• important host defense mechanism
• mechanism of action
  • blood in fluid state in normal vessles
  • hemostatic plug at site of vascular injury
  • complex system w/checks and balances

• endothelial injury
• venous stasis/turbulence of blood flow
• hypercoagulability

Processes are interrelated

1. platelets adhere
2. coagulations cascade initiated
3. platelet fibrin plug stops bleeding
4. mechanims limit plug to injury site and it does not occlude vessel lumen
5. plug dissovles
6. replaced by CT

• platelets
• fibrin
• entrapped cellular elements (WBCs, RBCs)

• hemostasis in the wrong place or inappropriate activation of normal hemostatic processes
• forming thrombis in uninjured vessel
• complet blockage of vessel after only minor injury

• hemodynamic stress assoc. w/HTN
• turbulent flow over scarred valves
• bacterial endotoxin
• hypoxia
• trauma
• atherosclerotic plaque

Plays critical role in init. of thrombosis, esp. in heart, arterial circ. Normal intact endothelium has antithrombotic properties.

• def.- flow in which velocity at given point changes erratically in maginitude and direction
• plays major role in arterial and cardiac thrombosis by:
  • causing endothelial injury
  • form countercurrents and create pockets of stasis

• w/o turbulence, major factor in venous thrombi
• ex: aneurysms, mural thrombi

• coag. protein deficiency
  • factor V mutation
  • prothrombin mut.
• anticoagulant proteins
  • antithrombin
  • protein C
  • protein S deficiency

• oral contraceptives
• late pregnancy
• cancer
• antiphospholipid Ab syndrome

• dep on:
  • site of origin
  • size
  • conditions under which they develop

• cardiac chambers
• cardiac valve cusps
• aorta
• arteries
• capillaries
• veins

• pt of attachment to underlying wall
• tail of thrombis may not be firmly attached
• may detach to cause embolism

• local vascular obstruction
• embolization of thrombi
• cause
  • congestion
  • edema
  • infarct

• atherosclerosis
• inflammation
• trauma

• adherent to injured wall
• usually occlusive in vessels
• composition
  • WBCs
  • RBCs
  • platelets
  • fibrin
• gray, white
• friable
• exhibit lines of Zahn

• characteristic
  • seen grossly and microscopically
  • laminations in thrombi made of alternating pale layers (platelets, fibrin) and darker layers (mainly RBC's)
• significance- imply thrombosis at site of blood flow
• prominent in large arteries, aorta, heart

• coronary A.
• cerebral A.
• femoral A.

• often occludes the affected vessel, leading to an infarction

• chambers of heart
• aorta

• heart
  • MI
  • dilated cardiomyopathy
  • arrhythmias
• aorta
  • ulcerated atherosclerotic plaque
  • aneurysmal dilation

• may embolize
• may cause local obstruction

• cause
  • bacterial or fungal blood borne infections damaging valve
  • hypercoagulant patients w/o infection (sterile vegetation)
• fate
  • local effects
  • embolize
    • infection spread further leading to septic infarct

• most common sites
  • superficial veins of leg
  • deep veins of leg
• main predisposing factor- site of stasis

• lines of Zahn NOT apparent
• assume shape of lumen of vein
• adherent to wall
• can have stasis/red thrombi
  • caused by high content of entrapped RBC's

• may cause:
  • obstruction
  • congestion
• less likely to cause infarction than arterial thrombi
  • bypass channels open rapidly to relieve obstruction and allow arterial inflow
• infarcts more likely in organs with single venous outflow (ex: kidney)

• location- usually in saphenous system, especially when there are varicosities (dilation of veins)
• may cause:
  • pain
  • tenderness
  • local congestion and edema distal to point of obstruction
  • predisposition of overlying skin to:
    • infections from slight trauma
    • development of ulcers

• stasis- CHF, post-op. state, reduced physical activity, immobility
• injury- trauma, surgery, burns
• hypercoagulability

• may cause local pain, edema
• impaired drainage relieved by opening of bypass channels
• DVT's that form in leg veins at or above knee may embolize

• not attached to underlying vessel wall
• gelatinous
• no lines of Zahn
• two layers
  • thin yellow "chicken fat"
  • dark red, heavy "currant jelly" (many RBC's)

• propagation
• dissolution
• organization
• recanalization
• enzymatic digestion/mycotic aneurysm
• embolization

1. activate fibrinolytic pathways via tPA
   1. activate plasminogen to cleave fibrin in thrombosis
   2. blood flow reestablished

• infiltration by macrophages and fibroblasts
• results in fibrosis

• new capillary channels formed that span from one end of thrombus to another
• allows thrombus to eventually be encorperated into the wall

