hemostasis Flashcards

1
Q

3 key components of normal hemostasis

A

vascular endothelium
platelets
clotting factors

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2
Q

define normal hemostasis

A

physiologic process by which blood vessel lining cells, platelets, and coagulation factors in blood work together to stop bleeding

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3
Q

define coagulation

A

process by which liquid blood converted to solid clot.

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4
Q

3 requirements for optimal function of normal hemostasis

A
  • normal blood tempp
  • normal pH
  • normal calcium concentration.
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5
Q

process of primary hemostasis

A
  1. exposed subendothelial cells. vWF sees and spreads like glue . vWF adheres and sticks to platelet via gp1b. = platellet adhesion
  2. platelet secretion -platelet secretes contents to attract more platelets
  3. platelet aggregation - via gp2b3a platelet binds fibrinogen to form blood clot
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6
Q

lab eval of primary hemostasis

A

platelets: number, size morphology, special platelet function tests, medication history
vWF = factor level & fxn

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7
Q

secondary hemostasis.

A

extrinsic 7–> 10 -> 5 -> 2 ->1
intrinsic 12 -> 11 -> 9_>(cofacotr 8) -> 10 -> 5 -> 2-> 1
after 1 - crosslinked qith 13.
activation of factor 2 AKA thrombin = key. converts fibrinogen to fibrin = stable clot formed.

factor 7 - extrinsic factor. quickly turns off pathway after beginning activation.
thrombin activates facotrs 11, 8, 5, in pathway. so factor 12 isnt really necessary for coagulation.

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8
Q

lab eval of secondary hemostasis

A

PTT = assess intrinsic pathway - activate factor 12 in lab.
PT = measure extrinsic pathway
converted to INR - international normalization ratio.
detecting clot formation in vivo = optical density, electromechanical.

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9
Q

define fibrinolysis

A

normal process that breaks down/lyses clot away in time.

plasminogen – activated to plasmin breaks down fibrin.

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10
Q

lab evaluation

A

test fibrinogen, d-dimers, other special tests

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11
Q

bleeding disorders

A

acquired or hereditray.
acquired more frequent.
categories? platelet, VWF, factor deficiencies
cause of acquired: meds, alcohol ,liver/kidney failure,

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12
Q

hereditary - primary hemostasis defect
cause
clinical presentation

A

causes: VWF disease; platelet dysfunction

clincial presentation: muco-cutaneous bleeding: nose bleeds, heavy periods.

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13
Q

secondary hemostasis defects
cause
clinical presentation

A

cause: low coagulation factors
x-linked - hemophilia A (deficient factor 8)
hemophilia B - deficient factor 9.
autosomal recessive - hemophilia C.
clinical presentation: deep tissue hematoma - bleeding in joints/muscles.

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14
Q

vWF disease

A

low or abnormal
autosomal dominant.
most common hereditary disorder.
presents: muco-cutanesous. usually mild or asymptomatic

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15
Q

hereditary platelet disorders

A

present w muco-cutaneous bleeding.
treatment = platelet transfusion.
- bernard-soulier: autosomal recessive, gp1b deficiency. no platelet adhesion. = severe bleeding

glanzmann’s thrombasthenia: autosomal recessive, gp2b3a deficiency. no platelet aggregation or binding to fibrinogen. = severe bleeding
platelet granule abnormalities/secretion defects = no granules to be secreted. cant recruit/activate other platelets to amplify platelet adhesion

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16
Q

hereditary coagulation factors disorders

A
hem A (x): facotr 9
hem B (X): facotr 8
presentation of above: mild (excess bleed w trauma); moderate (excess bleed w minor injury); severe = spontaneous bleeding.
treat: replace deficient factor. 
hem C (auto): factor 6
17
Q

antiplatelet agents & anticoagulants

A
antiplatelet = inhibit platelet function
anticoag = inhibit coagulation.
18
Q

clinical and lab approach to hemostasis and coagulation

A
  • screen? not rlly.
    clinical history is important. family history, bleeding history, meds, past medical, surgical history.
    physical exam
    lab evaluations = basline. if concerned about those - do VWF factor & function; platelet fxn, hematology consultation