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Heme > Hemostasis > Flashcards

Hemostasis Flashcards

0
Q

Dense vs. alpha granules

A
  • dense: serotonin, Ca, ATP, ADP
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1
Q

vWB disease

A
  • autosomal: I and II - dominant; III - recessive
    ~ ch 12
    ~ most common hereditary coag abnormality
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2
Q

Initial vasoconstriction (2)

A
  • neuro stimulated

- endothelin

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3
Q

Von willebrands factor

A
  • from platelets and (majority) and endothelial Weible Pilade bodies
  • binds GpIb
  • stabilizes factor VIII
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4
Q

GpIIa/IIIb

A
  • fibrinogen binder

- fibrinogen -> fibrin via Thrombin

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5
Q

Co-factors req vitamin K

A
  • II
  • VII
  • IX
  • X
  • C
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6
Q

Thrombin function

A
  • cleaves proteins off fibrinogen (fuzzy bits on top of bar bell) to activate it
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7
Q

Factor XIII

A
  • cross links polymerized fibrin proteins

- aka trans glutaminase

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8
Q

Tissue factor (factor III, thromboplastin)

A
  • initiates extrinsic coagulation

- in most cells in the body

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9
Q

PT test

A

Tests factors in extrinsic pathway

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10
Q

PTT (partial thromboplastin time)

A

Measures intrinsic pathway

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11
Q

Protein C

A
  • serine esterase
  • works along with protein S (co-factor)
  • PC sequesters F V and VIII
  • deficiency -> hypercoagulability
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12
Q

Warfarin paradox

A
  • warfarin decreases all factors including PC, but its short 1/2 life it’s is decreased first so initial administration of warfarin actually increases your risk of clotting
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13
Q

TTP

A

ADAMSTS13 deficiency

  • normally degrades vWF monomers; defect = thrombi
  • autoimmune process -> auto Ab -> adamsts13
    • typical pt. is 30 y/o female
  • corticosteroids, splenectomy
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14
Q

Verotoxin

A
  • E.Coli 0157H7

~ can cause HUS -> microangiopathic anemia

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15
Q

TTP/HUS lab findings

A
  • thrombocytopenia (using up platelets)
  • NORMAL PT/PTT
  • anemia schistocytes
  • increase MGKs on biopsy
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16
Q
  • Genetic GP1a deficiency

- mild tcytopenia and enlarged platelets

A
  • Bernard-Soulier syndrome

-

17
Q
  • GPIIb/IIIa defect; impaired platelet aggregation
A

Glanzmann Thrombasthenia

18
Q

TTP

A
  • ADAMSTS13 deficiency
  • vWF doesn’t get broken down -> microangiopathic hemolytic anemia (schistocytes)
  • usually auto-antibody: adult females
  • CNS effects predominate (over renal as in HUS)
19
Q

HUS

A
  • classically seen in EHEC 0157:H7
  • skin and mucosal bleeds, Microangiopathic HemeAneme
  • renal insufficiency
  • Tcyt, with increased bleeding time, normal PTT/PT, schistocytes,
20
Q

Secondary hemostasis

A
  • after fibrinogen binds GPIIb/IIIa to form soft clot -> intrinsic cascade is activated to thrombin -> crosslinks in into hard clot
21
Q

Disorders of secondary hemostasis signs

A
  • hemarthrosis, rebleeding, muscle bleeding

- measured by PT/PTT

22
Q

Hemophilia A

A
  • factor VIII deficiency
  • X linked or de novo
  • increased PTT
  • normal PT
  • decreased factor VIII
  • normal platelet count and bleeding time
23
Q

Hemophilia B

A
  • same as A but with factor IX
24
Q

Factor inhibitor

A
  • test with mixing study: factor deficiency will correct, inhibitor will not
25
Q

Newborns, long-term antibiotic therapy, malabsorption

- Liver failure can mimic due to the lack of production of epoxide reductase

A

Vitamin K deficiency

26
Q

Newborns, long-term antibiotic therapy, malabsorption

- Liver failure can mimic due to the lack of production of epoxide reductase

A
  • Vitamin K deficiency
27
Q

Heparin-induced thrombocytopenia

A
  • Platelet destruction secondary to heparin therapy may cause thrombosis
28
Q

Common causes of DIC

A
  • Amniotic fluid
  • Sepsis traditionally E. coli or N. meningitis (TNF IL1)
  • Adenocarcinoma mucin activating coagulation
  • Acute promyelocytic leukemia, MPO
  • Rattlesnake bite
29
Q

DIC lab findings

A
  • Decreased platelet counts
  • Increased PT/PTT (Getting used up in clots)
  • decreased fibrinogen (Getting used up in clots)
  • Microangiopathic hemolytic anemia
  • Elevated D dimer most specific for DIC (Split product of cross-linked fibrin)
30
Q
  • Resembles DIC but with negative D dimer And normal platelets
  • Due to plasmin overactivity
    ~ Radical prostatectomy
    ~ Liver Cirrhosis
A

Disorder of fibrinolysis

31
Q

Virchow Triad

A
  • Endothelial damage, venous stasis, hypercoagulability
32
Q

Lines of Zahn

A
  • Along with adherence to endothelial wall indicates premortem clock
33
Q

Heparin like molecules

A

Activates anti-thrombin three -> Activates protein C which sequesters factors V and VIII

34
Q

Endothelial protection against thrombus

A
  • Block exposure to sub endothelial collagen
  • Prostacyclin and nitrous oxide vasodilation
  • Heparin like molecule secretion
  • TPA secretion
  • Thrombomodulin secretion (modulates thrombin -> activate protein C)
35
Q

Elevated homocystine

A
  • Due to folate or B12 deficiency

- Results in endothelial damage -> Increasing risk for thrombus

36
Q

Considerations in pre-existing protein C or S deficiency

A
  • Administration of warfarin can lead to skin the necrosis, in addition to the increased risk for thrombus
37
Q

Most common inherited hypercoagulable state

A

Factor five leiden mutation

- Lacks binding site for deactivation by protein CNS

38
Q

No increase in PTT with standard heparin dosing

A

Anti-thrombin III deficiency

39
Q
  • Shortness of breath, hemoptysis, chest pain
  • VQ mismatch
  • Positive D dimer
A
  • Diagnostic for pulmonary embolism
  • Typically from right ventricle
  • Sudden-death from saddle embolus
40
Q

Extrinsic factor production

A
  • hepatic

- liver damage -> prolonged PT

Heme (7 decks)

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