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*med3* > Hematology - Hemostasis > Flashcards

Hematology - Hemostasis Flashcards

Coagulation Platelet Activation Hypercoagulable States Coagulopathies Platelet Disorders Antiplatelet Drugs Anticoagulant Drugs

1
Q

how does the body prevent blood loss when there is damage to a blood vessel?

A

thrombus formation

platelets are activated and fibrin crosslinks to form a clot

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2
Q

what is the first line of defense against bleeding?

A

vasoconstriction in response to endothelial damage

mediated by ENDOTHELINS

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3
Q

what are endothelins?

A

key mediator in the vasoconstrictor compensatory response to prevent blood loss

they are proteins

they are potent vasoconstrictors

they are released by endothelial cells near the damage

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4
Q

what are endothelin receptor blockers used for?

A

Pulmonary HTN

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5
Q

what are coagulation factors?

A

proteins synthesized by the liver

soluble in plasma

activated when endothelial damage occurs

forms fibrin => fibrin mesh => blood clot

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6
Q

what form do coagulation factors circulate in?

A

zymogens

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7
Q

what are serine proteases?

A

protein cleavage enzyme that contains serine

clotting factors can activate into a serine protease

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8
Q

what are the steps in the clotting cascade?

A
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9
Q

activation of what clotting factor will lead to fibrin formation?

A

X –> Xa

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10
Q

what drugs act on the clotting cascade?

A
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13
Q

what is the positive feedback associated with thrombin?

A

factor IIa activates factors V, XI, VIII

XIa activates IX —> IXa

IXa + VIIIa —> Xa

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15
Q

what activates factor X in the setting of endothelial damage?

A

tissue factor becomes activated by endothelial damage which interacts with factor VII to activate factor X

TF:VIIa complex activates Xa

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16
Q

what is tissue factor?

A

aka thromboplastin

glycoprotein expressed in SUBendothelial cells NOT endothelial cells => no contact with citculating blood unless exposed by endothelial damage

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18
Q

what is thrombin?

A

aka factor IIa

prothrombin is factor II

can activate factors V, XI, VIII

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19
Q

what are the components of extrinsic Xase?

A

phospholipid: TF-bearing cells

Enzyme: factor VIIa

co-factor: TF

substrate: factor X

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20
Q

what are the unique features of factor VIII?

A

produced in endothelial cells, not in the liver

circulates bound to vWF

released from vWF in response to vascular injury

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21
Q

what are the components of intrinsic Xase?

A

phospholipid: platelets
enzyme: factor IXa

co-factor: factor VIII (VIIIa)

substrate: factor X

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22
Q

what is vWF?

A

von willebrand factor

critical for platelet aggregation

binding to vWF increases VIII plasma half life

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23
Q

what cells produce vWF?

A

endothelial cells and megakaryocytes

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24
Q

what are the multicomponent complexes that activate X –> Xa?

A
  1. Extrinsic Xase
  2. Intrinsic Xase
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26
Q
A
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28
Q

what is calciums role in coagulation?

A

used to be called factor IV - required for the clotting cascade

activated platelets release calcium

EDTA binds calcium in blood samples and prevents clotting

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29
Q

what is the order of the intrinsic pathway?

A

XII

XI

IX

X

II

I

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30
Q

what is the order of the extrinsic pathway?

A

TF:VIIa

X

II

I

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31
Q

what is factor XIII’s job?

A

crosslink fibrin to stabilize plug

requires calcium as a co-factor

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32
Q

what activates factor XIII?

A

thrombin (IIa)

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33
Q

what happens in the absence of factor XIII?

A

inadequate clot formation

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34
Q

what is factor XII?

A

aka Hageman factor

used for PTT test

activted by contact with negative charges (silica)

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35
Q

what can activate factor XI?

A

thrombin and factor XII

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36
Q

what is PTT?

A

partial thromboplatin time

tests the intrinsic pathway

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39
Q

how does the PTT test work?

A

plasma is added to negatively charged substance, usually silica

measure how long it takes for a clot to form

tests intrinsic pathway

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40
Q

what is the PT test?

A

prothrombin time

add plasma to TF and measure how long it takes for a clot to form

tests extrinsic pathway

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41
Q

what does the intrinsic pathway require to function normally?

A

kinins

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42
Q

how does factor XII produce bradykinin?

A

activates PK –> Kallikrein

HMWK —–> bradykinin

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43
Q

what activates the intrinsic pathway?

