Thrombosis

Slide 1 · Thrombosis

Mechanisms, morphology, and clinicopathologic consequences

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Distinguish pathologic thrombosis from physiologic hemostasis.

Explain the interacting components of Virchow triad.

Relate arterial and venous risk factors to thrombus morphology.

Predict thrombus outcomes and major clinical consequences.

Slide 3 · Thrombosis is inappropriate intravascular clot formation

A thrombus is formed within the circulation or a cardiac chamber during life.

It may obstruct blood flow at its origin or become a source of emboli.

The affected vascular bed determines clinical severity.

Intravascular thrombus: Adherent luminal mass

Schematic vessel lumen

Schematic — not a clinical or histologic specimen

Slide 4 · Hemostasis protects; Thrombosis injures

Physiologic hemostasis

Pathologic thrombosis

Activated at a site of vascular injury

Occurs in intact or damaged vessels / cardiac chambers

Limits blood loss

May obstruct vessels or embolize

Spatially limited, regulated response

Unwanted clotting from local/systemic risk factors

Slide 5 · Virchow triad: Three principal thrombogenic abnormalities

Endothelial injury or prothrombotic activation.

Stasis or turbulent blood flow.

Hypercoagulability of circulating blood.

Endothelial injury

Abnormal blood flow

Hypercoagulability

THROMBOSIS

Schematic — not a clinical or histologic specimen

Slide 6 · The three components reinforce one another

Endothelial injury changes local flow and coagulation.

Stasis and turbulence favor endothelial activation.

Acquired or inherited thrombophilia magnifies local triggers.

Slide 7 · Arterial and venous thrombosis arise in different hemodynamic settings

Arteries / heart

Veins

High shear, rapid circulation

Lower flow velocities and stasis

Endothelial injury and disturbed flow predominate

Stasis and hypercoagulability predominate

Platelet-rich lesions common

Red-cell-rich thrombi common

Slide 8 · The intact endothelium is normally antithrombotic

Healthy endothelium separates blood from thrombogenic subendothelial matrix.

Antiplatelet, anticoagulant, and fibrinolytic activities oppose unwanted clotting.

Endothelial activation can reverse this local balance.

NO / PGI₂ · thrombomodulin · t-PA

Antiplatelet + anticoagulant + fibrinolytic

Schematic — not a clinical or histologic specimen

Slide 9 · Endothelium restrains platelet adhesion and activation

Prostacyclin (PGI₂) and nitric oxide inhibit platelet activation.

Adenosine diphosphatase reduces available platelet agonists.

Exposed von Willebrand factor and collagen promote adhesion after injury.

Loss of this barrier is particularly important under arterial shear.

Slide 10 · Thrombomodulin redirects thrombin toward anticoagulation

Endothelial thrombomodulin binds thrombin.

The resulting complex activates protein C.

Activated protein C, with protein S, suppresses factors Va and VIIIa.

Thrombin + thrombomodulin

Protein C activation

Factor Va / VIIIa inhibition

Protein S is a cofactor of activated protein C

Schematic — not a clinical or histologic specimen

Slide 11 · Endothelial regulation also promotes fibrinolysis

Tissue plasminogen activator (t-PA) drives plasmin generation.

Plasmin degrades fibrin within a thrombus.

Plasminogen activator inhibitors (PAIs) limit this pathway.

Endothelial t-PA

Plasmin generation

Fibrin breakdown

Slide 12 · Severe endothelial injury exposes a thrombogenic surface

Exposed subendothelial collagen and vWF recruit platelets.

Tissue factor initiates coagulation and thrombin production.

Fibrin formation consolidates platelet-rich material.

Exposed collagen + vWF + tissue factor

Platelet adhesion → thrombin → fibrin

Schematic — not a clinical or histologic specimen

Slide 13 · Endothelial activation is not necessarily endothelial denudation

Inflammatory mediators can induce a prothrombotic endothelial phenotype.

The endothelium may remain physically present but become dysfunctional.

Changes in gene expression shift the balance toward clot formation.

Slide 14 · Activated endothelium loses anticoagulant capacity

Inflammation reduces thrombomodulin expression.

Anticoagulant pathways, including protein C–related mechanisms, are impaired.

The net effect favors thrombin activity and coagulation.

