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My Pathology > Hemostatic Disorders > Flashcards

Hemostatic Disorders Flashcards

1
Q

Heparin/heparin-like molecules

A
  • Enhance anti-thrombin III

* Neutralize coagulation factors 7, 9-12, thrombin

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2
Q

PGI2

A
  • Synthesized from PGH2 in epithelial cells

* Vasodilator, inhibits platelet aggregation

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3
Q

Protein C

A
  • Vit K dependent

* Inactivates factors 5 and 8

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4
Q

Thromboxane A2

A
  • Synthesized from PGH2 by platelets

* Vasoconstrictor, enhances fibrinogen binding to GpIIb-IIIa receptors

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5
Q

What does aspirin do?

A

Irreversible COX inhibitor, inhibits TXA2 formation

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6
Q

vWF

A
  • Synthesized by endothelial cells and megakaryocytes
  • Aids platelet adhesion to exposed collagen by binding to Gp1b receptor
  • Prevents degradation of factor 8c
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7
Q

What does tissue thromboplastin (factor 3) do?

A

Activates factor 7

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8
Q

What is the platelet receptor for fibrinogen and which drugs interfere with it?

A
  • Gp2b-3a

* Ticlopidine, clopidigrel, abciximab

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9
Q

What is Glanzmann disease?

A

Deficiency in Gp2b-3a

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10
Q

What is in platelet dense bodies?

A
  • ADP, aggregating agent

* Calcium, binding agent for vit K-dependent factors

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11
Q

What is in platelet α-granules?

A

vWF, fibrinogen, PDGF, platelet factor 4 (neutralizes heparin)

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12
Q

What do platelets do?

A
  • Stabilize intercellular adherens jxns, esp. in postcapillary venules
  • Form fibrin thrombus in small vessel injury
  • PDGF stimulates smooth muscle hyperplasia (see: pathogenesis of atherosclerosis)
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13
Q

Why do petechiae appear?

A

Thrombocytopenia causes disassembly of intercellular jxns and RBCs leak out

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14
Q

How is the extrinsic coagulation system activated?

A

Damaged tissue activates factor 7, which activates factors 9 and 10

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15
Q

What does factor 12 do?

A
  • Initiates intrinsic coagulation system when exposed to subendothelial collagen
  • Activates factor 11, plasminogen (—> plasmin) and kiminogen (—> kallikrein, bradykinin)
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16
Q

What factors are involved in the intrinsic coagulation system?

A

Factors 8, 9, 11, 12

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17
Q

What factors are involved in the final common coagulation pathway?

A

Factors 1, 2, 5, 10

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18
Q

How is thrombin formed?

A

Prothrombin is cleaved by prothrombin complex (product of final common coagulation pathway) into thrombin

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19
Q

What are 4 functions of thrombin?

A
  • Converts fibrinogen —> fibrin
  • Activates factor 13, which enhances fibrin cross-linking
  • Activates factor 8
  • Activates protein C, which inactivates factors 5 and 8
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20
Q

Where is vitamin K activated and what does it do?

A
  • Activated in liver by epoxide reductase

* Along with calcium, activates factors 2, 7, 9, 10 and protein C

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21
Q

Which factors are consumed in clot formation?

A

1 (fibrinogen), 2, (prothrombin), 5, 8

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22
Q

Name 5 activators of the fibrinolytic system.

A

tPA, factor 12, streptokinase (from streptococci), urokinase, anistreplase

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23
Q

What does aminocaproic acid do?

A

Blocks plasminogen activation

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24
Q

What does plasmin do?

A

Breaks up cross-linked fibrin into fragments called D-dimers

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25
Q

What happens in the vascular phase?

A
  • Transient local vasoconstriction
  • Activation of factor 7 by TTP
  • Activation of factor 12 by exposed collagen
26
Q

What happens in the adhesion step of the platelet phase?

A

Platelet GpIb receptors adhere to vWF in damaged endothelial cells

27
Q

What is Bernard-Soulier disease?

