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39 Cards in this Set
- Front
- Back
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What is the Ivy Template Bleeding time?
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poke them with a little spring-spike, and time the bleeding.
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What is the PFA-100?
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can test clotting speed on flowing blood and differentiate between ADP and epinephrine
Gives "closure time" |
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Secondary Hemostasis is...
Where are the co-ag proteins made, primarily? What is the Trigger? |
... the formation of the fibrin clot.
Liver. Tissue Factor (TF), exposed from sub-endothelium at sites of injury. |
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What are zymogens?
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pro-enzymes that become serine proteases upon activations (IX-->IXa, X-->Xa)
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There is no factor...
Which factors are pro-cofactors? |
...VI.
V, VIII |
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What are the two ways of activating IX?
Which is not important in vivo? Which is helpful for understanding the aPTT? |
(VIIa + TF) & XIa
XIa XIa |
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Throbin (IIa) activates:
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V, VIII, XI, and XIII
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The 'intrinsic' pathW deals with...
extrinsic? |
...XI
TF |
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What are the three routine coag tests?
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Prothrombin Time (PT)
Activated Partial Thromboplastin Time (aPTT) Thrombin Time (TT) [= Thrombin clotting time (TCT)] |
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How is the thrombin time performed?
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Take citrated plasma, add excess of bovine thrombin, record the time until the clot forms.
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What is a PTT?
What is GURB? What does it supply? |
add GURB to citrated plasma, add calcium, record time till clot forms.
Ground up rabbit brains. TF. |
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What can make the PT time long? What is TT more sensitive to than PT?
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anything that makes the TT time long....
Something wrong with the Vitamin-K-related factors: II, VII, IX, X Not enough -- deficiency of one or more factor (inherited abnormalities rare) Vitamin K deficiency Warfarin Liver disease Something is wrong with V DIC Heparin, FDPs. |
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What vitamin do many co-ag enzymes depend on?
What are the fat-soluble vitamins? How do you get Vitamin K deficiency? |
Vitamin K.
ADEK Don’t eat Take antibiotics Malabsorb fat |
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What is Vitamin K required for?
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Required for synthesis of….
II (Prothrombin) VII (The Tissue Factor Partner) IX (Hemophilia B) X (Final Common Pathway) Also…. Protein C (Coag Regulatory Protein) Protein S (Protein C’s Cofactor) Some bone homeostatic enzymes |
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If you suspect Vitamin K def as the reason a PT is long, what can you do as a confirmatory test? Why?
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Test V lvls, it should be normal b/c it's not a K dependent factor.
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What is the INR?
What are normal values? Usual target range for warfarin? |
The usual way to report the protime
Goal is allow PT results to be more comparable from one lab to another Especially helpful in managing anticoagulation 1 +/- 0.12 2.0-3.0 |
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What is the PTT?
Which pathway does it trigger? What is a common activator? |
add activator that provides a negative charge, add partial thromboplastin, add calcium, record time.
Intrinsic pathway. Kaolin (clay) |
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What does XI turn on?
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VIII and IX = the accelerators
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What makes a PTT long?
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anything that makes a TT long
• Something wrong with the contact activation factors (XII, XI…. ) deficiency (inherited XII deficiency not all that uncommon) only XI deficiency is associated with some (milder) bleeding risk; no bleeding associated with deficiencies of XII, High MW kininogen, pre-kallikrein |
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What prolongs the TCT (TT)?
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1. Circulating heparin
2. Circulating direct thrombin inhibitor (Argatroban) 3. Fibrinogen deficiency 4. Abnormal fibrinogen 5. Inhibition of fibrin polymerization - high circulating fibrin degradation products |
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What is traditionally a test of the extrinsic pathW?
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PT (Protime)
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How is the PT (Protime) test performed?
Are results standard across the different reagents that may be used? What is used to assist in management of this problem? |
Protime reagent consists of TF + PL (‘complete thromboplastin’; ‘GURB’/’Ground Up Rabbit Brain’) added to citrated plasma. Reaction started by calcium and clotting time recorded. Usually about 12-15 secs.