↓ Thrombomodulin and anticoagulant function

↑ Procoagulant thrombin signaling

Schematic — not a clinical or histologic specimen

Slide 15 · Activated endothelium also suppresses fibrin removal

PAI secretion increases during endothelial activation.

T-PA expression decreases.

Reduced fibrinolysis permits persistence of fibrin-rich thrombi.

Endothelial activation

↑ PAI; ↓ t-PA

Reduced fibrinolysis

Thrombus persistence

Slide 16 · Common endothelial stressors act through different routes

Physical injury and disturbed flow can directly damage or activate endothelium.

Infectious agents and inflammatory mediators alter endothelial function.

Hypercholesterolemia, homocystinemia, and cigarette-smoke toxins are implicated.

The shared consequence is a more procoagulant vascular surface.

Slide 17 · Platelets are central in high-shear arterial thrombosis

High shear makes platelet adhesion an initiating step in arterial clot formation.

Platelet activation drives recruitment and aggregation.

This underpins antiplatelet treatment rationale in coronary disease.

High shear → platelet adhesion / aggregation

Schematic — not a clinical or histologic specimen

Slide 18 · Blood normally moves in organized laminar layers

Cellular elements tend to flow centrally within the lumen.

A marginal plasma layer ordinarily separates platelets from endothelium.

Disrupted flow changes cell–wall contact and local clotting-factor exposure.

Parallel streamlines; Cells centrally located

Schematic — not a clinical or histologic specimen

Slide 19 · Stasis favors thrombosis through several mechanisms

Slower flow reduces dilution and washout of activated coagulation factors.

Stasis encourages local accumulation of procoagulant substances.

Endothelial changes and altered platelet contact may follow.

Impaired washout and accumulation of clotting factors

Schematic — not a clinical or histologic specimen

Slide 20 · Turbulence predisposes to arterial and cardiac thrombi

Disturbed streams create countercurrents and pockets of relative stasis.

Abnormal shear can injure or activate vascular endothelium.

Atherosclerotic narrowing and aneurysmal dilation are characteristic settings.

Vortices and disturbed endothelial shear

Schematic — not a clinical or histologic specimen

Slide 21 · Both abnormal flow patterns amplify endothelial activation

Stasis and turbulence alter endothelial mechanosignaling.

Adhesion molecules and proinflammatory mediators are induced.

Thrombogenic blood elements interact more readily with the vessel surface.

Disturbed flow

Endothelial activation

Cell adhesion + coagulation

Thrombosis

Slide 22 · Atherosclerotic plaques combine injury with turbulence

Plaque ulceration exposes subendothelial thrombogenic material.

Local luminal narrowing generates disturbed flow.

The combined mechanism favors occlusive arterial thrombosis.

Plaque disruption + thrombus

Schematic — not a clinical or histologic specimen

Slide 23 · Aneurysms create regions of sluggish circulation

Dilated vascular segments permit local stasis.

Aortic aneurysms can contain mural thrombi.

The vascular lesion and thrombus may coexist over an extended period.

Dilation creates a low-flow recess

Schematic — not a clinical or histologic specimen

Slide 24 · Atrial fibrillation and atrial enlargement promote thrombi

Reduced coordinated atrial contraction contributes to stasis.

Left atrial dilation can accentuate the stagnant compartment.

Mural thrombi can subsequently become an embolic source.

Atrial dilation / fibrillation

Blood stasis

Cardiac thrombus

Potential embolization

Slide 25 · Impaired ventricular contraction promotes mural thrombosis

Myocardial infarction produces noncontractile or dyskinetic regions.

Stasis and endocardial injury may coexist over injured myocardium.

These conditions favor cardiac mural thrombus formation.

Myocardial injury

Dyskinesia + endocardial injury

Mural thrombus

Slide 26 · Viscosity and abnormal erythrocytes also disturb flow

Polycythemia vera

Sickle cell disease

Increased viscosity increases flow resistance

Deformed red cells impede small-vessel transit

Small-vessel stasis contributes to risk

Local stasis contributes to thrombosis

Contrast the mechanism, not merely the color or appearance.

Slide 27 · Hypercoagulability is an increased tendency of blood to clot

It often results from abnormalities in coagulation factors or their regulation.

It is especially important in venous thrombosis.

Inherited and acquired contributors frequently interact.

