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Fluids > Quick hits Coag > Flashcards

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
Q

Normal Plt? Critical values?

A

150,000-300,000

<50,000 increases surgical risk

<20,000 increases spontaneous bleeding

26
Q

What is bleeding time?

A

Monitors plt function and evaluates time to form a plug

Normal is 2-10 minutes

Aspirin and NSAIDS prolong

27
Q

Normal D-Dimer? What differentials?

A

<500mg/mL

DVT, PE, DIC

28
Q

How does Heparin work?

A

Binds to antithrombin which accelerates it by 1,000 fold

Inhibits intrinsic and final common pathways

Inhibits Plt function

29
Q

Why might Heparin not work?

A

Possible AT deficiency

30
Q

Which activated factors does Heparin neutralize?

A

2, 9,10,11,12

31
Q

Protamine dosage? Type of reactions?

A

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
Q

Where is endogenous heparin produced?

A

Liver, basophils, and mast cells

33
Q

What does warfarin inhibit? How does it work?

A

2, 7, 9, 10, protein C and S

Inhibits vit k epoxide reductase which inhibits Vit K dependent factors

34
Q

Why do infants need Vit K?

A

No gut flora which is also why any gut disease in adults lead to issues

35
Q

What is phytonadione?

A

Exogenously Vit K

Doesn’t work in liver failure

Takes 4 hours to work

SEVERE ANAPHYLAXIS - give slow 1mg/min

36
Q

Two antidotes for warfarin?

A

FFP and Vit k

37
Q

Examples of ADP receptor inhibitors? How long should they be stopped?

A

Ticagrelor - 7 days
Clopidogrel - 7 days
Prasugrel - 7 days
Ticlopidine - 14 days

Antiplatelet

37
Q

Examples of GpIIb/IIIA antagonists? How long should they be stopped?

A

Tirofiban - 1 day
Eptifibatide - 1 day
Abciximab - 3 days

Antiplatelet

38
Q

Examples of COX inhibitors? How long should they be stopped?

A

Aspirin - 7 days
NSAIDS - 1 day

Antiplatelet

39
Q

Examples of thrombin inhibitors? How long should they be stopped? What do they achieve?

A

Argatroban - 3 hours
Bivalirudin - 3 hours

Anticoagulant

40
Q

Examples of COX2 inhibitors? How long should they be stopped?

A

Coxib’s - don’t need to be stopped

-Don’t affect PLT function

41
Q

What drugs decrease bleeding?

A

Aminocaproic acid and TXA

Plasminogen activation inhibitor

42
Q

What is the best type of treatment for type 3 vWF disease? What is wrong?

A

vWF/factor 8 concentrate

Type 3 - do not make any vWF

DDAVP will have no effect

43
Q

Where is vWF synthesized? Two Key functions?

A

Vascular endothelium and megakaryocytes

Anchors PLT

Carries inactivated factor 8 in the plasma

44
Q

What products are contained in cryo?

A

1, 8, 13, vWF

(1 and 13 go together, 8 and vWF go together)

Can be used for any vWB disease

45
Q

What type of vWB should desmopressin be used for?

A

Type 1

46
Q

What lab findings are seen in vWB?

A

Increased PTT and bleeding time

(effects intrinsic pathway)

47
Q

What lab value is changed in hemophilia A and B?

A

Increased PTT

Bleeding time is the same

Doesn’t affect Plt function

48
Q

What is hemophilia A and B?

A

X-linked disorder

A - dysfunctional Factor 8
B - dysfunctional Factor 9

49
Q

Treatment for hemophilia A and B? What of that doesn’t work?

A

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
Q

What lab changes are seen in DIC?

A

Increased PT/PTT
Increased D dimer

Decreased Plt
Decreased Fibrinogen

51
Q

Which patients are at high risk for DIC?

A
  1. Sepsis - highest gram negative
  2. OB (preeclampsia, abruption, amniotic fluid embolism)
  3. Malignancy
52
Q

How is DIC treated?

A
  1. TREAT UNDERLYING CAUSE
  2. Hypovolemia - treat with fluids
  3. Coagulopathy - treat with ffp, Plt, cryo
  4. Microvascular thrombosis - IV heparin
53
Q

HIT type 1?

A

Induces Plt aggregation after large dose of heparin, 1-4 days after

Fairly safe

Resolves on own

54
Q

HIT type 2?

A

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
Q

How is Protein C and S deficiency treated?

A

Heparin then Warfarin

May or may not need lifelong

56
Q

What is Factor 5 Leiden mutation?

A

Causes resistance to protein C

Only needs lifelong if patient experiences recurrent thrombotic events

57
Q

Triggers for sickle cell disease?

A

Pain
Dehydration
Hypoxemia
Acidosis
Hypothermia

58
Q

What is the sickle cell trait?

A

Heterozygous trait - do not advance to crisis except with SEVERE HYPOXEMIA

59
Q

What complications are seen with sickle cell disease?

A

Vaso-occlusive crisis

Acute chest syndrome

Sequestration crisis

Aplastic crisis

Asthma

Pulm HTN

Pneumococcal Disease

60
Q

Which drug reduces the risk of vaso-occulsive crisis ?

A

Hydroxyurea

61
Q

What is the most common comorbidity with sickle cell?

A

Asthma

Fluids (5 decks)

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