STEP 1 — MCQs (NO answers here)

MCQ 1 — Effects of Turbulence

Turbulence contributes to thrombosis mainly by:

a. Increasing laminar flow

b. Causing endothelial injury/dysfunction and creating pockets of stasis

c. Reducing platelet-endothelium interaction

d. Enhancing fibrinolysis

e. Increasing NO and PGI₂ production

MCQ 2 — Major Factor in Venous Thrombosis

The most important contributor to venous thrombus formation is:

a. Turbulence only

b. Stasis

c. High systolic pressure

d. Hyperoxygenation

e. Lymphatic obstruction

MCQ 3 — Normal Laminar Flow

In normal laminar blood flow:

a. Platelets travel close to the vessel wall

b. Platelets remain mainly in the center of the lumen

c. Flow is chaotic and variable

d. Platelets constantly contact endothelium

e. Red cells only remain at the wall

MCQ 4 — Effects of Stasis & Turbulence

Which is NOT a consequence of stasis or turbulence?

a. Promotion of endothelial activation

b. Enhanced procoagulant gene expression

c. Slowed washout of activated clotting factors

d. Increased inflow of clotting factor inhibitors

e. Platelet and leukocyte contact with endothelium

MCQ 5 — Atherosclerotic Plaques

Ulcerated atherosclerotic plaques promote thrombosis because they:

a. Release anticoagulants

b. Increase blood viscosity

c. Expose subendothelial ECM and cause turbulence

d. Improve laminar flow

e. Release prostacyclin

MCQ 6 — Aneurysm Thrombosis

Aneurysms predispose to thrombosis primarily because:

a. They reduce blood pressure

b. They create areas of local stasis

c. They increase endothelial NO

d. They increase shear stress and fibrinolysis

e. They decrease blood viscosity

MCQ 7 — MI and Cardiac Mural Thrombi

Cardiac thrombi are more likely to form after acute MI because:

a. Myocardium contracts too strongly

b. Noncontractile myocardial segments create stasis

c. The infarcted region produces excess t-PA

d. Platelets are destroyed

e. Fibrinogen levels fall

MCQ 8 — Mitral Stenosis & A-Fib

Mitral stenosis contributes to thrombosis mainly by:

a. Increasing left atrial pressure → vasodilation

b. Causing left atrial dilation → stasis

c. Increasing NO release

d. Increasing fibrinolysis

e. Continuous laminar flow

MCQ 9 — Polycythemia Vera

Hyperviscosity syndromes predispose to thrombosis because:

a. They decrease RBC count

b. They accelerate blood flow

c. They increase resistance → stasis in small vessels

d. They activate protein C

e. They increase PGI₂ production

MCQ 10 — Sickle Cell Disease

Sickle cell anemia predisposes to thrombosis because:

a. Deformed RBCs cause vascular occlusions → stasis

b. RBC membranes release anticoagulants

c. t-PA levels increase

d. Fibrinogen levels fall

e. Platelets cannot function

STEP 2 — ANSWERS + SHORT EXPLANATIONS

MCQ 1 — b

Turbulence → endothelial injury + countercurrents + local pockets of stasis.

MCQ 2 — b

Stasis is the major contributor to venous thrombosis.

MCQ 3 — b

Normal laminar flow keeps platelets in the center, away from endothelium.

MCQ 4 — d

Stasis impedes inflow of clotting factor inhibitors — does NOT increase them.

MCQ 5 — c

Ulcerated plaques:

• Expose subendothelial ECM
• Create turbulence

→ thrombosis.

MCQ 6 — b

Aneurysms → local stasis → thrombosis.

MCQ 7 — b

Infarcted myocardium becomes noncontractile, causing stasis, → mural thrombi.

MCQ 8 — b

Mitral stenosis → left atrial dilation, worsened by atrial fibrillation → stasis.

MCQ 9 — c

Polycythemia vera → hyperviscosity → increased resistance → stasis.

MCQ 10 — a

Sickled RBCs obstruct small vessels → occlusion + stasis → thrombosis risk.

STEP 3 — HIGH-YIELD NOTES (EXAM-READY)

Abnormal Blood Flow → Stasis + Turbulence

1. Core Principle

Abnormal blood flow—stasis and turbulence—is one of the three pillars of Virchow’s Triad.

Both dramatically increase the likelihood of intravascular thrombosis by disrupting normal endothelial–blood interactions.

2. Normal Laminar Flow — Why It Protects

• Blood flows in smooth laminar layers.
• Platelets & leukocytes remain in the center of the lumen.
• A thin layer of fast-moving plasma lines the wall → prevents them from touching the endothelium.
• → No platelet activation, no unnecessary clot.

This protective architecture is lost in stasis and turbulence.

3. How Stasis & Turbulence Promote Thrombosis

A. Endothelial Activation (Most Important)

Both stasis and turbulence alter shear stress →

Endothelium shifts to a prothrombotic phenotype:

• ↑ Tissue factor
• ↑ vWF
• ↑ PAI-1(Plasminogen Activator Inhibitor-1)
• ↓ Thrombomodulin
• ↓ Protein C activation

Bottom line: Endothelium becomes procoagulant.

B. Increased Platelet & Leukocyte Contact with Endothelium

• Sluggish flow brings platelets close to the vessel wall.
• Platelets stick, activate, and aggregate → clot formation.
• Also enhances leukocyte adhesion → inflammation + thrombosis.

C. Failure to Wash Out Clotting Factors

Especially in stasis:

• Activated coagulation factors accumulate locally.
• Inhibitors (antithrombin, protein C/S) cannot enter effectively.
• → Runaway coagulation, large thrombus formation.

4. Clinical Settings Where Abnormal Flow Causes Thrombosis

A. Ulcerated Atherosclerotic Plaques

• Cause turbulence.
• Expose collagen + TF-rich necrotic core.
• → Powerful trigger for arterial thrombosis.

B. Aneurysms

• Dilated segments create pockets of stagnant blood.
• → Common site for mural thrombi in the aorta or large arteries.

C. Post–Myocardial Infarction

• Infarcted ventricle is akinetic/dyskinetic.
• Blood becomes stagnant → mural thrombus.
• Ventricular aneurysm formation later increases stasis even more.

D. Mitral Stenosis + Atrial Fibrillation

• Mitral stenosis → left atrial enlargement.
• Atrial fibrillation → no organized contraction → major stasis.
• → Extremely high risk of left atrial thrombi → systemic emboli (stroke!).

E. Hyperviscosity States

1. Polycythemia vera
• ↑ RBC mass → viscosity ↑ → flow ↓ → stasis → thrombosis.
2. Sickle cell disease
• Sickled RBCs occlude microcirculation.
• Stasis + endothelial injury → microvascular thrombosis.

5. High-Yield Clinical Applications

Abnormal blood flow is a major cause of:

• Deep venous thrombosis (DVT)
• Atrial thrombi in AF + MS
• Ventricular mural thrombi post-MI
• Thrombi on aneurysm walls
• Microthrombi in sickle cell disease
• Thrombosis in hyperviscosity syndromes

Exam-Ready Mnemonic

“FAST-T” → Flow Abnormalities Support Thrombus

• F – Fibrillation (AF)
• A – Aneurysm
• S – Stasis (immobility, hyperviscosity)
• T – Turbulence (atherosclerosis, plaques)
• T – Thrombosis follows