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Heme/Derm/MSK 1 > Hemostasis > Flashcards

Hemostasis Flashcards

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1
Q

3 parts of plateletfxn

A

(1) adherence- to exposed subendothelium (via vWF)
(2) activation- shape change and release of granule contents
(3) aggregation- recruitment of additional platelets

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2
Q

What is the most immediate response to vessel injury?

A

Vasoconstriction

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3
Q

What is primary hemostasis?

A

Platelet fxn including adherence, activation, and aggregation

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4
Q

What is secondary hemostasis?

A

Activation of coagulation (via tissue factor) and generation of thrombin (factor IIa)

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5
Q

Coagulation

(a) What initiates it
(b) What is the ultimate end product?
(c) What is this end product’s fxn?

A

Coagulation

(a) Initiated by tissue factor = membrane protein (not an enzyme)
(b) Ultimately terminates in thrombin (factor IIa)
(c) Thrombin converts fibrinogen into fibrin- the strand-like protein that provides tensile strength to a clot

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6
Q

What two factors does tissue factor directly activate?

A

Factor IX and factor X

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7
Q

What is the role of factor XIII?

A

Factor XIII is activated by thrombin to form covalent bridges btwn fibrin molecules

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8
Q

Where are coagulation factors produced?

A

In the liver

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9
Q

What is the function of factor VIII?

A

= cofactor for factor IXa

  • In response to injury factor VIII is activated and separates from vWF
  • active factor VIII (VIIIa) can then interaction w/ factor IX to set off additional reactions that end in formation of a blood clot
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10
Q

What is the function of factor V?

A

= Cofactor for Xa

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11
Q

What is the function of factor XI?

(a) What activates factor XI?

A

Factor XI activates the clotting cascade via an accessory pathway that is important in injury states

(a) Thrombin (factor IIa) activates factor XI

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12
Q

Describe the mechanism by which fibrinogen –> fibrin?

A

Cleavage of fibrinogen allows for assembly of fibrin

  • Thrombin (IIa) removes four fibrinopeptides to produce fibrin
  • then fibrin can polymerize end to end and side to side
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13
Q

What are protein C and protein S?

(a) What activates protein C?

A

Protein C and protein S are anticoagulation factors that together make a complex to inhibit factor VIII and V (cofactors that normally accelerate coagulation)

  • PS = cofactor to increased PC activity
    (a) Protein C is activates by thrombin (IIa)
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14
Q

What is thrombomodulin?

A

Thrombomodulin (TM) enhances the activation of protein C by IIa (thrombin)

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15
Q

What is the fxn of antithrombin?

A

Antithrombin = potent inhibitor of the coagulation cascade

-inhibits thrombin (IIa) and factor Xa

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16
Q

Action of TFPI

A

TFPI = tissue factor pathway inhibitor = natural coagulation inhibitor

-binds to Xa, then binds to and inhibits TF/factor VIIa complex and Xa

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17
Q

Mechanism of action for heparin

A

Heparin binds to AT (antithrombin) to make it a more potent inhibitor of Va and IIa (thrombin)

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18
Q

Describe how tpA and the fibrinolytic system work to lyse a clot

A

tPA (tissue plasminogen activator- released by various tissues) activates plasminogen to plasmin
-then plasmin can cleave cross linked fibrin molecules

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19
Q

What is the key terminal enzyme of the fibrinolytic system?

A

Plasmin

-cleaves up fibrin clots

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20
Q

What are D-dimers?

A

D-dimers are fibrin clot degradation particles that are measurable/visible in blood after plasmin breaks down a fibrin clot

-elevated in acute thrombosis

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21
Q

When is measuring D-dimer helpful?

A

Good negative predictive value (to rule out acute thrombotic event)

Ex: rule out DVT, PE, DIC

22
Q

What is hemophilia?

(a) A vs. B
(b) Mode of inheritance
(c) How can it cause arthropathies?

A

An increased tendency to bleed

(a) Hemophilia A = deficiency in factor VIII. Hemophilia B = deficiency in factor IX
(b) X-linked
(c) Can cause recurrent bleeding, recurrent bleeding into joints can cause arthropathies and permanent damage

23
Q

Is hemophilia seen more in males or females?

A

Males b/c it’s X-linked

24
Q

About how much coagulation factor do you required to function

(a) Normally
(b) Abnormally after major surgery or trauma
(c) Abnormally after minor injury or surgery

A

Coagulation factor levels

(a) Normal is > 40% (so you don’t need anywhere near 100% to be perfectly normal)
(b) Mild hemophilia: 5-40% coagulation factor => bleeding after major post-op and post-trauma bleeding
(c) Moderate hemophilia: 1-5% => bleeding after minor injury or surgery

25
Q

What is the manifestation of a coagulation factor level

A

= severe hemophilia

Clinical manifestation = spontaneous bleeding into soft tissue and joints

26
Q

What is the treatment for hemophilia?