1. center of thrombus undergo enzymatic digrestion
   • esp. in large thrombi in aneurysm or heart
2. degraded thrombus become ideal culture medium for bacteria
3. if bacteria infect, results in mycotic aneurysm

• droplets of fat (fracture long bone)
• bubbles of air (enter circ. during obstetric procedures or chest wall injury)
• atheroschlerotic debri
• tumor fragment
• fragment of bone marrow
• foreign bodies (ex: bullet)

1. carried by blood flow
2. eventually lodge in vessels too small to allow passage
3. lead to occlustion
4. infarction

1. DVT in leg at or above knee level
2. goes to larger veins
3. into right side of heart
4. into pulmonary vasculature

• size of embolism
• size of occluded vessel
• extent to which flow is obstructed
• availability of alternative source of blood flow
  • ex: bronchial A. in lung
• CV health

• main pulm. A. or its major branches
• lodge at bifurcation of main pulm. A = saddle embolus

1. more than 60% pulm. circulation occluded
2. sudden obstruction of right ventricular outflow
3. acute right ventricular HF
4. reduction in left ventricular CO
5. SHOCK

• most emboli in general are clinically silent because they are small
• if there is recurrent episodes of PE or multiple PE, you get pulm. HTN with right sided heart failure

• if normal CV function
  • usually no infarct due to blood supply from bronchial A.
• compromised CV function
  • may infarct

1. arise in venous circulation
2. go to right heart
3. go through heart defect (ex: patent foramen ovale)
4. enter left heart
5. go into systemic circulation

• cardiac mural thrombi
  • 2/3 in setting of LV wall infarcts
  • 1/4 in setting of dilated left atria
• remainder mainly through aneurysm

• legs (MAJOR)
• brain
• intestines
• spleen
• kidney

• size of embolus
• size of occluded vessel
• extent to which blood flow obstructed
• availability of alternative source of blood flow
• vulnerability of particular tissue to ischemia

• local vasopasm
• hemorrhage into atherosclerotic plaque
• compression of blood supply
• twisting of bv's
• rupture of bv aka hemorrhage

• range from insig. to fatal
• major det.
  • nature of vascular supply (alternatives)
  • vulnerability of given tissue to hypoxia
  • rate of development of occlusion
  • blood oxygen content

• the kidney has a single blood supply
• the lung has the pulm. A and bronchial A.
• liver has hepatic A. and portal V.

• if slow, less likely because you can increase your anastamoses to the area that is occluded enough to prevent infarction
• if sudden, acute MI will result

• neurons- irreversible damage after 3-4 minutes
• myocytes- die after 20-30 minutes
• fibroblasts- viable for many hours

• if you have a partial obstruction of blood flow in a small vessel
  • if anemic, you may have infarction
  • if not anemic, you wont have one

• wedge schaped with occluded vessel at apex
• when on serosal surface, there is frequent overlying exudate
• lateral margins of infarct are irregular
  • reflect pattern of vasculare supply from adjacent bv's
  • over time, margins become better defined (at first, poorly defined)
    • so if sudden death after infarct, no morphologic changes

• color- reflect amount of hemorrhage
  • red (hemorrhagic)
  • white
• presence, absence of microbial infection
  • bland (not infected)
  • septic (infected)

• venous occlusions
• previously congested tissue (decreased venous outflow)
• loose tissue
  • lack firmness, allowing blood to accumulate in necrotic areas
• tissues with dual circulation
  • unblocked circulation still flowing, but not enough to prevent infarction
• when flow re-established to site of previous infaction
  • ex: lyse thrombus

• never become pale
• over time:
  • firmer
  • more brown
  • less red

• arterial occlusions
• tissues with NO dual blood supply (ex: kidney)
• in solid organs (firmness limit amount of hemorrhage into infarcted area)
  • ex: heart, spleen, kidney

• progressively more sharply defined and paler with time as extravasted RBC's are broken down

• hallmark: ischemic coagulative necrosis
• at the edge of infarct, zone of hyperemia (active congestion) and inflammation develops
  • inflam. (in response to necrotic material) begin within hrs and well defined by 1-2 days
• gradual degradation of necrotic tissue followed by phagocytosis by neutrophils and macrophages
• reparative response in preserved margins
  • some tissues with preserved underlying stromal architecture intact can regen. infarct edges
  • most eventually replaced by fibrous scar

• NO FIBROUS SCAR
• ischemic injury cause liquefactive necrosis
  • complete digestion of necrotic cells

• micro-organisms seeding an infarct
• embolism of infected vegetation

• resembles abscess
  • localized collection of inflammatory cells (mainly neutrophils)
  • necrotic tissue