head is talled and prothrombotic (procoagulant) properties.

The balanca
Papilledrma: Swrlling of the optie
nerve

1he contentric inctease in ptessure between these two opposing endothelial properties deter.
as papilledrma. mines the thrombus formation.
enirinE 1hr optit nene produces stasis of venous
of the optic nerve head.
otflow whiuh leads to &wrling
The tauses a Antithrombotic Properties
of
-Comprrssion of the nerve (e.g. primay neoplasm
the optic nerve)
0.Write ashort note on antithrombotic properties of endothelium
Raiscd cerebrospinal fluid pressure surrounding the Normally, the endothelial cells have antiplatelet, anticoagu
nerne.
lant and fibrinolytic properties which prevent thrombosis
and also coagulation) (Figs. 5.6A andB).
Edema Excess fluid in the interstitial spaces within
tissues.

Antiplatelet Effects
Trensudate is a protein poor and cell-poor fluid. Exudate is
They prevent platelet adhesion and aggregation following
protein-rich and cell-rich fuid.
mechanism:
Anasarca. Severe form of generalized edema. Intact endothelium prevents adhesion of platelets (and
plasma coagulation factors) to the highly thrombogenic
Ynflammatory carcinoma of breast: Local lymphedema due to inva- subendothelial extracellular matrix (FCM).
cells.
sion and obstruction of subcutaneous lymphatics by
tumor
Production of inhibitors of platelet aggregation by
(PGI),
Nephrotic syndrome: Massive loss of albumin urine-decreased endothelial cells: These include: prostacyclin
serum albumin decreased plasma osmotic pressure nitric oxide (NO) and adenosine diphosphatase (which
generalized edema. degrades adenosinediphosphate--ADP

Angioneurotic edema: Anticoagulant Effects

Autosomal dominant The endothelium inhibits coagulation by following
Mediated by vasoactive peptides such as bradykinin
molecules:
Low ievels or abnormal function regulatory complement
of a molecules: Found in the endothelium
inhibitor (Ci INH deficiency). .Heparin-like
in the plasma, C1
protein and exert their anticoagulant effect indirectly through
thrombin and
content. antithrombin II1. They inactivate
Lymphatic edema: Fluid in edema has high protein
coagulation factors (Xa and Xa).
after modified radical Thrombomodulin: Present on the endothelial cells and
Lymphedema: Lymphatic obstruction
which inhibits
mastectomy, radiation and
filariasis. binds to thrombin and activates protein C,
clotting by proteolysis of factor Va andVIlla
of skin in the carcinoma breast: Inhibits tissue
Peau d 'orange appearance
blockage of subcutaneous
.Tissue factor pathway inhibitor (TFPI)
Lymphedema of breast due to
factor/factor VIlacomplexes. Extniwsto pabh
lymphatics by malignant cells.
failure is due to increased hydrostatic Fibrinolytic Effects
Pitting edema in right heart
pressure Endothelial cells synthesize tissue-type plasminogen
which degrades a thrombi whenever it is

is due to reduced osmotic pressure.

activator (-PA)
Pitting edema in cirhosis formed.
Cerebral edema:
the
In generalized edema,
I t may be localized or generalized. Prothrombotic Properties
and narrowed
is
brain swollen with distended gyri
grossly
compressed and the brain of endothelium.
suici. The ventricular cavities O. Write a short note on prothrombotic properties
are

expands, it may
herniate. activated by several
Endothelial cells may be damaged or
infectious
ways. These
include trauma, inflammation,
VFUNCTIONS OF NORMAL agents, hemodynamic forces,
plasma mediators, and

activated endothelial cells

ENDOTHELIUM cytokines. The damaged or

promote prothrombotic
state by its platelet, procoagulant
role in both homeostasis
Endothelial cells play an important and antifibrinolytic effects.
antithrombotic
thrombus formation. They have both
and
 VAV V i A

Anlicboqulant Heparin-ke
molectule
aritithrormbin f1
Anticoaguant.etec
Active protein C
Inavetivaneotemc
Antiplatelet
eftect
Fibrinolytic
effect

thrombin

Antilthrombin 1
Thrombin F t s r e t e p a d n

pGNOand PA
adenosine diphosphatase
tPA 45tg Cpe

Oteparin-lkehrombomoduiesue factor
molecule pathway inhibitor
Endothelial
cell

Platelet effects Procoagulant effects Antifibrinolytic effects

4oCoagulanl Synthesis
fissue
Platelets TF
1
O1A
factor
Secretes inhibitors of
plasminogen activator
plasi AIS
PA
PMAna hdgan
lbn.oiyled