No. INR |
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What is the INR?
What is the ISI? What does it account for? What should the INR be? |
International Normalized Ratio
(patients PT (seconds) / mean normal PT (seconds)) raised to the power of an exponent known as the 'ISI' - international sensitivity index. The ISI accounts from the properties of the particular thromboplastin being used. ~1.0 |
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What prolongs the PT? Is it sensitive to heparin?
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1. all conditions that prolong the TCT, though it is less sensitive to them.
2. Certain factor deficiency states. 3. Liver disease 4. DIC, due to consumption of factors 5. Vit K def 6. Warfarin therapy No, commercial reagents contain heparinase. |
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What factor deficits are associated with liver disease?
DIC? Vitamin K deficiency? Warfarin therapy? |
I, II, V, VII, and X
multiple factors are consumed, spans both the PT and PTT II, VII, IX, X II, VII, IX, X - it inhibits recycling of Vitamin K, so this makes sense. |
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How is the aPTT (PTT) performed?
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- Start with citrated plasma. Add ‘partial thromboplastin’ reagent, containing: a] an inert negatively charged activator of the contact factors (kaolin, celite, glass,…); and b] phospholipid that is devoid of TF.
- Add calcium, and measure clotting time. Normal range usually about 23-35 secs. |
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Is there a standardization of PTT times ala INR?
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No, there is not.
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What can prolong the PTT?
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1. Anything prolonging the TT (including heparin)
2. acquired factor-specific auto-antibodies 3. lupus inhibitor 4. single factor deficiency states. 5. Liver Disease 6. DIC 7. Vit K deficiency 8. Warfarin Therapy |
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What is a mixing study used for?
How is it performed? How is it read? |
differentiate deficiency of factor(s) from an inhibitor in plasma
Mix patient and normal plasma 1:1 and then repeat the clotting time tests (usually the aPTT) If the factor is just missing in the patient's sample, then the mix will supply the correct clotting time. If an inhibitor is the source of the problem, then a mix will not fix the problem. |
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What should be the first step in working up a PTT value that is elevated for unknown reasons?
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mixing study, to differentiate between "lack of" disorders and "inhibitor" disorders.
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What is a risk factor for thrombosis in vivo, but prolongs phosopholipin-dependent in vitro clotting tests?
Which is more sensitive to the inhibitors: PT, PTT, TCT? |
Lupus inhibitor
PTT > PT, TCT = 0 b/c phospholipins aren't required from the common pathway. |
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If a mixing study is run, and fails to correct - what jumps up on the DiffDx list?
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presence of an inhibitor, e.g., lupus inhibitor.
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What is an essential cofactor for carboxylase, which is required for the post-translational modification of a number of co-ag factors in the liver?
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Vit. K
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What is D-dimer?
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a fibrin split product such as d-dimer that can be measure in plasma after proteolytic degradation of the fibrin plug.
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What is the co-factor for the destruction of fibrin?
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itself; it is the cofactor for plasminogen activator (tPA or Urokinase)-mediated activation of plasminogen (a zymogen) to form plasmin (an active serine protease)
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Most coag reactions require 4 components - what are they?
What is an exception, and what implications does that have re: diag. testing? |
enzyme, cofactor in actv. form, calcium, certain phospholipids
Fibrinogen's activation by thrombin. This means that the common pathway doesn't use phospholipids, and thus that things like lupus inhibitor won't affect the TT (TCT). |
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Can thrombin have anticoagulant activ? When/how?
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when bound to endothelial thrombomodulin, it loses its procoagulant activities, and becomes an efficient activator of protein C (to form activated protein C).
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What two things prevents thrombin activation from going overboard?
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Thrombin's own anti-coag activ & antithrombin's direct-inactivating
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If aspirin/NSAIDs inhibit prostacyclin, why do they have an anti-coag effect?
Why did other COX-2 inhibitors cause MIs? |
They also inhibit TxA2, which is how platelets "call for help" after they adhere. The answer for why the net effect is anti-coag must lie in the balance between these two effects.
They blocked Prostacyclin w/o blocking TxA2 |