A

factor XII - aka the contact pathway because it becomes activated with contact to negatively charged substances

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44
Q

what are kinins?

A

peptide hormones/signaling molecules that link coagulation with inflammation

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45
Q

what do kinins circulate as and what activates them?

A

kininogens activated by kallikreins

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46
Q

what is bradykinin?

A

vasodilator

increases vascular permeability

can cause pain

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47
Q

what is bradykinin degraded. by?

A

ACE and C1 inhibitor protein

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48
Q

what happens to [bradykinin] with ACE inhibitors?

A

bradykinin levels increase

can cause angioedema

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49
Q

hereditary angioedema

A

C1 inhibitor protein deficiency

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50
Q

what does factor XII do?

A

activates clotting and produces bradykinin

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52
Q

what is prekallikrein deficiency?

A

rare condition that results in a markedly long PTT

factor XII an not activate normally

no bleeding problems bc the physiologic significance of factor XII is unkown

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53
Q

what is the relationship between protein C and S?

A

APC requires protein S as a co-factor

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54
Q

what are the important, naturally occurring, deactivators of coagulation?

A

antithrombin III

protein C & S

TF pathway inhibitor

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55
Q

what is antithrombin III?

A

a serpin - inhibts serine proteases

produced by the liver

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56
Q

what activates antithrombin III?

A

endothelium - endothelium makes heparan sulfate molecules that activate antithrombin

*basis for role of heparin drug therapy

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57
Q

antithrombin III deficiency

A

hypercoagulable state

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58
Q

what are the serine proteases?

A

factors II, VII, IX, X, XI, XII

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59
Q

What are proteins C and S?

A

glycoproteins synthesized in the liver

protein C: zymogen

active = APC (activated protein C)

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60
Q

what does APC do?

A

inactivates factors Va and VIIIa

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61
Q

what activates protein C?

A

thrombomodulin

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62
Q

what is thrombomodulin?

A

cell membrane protein found on endothelial cells

binds thrombin => complex activates protein C

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64
Q

what is protein S?

A

co-factor for APC to inactivate factors Va and VIIIa

circulates in active form so it can bind APC

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65
Q

how does protein C do its job?

A

thrombomodulin:thrombin complex activates protein C (APC)

when endothelium is healthy, it produces a lot of thrombomodulin which binds thrombin to activate protein C

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66
Q

what are steps for protein C to inactivate factors Va and VIIIa?

A

thrombomodulin binds thrombin

complex activates protein C (APC)

circulating Protein S binds APC

inactivation

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67
Q

what is the tissue factor pathway inhibitor?

A

TFPI

inactivates Xa

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68
Q

what are the 2 domains of fibrinogen and how are the involved in crosslinking fibrin?

A

E - central

D - side

factor XIII crosslinks fibrin and creates E linked to 2 D’s

plasmin breaks down fibrin into FDP’s and D-dimers

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69
Q

how does TFPI inactivate Xa?

A
  1. directly binds Xa —> deactivated
  2. binds TF/VIIa complex —> prevents X activation
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70
Q

what drug causes levels of TFPI to increase?

A

heparin - may contribute to antithrombic effect

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71
Q

once the clot is formed, what breaks it down?

A

plasminogen and plasmin

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72
Q

what is plasminogen

A

zymogen synthesized by liver

active form = plasmin

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73
Q

what does plasmin do?

A

breakdown fibrin (main job)

broad substrate specificity

also degreades clotting factors and fibrinogen

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74
Q

what are the naturally occurring plasminogen activators?

A

tPA and urokinase

streptokinase

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75
Q

what do tPA and urokinase do?

A

synthesized by endothelial ells, actiivate plasminogen to plasmin and clean up any fibrin that formed inside blood vessels

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76
Q

what plasminogen activtors can be used in the treatment of acute MI and stroke?

A

tPA

urokinase

streptokinase

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77
Q

streptokinase

A

streptococcal protein activates plaminogen

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78
Q

what are the breakdown products of fibrin?

A

FDPs and D-dimers

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80
Q

what are D-dimers?

A

special type of FDP

presence indicates clot breakdown

81
Q

what Dx can an elevated D-dimer indicate?

A

DVT/PE

82
Q

what is the only way to get D-dimers?

A

breakdown of CROSSLINKED fibrin from factor XIII

83
Q

What do FDPs indicate?

A

plasmin activity

plasmin can directly convert fibrin into FDPs without clot formation

84
Q

what is plasmin fibrinolysis?

