Quick hits Coag Flashcards

1
Q

4 steps of hemostasis?

A
  1. Vascular spasm
  2. Primary hemostasis (Plt plug)
  3. Secondary hemostasis (cascade)
  4. Fibrinolysis (when clot is no longer needed)
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2
Q

Which three mediators vasoconstrict?

A

Thromboxane A2
ADP
Serotonin

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3
Q

Which two mediators vasodilate?

A

Nitric oxide
Prostacyclin

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4
Q

What breaks down fibrin ?

A

Plasminogen

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5
Q

Which two fibrinolytics activate Plasmin?

A

tPA

Urokinase

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6
Q

Do Platelets contain a nucleus or DNA? Where are they made? What is the lifespan? Cleared by ?

A

NO

Made in bone marrow by megakaryocytes

8-12 days

Spleen and RNS

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7
Q

Three steps to create a platelet plug? How does the injured vessel initially activate the platelet plug?

A
  1. Adhesion
  2. Activation
  3. Aggregation

-Collagen

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8
Q

Where are all factors made? Which two aren’t? Where are they made?

A

All made in Liver except

  1. Tissue factor (3) made in vascular wall
  2. Calcium (4) through diet
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9
Q

What are the vitamin K dependent factors?

A

2, 7, 9, 10

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10
Q

Factors in the Extrinsic ? What lab values? What drug?

A

3 and 7. - Can create a clot in 15 seconds

-3 is activated first
-7 is the fastest coag factor
-PT
-Warfarin

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11
Q

What is the first factor to be depleted with a vitamin K deficiency ?

A

7 ( Stable factor )

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12
Q

A deficiency of what factor causes Hemophilia A? What about B?

A

A - factor 8
B - factor 9

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13
Q

How long does it take to form a clot via intrinsic pathway?

A

Up to 6 minutes

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14
Q

Which lab tests measures fibrin split products? What disease is this good to measure for?

A

D- Dimer

Helpful in DIC

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15
Q

What does antithrombin inactivate? Which factors do Protein C and S inactivate?

A

2, 9, 10, 11, 12

5, 8

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16
Q

How is a clot broken down?

A

Fibrinolysis

  1. Plasminogen is converted to Plasmin through tPa+Urokinase
  2. Plasmin cuts the fibrin
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17
Q

How is fibrinolysis turned off? Which two enzyme inhibitors?

A
  1. tPa Inhibitor stops plasminogen converting to plasmin
  2. Alpha-2 antiplasmin inhibits the action of plasmin on fibrin
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18
Q

What 4 mechanisms counterbalance a clot?

A
  1. Vasodilation and washout of ADP + TxA2
  2. Antithrombin inactivating thrombin
  3. Tissue factor inhibitor neutralizes tissue factor
  4. Protein C+S
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19
Q

What are the three steps to contemporary cell based cascade?

A
  1. Initiation
  2. Amplification
  3. Propagation
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20
Q

What is the best predictor of bleeding during surgery?

A

H&P

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21
Q

What is aPTT? Normal value? Therapeutic level?

A

-Intrinsic and final common pathways
- 30 seconds

1.5- 2.5 times normal

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22
Q

What is PT?

A

-Extrinsic and final common pathways
-12 seconds

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23
Q

What is INR?

A

Standardizes PT results

Normal is 1

Therapeutic is 2-3 times control

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24
Q

What is ACT? What is it affected by?