↑ Procoagulant activity

↓ Anticoagulant activity

Thrombotic tendency

Especially important in venous thrombosis

Schematic — not a clinical or histologic specimen

Slide 28 · Thrombophilias can be inherited or acquired

Primary (genetic)

Secondary (acquired)

Factor V Leiden

Immobilization; tissue injury

Prothrombin G20210A variant

Malignancy; pregnancy/postpartum

Antithrombin, protein C, protein S deficiency

APS; HIT; cardiac disease

Slide 29 · Factor V Leiden impairs physiologic factor V inactivation

A variant of factor V resists cleavage by activated protein C.

The impaired negative-feedback pathway permits increased thrombin generation.

This produces a predisposition to venous thromboembolism.

Normal factor Va

Factor V Leiden

Inactivated by APC

APC resistance

APC = activated protein C

Schematic — not a clinical or histologic specimen

Slide 30 · Factor V Leiden has dose-dependent clinical implications

Heterozygous and homozygous carriers differ in thrombotic risk.

Not all carriers develop thrombosis.

Clinical expression is strongly modified by acquired exposures.

Risk should not be inferred from genotype alone.

Slide 31 · Prothrombin G20210A increases prothrombin availability

The variant involves the noncoding 3′ region of the prothrombin gene.

Prothrombin expression is increased.

Greater substrate availability contributes to venous thrombosis risk.

G20210A variant

↑ Prothrombin

Increased thrombotic tendency

Slide 32 · Loss of endogenous anticoagulants predisposes to thrombosis

Antithrombin restrains activated coagulation proteases.

Protein C and protein S regulate activated cofactors Va and VIIIa.

Deficiencies can present as early or recurrent venous thromboembolism.

Antithrombin

Protein C / protein S

Restriction of clotting

Deficiency reduces inhibitory capacity

Schematic — not a clinical or histologic specimen

Slide 33 · Inherited thrombophilia acts together with acquired triggers

A thrombophilic genotype may remain clinically silent for years.

Bed rest, pregnancy, or other exposures can add venous stasis or hypercoagulability.

Combined factors may cross the threshold for a thrombotic event.

Genetic predisposition

Acquired risk factor

Combined thrombogenic pressure

DVT

Slide 34 · Acquired thrombophilia is usually multifactorial

Some conditions act mainly through impaired venous return or local injury.

Hormonal changes may increase procoagulant and reduce anticoagulant synthesis.

Neoplasms can release thrombogenic substances and induce inflammation.

Age, smoking, and obesity contribute to overall risk.

Slide 35 · Prolonged immobilization removes the leg-muscle pump

Leg-muscle contraction normally assists venous return.

Bed rest and prolonged inactivity produce venous stasis.

Prolonged stasis favors clot formation in lower-limb deep veins.

Reduced muscle contraction → slow venous return

Schematic — not a clinical or histologic specimen

Slide 36 · Trauma, surgery, and burns activate multiple elements of the triad

Tissue injury exposes or releases procoagulant factors.

Vascular injury and immobility add further prothrombotic pressures.

Inflammatory responses may compound the local and systemic effects.

Tissue injury

Procoagulant release + vascular injury

Immobility / stasis

Venous thrombosis

Slide 37 · Pregnancy creates both local and systemic thrombotic risk

Venous return from the lower extremities may be impaired.

Hormonal changes favor a systemic hypercoagulable state.

Thrombosis risk extends into the postpartum period.

Reduced leg venous return

Systemic hormonal change

Increased VTE risk

Schematic — not a clinical or histologic specimen

Slide 38 · Malignancy may produce a systemic procoagulant state

Tumor-associated inflammation supports coagulation activation.

Tumor tissue factor and mucin contribute to thrombogenic signaling.

Migratory thrombophlebitis is a classic manifestation (Trousseau syndrome).

Disseminated malignancy

Inflammation + tumor procoagulants

Venous thrombosis

Migratory thrombophlebitis

Slide 39 · Heparin-induced thrombocytopenia is paradoxically prothrombotic

Immune complexes recognize platelet factor 4 (PF4) in association with heparin.

Antibody-mediated platelet activation generates a procoagulant state.

Despite falling platelets, thrombosis can affect veins or arteries.

HIT is not merely a low platelet count.

Slide 40 · HIT: PF4 antibodies link platelet activation and clearance

Heparin forms complexes with released PF4.

IgG recognizing PF4-containing complexes triggers platelet Fc-receptor activation.

Platelet consumption and thrombin generation occur concurrently.