A

Absence of GpIb receptors

28
Q

What happens in the release reaction step of the platelet phase?

A

Platelet dense bodies release ADP, which primes GpIIb-IIIa receptors to bind fibrinogen

29
Q

What is the temporary platelet thrombus?

A

Held together with fibrinogen, marks end of bleeding time

30
Q

What happens in the coagulation phase?

A

Thrombin converts fibrinogen —> fibrin to form STABLE platelet thrombus

31
Q

What happens in the fibrinolytic phase?

A

Plasmin cleaves fibrin, breaking clot

32
Q

What does the PT (prothrombin time) test, and what are 3 of its uses?

A
  • Tests extrinsic coagulation system
  • Warfarin monitoring
  • Liver synthetic function
  • Detects factor 7 deficiency if PTT is normal
33
Q

What does the PTT (partial thromboplastin time) test, and what are 2 of its uses?

A
  • Tests intrinsic coagulation system
  • Heparin monitoring
  • Factor deficiencies in intrinsic coagulation system
34
Q

What does FDPs stand for and what does it test?

A
  • Fibrin(ogen) degradation products

* Tests plasma degradation of fibrin(ogen)

35
Q

What does a D-dimer test? What conditions is it used for? What are the major pro and con?

A
  • Specific for lysis of FIBRIN thrombi
  • Monitors fibrinolytic therapy OR tests for clot-related conditions (DVT, PE, DIC, etc.)
  • High sensitivity—can use to r/o diseases
  • Low specificity—frequent false positives with inflammation, liver disease, trauma, etc.
36
Q

Acute idiopathic thrombocytopenic purpura

A
  • Children 2-6 yrs
  • 1-3 weeks after viral infection
  • Epistaxis, easy bruising, petechiae
  • IgG vs. GpIIb-IIIa receptors (type II hypersensitivity)
  • Steroids or IV IG
37
Q

Chronic idiopathic thrombocytopenic purpura

A
  • Adults, esp. women 20-40 yrs
  • Gradual onset, may be caused by SLE, HIV, etc.
  • Epistaxis, easy bruising, petechiae
  • IgG vs. GpIIb-IIIa receptors (type II hypersensitivity)
  • Splenectomy; acute bleeding may be stopped w/ IV gamma-globulin
38
Q

Neonatal alloimune thrombocytopenia

A
  • Feto-maternal mismatch in platelet-specific PlA1 antigen
  • Maternal IgG crosses placenta and attacks PlA1
  • Neonate: few days of petechiae; in severe cases, CNS hemorrhage
39
Q

Post-transfusion purpura

A
  • Mothers who have developed anti-PlA1 IgG and receive PlA1-positive transfusion
  • Severe thrombocytopenia 7-10 days after transfusion
40
Q

Type I heparin-induced thrombocytopenia

A

Early in heparin course, self-limiting

41
Q

Type II heparin-induced thrombocytopenia

A
  • 5-14 days after heparin therapy
  • Activation of coagulation system + vessel thrombosis
  • Treat with thrombin antagonists
42
Q

Thrombotic thrombocytopenic purpura

A
  • Women 10-50 yrs old
  • Increased vWF multimers promoting platelet activation
  • Endothelial damage with drugs, infection, HTN, autoimmune disease, malignancy, radiation
  • Platelets are consumed
  • Clinical pentad: fever, thrombocytopenia, renal failure, schistocytes, CNS deficits
  • Plasma exchange therapy, steroids; in severe cases splenectomy
  • Mortality rate 10-20%
43
Q

How can portal HTN lead to thrombocytopenia?

A

Platelets become sequestered in spleen (hypersplenism)

44
Q

Name 3 common causes of thrombocytosis.

A

Chronic iron deficiency, malignancy, splenectomy

45
Q

What are 3 common signs of platelet dysfuncion?

A

Epistaxis, bleeding from superficial scratches, easy bruising (all may also occur with coagulation deficiency)

46
Q

What is senile purpura?

