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Heme/Lymph > Thrombosis & DIC > Flashcards

Thrombosis & DIC Flashcards

1
Q

What are physiologic coagulation control methods?

A

blood flow-wash away activated factors
natural anticoagulant processing
-antithrombin inactivates enzymes thrombin & Xa
-protein C digests cofactors V & VIII

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2
Q

What makes up Virchow’s triad?

A

endothelial injury *
abnormal blood flow
hypercoagulability

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3
Q

Is antithrombin or protein C system vitamin K dependent?

A

protein C/S system

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4
Q

Which type of thrombosis are primary hypercoagulable states associated with?

A

venous

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5
Q

What are the 3 types of primary hypercoagulable states?

A

deficiency of control proteins (AT, PC, PS)
subtle changes causing control mechanisms (leiden V)
increased coagulation factor levels (prothrombin gene variation G20210A)

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6
Q

When does the risk of thrombosis in AT/PC/PS deficiencies increase?

A

after puberty

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7
Q

How do you test for AT, PC/PS deficiencies?

A

functional AT, PS or PS assay

protein S free antigen

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8
Q

What happpens to PTT in a patient with resistance to activated protein C?

A

failture of PTT to prolong in response to addition of activated protein C

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9
Q

If PTT fails to prolong in response to addition of activated protein C what test do you perform next?

A

genetic defect of factor V test (gain of function mutation)

(factor V leiden: Arg 506 replaced wtih Gln

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10
Q

What are the key features of leidein factor V?

A

venous throbosis risk factor
causes DVT
common in caucasians

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11
Q

What are the key features of prothrombin gene variation?

A

G20210A mutation, leads to higher levels of transcription
associated with venous events DVT/PE
via elevated thrombin levels
(more freq than def of AT, PC, PS)
risk of venous thrombotic event similar to leiden factor V, weaker than AT/PC/PS

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12
Q

What is antiphospholipid antibody syndrome?
Key lab findings?
Symptoms?

A

venous &/or arterial thrombosis
recurrent fetal wastage/preg loss
evidence of antiphospholipid antibody/lupus like anticoag/positive antiphospholipid serology
may have thrombocytopenia

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13
Q

What is the mechanism of antiphospholipid antibody syndrome as understood to date?

A

auto-antibody to phospholipid-protein complex
-anti-cardiolipin/lupus antigoaculents present
inhibits phospholipid depenant in vitro coag assays
-inhibitor: failure to clot time to correct on 1:1 mix
-phospholipid dependence: clot time corrects with high PL
can cause false positive syphillis serology

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14
Q

Features of “lupus-like” anticoagulant

A

inhibitor of phospholipid dependent in vitro assays of coagulation

  • prolonged PL dependent clot time (dRVVT or PTT)
  • failture of correction on 1:1 mix study
  • correction occurs in lipid rich assay
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15
Q

What causes both arterial and venous thrombosis?

A

homocysteine

apla syndrome

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16
Q

What are acquired risk factors of thrombosis?

A 
obstruction to flow (pregnancy)
activation of hemostatic mechanism (spesis, neoplasm, foregin body)
damaged endothelium (infl, atherosclerosis, trauma, etc)
17
Q

What are risk factors for secondary hypercoagulable states?

A

post op
neoplasm
immobilizaiton

18
Q

What is DIC?

A

widespread acivation of thrombin nad plasmin mechanisms

  • overwhelmed control mechanisms
  • consumption of participants in hemostasis
  • pay present as bleeding or thrombosis
19
Q

What are syndromes associated with DIC?

A 
intro of extrinsic clot promoting material
intravascular elaboration of procoagulants
vascular injury (ie/sepsis)
20
Q

What is purpura fulminans?

A

presenting symptom of DIC caused by meningococcal spesis or severe protein C deficiency in a newborn

21
Q

Clinical presentation of DIC?

A

bleeding from venipunctures and other sites

purpura fulminans

22
Q

What is the screening test for DIC?

A

D-dimer

23
Q

Lab values for DIC

A

prolonged PT/PTT
decreased fibrinogen
low platelets
D-dimer elevated

24
Q

What are the consequences fo DIC?

A

microcirculatory failure leading to multiorgan dysfunction

25
Q

How do you treat DIC?

A

treat the triggering condition
restore tissue perfusion and acid/base balance
replacement therapy for bleeding

26
Q

What is a D-dimer?

A

a product from fibrinolysis of cross linked fibrinolysis

27
Q

What disorders are dissociated with increased D dimer?

A 
DIC
DVT
healing (post op/resolving hematoma)
Liver disease
cancer
28
Q

What are lab findings for liver failure?

A 
greatly increased PT
increased PTT
n/c or decreased fibrinogen
n/c or decreased platelets
increased FDP
jaundice
29
Q

What are lab findings for vit K deficiency?

A 
greatly increased PT 
increased PTT
n/c in fibrinogen
n/c in platelets
n/c in FDP
malabsorption, liver disease
30
Q

What are lab findings for Lupus anticoagulant?

A 
n/c or increased PT
increased PTT
n/c in fibrinogen
n/c or decrease in platelets
n/c in FDP thrombosis
31
Q

What type of feedback does thrombin exhibit on the clotting cascade?

A

positive-activates more thrombin

negative: activates Protein C

32
Q

What is accelerated by heparin?

A

inactivation of thrombin, Xa, IXa, XIa and AT

33
Q

What is the pentad of clinical manifestations of TTP?

A 
microangiopathic hemolytic anemia
thrombocytopenia
CNS/mental status changes
fever
renal insufficiency
34
Q

What does ADAMTS13 do? When is it deficient?

A

cleaves vWF multimers into monomers

deficient in TTP (acquired or congenital)

35
Q

What causes HIT?

A

IgG binds to PF-4 heparin complex, activates via FC receptor, leads to generation of procoag rich microparticles

36
Q

Symptoms of HIT?

A

moderate thrombocytopenia
5-10 days after initial heparin exposure
clots

37
Q

TX for HIT?

A

stop heparn
do not start LMWH or warfarin
begin alternate anticoag (direct thrombin inhibitor)

Heme/Lymph (18 decks)

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