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Block 6 > Hemostasis wk7t11 > Flashcards

Hemostasis wk7t11 Flashcards

1
Q

3 stages in thrombus formation

A
  • vascular constriction
  • primary hemostasis- platelets
  • secondary hemostasis- fibrin
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2
Q

hemostasis

  • immediate response
A

vasoconstriction

  • endothelin release causes vasoconstriction
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3
Q

primary hemostasis

A

platelets

  1. platelet adhesion via VWF
  2. shape change/ activation (stick out adhesion molecules)
  3. granule release (ADP, TXA2 potent vasoconstrictor)
  4. recruitment
  5. aggregation (hemostatic plug), assembly of factors in secondary hemostasis
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4
Q

secondary hemostasis

A

thrombin + fibrin

  • rapidly formed
  • localized to site of injury
  • ultimately degradable
  • formation of a temporary barrier at site of injury
  • fibrin on top ok platelets, some trappen pmns and rbcs
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5
Q

Four enzymes in coagulation cascade

A

7,9,10,2 (thrombin)

serine proteases

synthesized in lover

vitamin K dependent

Ca2+ dependent

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6
Q

vitamin K

A
  • co-factor for a liver carboxylase enzyme
  • carboxylase adds COO- group to 4 proteases
  • COO- on proteases alows Ca+2 binding
  • coumadin inhibits carboxylase reaction
  • Vit K deficiencies seen in newborns, malnutrition, gut sterilization
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7
Q

Cofactors in coagulation cascade

A

Factor VIII, cofactor for factor IX

Factor V, co-factor for factor X

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8
Q

Corollaries

A

Neither enzymes nor co-factors are consumed in a reaction

Diminution of an enzyme or co-factor does not impair coagulation until the plasma level is very low (<30%) – phenotypes are recessive or X-linked

Fibrinogen and vWF are consumed in this reaction, so fibrinogen mutations and vWD can act as autosomal dominant

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9
Q

clinical findings of platelet defects

A
  • petechiae and purapura- usually symetric
  • hx of easy or spontaneous bruising
  • mild to moderate mucosal membrane bleeding
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10
Q

Platelet disorders

A
  • thrombocythemia- primary or secondary
  • thrombocytopenia- production or destruction
  • loss of platelet function- congenital (rare) vs. acquired (more common)
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11
Q

Thrombocythemia

A

** primary**- a myeloproliferative disease, essential thrombocythemia

  • platelets can have norma or abnormal function

secondary- increased release from bone marrow due to steriods or stress

  • platelets have normal function
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12
Q

thrombocytopenia

A

production

  • marrow replacement, aplasia, viral infections, drugs, rare congenital disorders

destruction

  • prosthetic valves, hypersplenism, immune mediated, DIC
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13
Q

causes of immune thromocytopenia

A

autoImmune (ITP)- acute and chronic

Alloantibodies - neonatal, transfusion (MHC)

Drug induced (drug as hapten), e.g. HIT

Disease associated

Other autoimmune

Lymphopholiferative

Solid tumors

Infection - viral, bacterial, parasitic

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14
Q

Acute vs chronic ITP

idiopathic thrombocytopenic purapura

A

acute:

2-9 years
Abrupt onset
Antecedent infection
<20,000 plts
2-6 weeks
80% spontaneous remission
variable response to immunosuppression or splenectomy

chronic:

20-40 yrs, 3F:1M
Gradual onset
no clear antecedent
20-100,000 plts
years
spontaneous remission rare
commonly respond to immunosuppression or splenectomy

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15
Q

Loss of platelet function

A
  • uremia
  • liver disease
  • prosthetic valves
  • aspirin or NSAIDS or other drugs
  • essential thrombocythemia
  • congenital- VWD, intrinsic platelet defects
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16
Q

lab tests to assess platelet type bleeds

A
  • platelet count
  • bone marrow evaluation: problem of production or destruction
  • bleeding time- only if platelet count is >100K
  • platelet aggregation assays- to test for specific defects
17
Q

Thrombocytopenia ranges

A
  • <5K imminent risk of GI or cerebral hemorrhage
  • <20K risk of spontaneous bleeding
  • <50K risk of excess bleeding with surgery
18
Q

Bleeding time

A
  • poor screening test
  • bleeding time prlongs when platelet count <100K

- bleeding time abnormalities:

liver disease, uremia, collagen vascular disease, ess T’themia, VWD

19
Q

Coagulation disorders- hemorrhagic

A

**1. Decreased Factor production: **

Acquired – liver disease, vitamin K deficiency
Congenital – hemophilia (lack of specific factors)

2. Increased Factor consumption:

Acquired – DIC
Congenital – some rare congenital deficiencies, e.g. a2-anti-plasmin (continue to degrade clots with plasmin, so more clots form and consume factors)

20
Q

Congenital bleeding disorders

A

Von Willebrand’s Disease – autosomal dominant

Hemophilia A (F VIII) or B (F IX) – X-linked

All other factors – autosomal recessive

Fibrinogen – dominant or recessive, depending on mutation

21
Q

Von Willebrand’s factor

A

made in endothelial cells

glues platelets down to exposed collagen to start primary hemostasis (so consumed in reaction, acts as autosomal dominant)

also stabilizes FVIII- so can affect secondary hemostasis

  • mutations affect amount or affect function
22
Q

Hereditary hemorrhagic disease

A

Factor VIII- Hemophila A- x linked rec

factor IX- hemophila B- x-linked rec

VWF- VWD- auto dom

23
Q

Clinical findings in factor deficiencies

A

common:

Bleeding in major muscles and joints
Large bruises

rare:

Mucosal hemorrhage
Intracranial bleeds
Bleeding from minor cuts and abrasions

24
Q

regulators of coagulation

A

Plasmin – degrades fibrin

Protein C/Protein S – enzyme/co-factor that degrade FVIII and FV

Anti-thrombin III (ATIII) – serine protease inhibitor. In presence of heparin/heparan, inhibits FII, X, IX (not FVII).

25
Q

Coagulation disorders- thrombotic

A

Antiphospholipid syndrome (autoimmune, often seen in lupus)

FVLeiden mutation- resistance to Protein C

Protein C deficiency

Protein S deficiency

ATIII deficiency

Prothrombin mutation

Homocysteinemia

All are autosomal dominant with incomplete penetrance - most symptomatic patients have >1 mutation and other contributing factors

26
Q

Trigger mechs in DIC

A

Direct intravascular factor activation by proteases - snake venoms, proteases released in acute pancreatitis, crude factor concentrates

Release of cellular procoagulants, e.g. Tissue Factor - intravascular cell lysis (hemolysis, leukemia, granulocyte lysis in sepsis), extravascular cell lysis (tumor, trauma, surgery), ascitic or amniotic fluid emboli

Vascular factors - endothelial cell damage by endotoxin, hypotension and stasis (shock), hemangiomas

27
Q

Microvascular thrombi

A
  • glomerular capillaries frequently affected
  • fibrin-platelet thrombi in DIC

0 widespread focal ischemia

28
Q

Lab tests to evaluate hemorrhagic and thrombotic diseases

A

Prothrombin Time (PT) 9-12 sec

Partial Thromboplastin Time (PTT) 22-33 sec

**Fibrinogen ** 200-400 mg/dl

Specific factor/co-factor assays >50% activity

APC resistance/ FVLeiden negative

D-dimer assay negative

Block 6 (17 decks)

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