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IHO Week 6 > General Principles of Hemostasis > Flashcards

General Principles of Hemostasis Flashcards

1
Q

What two things is hemostasis a balancing act between?

A
  1. Pro-clotting - plugs up holes in blood vessels

2. Anti-clotting - keeps clotting under control

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2
Q

What is the very basic order of clotting?

A

(1) Vascular constriction = vessels
(2) Platelets come together for a plug = platelets [Primary hemostasis]
(3) Make fibrin = clot/cascade [Seconday hemostasis]

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3
Q

What happens in the first stage of clotting?

A

Blood vessel constricts

  • Blood loss decreases
  • Platelets and factors meet
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4
Q

What happens in the second stage of clotting?

A 
[Primary hemostasis]
Platelets form a plug
-Proteins are exposed
-Platelets adhese
-Granules release contents
-Platelets aggregate
-Phospholipids are exposed
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5
Q

What happens in the third stage of clotting?

A 
[Secondary hemostasis] 
Fibrin seals up plug
-Tissue factor is exposed
-Cascade makes fibrin
-Fibrin solidifies plug
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6
Q

What are the two stages of anti-clotting?

A
  1. Cascade inhibition

2. Clot lysis

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7
Q

What happens during cascade inhibition?

A

Three things inhibit the clotting cascade:

  • TFPI
  • ATIII
  • Proteins C, S
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8
Q

What happens during clot lysis?

A

This is the remodeling of the clot

  • t-PA is used
  • Plasmin is used
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9
Q

What does the coagulation cascade NEED to run?

A

Calcium!

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10
Q

What granules are present in the platelet? (EXAM!!)

A
  • Alpha (fibrinogen, vWF)

- Delta (serotonin, ADP, Ca2+)

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11
Q

What factors are in the membrane of platelets? (EXAM!!)

A
  • Phospholipids (activate coag. factors)
  • GP Ia (binds collagen)
  • GP Ib (binds vWF)
  • GP IIb-IIIa (binds fibrinogen)
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12
Q

What are the two branches of the coagulation cascade?

A
  1. Intrinsic

2. Extrinsic

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13
Q

What is the intrinsic pathway?

A

Less simple, more complex

-Everything you need to get this pathway to run is already in the bloodstream and can be initiated in the lab

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14
Q

What is the extrinsic pathway?

A

Very simple, clean

-You need to add an extrinsic factor to get this pathway to run in the lab

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15
Q

What happens in the extrinsic pathway leading up to the final common pathway (X)?

A

Exposed TF combines with VII and makes TF VIIa.

Then TF VIIa promotes X —> Xa

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16
Q

What happens in the intrinsic pathway leading up to the final common pathway (X)?

A
  1. Factor XII becomes activated to XIIa.
  2. Factor XIIa and thrombin convert XI to XIa.
  3. Factor XIa helps convert IX to IXa.
  4. VIII becomes VIIIa (bam!) which combines with IXa to initiate the change from X —-> Xa. [final common pathway]
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17
Q

What is the final common pathway?

A
  1. Either VIIIa & IXa or TF VIIa promote Factor X —> Factor Xa
  2. Then Factor V becomes Va (bam!) which combines with Xa.
  3. Factor Va and Xa promote the conversion of Prothrombin to thrombin
  4. Thrombin promotes the conversion from fibrinogen to fibrin.
  5. Fibrin becomes a CLOT!
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18
Q

Where does tissue factor (TF) come from?

A
  • Still kind of mysterious where it comes from
  • “Hidden” cells exposed during injury
  • Microparticles floating in blood
  • Endothelial cells and monocytes (during inflammation)
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19
Q

What does tPA do and what is it used for?

A
  • Used for Stroke (type caused by clot only)

- Promotes the creation of plasmin from plasminogen, then the plasmin breaks up the clot!

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20
Q

What does plasmin do?

A

It busts up clots and forms FDPs

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21
Q

What is probably the reason Factor VII becomes TF Factor VIIa?

A

Thrombin production

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22
Q

What happens as soon as you make a little Factor Xa from the Extrinsic arm?

A

The extrinsic arm is turned off by Factor Xa

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23
Q

What does a little bit of pre-made thrombin do?

A

It can kick off the intrinsic or the extrinsic sides of the clotting cascade.

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24
Q

What are the two “cofactors”? Why are they called that?

A

VIIIa
Va
-They aren’t considered factors bc they aren’t exactly in the process, BUT they make the process run much more ‘robustly’
-Ex: Factor VIIIa binds to IXa and this accelerates the process!

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25
Q

What are FDPs?

A

Fibrin Degradation Products - busted up clots

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26
Q

How does tPA fit into the anti-clotting mechanism?

A

t-PA helps convert plasminogen into plasmin. Then plasmin acts on the clot to break it up into FDPs.

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27
Q

What three things can stop the clotting cascade?

A
  1. Protein C - acts on protein cofactors VIIIa, Va
  2. ATIII (antithrombin III- potentiated by Heparin) - Inhibits actions of Xa, XIa, TF VIIa and thrombin
  3. TFPI - inhibits TF VIIa
28
Q

Platelet Count Lab Test

A
  • Done by particle counter

- Normal: 150-450 x 10^9/L (don’t memorize)

29
Q

Platelet Morphology Test

A

Look at: Size, Granulation

30
Q

What two parts do normal platelets have?

A

Granulomere (where granules hang out) & Hyalomere (homogenous, no granules)

31
Q

What can odd platelets be?