WF

Fibrin Endothelial
cell

Collagen
Figs. 5.6A and B: Endothelial factors that (A) inhibit and (B) favor thrombosis. factor)
von Willebrand
(PGl:prostacyclin; NO: nitric oxide; t-PA: tissue plasminogen activator; vWF:

Platelet Effects Table 5.3: Antithrombotic and prothrombotic properties

Endothelial damage exposes the subendothelial of endothelium.
thrombogenic ECM and allows adhesion of platelets
Antithrombotic properties Prothrombotic properties
fromcirculation to ECM. Antiplatelet effects Platelet effects
von Willebrandfactor (vWF) produced by normal
Acts as a barrier Endothelial damage
endothelial cells is essential cofactor that helps platelet between platelets exposes the subendothelial
binding to matrix elements. and subendothelial thrombogenic ECM
thrombogenic ECM von Willebrand factor
Procoagulant Effects Produce inhibitors of (vWF) produced by normal
platelet aggregation (e.g. endothelial cells helps
Endothelial cells synthesize tissue factor in response PGl2, NO and adenosine platelet binding to ECM
to cytokines le.g. tumor necrosis factor (TNE) or diphosphatase
interleukin-1 (IL-1)] or bacterial endotoxin. Tissue factor Anticoagulant effects Procoagulant effects
activates the extrinsic coagulation cascade. . Heparin-like molecules Synthesis of tissue factor
Activated endothelial cells increases the catalytic Thrombomodulin activates the extrinsic
lunctionof activated coagulation factors IXa and Xa. Tissue factor pathway
inhibitor (TFP)
coagulation cascade
Activated endothelial
Antifibrinolytic Effects cells increase the catalytic
function of factors IXa and Xa
Endothelial cells secrete inhibitors of plasminogen ac Fibrinolytic effect through Antifbrinolytic effects
vator (PAls), They reduce fibrinolysis and tend to favor tissue-type plasminogen through secretion of inhibitors
thrombosis. activator(t-PA)->conversion
of plasminogen to
of plasminogen activator
Antithrombotic and prothrombotic properties of endo- (PAIs)reduce fibrinolysis
theliumare listed in Table 5.3. plasmin-cleaves fibrin
 ror Ondergraduates-Patholoo

A Eram Preparatory Nanual

Intact
nactivated endothelial cells inhibit thrombus whereas Injury to Endothelium (Changes in the
dothelial injury or activationpromotes thrombus formation Vessel Wall)

Ultrastructurally, endothelialcells contain Weibel Palade bodies Endothelial injury may be either physical damageo
endothelial dysfunction (or activation) or

THROMBOSIS Physical Endothelial Injury

n Defineanddescribe the pathogenesisof thrombus. Add a note on lt is important for formation of thrombus in the hearto
fate of thrombus. the arterial circulation. Normally, high flow ratesin the
heart and arterial circulation prevent adhesion of plateler
Q Define thrombus.
Discussthe etiopathogenesis and pathology of
to endocardium/endothelium and wash out any activated
Add a note on fate of thrombus
thrombosis., coagulation factors. The endothelial cellinjury promotes
Define thrombus. adhesion of platelets at the site of injury.
Defnition: Thrombosis is defined as the process of formation
ofa solid mass in the circulating blood from the constituents
Causes
Heart:
offlowing blood.
Chambers of heart (e.g. endocardial injury due to
Thesolid mass formed is called as thrombus and it consists
myocardial infarction with damage to the adjacent
ofan aggregate of coagulated blood containing platelets, fibrin,
endocardium, catheter trauma).
andentrapped cellular elements of blood. Valves: Small thrombi on the valves are called as
vegetations.
Etiology Infective endocarditis: Thrombi on valves (e.g.
mitral, aortic valve) damaged by a blood-borne
Q What is Virchow's triad? List its components.
bacteria or fungi
Q Describe the etiopathogenesis of thrombus. Damaged valves (e.g. due to rheumatic heart
Threeprimary abnormalities can lead to formation of a disease, congenital heart disease)
thrombus and constitute Virchow's triad (Fig. 5.7). These Libman-Sacks endocarditis in systemic lupus
include: erythematosus
1. Injury to endothelium (changes in the vessel wall). Nonbacterial thrombotic endocarditis: They are
2. Stasis or turbulent blood flow (changes in the blood flow). sterile vegetations on noninfected valves with
3. Hypercoagulability of the blood (changes in the blooditself) hypercoagulable states.
Arteries e.g.ulcerated atherosclerotic plaques, traumatic
or inflammatory vascular
injury (vasculitis)].
Capillaries: Causes include acute inflammatory lesions,
vasculitis and disseminated intravascular
coagulation
(DIC).
Endothelial Mechanism: Physical loss of endothelium exposes
injury
thrombogenic subendothelial ECM. Platelets adhere to
the site of endothelial injury and release
prothrombotic
tissuefactor. There is local depletion of antithrombotic
factors like PGl.