A

overactive plasmin

increased FDPs; normal D-dimer****

85
Q

what happens to result in plasmin fibrinolysis?

A

aka hyperfibrinolysis

plasmin breakdown of fibrinogen - not fibrin - forms FDPs

plasmin can deplete clotting factors

86
Q

why are D-dimers normal (0) in primary fibrinolysis?

A

no clot or crosslinked fibrin = no D-dimers

87
Q

what will PT/PTT show in primary fibrinolysis?

A

increased with bleeding

similar to DIC

88
Q

why is prostate cancer a risk factor for primary fibrinolysis?

A

cancer cells release urokinase

89
Q

how can cirrhosis lead to primary fibrinolysis?

A

loss of α-2 antiplasmin from liver causing overactive plasmin

90
Q

FDPs & D-dimers key points

A

clot breakdown - increased FDPs & D-dimers

hyperfibrinolysis - increased FDPs w/ normal D-dimer

increased D-dimer used to Dx thrombotic disorders

elevated levels of D-dimer seen in DVT/PE - sensitive, not specific

91
Q

what are the vitamin K dependent clotting factors?

A

II

VII

IX

X

protein C

protein S

92
Q

vitamin K deficiency

A

bleeding

93
Q

what drug is a vitamin K antagonist?

A

warfarin

94
Q

what is ESR?

A

erythrocyte sedimentation rate

the rate of RBC sedimentation in test tube

increased in inflammatory conditions

95
Q

what is normal ESR?

A

men = 0-22 mm/hr

women = 0-29 mm/hr

96
Q

why is ESR increased in inflammatory conditions?

A

during inflammation, protein levels in the plasma increase –> the proteins are sticky and cause the RBCs to clump together

the clumps will settle faster

97
Q

acute phase reactants

A

serum proteins tht rise in inflammation or tissue injury

driven by cytokines

synthesized in liver

98
Q

what are the proteins in plasma that cause ESR to increase in inflammatory conditions?

A

acute phase reactants:

fibrinogen

ferritin

CRP

99
Q

what does CRP do?

A

binds bacteria and activates complement

100
Q

where do platelets come from? how long do they live?

A

megakaryocytes

8-10 days

101
Q

what regulates platelet production?

A

thrombopoietin (TPO)

102
Q

what is thrombopoietin?

A

glycoprotein produced mainly in the liver

103
Q

what do platelets do?

A

aid in hemostasis after vascular injury

activated platelets seal damaged vessels

104
Q

platelets circulate in their inactive form, what activates them?

A

endothelial injury

stimuli from other activted platelets

105
Q

describe the steps in making a platelet plug

A
  1. adhesion to sub-endothelium
  2. aggregation - platelet-platelet binding
  3. secretion - release of granule contents
106
Q

what is Von Willebrand factor?

A
  • a large glycoprotein that is synthesized by endotheial cells and megakaryocytes
  • present in platelets
  • some found in plasma
  • released on vascular injury
107
Q

where is vWF stored?

A

Weibel-Palade bodies in endothelial cells

alpha granules in platelets

108
Q

when is vWF released?

A

on vascular injury activated platelets degranulate and endothelial cells release vWF

109
Q

what are Weibel-Palade bodies?

A

where platelets are stored in endothelial cells

releases vWF and P-selectin

110
Q

what are the 3 main roles of vWF?

A
  1. carrier protein for factor VIII
  2. binds platelets to damaged endothelium
  3. binds activated platelets together (aggregation)
111
Q

when is factor VIII released?

A

in the presence of thrombin (VIIIa)

112
Q

what are membrane glycoproteins?

A

amino acid and glucose molecules

on the surface of platelets

interact with other structures/molecules

113
Q

what are the membrane glycoproteins important for hemostasis?

A

GPIb, GPIIb/IIIa

114
Q

what happens during platelet adhesion?

A

vascular damage = exposure to sub-endothelial collagen –> binds vWF

once vWF is bound to the sub-endothelial collagen, it can then bind the GPIb R on patelets

115
Q

what happens during platelet aggregation?

A

GPIIb/IIIa changes confromation when platelets are activated

116
Q

what is the most abundant surface R on platelets?

A

GPIIb/IIIa

117
Q

what is inside out signaling?

A

refers to the process of platelet aggregation where cell activity (platelet activation) leads to an altered R

GPIIb/IIIa R will not bind unless platelets are activated

usually the R is altered then some cell activity is triggered

118
Q

what can activated GPIIb/IIIa R bind to?

