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FOD > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

coagulopathy

A

A condition characterized by impaired clotting of blood

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2
Q

Hypercoaguability (thrombophilia)

A

A condition characterized by an increased tendency toward blood clotting

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3
Q

Reflex vasoconstriction

A

1st step of primary hemostasis

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4
Q

2nd step of primary hemostasis

A

vWF line surface of disruption at subendothelial collagen, platelets bind to vWF

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5
Q

3rd step of primary hemostasis

A

Platelets activate and degranulate

Binding to vWF causes change in platelet shape -> dump mediators from granulation. Mediators are ADP and TXA2.

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6
Q

Platelet aggregation

A

4th step in primary hemostasis

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7
Q

Primary hemostasis

A

Form a weak platelet plug. Mediated by platelet wall interactions

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8
Q

Secondary hemostasis

A

Stabilizes platelet plug by forming a fibrin meshwork. Mediated by coagulation cascade.

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9
Q

Tertiary hemostasis

A

clot limitation and fibrinolysis - need to limit clot size and contain the reaction

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10
Q

Plasmin

A

In fibrinolysis, this molecule removes the thrombus by cleaving fibrin and fibrinogen, destroys coagulation factors and blocks platelet aggregation

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11
Q

tPA

A

converts plasminogen to plasmin to start fibrinolysis

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12
Q

Normal endothelium

A

Expresses proteins that inhibits platelet aggregation, act as vasodilators, facilitate the inactivation of thrombin

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13
Q

vWF

A

Line surface of endothelial disruption at subendothelial collagen. Attach to platelets

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14
Q

Bone marrow by megakaryocytes

A

Where are platelets made?

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15
Q

Factor VIII

A

vWF protects which factor

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16
Q

Liver

A

Coagulation cascade proteins are made here except VIII

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17
Q

VIII

A

Only factor made in endothelial cells

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18
Q

II, VII, IX, X

A

Vitamin K dependent factors

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19
Q

V, VIII, XI, XIII, platelets and fibrinogen

A

Thrombin activates

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20
Q

XIII

A

Enzyme that crosslinks fibrin and helps to stabilize clot, activated by thrombin

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21
Q

X

A

Active form of this factor activates thrombin, intrinsic and extrinsic pathways feed together to this factor

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22
Q

V and VIII

A

Thrombin can be an inhibitor to stop clotting cascade. Bind thrombomodulin, protein C, protein S which inactivate these factors

23
Q

Antithrombin

A

Inhibits all the serine proteases (Xa, XIa, IXa, XIIa, VIIa) but especially thrombin

24
Q

Heparin

A

Binds to antithrombin and makes it a much more potent inhibitor of thrombin
Works mostly on thrombin, but also XI and X. Major effect is intrinsic so PTT effects more striking

25
Q

TFPI

A

Inhibits Xa and VIIa

26
Q

PT

A

When extrinsic pathway is affected, this time is abnormal

27
Q

PTT

A

When intrinsic pathway is affect, this time is abnormal

28
Q

Abnormal PT

A

Defect in factor VII shows

29
Q

Abnormal PTT

A

Defect in factor XII, XI, IX, or VIII shows

30
Q

Abnormal PT and PTT

A

Defect in factor II, V, X, or fibrinogen shows

31
Q

TEG (thromboelastography)

A

Mechanical test of clotting strength development. Assesses ability of platelets to pull the fibrin clot into a tight mesh and of desolution

32
Q

Defects in primary hemostasis

A

Platelet problems, Von Willebrand disease

33
Q

Defects in secondary hemostasis

A

Hemophilia, vitamin K deficiecny, anticoagulation

34
Q

von Willebrand’s disease

A

Most common inherited bleeding disorder. Autosomal DOMINANT. Causes “mucosal” bleeding (nosebleeds, prolonged bleeding with dental work, heavy menses, easy bruising, etc) Usually type 1 is mild, but potentially a problem with major injury or surgery
Unlike most platelet problems, it is inherited, life-long, a/w family history

35
Q

von willebrand testing

A

Measure antigen level, activity (ristocetin cofactor activity), factor VIII level, multimer assay

36
Q

Petechiae, bruising, mucosal bleeding

A

Clinical presentation of platelet problems (primary hemostasis)

37
Q

ITP

A

Immune reaction to platelets. Very low platelet counts, but normal bleeding time. Platelets produced are young and super functioning

38
Q

VIII, IX

A

X-linked recessive defects in these factors (hemophilia)

39
Q

XII

A

If defect in this factor, thrombin will still activate the next step (XI)

40
Q

Hemophilia A

A

X-linked recessive, factor 8 deficiency

Bleeding deep and delayed

41
Q

Hemophilia B

A

X-linked recessive, factor 9 deficiency

Bleeding deep and delayed

42
Q

Acquired factor VIII inhibitor

A

Acquried hemophilia, antibody against this factor. Occurs most commonly in elderly patients, also seen postpartum, in rheumatologic disease, and malignancy. Presents most commonly with soft tissue bleeding
Prolonged PTT

43
Q

Vitamin K deficiency

A

See a prolonged PT and PTT, but more commonly you will see only a prolonged PT
From a dietary deficiency (rare), antibiotics, malabsorption, newborn, and coumarins
To treat, give supplements (carefully if back on Warfarin), plasma (short term fix to get factors), and Kcentra (for emergencies)

44
Q

Warfarin

A

Followed using the PT. Blocks recycling of vitamin K and causes deficiency

45
Q

Causes of a prolonged PT

A

Warfarin use, liver disease, Vit K deficiency, Factor VII deficiency

46
Q

Causes of a prolonged PTT

A

Heparin use, factor deficiency (VIII, IX, XI, XII, von willebrand (protects 8)), antiphospholipid antibody (lupus inhibitor), DIC

47
Q

Lupus anticoagulant phenomenon

A

Prolonged phospholipid-dependent coagulation tests caused by autoantibodies against phospholipid-binding proteins- cause hypercoagulable state. Anti-phospholipid syndrome is associated with thrombosis, not bleeding (more prone to thrombosis)
In vitro phenomenon - test makes it look like a bleeding problem with prolonged PTT
In vivo they are not anticoagulants but promote thrombosis

48
Q

DIC

A

Coagulation system is activated everywhere. From sepsis, viral hemorrhagic fevers, trauma, cancers, OB complications, toxins (rattlesnakes), vascular disorders, immunologic disorders,etc
Usually a SECONDARY disease
Intravascular deposition of fibrin leads to trombosis of small vessels (microangiopathic hemolysis), depletion of platelets and coag factors leads to bleeding

49
Q

Schistocytes or helmet cells

A

Types of cells seen in DIC and TTP from microangiopathic hemolysis

50
Q

Lab findings for DIC

A

Prolonged PT, PTT
Decreased platelet count and fibrinogen
Increased D- dimers***** seen here because fibrin is being cut
Abnormalities on peripheral smear (like schistocytes)

51
Q

Anti-thrombin III deficiency

A

Most common severe inherited thrombophilic disorder. Can cause venous thrombosis and embolism

52
Q

Antithrombin, Protein C, Protein S deficiencies

A

Uncommon causes of inherited thrombophilia associated with high thrombotic risk

53
Q

Factor V Leiden

A

Common cause of inherited thrombophilia associated with lower thrombotic risk- mutation that keeps factor activated longer than it should be

54
Q

Liver disease

A

Have a hard time forming clots because of loss of all factors but 8, can’t activate Vit K
ALSO have a hard time inhibiting clots so have prolonged PT and PTTs but may actually be prone to thrombosis

FOD (5 decks)

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