Heparin + PF4

Anti-PF4 IgG

Platelet activation

Thrombosis + low platelets

Schematic — not a clinical or histologic specimen

Slide 41 · HIT illustrates thrombosis in the setting of thrombocytopenia

Platelet count

Thrombotic potential

Falls owing partly to immune-mediated clearance

Rises because remaining platelets become activated

Does not quantify the entire clinical danger

Veins and arteries can both be affected

Contrast the mechanism, not merely the color or appearance.

Slide 42 · Vaccine-induced thrombotic thrombocytopenia also targets PF4

VITT after certain adenoviral-vector COVID-19 vaccines.

Anti-PF4 antibodies can be present without heparin exposure.

Reported thrombi include cerebral venous sinuses and splanchnic vessels.

This is distinct from ordinary post-vaccination symptoms.

Slide 43 · Antiphospholipid syndrome links autoimmunity to thrombosis

APS involves antiphospholipid autoantibodies and characteristic clinical disease.

Venous or arterial thrombosis and obstetric complications are prominent.

The syndrome may occur with or without systemic autoimmune disease.

Antiphospholipid antibodies

Cellular activation

Thrombosis / pregnancy morbidity

Schematic — not a clinical or histologic specimen

Slide 44 · APS may be primary or associated with autoimmune disease

Primary APS

Secondary APS

No accompanying established systemic autoimmune disease

Occurs with autoimmune disease, often SLE

Thrombotic / pregnancy manifestations dominate

Similar APS manifestations plus background autoimmune disease

Contrast the mechanism, not merely the color or appearance.

Slide 45 · Anti-β₂-glycoprotein I participates in APS pathogenesis

Relevant antibodies recognize phospholipid-associated proteins.

Endothelial cells, monocytes, neutrophils, and platelets may become activated.

Complement activation and impaired fibrinolysis further promote thrombosis.

Anti-β₂-glycoprotein I antibodies

Cellular activation

Complement / impaired fibrinolysis

Thrombosis

Slide 46 · APS pregnancy morbidity is not explained solely by clotting

Early fetal loss is linked to antibody effects on trophoblast differentiation and placentation.

Later pregnancy complications may involve trophoblast injury and inflammation.

A purely vascular-occlusion explanation is therefore inadequate.

Slide 47 · The lupus anticoagulant creates an in vitro paradox

Some antiphospholipid antibodies prolong phospholipid-dependent clotting assays in vitro.

In patients they are associated with hypercoagulability and thrombosis.

A prolonged aPTT in this setting does not imply protection from clot formation.

In vitro

In vivo

Clotting assaysmay be prolonged

Thrombotictendency rises

Schematic — not a clinical or histologic specimen

Slide 48 · APS clinical manifestations depend on vascular territory

Recurrent venous thrombosis or pulmonary thromboembolism.

Stroke, bowel infarction, and renal vascular complications.

Valvular vegetations and thrombocytopenia.

Recurrent pregnancy loss or other placental complications.

Slide 49 · Thrombus morphology depends on its site of formation

Cardiac and arterial thrombi often begin at injury or turbulence.

Venous thrombi frequently begin where blood flow stagnates.

A thrombus is typically attached to vascular or endocardial surfaces.

Different initiating sites; Shared luminal thrombus

Schematic — not a clinical or histologic specimen

Slide 50 · Lines of Zahn indicate layered deposition during blood flow

Pale platelet/fibrin layers alternate with darker erythrocyte-rich layers.

The laminated architecture is evidence of antemortem formation under flow.

Layering may be evident grossly or microscopically.

Alternating platelet/fibrin and red-cell layers

Schematic — not a clinical or histologic specimen

Slide 51 · Thrombus attachment is a useful morphologic clue

The point of origin is usually firmly attached to the vessel wall.

The extending portion may be relatively loosely attached.

This explains why propagation can increase embolic potential.

Adherent base; Mobile propagating portion

Schematic — not a clinical or histologic specimen

Slide 52 · Arterial and venous thrombi grow differently

Arterial thrombus

Venous thrombus

Extends retrograde from initiation site

Extends in direction of blood flow

Growth is commonly toward the heart

Growth is commonly toward the heart

Often begins at endothelial injury

Often begins with stasis

Slide 53 · Arterial thrombi are often platelet-rich and occlusive

Frequently superimposed on disrupted atherosclerotic lesions.

