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Medical Physiology > Exam #2: Hemostasis > Flashcards

Exam #2: Hemostasis Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the 5 different components of the hemostasis system? What are their main functions?

A

1) Vascular= constriction that reduces blood flow to prevent blood loss & slows platelets for better adherence
2) Platelet= form platelet plugs to prevent blood loss & secrete vasoconstrictors
3) Coagulation= forms fibrin clots & further activates platelets
4) Anti-coagulation= reduce coagulation
5) Fibrinolytic= dissolves unnecessary clots

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2
Q

What can a deficiency in any of the 5 systems cause?

A

Hemorrhaging (Hemophilia)

Clotting (Thrombosis)

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3
Q

What responds first when there has been tissue damage?

A

Vascular System

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4
Q

Outline the vascular response to tissue damage.

A

1) Damaged tissue secretes factors that cause vasoconstriction
2) Platelets become activated
3) Activated platelets secrete Thromboxane A2 & Serotonin, leading to further vasoconstriction

Vasoconstriction prevents blood loss & slows flow to give platelets a better chance of adhering.

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5
Q

How does the vascular response to tissue damage interact with the coagulation system?

A
  • The coagulation system is also activated in response to tissue damage, and produce thrombin.
  • Thrombin induces vascular endothelial cells to secrete Endothelin-1, which produces further vasoconstriction.
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6
Q

Outline the platelet system response to tissue damage.

A

1) Tissue damage exposes collagen & vFW in the subendothelial matrix
2) Platelet GP1ba binds vFW, leading to platelet tethering at the site of injury
3) Platelet GPVI binds collagen, strengthening adhesion & activating platelets
4) Active platelets develop finger-like projections & secrete: ADP, Thromboxane A2 & 5-HT
5) These factors bind G-protein coupled receptors on already adherent platelets

Binding to GPCRs results in three things:

  • Further activation of adherent platelets
  • Further vasoconstriction
  • And, a conformational change in GP IIb/IIIa, which binds fibrinogen in plasma
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7
Q

What happens is von Willebrand’s disease?

A

Decreased amount of vFW prevents the proper formation of a platelet plug

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8
Q

What is the function of fibrinogen?

A

Fibrinogen acts as molecular “glue” between activated GPIIb/IIIa platelets, forming the platelet plug

*Note that the platelet plug is not very strong; the coagulation system is needed to form a secure fibrin clot

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9
Q

What are the factors released by platelets? What is their function?

A

Platelets release three groups of chemical mediators:

1) Chemokines
2) Dense granules (ADP & 5-HT)
3) Alpha granules, which includes Factor V

Factor V links the platelet system to the coagulation cascade

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10
Q

What is the difference between GPIba, GPVI, GPIIb/IIIa

A
  • GPIba binds vFW to mediate platelet tethering
  • GPVI binds collagen for strong platelet adhesion & activation
  • GPIIb/IIIa binds fibrinogen, forming the platelet plug
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11
Q

What is the P2Y12 receptor? What drug antagonises this receptor?

A

Is the receptor for ADP on platelets, which leads to platelet activation

*Plavix is a P2Y12 antagonist

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12
Q

What are PARs? Why are PARs important?

A

PAR stands for “Protease activated receptors,” which are GPCRs on the surface of platelets that are activated by thrombin

*Activation of PARs leads to further platelet activation & is important because this links the platelet & coagulation systems

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13
Q

What is the Thromboxane A2 receptor?

A

A platelet receptor

Thromboxane A2 works in an autocrine fashion, increasing platelet activation; it also is a vasoconstrictor

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14
Q

What are Collagen, vWF, and fibrinogen ligands for?

A 
Collagen= GPVI 
vFW= GPIba 
Fibrinogen= GPIIb/IIIa
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15
Q

What are Thromboxane A2, ADP, & thrombin ligands for?

A

TXA2R
P2Y12R (plavix antagonist)
PARs

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16
Q

What mechansisms prevent unnecessary platelet adhesion & activation in nearby uninjured endothelium?

A

Healthy vasculature has anti-platelet adhesion properties

- Vascular endothelial cells release NO & prostacylin 2, both of which induce vasodilaiton

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17
Q

How does the Blood coagulation system differ from the platelet coagulation system?

A

Coagulation system forms Fibrin clots, which are much more secure than platelet plugs

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18
Q

How is fibrin made?

A
  • Thrombin is a protease cleaves fibrinogen into fibrin monomers (fibrinogen is synthesized in the liver)
  • Fibrin monomers spontaneously form fibrin fibers
  • Thrombin also activates Factor XIII, which induces fibrin cross-linking (forming a stable & strong clot)
19
Q

What are the three general steps of the coagulation cascade? What is the ultimate goal of the coagulation cascade?