A

fibrinogen or vWF

119
Q

what happens after GPIIb/IIIa is activated?

A

binds fibrinogen or vWF which allows for platelet aggregation

120
Q

how do platelets aggregate?

A

uses fibrinogen or vWF as a link between platelets, connects platelets together by their GPIIb/IIIa R’s

121
Q

what are the 2 ways platelets can be activated?

A

binding to subendothelial collagen

stimulation by activating substances released from other platelets

122
Q

what happens during platelet secretion?

A

when one platelet is activated it will release its stored contents which can then go and activate other platelets

this is how the activation of 1 platelet can lead to the activation of many others

123
Q

what are the platelet granules?

A

alpha granules (most abundant)

&

dense granules

124
Q

what are contained in alpha granules?

A

fibrinogen

vWF

platelet factor 4

125
Q

what are the contents of dense granules?

A

ADP

Calcium

Serotonin

126
Q

what is platelet factor 4?

A

PF4

released from alpha granules, binds to endothelial cells

127
Q

what is the role of PF4 in heparin induced thrombocytopenia?

A

antibodies formed to PF4 complexed with heparin

antibodies bind PF4-heparin –> platelet activation

=> diffuse thrombosis

=> low platelets from consumption

life threatening S/E of heparin

128
Q

what is the role of serotonin in platelet activation?

A

stored in dense granules, released on platelet activation

basis for serotonin release assay

129
Q

what is the serotoning release assay?

A

screening test for HIT

donor patelets radiolabeled with radioactive serotonin

patient serum (person screening for HIT) and heparin added

if HIT antibodies are present, excessive serotonin will be released from the donor platelets

130
Q

what is the role of ADP in platelet activation?

A

stored in dense granules

released by RBCs when damaged

binds to 2 GPCR’s - P2Y1 & P2Y12

131
Q

when ADP binds to P2Y1 or P2Y12 what happens?

A

decreased cAMP inside of platelets leading to platelet activation

132
Q

what class of anti-platelet drugs increase cAMP?

A

phosphodiesterase inhibitors

133
Q

how do phosphodiesterase inhibitors work?

A

increase in cAMP inside of platelets blocks activation

134
Q

ADP binds P2Y1

A

calcium is released

change in platelet shape

135
Q

ADP binds P2Y12

A

platelet degranulation => increased aggregation

136
Q

what do P2Y12 receptor blocking drugs do?

what are they?

A

“ADP R blockers”

inhibit platelet activity

clopidogrel

prasugrel

ticlopidine

ticagrelor

137
Q

what is TXA2?

A

thromboxane A2

powerful platelet activator

TXA2 R found on platelets

basis for aspirin therapy

138
Q

what is TXA2 derived from?

A

lipids in cell membranes

139
Q

what does aspirin block?

A

TXA2 formation

140
Q

what does phospholipase A2 do?

A

enzyme that takes lipids from the cell membrane and converts them into arachadonic acid

141
Q

what is an INR?

A

international normalized ratio

142
Q

where is arachadonic acid released?

A

sites of vascular injury

also stored in platelets

143
Q

aracadonic acid —> TXA2

A

converted by platelets with the enzyme cyclooxygenase (COX)

TXA2 is then released by platelets to activate more platelets

144
Q

MOA of aspirin?

A

inhibits COX –> decreased TXA2 –> platelet activation

145
Q

what is bleeding time? how is it performed?

A

test of platelet function

small cut to patients arm –> filter paper applied/removed until bleeding stops –> record time

rarely done in modern era

146
Q

prolonged bleeding time

A

platelet function problem

147
Q

what are coagulopathies?

A

bleeding disorder within the clotting cascade

148
Q

what bleeding disorders have an abnormality of the coagulation cascade?

A

hemophilia

vitamin K deficiency

149
Q

how are bleeding disorders classified?

A

abnormal coagulatin cascase

abnormal platelets

mixed disorers

150
Q

what bleeding disorders have abnormal platelets?

A

Bernard-Soulier

Glanzmann’s thrombasthenia

ITP; TTP

uremia

151
Q

what bleeding disorders are mixed?

A

Von Willebrand disease

DIC

liver disease

152
Q

normal PT

A

~10s

154
Q

what is thrombin time?

A

add thrombin to samlpe and record time to form clot

the only way this test will be abnormal is if there is a thrombin inhibitor in the plasma or if the patient has a very low fibrinogen level

155
Q

how do abnormal platelet disorders present?