A

Guides Heparin dosing

Normal is 90-120

CPB > 400

Check in 3 minutes and every 30 after

Tends to be more accurate

Hypothermia, thrombocytopenia, deficiency in fibrinogen, factor 7, factor 12

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25
Normal Plt? Critical values?
150,000-300,000 <50,000 increases surgical risk <20,000 increases spontaneous bleeding
26
What is bleeding time?
Monitors plt function and evaluates time to form a plug Normal is 2-10 minutes Aspirin and NSAIDS prolong
27
Normal D-Dimer? What differentials?
<500mg/mL DVT, PE, DIC
28
How does Heparin work?
Binds to antithrombin which accelerates it by 1,000 fold Inhibits intrinsic and final common pathways Inhibits Plt function
29
Why might Heparin not work?
Possible AT deficiency
30
Which activated factors does Heparin neutralize?
2, 9,10,11,12
31
Protamine dosage? Type of reactions?
1mg for every 100 units of heparin (GIVE SLOW) Hypotension Bronchoconstriction Increased airway pressures Neutralized heparin through being VERY positively charged and heparin being negatively charged
32
Where is endogenous heparin produced?
Liver, basophils, and mast cells
33
What does warfarin inhibit? How does it work?
2, 7, 9, 10, protein C and S Inhibits vit k epoxide reductase which inhibits Vit K dependent factors
34
Why do infants need Vit K?
No gut flora which is also why any gut disease in adults lead to issues
35
What is phytonadione?
Exogenously Vit K Doesn't work in liver failure Takes 4 hours to work SEVERE ANAPHYLAXIS - give slow 1mg/min
36
Two antidotes for warfarin?
FFP and Vit k
37
Examples of ADP receptor inhibitors? How long should they be stopped?
Ticagrelor - 7 days Clopidogrel - 7 days Prasugrel - 7 days Ticlopidine - 14 days Antiplatelet
37
Examples of GpIIb/IIIA antagonists? How long should they be stopped?
Tirofiban - 1 day Eptifibatide - 1 day Abciximab - 3 days Antiplatelet
38
Examples of COX inhibitors? How long should they be stopped?
Aspirin - 7 days NSAIDS - 1 day Antiplatelet
39
Examples of thrombin inhibitors? How long should they be stopped? What do they achieve?
Argatroban - 3 hours Bivalirudin - 3 hours Anticoagulant
40
Examples of COX2 inhibitors? How long should they be stopped?
Coxib's - don't need to be stopped -Don't affect PLT function
41
What drugs decrease bleeding?
Aminocaproic acid and TXA Plasminogen activation inhibitor
42
What is the best type of treatment for type 3 vWF disease? What is wrong?
vWF/factor 8 concentrate Type 3 - do not make any vWF DDAVP will have no effect
43
Where is vWF synthesized? Two Key functions?
Vascular endothelium and megakaryocytes Anchors PLT Carries inactivated factor 8 in the plasma
44
What products are contained in cryo?
1, 8, 13, vWF (1 and 13 go together, 8 and vWF go together) Can be used for any vWB disease
45
What type of vWB should desmopressin be used for?
Type 1
46
What lab findings are seen in vWB?
Increased PTT and bleeding time (effects intrinsic pathway)
47
What lab value is changed in hemophilia A and B?
Increased PTT Bleeding time is the same Doesn't affect Plt function
48
What is hemophilia A and B?
X-linked disorder A - dysfunctional Factor 8 B - dysfunctional Factor 9
49
Treatment for hemophilia A and B? What of that doesn't work?
A - Factor 8, FFP, Cryo B - Factor 9 Recombinant factor 7 - but can increase the risk of arterial + venous thrombosis (Also used for unexplained bleeding)
50
What lab changes are seen in DIC?
Increased PT/PTT Increased D dimer Decreased Plt Decreased Fibrinogen
51
Which patients are at high risk for DIC?
1. Sepsis - highest gram negative 2. OB (preeclampsia, abruption, amniotic fluid embolism) 3. Malignancy
52
How is DIC treated?
1. TREAT UNDERLYING CAUSE 2. Hypovolemia - treat with fluids 3. Coagulopathy - treat with ffp, Plt, cryo 4. Microvascular thrombosis - IV heparin
53
HIT type 1?
Induces Plt aggregation after large dose of heparin, 1-4 days after Fairly safe Resolves on own
54
HIT type 2?
IgG attacks immune which causes Plt aggregation 5-14 days after ANY dose of heparin High risk of amputation and death MUST STOP HEPARIN AND USE A DIFFERNT ANTICOAGULANT
55
How is Protein C and S deficiency treated?
Heparin then Warfarin May or may not need lifelong
56
What is Factor 5 Leiden mutation?
Causes resistance to protein C Only needs lifelong if patient experiences recurrent thrombotic events
57
Triggers for sickle cell disease?
Pain Dehydration Hypoxemia Acidosis Hypothermia
58
What is the sickle cell trait?
Heterozygous trait - do not advance to crisis except with SEVERE HYPOXEMIA
59
What complications are seen with sickle cell disease?
Vaso-occlusive crisis Acute chest syndrome Sequestration crisis Aplastic crisis Asthma Pulm HTN Pneumococcal Disease
60
Which drug reduces the risk of vaso-occulsive crisis ?
Hydroxyurea
61
What is the most common comorbidity with sickle cell?
Asthma