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Forget Nots > Heme > Flashcards

Heme Flashcards

1
Q

What factor is prothrombin?

A

Factor II

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2
Q

What is pradaxa?

How do you reverse it?

A

It’s dabigatran. a direct thrombin inhibitor

Praxbind (idarucizumab) or HD

Caution with renal insufficiency. Metabolized by the kidneys

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3
Q

What is Xarelto?

How do you reverse?

A

Rivaroxaban. Factor Xa inhibitor

K-centra

Metabolized by the kidneys

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4
Q

What is eliquis?

How do you reverse it?

A

Apixaban. Factor Xa inhibitor

K-centra

Metabolized by liver. Safe in kidney pts

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5
Q

Protein C and S

Which one is the helper and which one is the primary actor?

What is their role?

A

Protein C is the hancho. Protein S helps. Or Supplements.

They degrade factors V and VIII

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6
Q

In antithrombin III deficiency do you bleed or clot?

A

No anti-thrombin. You don’t have a counteractor for thrombin -> you thrombose. Resistant to heparin because heparin augments anti-thrombin.

Rx: give ffp then heparin

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7
Q

1?

What is the 2nd most common congenital hypercoagulability?

A

1: factor V leiden

Protein C deficiency. No inhibition of factors V and VIII

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8
Q

What is dabigatran? Reversal?

A

Direct thrombin inhibitor

Pradaxa

Praxbind or HD

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9
Q

What is rivaroxaban? Reversal?

If you stop it, how long until the coat profile normalizes?

A

Xarelto.

Factor Xa inhibitor

4 factor PCC

Half life is 9-13 hrs. 4-5 half lives ~ 36hrs

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10
Q

Apixaban. Reversal?

A

Eliquis. Factor Xa inhibitor

4 factor PCC

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11
Q

What is the P2Y12 assay?

A

Measures degree of platelet inhibition from plavix.

Inhibition of <20% is preferred in the preop setting

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12
Q

Collagen types.

  • Which one is the most common overall?
  • which one is the most dominant during proliferative phase?
  • at the end of wound healing
A
  • overall: type I
  • during proliferative: type III
  • most type III’s are replaced by type I at the end of wound healing
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13
Q

What are the timings of the three phases in wound healing?

A

Inflammatory: 4-6 days
Proliferative: 4-24 days
Remodeling: 21 days - 2 yrs

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14
Q

Why do smokers suck at wound healing?

A

They don’t have appropriate neovascularization capability

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15
Q

Scar Bounded by the original incision.

Treatment?

A

Hypertrophic scar -> excision and reclosure can be helpful

Keloid: not bounded by the original incision

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16
Q

Steroids woundm vitamins A or E?

A

Vitamin A

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17
Q

What is the best treatment for ABO incompatibility after stopping the transfusion?

A

1L saline bolus

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18
Q

Non-hemolytic febrile reactions are the most common transfusion reaction. What is the overall incidence?

What is the pathophys of this?

A

1-2%

Wbcs in the DONOR blood

19
Q

What medication has shown benefit in treating refractory small bowel AVM bleeding?

A

Thalidomide

20
Q

What’s wrong with the factor V in factor V leiden?

A

Resistant to activated protein C so uncontrolled factor V -> clots more

21
Q

What is the confirmatory test for HIT?

A

serotonin release assay. gold standard

also can use PF4 antibody test

22
Q

T/F: in vWF disease, bleeding is due to poor platelet-platelet aggregation

A

False. vWF links platelets to collagen on the endothelium

23
Q

Can type III vWF be treated with cryo?

A

All three types can be rx with cryo

type I & II: desmopressin

24
Q

What is the transmission rate for HBV, HCV, and HIV from blood transfusion?

A

HBV: 1/200,000
HCV: 1/2,000,000
HIV: 1/2,000,000

25
Q

Dabigatran vs argateoban. What’s the difference?

