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B&L Unit 3 > Hemostasis: Approach to Patient (complete) > Flashcards

Hemostasis: Approach to Patient (complete) Flashcards

1
Q

What are the events occurring during primary hemostasis?

A
  • Adhesion
  • Activation
  • Aggregation of platelets

forms a platelet plug

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2
Q

What are the events occurring during secondary hemostasis?

A
  • Formation of fibrin network (generated by coag cascade)

Stabilizes the platelet plug

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3
Q

Describe the structure of a mature platelet. Include dense granules, alpha granules, and phospholipids

A
  • No nucleus, but they have mitos
  • Three kinds of granules: dense, alpha, lysosomal
  • Phospholipid membrane
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4
Q

What do dense granules contain?

A
  • ATP
  • ADP
  • Serotonin
  • Calcium
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5
Q

What do alpha granules contain?

A

Proteins essential for platelet function:

  • procoag proteins (fibrinogen, Factor 5, vWF)
  • platelet factors for activation
  • growth factors
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6
Q

What do lysosomal granules contain?

A

Acid hydrolases

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7
Q

What are the 3 functions of platelets?

A

1) Adhesion to vascular subendothelium at injury sites
2) Activation of intracellular signaling pathways
3) Platelet aggregation to form the platelet plug

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8
Q

Describe the process of platelet adhesion. Include subendothelial collagen, von Willebrand factor, and glycoprotein 1b.

A
  • w/ injury, subendo components exposed => vWF adheres to this
  • circulating platelets adhere to exposed subendo via interaction w/ GP1b
  • GP3 and 4 also interact w/ exposed subendo (collagen) => ligands form

LEADS TO: firm adherence of the platelet to subendo surface

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9
Q

Explain why platelet adhesion to blood vessels does not occur under normal circumstances

A
  • Only happens when subendothelium is exposed

- Can only happen during vessel injury

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10
Q

Describe the process of platelet aggregation, including the release reaction (ADP), thromboxane synthesis, ADP and thromboxane receptors, glycoprotein IIb/IIIa, and fibrinogen.

A
  • New platelets sick to activates plateless => new ones are activated through release of thromboxane A2 and ADP
  • That process puts GP2b/3a in high affinity state
  • GP2b/3a are on each platelet
  • GP2b/3a binds fibrongen => bridge to lace platelets together
  • GP1 is bound to vWF
  • Thrombin converts fibrinogen to fibrin
  • stable clot formed
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11
Q

What are the 3 mechanisms that can lead to thrombocytopenia?

A

1) Decreased platelet production
2) Increased platelet destruction
3) Increased consumption/sequestration of platelets in spleen

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12
Q

What are the causes of decreased platelet production as a mechanism that leads to thrombocytopenia

A
  • BM disorders
  • Myelodysplasia
  • Leukemia
  • BM invasion (cancer, TB)
  • Chemo
  • Severe nutritional deficiency (B12, folate)
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13
Q

What are the causes of increased platelet destruction as a mechanism that leads to thrombocytopenia

A

Common cause: ITP

  • AutoAbs made directed at platelets => removal by macros
  • These AutoAbs are produced in spleen, macros are from spleen

Acute: children, nosebleeds, viral infection => resolves in 2-6 wks

Chronic: adults w/autoimmune disorders, requires tx

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14
Q

What are the causes of consumption/sequestration of platelets as a mechanism that leads to thrombocytopenia

A

Thrombotic thrombocytopenia purpura (TTP)

  • Endo damage => abnormal release of vWF => increased consumption of platelets
  • vWF is large b/c ADAMTS13 (normally breaks large vWF to small ones) is absent
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15
Q

What are 3 methods of treating ITP?

A

1) Corticosteroids
2) IVIG
3) Splenectomy

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16
Q

What is the mechanism by which corticosteroids increases the platelet count?

A
  • Stunt proliferation of the B cell clone that makes autoAb

- Effect in 7-10 days of tx

17
Q

What is the mechanism by which IVIG increases the platelet count?

A
  • blocks splenic Fc receptors => prevents binding to autoAb coated platelets

Remember pathoma example: like you’re throwing a stick at a dog to distract them from something else

18
Q

What is the mechanism by which splenectomy increases the platelet count?

A
  • Stops formation of autoAb (spleen did this before)

- Stops production of macros that eat the platelets (spleen did this)

19
Q

Describe the molecular defect of von Willebrand Disease

A
  • Acquired: Abs develop against vWF
  • Congenital: inadequate amount or mutations in vWF gene that cause abnormal protein function

Leads to:

  • abnormal platelet/endo interaction => 1ary bleeding disorder, mucosal/skin bleeding
  • decrease in Factor 8
20
Q

Describe the typical clinical course for a patient with von Willebrand Disease

A

Tests:

  • Bleeding time
  • PFA-100 (prolonged w/vWD)
  • Factor 8 level
  • vW Ag test
  • Ristocetin cofactor activity (measures vWF activity)
21
Q

Describe the general approach to treatment for a patient with von Willebrand Disease

A

DDAVP
- Synthetic (arginine) vasopressin

Factor 8 replacement

Must avoid aspirin/other platelet inhibiting agents

22
Q

What are the important questions to ask when obtaining a bleeding history in a pt w/ excessive bleeding?

A

1) Abnormal bruising?
2) Prolonged bleed after laceration/surgery?
3) Prolonged menstrual bleeding?
4) H/o unusual hematoma, unexplained arthritis
5) Family history
6) Drugs/meds

23
Q

What are the important lab studies to obtain when evaluating a pt w/ excessive bleeding?

A
  • Platelet count – blood smear
  • Bleeding time, PFA
  • APTT
  • PT/INR
  • Thrombin clotting time
  • Fibrinogen level
24
Q

What do an abnormal platelet count and blood smear indicate?

A

Thrombocytopenia!!

Other hematologic abnormalities

25
Q

What does bleeding time evaluate?

A

Primary hemostasis

26
Q

What does PFA-100 (platelet function analyzer) evaluate?

A

Primary hemostasis

27
Q

What does aPTT screen for?

A
  • Abnormal intrinsic pathway

Hemophilia

28
Q

What does PT/INR screen for?

A
  • Abnormal extrinsic pathway

Factor 7 deficiency

29
Q

What does thrombin clotting time (TCT) evaluate?

A
  • Fibrinogen defects
  • Presence of fibrin split products
  • Heparin effects

B&L Unit 3 (12 decks)

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