(a) Primary prophylaxis
(b) On demand treatment

A

Treatment = IV injections of factor VIII (type A) or IX (type B)

(a) primary prophylaxis = give continuous factor VIII/IX especially in children to prevent permanent damage to joints and muscle
(b) Most adults get on demand treatment- injections when they feel a bleed coming on

27
Q

What are some improvements to infusing pure human produced factor VIII/IX?

A
  • recombinant therapy so don’t risk any transmissions btwn donor/host
  • longer half-life products so the pts can infuse less frequently
28
Q

Factor XI deficiency

(a) mode of inheritance
(b) severity

A

Factor XI deficiency- rare but seen in Ashkenazi jews

(a) Autosomal dominant
(b) Mild disorder- factor XI not part of the main coagulation cascade, part of accessory pathway

29
Q

Describe how the PT is evaluated in lab?

A

PT = prothrombin time

(i) Draw blood into tube w/ sodium citrate (anticoagulation factor)
(ii) Add calcium to reverse the sodium citrate
(iii) Add tissue factor to activate the extrinsic coagulation pathway- time how long it takes the blood to clot after adding TG

30
Q

Reduction of what factors will prolong PT?

A

Reduction of the factors involved in the extrinsic clotting pathway: VII, X, V, and II (and fibrinogen)

31
Q

What clotting factors are not tested by PT?

A

Factors VIII, IX, XI, XIII

Therefore, to test these factors use the PTT

32
Q

What is PTT?

(a) What clotting factors does it measure the activity of?

A

PTT = partial thromboplastin time- measure how long it takes the intrinsic clotting pathway to work => evaluates more of the clotting factors than PT

(a) PTT is prolonged if any factor except factor VIII is low

33
Q

Which test: PT or PTT is used to test factor VIII?

A

Neither! Level of factor XIII doesn’t affect the PT or PTT

34
Q

Normal PT value

A

11-14 seconds

35
Q

Normal PTT value

A

30-38 seconds

36
Q

How does liver dysfunction cause a bleeding disorder?

A

All coagulation factors are made in the liver => liver dysfunction = coagulopathy

37
Q

What coagulation factors require vitamin K?

(a) Mechanism

A

Factors II, VII, IX, and X

  • also protein C and S
    (a) Vitamin K needed as a cofactor for coagulation factors so they can bind calcium and bind phospholipid membranes
38
Q

What is thrombophilia?

(a) Increased risk of MI

A

= an increased tendency to clot/thrombose

(a) Doesn’t really increase risk of stroke/MI b/c the clotting is usually venous => increases risk of DVTs/PE

39
Q

Deficiency in what three enzymes may cause inherited thrombophilia?

A

Antithrombin, protein C, or protein S deficiency

40
Q

What is factor V Leiden?

A

Mutated form (variant) of factor V that cannot be inhibited by protein C (the APC/PS complex) => increased clotting

-one of the most common inherited thrombophilias

41
Q

Mechanism of Heparin

A

Indirect acting anticoagulant

-enhances the inhibitor effect of antithrombin on thrombin

42
Q

What are two new direct anticoagulant meds?

A
  • direct thrombin inhibitor = Dabigatran

- direct Xa inhibitor = Apixaban and Rivaroxaban

43
Q

What is the INR?

(a) What is its function

A

INR = international normalized ratio

INR = (PT value of pt) / (PT normal)

(a) Way of standardizing PT values among different labs

44
Q

Normal/expected INR value for

(a) Unmediated pt
(b) Pt on warfarin/coumadin

A

Expected INR value for

(a) Unmedicated pt = 1.0
(b) Pt on warfarin/coumadin = 2-3

45
Q

Which anticoagulant medication is safe for pts w/ mechanical heart valves?

A

Warfarin

46
Q

Mechanism of warfarin

A

Warfarin inhibits enzyme used in vitamin K synthesis => inhibits the vitamin-K activation/synthesis of the Ca2+ dependent clotting factors = factors II, VII, IX, and X

47
Q

How to treat DIC

A

Treat the underlying condition

-treat the bacterial sepsis, burn etc

48
Q

Why was APC previously used to treat sepsis

(a) Why was this stopped?

A

APC (activated protein C) inhibits the coagulation cascade, but also has an anti-inflammatory effect

  • this highlights the strong link/association btwn coagulation and inflammatory pathways
    (a) APC no longer given for sepsis b/c of its anti-coagulation effects and pts w/ sepsis are at risk for bleeding
49
Q

Describe the mechanism of the following in DIC

(a) Coagulation
(b) Bleeding

A

DIC = disseminated intravascular coagulation

(a) Coagulation: blood exposed to tons of tissue factor (due to endothelial injury) which activates the coagulation cascade in vessels, causing occlusion of capillaries w/ fibrin thrombi.
- microthrombi in vascular beds

(b) Bleeding when coagulation factors are activated faster than they’re synthesized

50
Q

What is the blood marker of DIC?

A

Positive D-dimer

-D-dimer (+) due to systemic activation of the fibrinolytic system => fibrin in vessels are lysed so D-dimer levels are measurable in the blood

Heme/Derm/MSK 1 (7 decks)

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