A

Both direct thrombin inhibitor. Dabigatran is pradaxa. It is PO. argatro is IV. use argatro for HIT

Dabigatran should be used with caution in pts with renal insufficiency

26
Q

Rivaroxaban vs apixaban

Which one for pts with renal disease?

A

Use eliquis/apixaban for renal disease. It is hepatically cleared.

Xarelto/rivaroxaban for pts with normal creatinine clearance

27
Q

What is idarucizumab?

A

Monoclonal antibody that binds dabigatran (praxbind)

28
Q

What should you use to monitor von willebrand pts post-op?

A

Factor VIII activity. It is better than vWF activity level which is determined by restocetin cofactor activity, which is an indirect measure of platelet aggregation

29
Q

What is the difference between HIT I vs. HIT II?

How do you differentiate the two clinically?

A

HIT I: non-immune response. It’s a direct interaction between heparin and circulating platelets causing clumping and sequestration. Plt rarely < 100,000. Self limited. Continue unfractionated heparin.

Timing: within the first 48-72 hrs

HIT II: IgG against platelet factor 4. Stop UFH, start argatroban

Timing: 4-5 days after starting

30
Q

For what range of anticipated blood loss is intra-op red cell salvage appropriate for consideration?

A

500-1000cc

31
Q

What is the half life of heparin?

Does heparin inhibit thrombin? Does it inhibit factor Xa?

A

30-90 minutes

Both thrombin and factor Xa.

32
Q

Abciximab. What is it? Mechanism of action?

A

Blocks glycoprotein IIb/IIIa receptor

33
Q

What is the mechanism of action of clopidogrel?

A

Blocks ADP activation of the IIb/IIIa complex

34
Q

A man has prolonged PTT. he’s had an uneventful appy in the past. VWF or hemophilia A?

A woman has prolonged PTT. She’s had an uneventful appy in the past. VWF or hemophilia A?

A

VWF. If he had hemophilia A, it’s unlikely that his appy was uneventful

VWF. hemophilia is x-linked recessive. It’s manifested only in makes

35
Q

5 things you see in TTP

A 
purpura
Neuro
Kidney injury/hematuria
Anemia
Fever
36
Q

Which factor has the shortest half life?

A

Factor VII (5 hrs)

37
Q

What’s the difference between vasopressin and desmopressin?

A

Desmopressin is a synthetic analog of vasopressin but it doesn’t have any vasopressor activity.

Desmopressin, not vasopressin, is the 1st line prophylactic treatment for vWD I, II

38
Q

What is the treatment of TTP?

A

plasmapheresis

39
Q

T/F: pts with renal disease are at increases risk of DVT/PE

A

True

Thought to be related to elevated levels of factor VII and vWF and decreased lvls of antithrombin in pts with nephrotic syndrome

40
Q

What drug is a reversible platelet aggregation inhibitor?

Mechanism of action for plavix? Aspirin?

A

Ticagrelor. Reversibly binds the ADP receptor on platelets.

Plavix and prasugrel also binds ADP but irreversible

Aspirin inactivates COX1 which then decreases production of thromboxane which binds to the txa2 receptors on platelets.

41
Q

Budd chiari syndrome

  • when can you do thrombolytic therapy?
  • what is the prognosis without any treatment?
A
  • thrombolytic within 3-4 wks of presentation

- prognosis poor. 90% mortality within 3 years

42
Q

For acute limb ischemia,

  • what is the heparin bolus dose?
  • what is the drip dose?
  • aPTT should be aimed for what?
A
  • 80u/kg
  • 18u/kg
  • b/w 60-90 seconds for high dose
43
Q

Transfusion of ABO incompatible blood. Do you use high dose steroids?

A

No. You can use it for the non-hemolytic febrile reaction.

ABO incompatibility: stop transfusion + IV fluids

44
Q

hemophilia A vs. B trauma case. when to give cryo vs. FFP?

A

give cryo to hemophilia A. cryo has more factor VIII than FFP.

give FFP to hemophilia B

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