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Coagulation > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

What is localized bleeding? What is an example of it?

A

Bleeding from a single location such as an ineffectively sutured surgical site or AVM

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2
Q

What is generalized bleeding? Example?

A

Bleeding from multiple sites, spontaneous/recurring bleeding such as disorders of primary or secondary hemostasis

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3
Q

What is mucocutaneous bleeding? Example?

A

Bleeding in skin or at body orifices such as petechiae, purpura, ecchymoses associated with defects of primary hemostasis

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4
Q

What is anatomic bleeding? Example?

A

Bleeding in soft tissue, muscles, joints, deep tissues seen in secondary hemostasis - INTERNAL bleeding

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5
Q

What are the most common congenital coagulation deficiencies in order?

A
  1. VWD
  2. Factor VIII (Hemophilia A)
  3. Factor IX (Hemophilia B)
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6
Q

Acquired vs congenital bleeding disorders (how to differentiate)

A

Acquired: episodes begin after childhood
Congenital: relatives with similar symptoms, onset in infancy

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7
Q

What factors are decreased in liver disease?

A

Factor VII first, then Factor V

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8
Q

If you have a decrease in factor VII, but not factor V, is this liver disease?

A

NO

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9
Q

What factor decrease is a specific marker of liver disease?

A

Factor V

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10
Q

What increases with liver disease?

A

Fibrinogen, VWF, Factor VIII, Factor XIII

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11
Q

Chronic DIC - caused by decreased liver production of what?

A

Antithrombin, protein C, protein S

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12
Q

What test can be used to differentiate between liver disease and vitamin K deficiency? What are the results for each?

A

Factor V and Factor VII assays - both will be decreased in liver disease and only factor VII will be decreased in vitamin K deficiency

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13
Q

What test confirms dysfibrinogenemia?

A

Reptilase time test

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14
Q

How can renal disease lead to bleeding tendancies?

A

Renal failure is associated with PLT dysfunction and mucocutaneous bleeding leading to anemia and thrombocytopenia

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15
Q

How does a vitamin K deficiency or Coumadin treatment lead to bleeding?

A

Vitamin K deficiency will lead to decreased vitamin K dependent factors leading to increased bleeding, and coumadin treatment is an anticoagulant so too much can lead to bleeding

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16
Q

What is the treatment to overdose of coumadin?

A

administration of vitamin K

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17
Q

Briefly describe acquired hemophilia

A

Caused by autoanti-factor VIII often seen in elderly and associated with RA, IBD, and SLE

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18
Q

What is the most common factor inhibitor?

A

Factor VIII

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19
Q

What is the most prevalent congenital mucocutaneous bleeding disorder?

A

VWD

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20
Q

What is the cause of VWD?

A

Quantitative (type 1) and qualitative (type 2) VWF abnormalities

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21
Q

What is the result of VWD?

A

Decreased PLT adhesion to vessel walls leading to impaired primary hemostasis

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22
Q

Describe Type 1 and Type 2 VWD and which is more common?

A

Type 1 is a quantitative deficiency and is more common
Type 2 is a qualitative deficiency due to VWF function reduced

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23
Q

What is included in the VWD test panel?

A

VWF:Ag
VWF activity by ristocetin cofactor assay
Coagulation factor VIII assay

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24
Q

Hemophilia A

A

Factor VIII deficiency

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25
Q

Hemophilia A occurs mostly in _____ because the gene is present on the _________.

A

Males; X chromosome

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26
Q

Factor VIII deficiency significantly slows coag pathway’s production of ______.

A

Thrombin

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27
Q

Test results for Hemophilia A

A

PTT prolonged; PT, FBG, TT normal

28
Q

Hemophilia B

A

Christmas Disease - Factor IX deficiency

29
Q

Test results for Hemophilia B

A

PTT prolonged; PT, FBG, TT normal

30
Q

Hemophilia C

A

Rosenthal Syndrome (Factor XI deficiency)

31
Q

Hemophilia C inheritance

A

Autosomal dominant

32
Q

Hemophilia B inheritance

A

Sex linked

33
Q

Hemophilia A inheritance

34
Q

What population is greatly affected by Hemophilia C?

A

Ashkenazi jews

35
Q

Lab results for Hemophilia C

A

PTT prolonged; PT normal

36
Q

T/F: Frequency and severity of bleeding in hemophilia C is linked to factor XI levels.

