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Hem/Onc > Hemostasis 0502 > Flashcards

Hemostasis 0502 Flashcards

1
Q

hemophilia A

A

factor VIII deficiency

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2
Q

hemophilia B

A

factor IX deficiency

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3
Q

vit K deficiency

A

decreased synthesis of factors II, VII, IX, X, protein C, protein S

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4
Q

antithrombin

A 
inhibits thrombin (II) and factors VII, IX, IX, XI, XII (active forms).
activated by HEPARIN.
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5
Q

what protects factor XIII?

A

vWF

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6
Q

protein C

A

activated by thrombomodulin (from endo cells).

along with protein S, inactivates factor V and VIII.

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7
Q

tissue plasminogen activator (tPA)

A

converts plasminogen to plasmin.

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8
Q

plasmin

A

cleaves fibrin mesh (THROMBOLYTIC)

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9
Q

what activates factor XII (intrinsic)?

A

subendothelial collagen, basement memb, activated plts

*also HMWK

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10
Q

what activates factor VII (extrinsic)?

A

tissue thromboplastin

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11
Q

what does plasmin do?

A
  1. break down fibrin mesh into fibrin degradation products

2. cleave C3 into C3a in complement cascade

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12
Q

what converts prekallikrein to kallikrein?

A

activated factor XII

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13
Q

what does kallikrein do?

A

convert high molec weight kininogen (HMWK) to bradykinin

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14
Q

actions of bradykinin

A
  1. increase vasodilation
  2. increase permeability
  3. increase pain
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15
Q

which cells release pro-aggregation factors?

A

plts - release TXA2 (decrease bld flow, increase agg)

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16
Q

which cells release anti-aggregation factors?

A

endo cells - release PGI2 and NO (increase bld flow, decrease agg)

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17
Q

what facilitates plt adhesion?

A

vWf binds injured endo first.

plt binds to vWf via GpIb receptor.

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18
Q

what facilitates plt aggregation?

A

plts release ADP which induce expression of GpIIbIIIa receptor.
fibrinogen binds GpIIbIIIa and link plts.

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19
Q

what drug inhibits TXA2 synthesis?

A

aspirin - inhibits COX, which converts arach acid to TXA2

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20
Q

what drugs inhibit ADP-induced expression of GpIIbIIIa?

A

ticlodipine and clopidogrel

21
Q

what inhibits GpIIbIIIa directly?

A

abciximab

22
Q

what increases ESR?

A 
infection
inflamm dz (temporal arteritis, polymyalgia rheumatica)
malignant neoplasm
GI dz (UC)
pregnancy

*acute phase reactants can cause RBC aggregation and thus, increased ESR

23
Q

what decreases ESR?

A 
polycythemia
sickle cell anemia
CHF
microcytosis
hypofibrinogenemia
24
Q

what lab is changed in hemophilia A and/or B?

A

increased PTT

25
Q

what lab is changed in vit K deficiency?

A

increased PT and PTT

26
Q

what lab is changed in Bernard Soulier disease?

A

decreased PC
increased BT

*GpIb deficiency - plt adhesion

27
Q

what lab is changed in Glanzmann thrombasthenia?

A

normal PC
increased BT
no plt clumping on smear

*GpIIbIIIa deficiency - plt aggregation

28
Q

what lab is changed in idiopathic thrombocytopenic purpura?

A

decreased PC
increased BT
increased megakaryocytes in BM

*anti-GpIIbIIIa Abs decrease plt survivial

29
Q

what lab is changed in TTP?

A

decreased PC
increased BT
schistocytes, increased LDH

30
Q

cause of TTP

A

deficiency of ADAMTS13 vWf metalloproteinase - increase in vWf multimers that increase plt aggregation (micro thrombi)

31
Q

what are the sx of TTP?

A
  1. neuro sx
  2. renal sx
  3. fever
  4. thrombocytopenia
  5. microangiopathic hemolytic anemia
32
Q

what lab is changed in vWf disease?

A 
PTT increase (due to loss of F VIII protection)
BT increase
33
Q

vWf manifestations

A

defective plt plug formation (adhesion).
mild mucosal and skin bleeding.
AD inheritance. most common inherited bleeding d/o - mixed plt and coag d/o.

34
Q

ristocetin test with vWf

A

normally ristocetin induces plt agg by causing vWf to bind GpIb.

without vWf, plt agg is impaired and test is abn.

35
Q

tx of vWf

A

DDAVP (desmopressin) - releases vWf from endo cells

36
Q

DIC definition

A

= disseminated intravascular coagulation.
widespread activation of clotting cascade.
leads to deficiency in clotting factors and consequent bleeding state.

mixed plt and coag d/o.

37
Q

what lab is changed in DIC?

A 
PC decrease (used in microthrombi)
BT increase
PT increase
PTT increase
schistocytes
D-dimers (fibrin split product)
decrease fibrinogen
decrease factors V,VIII
38
Q

causes of DIC

A 
"STOP Making New Thrombi"
Sepsis (gm neg)
Trauma
Obstetric complications
acute Pancreatitis
Malignancy
Nephrotic syndrome
Transfusion
39
Q

factor V Leiden

A

hereditary thrombosis syndrome leading to hypercoag - most common cause.

production of mutant factor V that CANNOT be degraded by protein C.

40
Q

prothrombin gene mutation

A

hereditary thrombosis syndrome leading to hypercoag.

mutation in 3’ untranslated region.
increased gene expression.
increased prothrombin = increased thrombin.
assoc. w/ venous clots.

41
Q

antithrombin deficiency

A

hereditary thrombosis syndrome leading to hypercoag.

less increase in PTT after heparin admin.
*ATIII is normally activated by heparin

42
Q

protein C or S deficiency

A

hereditary thrombosis syndrome leading to hypercoag.

decreased ability to inactivate factors V, VIII.

43
Q

thrombotic skin necrosis with warfarin

A

normally, warfarin initiation leads to temporary deficit in prot C and S (shorter half life) relative to factors II, VII, IX, X.

increased risk in prot C or S deficiency - more severe deficit is seen with warfarin initiation, leading to increased thrombosis in skin (about 1 wk later)

44
Q

bld transfusion: packed RBCs

A

increase Hb and O2 carrying capacity.

for acute bld loss, severe anemia.

45
Q

bld transfusion: plts

A

increase plt count.
usu given in “6 pack” or more for therapeutic effect.
stops significant bleeding (thrombocytopenia, qualitative plt defects).

46
Q

bld transfusion: fresh frozen plasma

A

increase coag factor levels by about 20%.

for DIC, cirrhosis, warfarin OVER-anticoagulation.

47
Q

bld transfusion: cryoprecipitate

A

contains fibrinogen, factor VIII, factor XIII, vWF.

to treat coag factor deficiencies involving fibrinogen and factor VIII.

48
Q

risks of bld transfusion

A

infection transmission -low.
transfusion rxns.
iron overload.
hypocalcemia -citrate used as anticoagulant but may also chelate calcium (paresthesias).
hyperkalemia -RBCs may lyse in old bld units.

Hem/Onc (9 decks)

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