A

Hypogranular and Agranular. A few can also be Large, even bigger than the size of a RBC but this is pretty rare.

32
Q

What is template bleeding time?

A

Two incisions are made in the wrist of a person with a blood pressure cuff on and the time required for clotting to occur is recorded.
-Done frequently

33
Q

Why do we use the Template Bleeding Time test?

A
  • Evaluate platelet response to vascular injury

- Some platelet disorders have a long bleeding time

34
Q

How does the Template Bleeding Time test work?

A
  • Inflate the blood pressure cuff
  • Make incision in arm
  • See how much time it takes to stop bleeding
35
Q

Why do you have to be careful with Template Bleeding Time?

A
  • Lots of factors affect the test

- Due to this, some consider the test unreliable

36
Q

What is Closure Time (CT?

A
  • An alternative to bleeding time
  • More reliable
  • Platelet function analyzer-100 (PFA-100) measures how quickly platelets occlude small holes in a membrane. Sometimes this is called the “in-vitro bleeding time”
37
Q

What is Closure Time (CT) better at detecting than Template Bleeding Time (TBT)?

A

-Detecting aspirin-related bledding and von Willebrand’s disease

38
Q

Why do we use the platelet aggregation test?

A
  • To find platelet function abnormalities

- Not done frequently

39
Q

How is the platelet aggregation test done?

A
  • Add aggregating agents to patient’s sample
  • See if platelets aggregate
  • Measure decrease in sample turbidity (its a trace)
  • You look at the pattern of patients platelet reactions and this can tell you what molecule, enzyme, etc. they’re missing
40
Q

Why do you need to be careful with the platelet aggregation test?

A

-Always repeat an abnormal test

41
Q

How do coagulation lab tests work?

A
  1. Draw blood into citrate tube
  2. Spin tube, decant plasma
  3. Add reagents to plasma
  4. Watch for formation of fibrin
42
Q

What two tests are VERY important?

A

PT and PTT

43
Q

What is PT?

A

Prothrombin time

  • Add plasma to thromboplastin
  • This test measure the extrinsic pathway [want to know how fast you make fibrin]
44
Q

What is important to know about Factor VII?

A
  • Made by liver
  • Needs K
  • Dec. by Coumadin
  • Short half-life
45
Q

What things could cause PT to be increased?

A
  • Dec. VII, X, V, II, I
  • Coumadin
  • Heparin - works with Antithrombin III
  • DIC - disseminated intervascular coagulation
46
Q

When should you order a PT?

A

NEVER

-Order an INR instead

47
Q

What is an INR?

A

A corrected PT.

48
Q

When should you order an INR?

A
  • To assess liver function (maybe?)
  • To monitor coumadin thearpy
  • To diagnose DIC = disseminated intravascular coagulation
  • To assess pre-op status
49
Q

How do you do a Partial Thromboplastin Time (PTT)?

A
  1. Add Plasma + Phospholipid
    - Measures intrinsic pathway
    - APTT = same thing
50
Q

When can PTT be increased?

A
  • Hemophilia A
  • Hemophilia B
  • DIC
  • Heparin
  • Inhibitors
51
Q

When should you order a PTT?

A
  • To investigate a history of abnormal bleeding
  • To monitor heparin therapy
  • To diagnose an antiphospholipid antibody
  • To assess pre-op status
52
Q

What is the Thrombin Time (TT) test?

A
  • Add plasma to thrombin (and see how long it takes to clot/if it clots)
  • Measures conversion of fibrinogen to fibrin
  • Bypasses intrinsic and extrinsic pathways [Just measures Final Common Pathway]
53
Q

When is Thrombin Time (TT) increased?

A
  • Dec. fibrinogen

- Inc. FDPs

54
Q

When should you order a Thrombin Time?

A

When the PTT is prolonged and you want to rule out a fibrinogen problem (rare!)

55
Q

What happens in a PTT Mixing Study?

A
  • Pooled plasma (mixed/normal plasma from large population) + patient plasma + phospholipid
  • If PTT corrects: something missing
  • If PTT doesn’t correct: inhibitor (PTT still prolonged indicates that an inhibitor is present)
56
Q

When should you order a PTT mixing study?

A
  • When PTT is prolonged, but TT is normal
  • If PTT corrects = factor deficiency
  • If PTT doesn’t correct = inhibitor present
57
Q

What is the Fibrin Degradation Product Assay?

A
  • Measures FDPs (including D-dimers)

- VERY sensitive!

58
Q

What do you still need after thrombin turns fibrinogen into fibrin?

A

Factor XIII!! (need this or you will have bad bleeding problems) It cross-links fibrin.

59
Q

What does the D-dimer test do?

A

Measures the cross-linked fibrin present!

60
Q

What does plasmin do?

A
  1. Degrades fibrinogen into FDPs

2. Degrades cross-linked fibrin into D-dimers

61
Q

When are FDPs increased?

A
  • Thrombi

- Minor clotting

62
Q

When should you order an FDP assay? (EXAM!!)

A
  • NOT to RULE IN a clot

- but to RULE OUT a clot

63
Q

What does a fibrinogen assay do?

A

Measures fibrinogen

64
Q

What does decreased fibrinogen indicate?

A
  • DIC

- Massive bleed

65
Q

When should you order fibrinogen level?

A
  • To diagnose DIC (bc this uses up all of your coagulation factors)
  • To follow patients with massive bleed

IHO Week 6 (16 decks)

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