombi

A

venous thrombi usually form d/t blood stasis –> pooling of RBCs & activation of the coagulation pathway

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13
Q

Antiplatelet drugs

A

ex: clopidogrel, baby aspirin
target the platelet plug by inactivating receptors
indicated for conditions where risk of coagulation activation is low

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14
Q

Anticoagulant drugs

A

ex: warfarin, heparin, DOACs, LWMH
interfere with the coagulation pathway preventing the formation of a clot
indicated for conditions where coagulation is likely to occur

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15
Q

Required components for clotting

A

platelets
clotting factors
calcium
Vitamin K

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16
Q

Laminar blood flow

A

normal flow of blood where formed elements are located centrally & plasma maintains contact with the endothelium

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17
Q

Alpha granules

A 
fibrinogen
clotting factors
plasminogen
PA inhibitor 
platelet derived growth factor
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18
Q

Dense granules

A

calcium
ADP
serotonin
histamine

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19
Q

TXA2 release

A

platelet activation –> activate phospholipase A2
PLA –> arachidonic acid –> COX-1 –> thromboxane A2
TXA2 acts on platelet receptors to stimulate platelet activation & aggregation

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20
Q

Time for platelet plug formation

A

3-7 minutes

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21
Q

Clopidogrel MOA

A

antiplatelet drug that blocks ADP receptors on platelets –> prevents binding w/ fibrinogen

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22
Q

Clopidogrel MOA

A

antiplatelet drug that blocks ADP receptors on platelets –> prevents binding w/ fibrinogen

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23
Q

Aspirin MOA

A

irreversibly locks COX-1 preventing TXA2 synthesis –> prevents platelet activation & aggregation

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24
Q

Where is tissue factor located

A

on subendothelial cells –> fibroblasts, smooth muscle cells
exposed following vascular injury

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25
Q

Extrinsic pathway mechanism

A

tissue factor activates Factor VII

TF/VIIa enzyme complex –> activates factor X (common) and Factor IX (intrinsic)

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26
Q

What is factor Xa

A

prothrombinase

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27
Q

Intrinsic pathway mechanism

A

Factor XII activated by contact with a foreign substance (subendothelial collagen) –> eventually leads to activation of IXa
Factor IX can also be activated by the TF/VIIa complex from the extrinsic pathway
IXa/VIIIa enzyme complex activates factor X

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28
Q

Common pathway mechanism

A

Xa & Va form an enzyme complex that converts prothrombin –> thrombin

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29
Q

Primary hemostatic plug

A

temporary blood clot formed from activated platelets & fibrinogen

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30
Q

Secondary hemostatic plug

A

blood clot formed from activation of the coagulation cascade

fibrin + platelets

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31
Q

Thrombin function

A

converts fibrinogen –> fibrin
amplifies the intrinsic pathway by acting on factors V, VIII, XI
activates platelets –> promoting activation/aggregation

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32
Q

Sources of Vitamin K

A

fat-soluble vitamin
green, leafy vegetables, grains + organ meats
synth by bacteria in the colon

33
Q

Vitamin K dependent clotting factors

A

II, VII, IX, X

prothrombin

34
Q

Calcium function

A

bridges binding of gla residue of clotting factors to platelet surface (platelet surface is negatively charged)

35
Q

Gla residue

A

negatively charged carboxyl group added to glutamate

binds with calcium

36
Q

Endogenous anticoagulants

A

proteins C & S
antithrombin
tissue factor pathway inhibitor

37
Q

Antithrombin function

A

binds & inactivates thrombin & Xa –> prevents FURTHER clot growth
amplified by heparin

38
Q

Heparin function

A

released from mast cells

causes a conformational change in antithrombin –> enhances binding of AT to clotting factors thrombin & Xa

39
Q

Fibrinolysis

A

system responsible for breaking down blood clots

40
Q

Plasmin

A

plasminogen –> plasmin

enzyme responsible for breaking down fibrin

41
Q

Plasminogen activators

A

tPA

urokinase

42
Q

D-dimer

A

fibrin degradation product

D-dimer levels in blood indicate existence of blood clots

43
Q

Warfarin MOA

A

blocks the enzyme needed to reactivate Vitamin K for clotting factor synthesis
blocks all pathways of the coagulation cascade

