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Heme and Lymph Final > DSA: Thrombosis and Hemostasis > Flashcards

DSA: Thrombosis and Hemostasis Flashcards

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1
Q

What is platelet adhesion mediated by?

A

vWF

  • it sticks circulating platelets to the area of damaged vessel wall
  • binds to platelet membrane glycoprotein 1b
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2
Q

What do platelets release when they adhere to the damaged endothelium?

A

-ADP
-TXA2
-

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3
Q

What cleaves prothrombin into thrombin?

A

activated Xa

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4
Q

What are the physiologic antithrombotic systems that inhibit platelet activation?

A
  • aniththrombin III
  • Ptn C and S
  • tissue factor pathway inhibitor (TFPI)
  • the fibrinolytic system
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5
Q

What does the ptn C and Ptn S do?

A

destroy factor Va and VIIIa

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6
Q

What does the PT measure

A

the integrity of the etrinsic and common pathway sof coagulation

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7
Q

What does PTT measure?

A

the integrity of the intrinsic and common pathways of coagulations

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8
Q

What is TT?

A

a screen for quantitative deficiencies and qualitative defects of plasma fibrinogen

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9
Q

What does it mean if we have a pronlonged PT or PTT?

A

-deficiency in one or more coagulation factors or the presence of an inhibitor (usually antibody)

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10
Q

Why do we do that weird 1:1 test?

A

if the PT or PTT is corrected, that confirms that something was missing in the person’s serum
-we mixed it with normal serum

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11
Q

what if the 1:1 test does correct the PTT and PT?

A

we need to assay for specific coagulation factors

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12
Q

What if the 1:1 test doesn’t correct the PT PTT values?

A

and inhibitor is probably there in the patient’s plasma

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13
Q

What does prolonged TT mean?

A

quantitative deficiency or qualitative defect of fibrinogen

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14
Q

In a preop patient, do we automatically want to run the coagulation tests on them?

A

no, not unless they have a bad history

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15
Q

How is a venous thromboembolism often precipitated?

A

by the combo of an underlying hypercoagulable genotype and an acquired prothrombotic, hypercoagulable state such as pregnancy, immobilization, or the postoperative state

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16
Q

What are patients who present with VTE at increased risk for?

A

an occult malignancy

-occult= not accompanied by readily discernable signs and symptoms

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17
Q

What is spontaneous miscarriages characteristic of?

A

antiphospholipid syndrome

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18
Q

inheritance of vW disease

A

auto dominant

-remember hemophilia is X-linked recessive

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19
Q

What happens in VWD?

A

VWF is decreased

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20
Q

What does vWF normally do?

A
  • mediates platelet adhesion and aggregation

- carries and stabilizes factor VIII

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21
Q

What is the stored reservoir of multimerized VWF in vascular endothlial cells?

A

Weibel-Palade bodies

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22
Q

What normally cleaves VWF?

A

ADAMTS13

-deficiency of this is TTP

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23
Q

Type 1 and 3 VWD

Study These Flashcards
A

quantitative

-3 is virtually absent

24
Q

Type 2 VWD?

