Hematology Flashcards

0
Q

What is secondary hemostasis?

A

Formation of the fibrinogen clot I.e. factors

  1. Extrinsic
  2. Intrinsic
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1
Q

what is primary hemostasis?

A

Platelets binding

  1. Adhesion
  2. Activation
  3. Aggregation
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2
Q

What is adhesion of primary hemostasis?

i.e. How do platelets bind to broken down endothelium?

A

Von wilibrands factor (vWF) on the endothelium binds to glyc Ib on platelets

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3
Q

What are two diseases associated with adhesion problems of platelets?

A

Bernard Soliers dz ( malfunctioning glyc Ib)

Von Wilibrands disease (malfunctioning vWF)

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4
Q

In primary hemostasis, once adhesion has occurred how are platelets activated?

A

They express thromboxane A2 (TXA2) and ADP which in turn activates other platelets.

Two drugs that inhibit activation are aspirin (blocks TXA2) and Plavix (inhibits ADP)

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5
Q

In primary hemostasis once platelets are adhesive and activated they need to aggregate. How does this occur?

A

Platelets bind to each other via glyc IIb/ IIIa, and covered with fibrinogen.

Abciximab inhibits this and it’s malfunctioning in Glanzmans Thrombasthenia

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6
Q

In secondary hemostasis what are the three pathways?

A

Common: 1,5,2,10
Extrinsic: 7
Intrinsic: the rest

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7
Q

What’s the name of factor 2

A

Thrombin

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8
Q

What’s the name of factor 1

A

Fibrinogen

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9
Q

Factor 1 (fibrinogen) -> Factor 1a (Fibrin). What breaks down fibrin to D-dimers?

A

Plasmin. Which is activated from plasminogen by tPA

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10
Q

What factors does Coumadin inhibit?

A

2,7,9,10

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11
Q

What drugs inhibit factor 10a?

A

Apixiban,

Rivaroxiban (xarelto)

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12
Q

What drugs inhibit thrombin (Factor 2)?

A

Dabigatran,
Lepirudin,
Argatroban

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13
Q

What is the mechanism of action of heparin?

A

Binds to Antithrombin III. Which inactivates Thrombin (Factor 2)

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14
Q

How do you approach a bleeding patient (non life threatening)?

A

Is it primary or secondary hemostasis?

Primary: vag bleed, oral bleed, petechiae

Secondary: hematoma, hemarthroses

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15
Q

If a patient is bleeding with petechiae, oral bleed or vaginal bleed etc. (primary hemostasis) what lab do you want?

A

Platelet count

16
Q

A bleeding patient with decreased platelets has thrombocytopenia. What are the three causes of thrombocytopenia?

A
  1. Production: BM, Aplastic anemia, Ca infiltrate, Cirrhosis
  2. Consumption: DIC, HIT, TTP, ITP
  3. Sequestration: spleen
17
Q

A bleeding patient with vaginal bleeding oral bleed petechiae etc. and a normal platelet count has platelet dysfunction. Name five causes of platelet dysfunction

A
vWD
NSAIDs
ASA
Clopidogrel
Uremia (100s)
18
Q

A “bleeding” pt comes in with hematoma or hemarthroses (secondary hemostasis). What lab study would you want first?

A

Mixing study

19
Q

A bleeding patient comes in with hematoma hemarthroses and the mixing study corrects. What type of problem is there?

A
Factor deficiency:
Vit K def
Coumadin
Cirrhosis
DIC
vWD
20
Q

I’m bleeding patient comes in with hematoma and hemarthroses and the mixing study does not correct. What type of problem is there?

A

And inhibitor problem:
Hemophilia A/B
Sickle cell

21
Q

Diagnose: A patient comes in with fever, autoimmune hemolytic anemia, thrombocytopenia, renal failure, Neuro symptoms

A

FATRN= TTP

22
Q

What’s the difference between TTP and DIC?

A

TTP has decreased platelets and everything else normal in the DIC panel. DIC has everything abnormal in the DIC panel.

23
Q

What’s the treatment for DIC?

A

Treat the underlying disease and give blood products including: platelets, cryo (fix dec fibrinogen), FFP (fix PT PTT INR), PRBCs (schistocytes)

24
Q

How do you treat TTP

A

Exchange transfusion. never give blood products

25
Q

Diagnosis: A patient comes in on heparin and starts to clot worse.

A

HIT

26
Q

How do you treat HIT?

A

Lepirudin or Argatroban. Bridge to Coumadin

27
Q

Diagnosis: A patient comes in asymptomatic and has extremely low platelets in the single digits

A

ITP

28
Q

How do you diagnose and treat ITP?

A

This is a diagnosis of exclusion

Tx: platelets, corticosteroids, IVIG, RhoGAM, splenectomy, Rituximab