Contain platelets, fibrin, trapped red cells, and leukocytes.

Coronary and cerebral arterial occlusion can rapidly injure vital tissues.

Platelets + fibrin; Often associated with plaque

Schematic — not a clinical or histologic specimen

Slide 54 · Venous thrombi commonly form red, occlusive casts

Slow circulation permits abundant red-cell trapping.

The thrombus often forms a long cast of the affected venous lumen.

Focal attachment to the vein wall helps distinguish it from a postmortem clot.

Erythrocyte-rich occlusive luminal cast

Schematic — not a clinical or histologic specimen

Slide 55 · Arterial and venous thrombi: Morphology at a glance

Arterial / cardiac

Venous

Platelet/fibrin prominent

More erythrocytes enmeshed

Frequently friable and occlusive

Usually occlusive long luminal cast

Injury and flow disturbance prominent

Stasis prominent

Ischemic tissue injury often dominant

Congestion and pulmonary embolic risk dominant

Slide 56 · Postmortem clots can resemble venous thrombi

Antemortem thrombus

Postmortem clot

Attached at least focally to vessel wall

Usually not firmly attached

May show lines of Zahn

Typically unlaminated

Firm / friable organization varies

Gelatinous “currant jelly” dependent portion

Produced under flowing blood

Can show yellow “chicken-fat” supernatant

Slide 57 · Cardiac and aortic mural thrombi reflect local flow defects

Mural thrombi attach to chamber or aortic walls without necessarily filling the lumen.

Dyskinesia, myocardial scar, and endocardial injury predispose cardiac sites.

Aortic atherosclerosis and aneurysm are typical structural substrates.

Adherent mass projecting into cavity or lumen

Schematic — not a clinical or histologic specimen

Slide 58 · Valvular vegetations can be infected or sterile

Infective vegetations

Sterile vegetations

Bacterial/fungal colonization on damaged or infected valve

Nonbacterial thrombotic endocarditis with hypercoagulability

Valve damage with platelet/fibrin deposits

Libman–Sacks lesions can occur with SLE

Contrast the mechanism, not merely the color or appearance.

Slide 59 · Superficial venous thrombosis mainly produces local effects

Commonly involves saphenous veins associated with varicosities.

May produce pain, tenderness, swelling, and congestion.

Embolization is relatively uncommon compared with proximal DVT.

Venous drainage impairment can predispose to skin changes and ulceration.

Slide 60 · Proximal deep vein thrombosis carries major embolic risk

Thrombi in popliteal, femoral, or iliac veins may embolize to the lungs.

DVT can cause pain or swelling, but collateral veins may mask obstruction.

Absence of symptoms does not exclude clinically important DVT.

Deep venous obstruction; Possible embolus source

Schematic — not a clinical or histologic specimen

Slide 61 · Why a deep venous thrombus can be clinically silent

Venous collaterals may maintain partial return around an obstructed segment.

Pain and edema are not obligatory.

The first recognized complication may be pulmonary thromboembolism.

Deep venous thrombus

Collateral venous channels

Few local symptoms

Potential embolization

Slide 62 · Arterial occlusion threatens downstream tissue perfusion

A local arterial thrombus reduces oxygen delivery distal to its site.

Coronary or cerebral vessel occlusion has serious consequences.

Arterial fragments can also embolize and produce infarction.

Arterial thrombosis

Reduced tissue perfusion

Ischemia

Infarction risk

Slide 63 · Thrombus fate includes four principal pathways

Propagation: Growth through further platelet and fibrin deposition.

Embolization: Detachment and transport to distant vessels.

Dissolution: Fibrinolytic degradation, particularly in recent thrombi.

Organization/recanalization: Cellular ingrowth and partial restoration of flow.

Propagation

Embolization

Dissolution

Organization /recanalization

Schematic — not a clinical or histologic specimen

Slide 64 · Propagation increases mass and risk of obstruction

Additional platelets and fibrin accumulate on the initial thrombus.

The extension may have a weak attachment to the original site.

Larger clot burden raises the risk of occlusion or fragmentation.

Initial thrombus

Platelet + fibrin deposition

Propagation

Obstruction / embolic risk

Slide 65 · Embolization converts a local lesion into a distant one

A thrombus fragment breaks loose from its site of formation.

It travels with the bloodstream until obstructed by a smaller vessel.