Study These Flashcards
A

qualitative defect

25
What is more rapidly cleared from the blood in VWD (2nN)?
factor 8 | -the protein on vWF that binds it is screwed up
26
How does VWD present?
they bleed a lot
27
What labs are recommended for initial evaluation if you think someone might have VWD?*
- VWF Ag - ristocetin cofactor activity - factor VIII coagulant activity
28
What 3 things do we need to do when managing someone with VWD?
- increase plasma concentration of VWF and FCIII - replace or supplement VWF and FVIII by using human plasma-derived, viral-inactivated concentrates - promote hemostasis using hemostatic agents that dont use the VWF mechanism
29
What do we suspect if someone has abnormal VWF test results and bleeding symptoms without a personal or family history consistent with hereditary VWD?
Acquired von Willebrand syndrome | -AVWS
30
Bernard-Soulier syndrome and Glanzmann Thrombasthenia
- BSS results from deficiency of platelet membrane glypoprotein Ib-IX-V complex that is the principal receptor for binding VWF... platelets can't adhere to vessels now - GT: deficiency of platelet GPIIb-IIIa complex that is the principal receptor for binding plasma fibrinogen.... platelets can't aggregate now
31
Which disorder has enlarged platelets?
BSS | -platelets are normal in GT
32
If we add ristocetin and we have BSS, what will happen?
nothing - means it's BSS - GT has normal response to ristocetin, but don't respond to anything else
33
Platelet storage pool disorders | -platelet dense granule storage pool deficiency (DG-SPD)
-HErmansky Pudlak syndrome: ocluocutaneous albinism
34
DG-SPD with Wiskott Aldrich
associated with microthrombocytopenia
35
DG-SPD with Chediak-Higashi syndrome
partial albinism and leukocyte inclusions
36
gray platelet syndrome
- auto recessive - DG-SPD - enlarged platelets that are gray
37
Hereditary hemorrhagic telangiectasia | -Osler weber rendu syndrome
- auto domninant - severe recurring nosebleeds and GI bleeds - resulting in chronic anemia nd iron deficiency - HHT genes mutated - bevacizumab normalizes cardiac index
38
Ehlers-Danhlos syndrome
- mutations in genes encoding fibrillar collagen - auto dominant - skin or join hyperextensibility - bleeding tendency and easy bruisability
39
Henoch-Schonlein purpura
- children - rash on legs - arthralgias - abdominal pain - deposition of IgA immune complexes in the skin, GI tract, and kidneys
40
Antithrombin III deficiency
- accumulation of fibrin | - lifelong propensity to thrombosis
41
What 3 things are the hypercoagulable states associated with a deficiency of antithrombotic factors?
- Antithrombin III deficiency - Protein C deficiency - Protein S deficiency
42
What things are associated with increased prothrombotic factors?
- Factor Va (Leiden, ptn C resistance) - Prothrombin (G20210A mutation) - Factor IX Padua
43
Protein C deficiency
-leads to unregulated fibrin generation because of impaired incactivation of factors VIIIa and Va, -auto dominant -
44
Protein S deficiency
- principal cofactor of activated protein C - looks just like protein C when it's gone - no regulation of fibrin generation
45
Activated Protein C Resistance (Factor V Leiden)
- frequent in european ancestry - point mutation for factor V - Arg to Gln mutation renders factor Va incapable of being inactivated by APC
46
Prothrombin Gene Mutation (prothrombin G20210A)
- sub G for A in prothrombin gene - elevated levels of prothrombin - increased risk for venous thrombosis
47
What do Protein S and C depend on for their activity?
Vitamin K! | -so warfarin is a Vit K antagonist and really screws us over... warfarin induced skin necrosis
48
should you test someone for a primary hypercoagulable state immediately after a major thrombotic eve?
no - all the antithrombotic proteins are consumed - leads to erroneous diagnosis of inherited antithrombin, Ptn C, or Ptn S deficiency
49
hyperhomocysteinemia
- premature atherosclerotic disease and VTE | - can cause vascular endothelial injury
50
What kind of cancer is hypercoagulability most prominent in?
panreatic cancer
51
What are the most frequent thrombotic manifestations in patients with neoplasms?
DVT and PE
52
What is highly associated with adenocarcinomas?
Trousseau's syndrome and nonbaterial thrombotic endocarditis
53
Antiphospholipid syndrome
- venous and arterial thrombosis - recurrent spontaneous preggo loss - thrombocytopenia
54
Hereditary Hemorrhagic telangiectasia EOD | -Osler-Weber-Rendu syndrome
- recurrent epistaxis - Mucocutaneous telangiectases - Visceral arteriovenous malformations (especially lung, liver, brain, bowel)
55
Genetics of HHT?
- Auto dominant | - ENG, ALK1, SMAD4
56
What does HHT look like?
- they bleed a lot | - AVMs
57
Tx of HHT?
- if you think it's there, do an MRI of the brain with contrast - if AVM 1-2 mm in diameter, do embolization - after that, do CT angiogram in 6 months and 3 years

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