A

False; they do not correlate

37
Q

Thrombosis

A

inappropriate formation of a PLT or fibrin clot that obstructs a blood vessel

38
Q

Thrombophilia

A

hypercoagulability; predisposition to thrombosis secondary to a condition

39
Q

Emboli

A

fragments of thrombi that move through the circulatory system and lodge in vasculature

40
Q

Ischemia

A

loss of blood supply

41
Q

Necrosis

A

tissue death

42
Q

Types of venous thromboembolic disease

A

DVT (deep vein thrombosis)

43
Q

Types of arterial thrombosis

A

MI, stroke

44
Q

Risk factors for thrombosis

A

Age, immobilization, diet, oral contraceptive use, pregnancy, lipid metabolism imbalance, smoking, inflammation, hormone replacement therapy, etc

45
Q

What is the most common inherited thrombosis risk factor?

A

Factor V Leidein (FVL) gene mutation

46
Q

What is the second most common inherited thrombosis risk factor?

A

Prothrombin G20210A gene mutation

47
Q

What are antiphospholipid antibodies (APLAs)?

A

immunoglobulins that bind protein-phospholipid complexes

48
Q

What are the 3 types of antiphospholipid antibodies?

A

LACs (lupus anticoagulants)
Anticardiolipin antibodies (ACL)
Anti-B2-GPI antibodies

49
Q

What does FVL gene mutation lead to?

A

APC resistance

50
Q

What is used to differentiate between a LAC and a factor deficiency?

A

mixing studies

51
Q

What are the 2 most common tests required for a LAC profile?

A

Dilute russel viper venom time (DRVVT) and silica based PTT (SCT)

52
Q

Describe the pathway of mixing studies.

A

Prolonged PTT –> TT normal –> perform mixing study
If mixing study corrects, move to incubated mixing study. If that corrects, assay for factor deficiency. If that does not correct, assay for specific factor inhibitor or LAC

53
Q

What are LACs? How do they affect clot based testing? How do they affect the patient’s hemostasis?

A

LACs are lupus anticoagulants (non-specific inhibitors, anti-phospholipid antibodies)
Presence of LACs = more at risk of thrombosis
They affect PTT by prolonging it.

54
Q

Describe the association between FVL and APC resistance. How does FVL affect hemostasis?

A

FVL mutation in factor V gene lacks arginine which is the usual cleavage site for APC so the substitution of arginine for glutamine slows or resists APC hydrolysis. Resistant factor V remains active and raises production of thrombin.
Mutated factor V will not be inactivated by protein C, so it will continue with the coag cascade and patient is at risk of clot.

55
Q

How does prothrombin G20210A lead to clotting?

A

Leads to elevated factor II (prothombin)

56
Q

How does AT (antithrombin) lead to clotting?

A

AT is a serine protease inhibitor, so less AT leads to less inhibition - increasing factors, so leads to more clotting

57
Q

How do PC and PS deficiencies lead to clotting?

A

PC and PS slow down clot formation, so having a deficiency will cause too much clots

58
Q

At onset of Coumadin therapy, ____ activity will drop rapidly. What can this lead to?

A

PC; can lead to Coumadin-induced skin necrosis because PC activity drops more rapidly than other vitamin K dependent factors

59
Q

How does lipoprotein a lead to clotting?

A

Increased lipoprotein a = increased thrombosis

60
Q

How does C-reactive protein lead to clotting?

A

Increased CRP = increased thrombosis

61
Q

How does fibrinogen lead to clotting?

A

Increased fibrinogen = increased clotting

62
Q

How does homocysteine lead to clotting?

A

increased MTHFR gene mutations = increased homocysteine = increased thrombosis

63
Q

How are D-dimer results used in DVT/PE diagnosis?

A

Increased D-dimers can be from DVT or PE. Normal D-dimer results rules out DVT and PE

64
Q

What is HIT?

A

Heparin-induced thrombocytopenia caused by anti-PF4, patients are more likely to clot

65
Q

In DIC, which of the following are increased/decreased: PLT count, coag factors, PT/PTT/TT, FSP, D-dimers, what is seen in lab smear

A

PLT count: decreased
Coag factors: decreased
PT/PTT/TT: prolonged
FSP: increased
Fibrinogen: decreased
D-dimer: increased
Schistocytes in lab smear

Coagulation (5 decks)

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