A

1) Formation of the Prothrombin Activator Complex, which converts prothrombin to thrombin
2) Thrombin conversion of fibrinogen to fibrin
3) Factor XIII production to cross-link fibrin

Ultimate goal: Make fibrin & Factor XIII

*Note that prothrombin is continuously synthesized by the liver

20
Q

What is Factor I called?

A

Fibrinogen

21
Q

What is Factor II?

A

Prothrombin

22
Q

What is Factor III?

A

Tissue factor

23
Q

What is factor IV?

A

Ca++

24
Q

Outline the intrinsic pathway. When is the intrinsic pathways activated?

A
  • Initiated when Factor XII binds to exposed collagen at the site of injury & is activated.
  • Consequently, Factors XI & IX are activated
  • Factor IXa slowly activates Factor X, which cleaves prothrombin to thrombin
  • Thrombin feeds back to form Factor VIIIa, which forms the “Tenase Complex” with factor IXa, and by activating Factor V or the Prothrombin Activator Complex–BOTH of these SIGNIFICANTLY accelerate activation thrombin

XII, XI, IX, VIII

25
Q

Outline the extrinsic pathway. When is the extrinsic pathways activated?

A
  • Sub-endothelial tissue constitutively expresses Tissue Factor (Factor III)
  • Tissue damage exposes Factor III to Factor VII, forming Factor VIIa
  • Tissue Factor (Factor III), Factor VIIa, & Ca++ form a complex that activates Factor X
26
Q

Where do the intrinsic & extrinsic pathways converge?

A

Factor Xa

27
Q

What is the tenase complex?

A

Factor VIIIa
Factor IXa
Ca++
Platelet phospholipids

These significantly increase the formation of Factor Xa, which then cleaves prothrombin to thrombin

28
Q

What deficiency causes Hemophilia A?

A

Factor VIIIa reduction

29
Q

Outline the common pathway.

A
  • Factors Xa & Va cleave Prothrombin to Thrombin
  • Thrombin cleaves fibrinogen to fibrin
  • Thrombin also activates XIIIa, which stabilizes the Fibrin clot
30
Q

What are the four coagulation factors that require Vitamin K?

A

X
IX
VII
II

Remember “Vitamin K was born in 1972 (1 is a 10)”

31
Q

What is the function of Vitamin K?

A

Reduced vitamin K is a cofactor in the carboxylation of key glutamate residues in coagulation factors, which allows Ca++ to bind & activate the factor

32
Q

What is the mechanism of action of Warfarin?

A

Warfarin blocks the reduction of Vitamin K

33
Q

How is coagulation time measured? What is the difference between an aPTT & PT?

A

1) aPTT= activated partial thromboplastin time, which measures the speed of the intrinsic pathway
2) PT= Prothrombin time, which is a measure of the extrinsic pathway

34
Q

What is the function of the anticoagulation system?

A

Reduction of coagulation system activity to prevent it from running out of control

35
Q

What are the two mechanisms of the anticoagulation system?

A

1) Prevention of thrombin-mediated fibrin clot formation, by inhibiting coagulation factors
2) Destruction of formed thrombin

36
Q

Outline the pathway of the reduction in thrombin production.

A
  • Thrombin can decrease further production of itself by interacting with Thrombomodulin
  • Thrombomodulin is an integral membrane protein of endothelial cells
  • Thrombomodulin can bind thrombin & protein C (blood plasma protein) to form APC (activated protein C)
  • APC interaction with a cofactor, protein S, to form a serine protease that degrades Factors VIIIa & Factor Va
37
Q

What is Factor V Leiden thrombophilia?

A

A mutation in Factor V prevents it from being inactivated & leads to a hypercoagulable state

38
Q

What is the consequence of a deficiency in protein C?

A

Hypercoaguable state

39
Q

Outline that mechanism by which activated thrombin is destroyed.

A

Tissue Factor Pathway Inhibitor (TFPI) is secreted by the vasculature
- TFPI reduces thrombin formation by inhibiting the Factor VIIa/Tissue factor complex

Antithrombin is a circulating plasma protease produced by the liver; it inhibits thrombin production & destroys thrombin already produced

40
Q

What is the role of Heparin sulfate in anticoagulation?

A

Heparin sulfate binds to antithrombin & speeds thrombin proteolysis (x1000)

*Note that Heparin has NO DIRECT ANTICOAGULATION effect

41
Q

How do platelets interact with Heparin?

A

Activated platelets negatively regulate the anticoagulation system by heparin neutralizing factor

42
Q

What is the function of the fibrinolytic system?

A

Degradation of fibrin clots after an injury has healed

Degradation of fibrin clots that form at inappropriate sites

43
Q

Outline the Fibrinolyitc system.

A
  • Plasmin is created by the cleavage of plasminogen by tPA (Tissue Activating Factor)
  • Plasmin is a serine proteases the cleaves fibrin; thus, degrading clots

Medical Physiology (74 decks)

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