44
Q

LWMH properties

A

small molecules = 100% bioavailability
longer HL than unfractionated heparin
does not require lab monitoring
less risk of heparin-induced thrombocytopenia

45
Q

Antidote for heparin

A

protamin sulfate

46
Q

Antidote for warfarin

A

Vitamin K

47
Q

Antidote for DOAC

A

none

48
Q

aPTT test

A

assess intrinsic & common pathways

used to measure heparin

49
Q

PT test

A

assess extrinsic & common pahways

used to measure warfarin

50
Q

INR test

A

international normalized ratio –> standardized PT value

used to measure warfarin

51
Q

Therapeutic INR for warfarin

A

2.0-3.0

52
Q

Normal INR range

A

0.9-1.2

53
Q

Therapeutic INR for mechanical heart valves

A

2.5-3.5

54
Q

Risk factors for thrombosis

A 
genetics
immobility
atrial fibrillation
cigarette smoking
medications
55
Q

Risk factors for bleeding

A

thrombocytopenia
genetics
liver disease
medications

56
Q

Consequences of thrombosis

A 
blood vessel occlusion, impaired tissue perfusion
ischemia & infarction
back up of blood --> edema
pain
embolism
57
Q

Consequences of excessive bleeding

A 
hemorrhage
hypovolemia & hypotension 
impaired central & tissue perfusion
anemia
hypovolemic shock
58
Q

VTE

A

venousthromboembolic disorders

includes DVT & PE

59
Q

Virchow’s triad

A

indicators three conditions that increase risk for clotting

1) endothelial injury
2) blood stasis
3) hypercoagulabiltiy

60
Q

RF for endothelial injury

A

*exposes collagen & tissue factor –> platelet plug & clotting

smoking
hypertension
indwelling venous catheters
fractures
surgery (esp orthopedic)
61
Q

RF for blood stasis

A
  • blood pooling –> activates coagulation pathway

immobility
A. fib
neurologic/spinal injury

62
Q

RF for hypercoagulability

A
  • increased procoagulants or reduced anticoagulants
estrogen
alcohol 
polycythemia
dehydration 
PSR (increased production of clotting factors)
63
Q

Medication for arterial thrombi

A

antiplatelet

64
Q

Medication for venous/mural thrombi

A

anticoagulants

65
Q

Fibrin polymerization

A

thrombin cleaves fibrinogen into fibrin monomers

these monomers combine to form a fibrin polymer that stabilize the clot

66
Q

S/S of bleeding

A

gum bleeding
nose bleeds
easy bruising
prolonged bleeding after trauma, surgery, dental work
hematuria
melena/hematochezia
petechiae, purpura
fatigue, weakness, dizziness, dyspnea, HR, decreased BP, oliguria (internal bleeding)
labs - decreased Hgb, Hct, increased INR/PTT

67
Q

S/S of a DVT

A 
unilateral swelling >3cm in diameter
discoloration 
warm skin
tenderness/pain d/t phlebitis 
dilated superficial veins
paresthesia (edema causing nerve compression)
low grade fever (systemic inflammation)
68
Q

DVT diagnostic tests

A

D-dimer

ultrasonography

69
Q

Heparin-induced thrombocytopenia

A

transinet, immune-mediated reaction to heparin
causes antibody complexes that form platelet aggregations or sent to spleen for destruction–> thrombocytopenia
can lead to paradoxical clotting

70
Q

HIT mechanism

A

PF4 released from activated platelets binds with heparin
antibodies form against PF4-heparin complex
complex binds to platelet surface

71
Q

Petechiae

A

pin point hemorrhages look like a rash

72
Q

Purpura

A

larger hemorrhages <1cm on skin

73
Q

DVT duration of therapy

A

minimum 3 months

74
Q

Vena cava filter

A

venous mesh that is inserted into the inferior vena cava a the level of the renal veins
catch any potential emboli from a proximal DVT
used when anticoagulation is contraindicated

75
Q

DVT prevention

A

anticoagulation
mobilize
leg exercises
mechanical prophylaxis

76
Q

DVT treatment

A

anticoagulants (prevent clot propagation & recurrence)
IVC filter
thromboltics/thrombectomy

77
Q

How long does warfarin take to become therapeutic

A

36-72 hours

78
Q

Location of superficial veins

A

adipose tissue

79
Q

Location of deep veins

A

in skeletal muscle, along bones

BSNC 3000 (11 decks)

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