A

Purpura in elderly associated with trauma; normal result of aging

47
Q

What are 2 common signs of coagulation deficiency?

A

Late rebleeding after surgery, hemarthroses (severe deficiency)

48
Q

Hemophilia A

A
  • XLR
  • Factor 8 deficiency (intrinsic coagulation system)
  • Increased PTT
  • Treat mild cases with desmopressin acetate
  • Treat severe cases with factor 8 infusion
49
Q

Hemophilia B (Christmas disease)

A

Factor 9 deficiency; clinically indistinguishable from hemophilia A

50
Q

Classic von Willebrand disease

A
  • Autosomal dominant
  • May be produced by angiodysplasia or severe aortic valve stenosis (repaired with AV replacement)
  • Increased PTT in 50% or fewer of cases; gene analysis to confirm diagnosis
  • Treat with desmopressin acetate or OCPs (increases vWF release, stabilizes factor 8)
  • In severe cases, infuse cryoprecipitate
51
Q

Antibodies against coagulation factor(s)

A
  • Most common vs. factor 8, can occur postpartum or in hemophiliacs receiving factor 8 transfusion
  • Increased PT and/or PTT; mix with normal plasma to differentiate immune destruction (no correction of PT/PTT) from decreased factor quantity (correction of PT/PTT)
52
Q

Cirrhosis-caused hemostasis disorders

A
  • Decreased synthesis of coagulation factors, anticoagulants, fibrinolytic agents
  • Decreased clearance of fibrin(ogen) degradation products, D-dimers, tPA
  • Increased PT/PTT, FDPs, D-dimer
53
Q

DIC (disseminated intravascular congestion)

A
  • Fibrin thrombi throughout microcirculation —> ischemia (mostly composed of RBCs with trapped leukocytes and platelets)
  • Bleeding from nose, GI tract, puncture sites —> anemia w/ schistocytes
  • May be caused by damaged tissue (massive trauma, shock, malignancies, obstetrical problems, ARDS, acute pancreatitis, rattlesnake bite)
  • May be caused by endothelial cell injury (Gram-negative septicemia [MCC], deposition of immune complexes [ex. SLE], severe temp. alterations)
  • Bleeding from consumption and trapping of platelets, activation of fibrinolytic system
  • Increased PT/PTT thrombocytopenia, positive FDPs/D-dimer
  • TREAT UNDERLYING CAUSE!
  • Infuse frozen plasma, packed RBCs, cryoprecipitate for fibrinogen deficiency
54
Q

Primary fibrinolysis

A
  • Causes: open heart surgery, radial prostatectomy, cirrhosis
  • Increased PT/PTT, FDPs; NEGATIVE D-dimer, normal platelets
  • Treat w/ aminocaproic acid to block plasminogen
55
Q

Secondary fibrinolysis

A
  • Compensatory reaction in DIC

* Increased FDPs, D-dimer; thrombocytopenia

56
Q

Antiphospholipid syndrome

A
  • Commonly associated w/ SLE, other autoimmune disorders
  • Venous and arterial thrombi
  • May cause false positive syphilis serology test with anticardiolipin Ab (ACA)
  • Sx include DVT, stroke
  • Best test is ACA
  • Treat w/ warfarin therapy
57
Q

Name 5 acquired causes of thrombosis syndromes.

A

Stasis of blood flow, malignancy, folic acid/B12 deficiency, OCPs, hyperviscosity

58
Q

Factor 5 Leiden disorder

A
  • Autosomal dominant; clots at early age

* Factor 5 cannot be degraded

59
Q

Antithrombin 3 deficiency

A
  • Autosomal dominant; clots at early age
  • ATIII normally neutralizes several factors (serine proteases)
  • Normal PTT after heparin
60
Q

Proteins C and S deficiency

A
  • Autosomal dominant; clots at early age
  • Activated factors 5 and 8 cannot be inhibited
  • Warfarin therapy, but at low dose to avoid cutaneous vessel thrombosis and skin necrosis

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