Resulting dysfunction depends on embolus size and destination.

Detached fragment travels downstream

Schematic — not a clinical or histologic specimen

Slide 66 · Recent thrombi are more susceptible to dissolution

The fibrinolytic system can remove new fibrin-rich material.

Older thrombi become more cross-linked and resistant to lysis.

This temporal difference is relevant to thrombolytic treatment rationale.

Recent thrombus

Plasmin activity

Fibrin dissolution

Potential flow restoration

Slide 67 · Organization replaces thrombus with fibrovascular tissue

Endothelium, smooth muscle cells, and fibroblasts grow into thrombus.

Connective tissue gradually incorporates the mass into the vascular wall.

The original clot may become a residual fibrous lesion.

Fibrovascular ingrowth forms organized tissue

Schematic — not a clinical or histologic specimen

Slide 68 · Recanalization creates new channels through an organized clot

Small capillary channels form through organized thrombotic tissue.

These channels restore luminal continuity to a variable degree.

Recanalization does not necessarily restore a normal vascular caliber.

Ingrowth + new channels through thrombus

Schematic — not a clinical or histologic specimen

Slide 69 · DIC combines diffuse microvascular thrombosis and bleeding

Systemic thrombin activation forms numerous microvascular thrombi.

Diffuse occlusion produces tissue hypoperfusion and organ injury.

Platelet and coagulation-factor consumption can cause severe hemorrhage.

Diffuse microvascular clotting

Schematic — not a clinical or histologic specimen

Slide 70 · DIC demonstrates that coagulation and bleeding can coexist

Pathologic systemic coagulation is not effective localized hemostasis.

Consumption depletes platelets and coagulation factors.

Fibrinolysis and organ dysfunction complicate the clinical course.

Systemic thrombin activation

Widespread microthrombi

Consumption + fibrinolysis

Bleeding and organ injury

Slide 71 · Case: Postoperative leg swelling and immobilization

A patient has prolonged bed rest after major surgery and develops unilateral leg swelling.

Which components of Virchow triad are activated, and why?

What important complication should be anticipated?

Slide 72 · Case analysis: Venous thrombosis is multifactorial

Reduced calf-muscle pumping favors venous stasis.

Operative tissue/vascular injury adds a procoagulant stimulus.

A proximal deep vein thrombus is a potential source of pulmonary emboli.

Slide 73 · Case: Arterial thrombosis over a disrupted plaque

A patient develops abrupt myocardial ischemia in the setting of advanced coronary atherosclerosis.

Why do platelet adhesion and endothelial injury dominate?

How does disturbed arterial flow augment the event?

Slide 74 · Case analysis: Plaque injury plus high-shear platelet activation

Plaque disruption exposes collagen, vWF, and tissue factor.

High shear favors platelet-dependent thrombus initiation.

Turbulence and coagulation generate an increasingly occlusive lesion.

Slide 75 · Case: Low platelets and new thrombosis after heparin

A hospitalized patient exposed to heparin develops falling platelets and a new thrombosis.

Why does thrombocytopenia not imply reduced thrombotic risk?

What immune target is characteristic?

Slide 76 · Case analysis: Immune platelet activation in HIT

Anti-PF4/heparin antibodies activate platelets through Fc receptors.

Activated platelets promote coagulation and are also cleared from blood.

HIT therefore produces the dangerous combination of thrombocytopenia and thrombosis.

Slide 77 · Integrated mechanism–morphology–consequence map

Injury, abnormal flow, and hypercoagulability initiate a thrombus.

Hemodynamics shape platelet-rich arterial versus red-cell-rich venous morphology.

Obstruction, embolization, and organization govern clinical outcomes.

Virchow triad

Thrombus formation

Morphology + propagation

Ischemia / congestion / emboli

Slide 78 · Thrombosis: High-yield synthesis

Virchow triad is a causal framework, not three mutually exclusive diagnoses.

Arterial disease emphasizes endothelial injury, disturbed flow, and platelets.

Venous disease emphasizes stasis and hypercoagulability.

Attachment, lamination, location, and fate explain clinical behavior.

Slide 79 · References

Robbins, Cotran & Kumar: Pathologic Basis of Disease. 11th ed. (2026). Chapter 4, pp. 102–114.

For extended clinicopathologic context: cardiovascular chapters addressing blood vessels and the heart.