BIO230 Chapter 11 Extended

1. Big Picture Framework (START HERE)

Hemostasis = the regulated process that:

  1. Stops bleeding

  2. Stabilizes the injury

  3. Removes the clot once healing occurs

⚖ Balance is everything

  • Too little activity → bleeding

  • Too much activity → thrombosis

This is why your slides emphasize balance imagery and not just the cascade.

2. The Four Components of Hemostasis

You should ALWAYS think in this order:

1⃣ Vascular Component

What happens first after injury

  • Immediate vasoconstriction

  • Exposure of collagen and tissue factor

  • Endothelium shifts from anti-clotting → pro-clotting

Why this matters

  • Collagen exposure is the trigger for:

    • Platelet activation

    • Intrinsic coagulation pathway

📌 Clinical links:

  • Scurvy (vit C deficiency) → weak collagen → fragile vessels

  • Ehlers-Danlos syndrome → connective tissue defect
    Bleeding occurs even if platelets & factors are normal

    BIO 230 Sp 2026 Chapter_011.pptx

2⃣ Platelet Component → Primary Hemostasis

Platelets form the initial plug.

Platelet origins

  • Derived from megakaryocytes in bone marrow

Key platelet functions

  1. Adhere to damaged vessel

  2. Aggregate with each other

  3. Provide surface for coagulation factors

Step-by-step platelet plug formation

  1. Vessel injury → collagen exposed

  2. vWF binds collagen

  3. Platelets bind vWF via GpIb

  4. Platelets activate → shape change + granule release

  5. GpIIb/IIIa receptors bind fibrinogen

  6. Platelets aggregate → primary platelet plug

⚠ This plug is temporary and unstable

3⃣ Coagulation Component → Secondary Hemostasis

This stabilizes the platelet plug with fibrin.

Important rules

  • Roman numerals ≠ order of reactions

  • Activated factors have an “a” (Xa, VIIa, etc.)

  • Calcium (Ca²⁺) and platelet phospholipid (PF3) are required

3. Coagulation Pathways (EXAM CRITICAL)

🔹 Extrinsic Pathway

  • Trigger: Tissue factor

  • Key factor: VII

  • Test: PT / INR

  • Drug association: Warfarin

  • Fast pathway

🔹 Intrinsic Pathway

  • Trigger: Collagen contact

  • Factors: XII → XI → IX → VIII

  • Test: aPTT

  • Drug association: Heparin

🔹 Common Pathway

  • Begins at Factor X

  • Xa + Va → prothrombin → thrombin

  • Thrombin converts:

    • Fibrinogen (I) → fibrin

  • Factor XIII cross-links fibrin → stable clot

📌 Exam distinction:

  • Platelet plug = primary hemostasis

  • Fibrin stabilization = secondary hemostasis

    BIO 230 Sp 2026 Chapter_011.pptx

4. Fibrinolysis (Controlled Clot Removal)

Once healing occurs:

  • Plasmin breaks down fibrin

  • Produces fibrin degradation products (D-dimer)

Clinical importance:

  • Elevated D-dimer helps rule out:

    • DVT

    • PE

    • MI

    • Stroke

    • DIC

⚠ If fibrinolysis fails → dangerous clots persist

BIO 230 Sp 2026 Chapter_011.pptx

5. Platelet Disorders

Quantitative Disorders (NUMBER problem)

Thrombocytopenia

  • ↓ platelet count (<150 × 10⁹/L)

Symptoms:

  • Petechiae

  • Purpura

  • Epistaxis

  • Ecchymosis

  • Mucosal bleeding

Causes:

  • Decreased production

  • Increased destruction

  • Sequestration/dilution

Qualitative Disorders (FUNCTION problem)

  • Normal platelet count

  • Prolonged bleeding time

Causes:

  • Aspirin

  • Uremia

  • Liver disease

  • von Willebrand disease

📌 Pattern:

  • Surface bleeding = platelet problem

6. Coagulation Disorders

Hemophilia (Classic Factor Defect)

Hemophilia A

  • Factor VIII deficiency

  • X-linked recessive

  • Normal platelets

  • Normal PT

  • ↑ aPTT

Bleeding pattern:

  • Deep bleeding

  • Joints (hemarthrosis)

  • Muscles

  • Internal organs

Severity based on factor activity:

  • Severe: <1%

  • Moderate: 1–5%

  • Mild: 6–24%

von Willebrand Disease

  • Defective platelet adhesion

  • ↓ factor VIII stability

  • Milder than hemophilia A

  • Bruising + mucosal bleeding

    BIO 230 Sp 2026 Chapter_011.pptx

7. Lab Tests You Must Interpret

Screening Tests

Test

Evaluates

PT / INR

Extrinsic + common

aPTT

Intrinsic + common

TT

Fibrinogen → fibrin

D-dimer

Clot breakdown

Mixing Studies

  • Abnormal PT/aPTT → mix with normal plasma

    • Corrects → factor deficiency

    • Does not correct → inhibitor present

8. High-Yield Pattern Recognition (EXAM FAVORITE)

  • Petechiae + normal PT/aPTT → platelet disorder

  • ↑ aPTT only → intrinsic pathway defect

  • ↑ PT only → extrinsic pathway defect

  • Normal platelets + joint bleeding → hemophilia

  • Elevated D-dimer → active clot breakdown