A

bleeding is very superficial - mucosal, skin, petechiae

156
Q

how do abnormal coagulation factor disorders present?

A

joint bleeding

deep tissue bleeding

157
Q

what is the inheritance of hemophilia?

A

X-linked recessive –> occur more in males

158
Q

what causes hemophilia?

A

gene mutations that often run in families, can occur de novo so no FHx of hemophilia does not r/o

159
Q

what are the 2 typs of hemophilia?

A

A = deficiency of factor VIII

“hemophilia eight”

B = deficiency of factoe IX

160
Q

what is christmas disease?

A

hemophilia B

deficiency of factor IX

161
Q

patient presents with spontaneous or easy bruising, recurrent joint bleeds, prolonged PTT, all other bleeding tests were normal.

A

hemophilia

162
Q

how can you screen for hemophilia?

A

PTT will be prolonged

factor VIII & IX are both part of intrinsic pathway

163
Q

what is the main treatment for hemophilia?

A

replacement factor VIII or IX

164
Q

what is Desmopressin?

A

dDAVP

analog of ADH with no pressor activity (no increase in BP)

increases vWF and factor VIII

used in mild hemophilia A

165
Q

what triggers the release of factor VIII and vWF from Weibel-Palade bodies?

A

desmopressin

166
Q

what is a key s/e of desmopressin?

A

flushing, headache from vasodilation

167
Q

what else can desmopressin be used for?

A

von Willebrand disease

Central DI (mimics ADH)

bedwetting - decreaseses urine volume

168
Q

aminocaproic acid

A

antifibrinolytic drug

plasminogen can’t be activated to plasmin

less breakdown of formed clots - allows for whatever factor VIII or IX is available in the patients plasma to work more effectively because plasmin is not breaking down whatever fibrin clots can be formed

169
Q

what is cryoprecipitate?

A

obsolete therapy for hemophilia A before factor VIII was readily available

precipitate that forms when FFP is thawed

separated from plasma by centrifugation

170
Q

what clotting factors does cryoprecipitate contain?

A

factor VIII, fibrinogen (mostly)

also factor XIII and vWF

171
Q

cryoprecipitate is often used as a source of what in the event of DIC, or massive trauma with blood transfusions?

A

fibrinogen

172
Q

what are coagulation factor inhibitors?

A

antibodies directed against a clotting factor

either inhibit activity or increase clearance of clotting factor

inhibitors of factor VIII most common

173
Q

coagulation factor inhibitors often occur in association with what?

A

malignancy

post-partum

autoimmune disorders

174
Q

how can coagulation factor inhibitors be treated?

A

prednisone

175
Q

how can you tell the difference between hemophilia A and coagulation factor inhibitors?

A

mixing study

patients serum is mixed with normal serum to see if the PT and PTT normalize

if prolonged PTT, then it is a coagulation factor inhibitor

176
Q

what does vitamin K deficiency result in?

A

bleeding

177
Q

what are the vitamin K dependent factors?

A

II, VII, IX, X

178
Q

key lab findings of vitamin K deficiency

A

elevated PT/INR

can see elevated PTT

normal bleeding time

179
Q

why is PT/INR the most sensitive test for vitamin K deficiency?

A

all the vitamin K dependent factors are part of both extrinsic and extrinsic pathways, but factor VII has the shortest half life, so the factor VII level will be the first to fall when a patient becomes vitamin K deficient, making the extrinsic pathway much more sensitive to vitamin K deficiency

180
Q

vitamin K deficiency causes

A

dietary deficiency is rare bc GI bacteria produce sufficient quantities

warfarin (antagonizes vit. k)

antibiotics (deplete GI bacteria)

newborns (sterile GI tract)

malabsorption (vit. K is fat sol.)

181
Q

how can blood transfusions cause a coagulopathy?

A

large volume of transfusions –> dilution of clotting factors

packed RBCs are used for blood transfusions which are devoid of plasma/platelets

administered saline or IVF with packed RBCs - no clotting factors

treated with FFP

182
Q

how does liver disease result in a coagulopathy?

A
  1. loss of clotting factors:
    * advanced liver disease decreases clotting factor synthesis – except for factor VIII because it is produced in endothelial cells
  2. thrombocytopenia
  • decreased hepatic synthesis of thrombopoietin
  • platelet sequestration in spleen from portal HTN
183
Q

what bleeding test is more sensitive to liver disease?

A

PT (vitamin K)

*med3* (21 decks)

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