THROMBOSIs
ondothuuv Y
Endothelial Dysfunction rembeqwc
Definition: Endothelial dysfunction is defined as an altered state
Alteration in Hypercoagulability which induces an endothelial surface that is thrombogenic or
normal bloodflow abnormally adhesive to inflammatory cells. Thus, thrombus
can develop without any denudation or
physical disruption of
endothelium.

Fig.5.7: Virchow's triad in thrombosis. (1) Endothelial injury is the most Causes: Hypertension, turbulent blood flow,toxins (e.g
importantfactor,(2) Alteration in blood flow (stasis or turbulence) and bacterial endotoxins, toxinsfrom cigarettesmoke),radiation
(3) Hypercoagulability.
 349)
metabolic abnormalities (e.g.homocystinemia.or Hypercoagulability (refer page
injury,
Q.Write short note on causes ofcoagulable
hypercholesterolemia). state.
with increased
Mechanism Endothelial dysfunction can disturb the
Q.Write short note on primary conditions associated
between prothombotic and antithrombotic risk of thrombosis.
balance
activities of endothelium by:
known as thrombophilia)
Definition: Hypercoagulability state (also
Producing more procoagulant factors, e.g. platelet with increased
systemic disorder associated
.
defined as a
adhesion molecules, tissue factor, PAls or is
tendency to develop thromboembolism.
throm-
Synthesizing less anticoagulant effectors, e.g. of thrombosis. Causes can
bomodulin, PGI, t-PA.
TiAnbuunLCauses: It frequent
is a less cause

be divided into primary (genetic)

and secondary (acquired)
in Normal Blood Flow disorders (Box 5.1)
Alterations Srnpn

Normal blood flow which platelets (and

is laminar, in
state.
other blood cellular elements) flow centrally, separated
Box 5.1:Major causes
of hypercoagulable
slower moving layer of plasma. A. Primary (genetic)
from endothelium by a
(anticoagulant) factors
Deficiency of antithrombotic
Antithrombin ll deficiency
Causes Protein C deficiencyy
.Turbulence (disturbed movement of blood): It can Protein S deficiency
produce thrombus in the arteries and heart. MTHFR gene mutation
for thrombosis.
.Stasis: It is a major cause venous Increased prothrombotic factors

Activated protein C (APC)

resistance (factor Vmutation/ factor
Va/ factor V Leiden)
Mechanism (prothrombin G2021OA
the following
.Excessive levels of prothrombin
Stasis and turbulence produce thrombus by mutation)
Willebrand factor:
High levels of factors VIl, XI, X, VIl;
von
mechanism:
Promote endothelial injury/activation and increases fibrinogeen
the procoagulant activity. Homocystinuria
the endothelium. B. Secondary (acquired)
Brings platelets into contact with
Preventcleansing and dilution of activated clottingHigh-risk for thrombosis
factorsby fresh flowing blood. Prolonged bed rest or immobilization
.Myocardial infarction, atrial fibrillation
.(Prevents flowing in of clotting factor inhibitors. Tissue injury (e.g. surgery, fracture, burn)
stasis: Disseminated intravascular coagulation DI
Clinical disorder associated with turbulence and
Heart Cancer, prosthetic cardiac valves, heparin-induced thrombo-
Acute myocardial infarction cytopenia
Antiphospholipid antibody syndrome APL-A
Arrhythmias/atrial fibrillation [e.g. rheumatic mitral
Lower risk for thrombosis
stenosis in conjugation with disordered atrial rhythm
Nephrotic syndrome
(atrial fibrillation), it predisposes to mural thrombi Hyperestrogenic states (pregnancy and postpartum), oral
in atria. contraceptive use
Dilated cardiomyopathy Cardiomyopathy, smoking, sickle cell anemia
Arteries
Arterial thrombi: Seen in
Ulceration of atherosclerotic plaques
Aneurysms: They cause local stasis. Homocysteinemia: Inherited or acquire disorder associated with
Veins: Thrombi develop in the saphenous veins with both arterial and venous thrombosis.
When thrombosis develops in patient below the age of 50 years,
varicosities or in deep veins.
genetic causes of hypercoagulability must be considered, even
Other causes if there are acquired risk factors.
Hyperviscosity, e.g. with polycythemia vera
RBC disorders, e.g. sickle cell anemia can cause vascular Hypercoagulability due to defective factor V gene is called Leiden
mutation. It is the common inherited cause of hypercoagulability.
Occlusions and stasis.
 Secondary/acquired disorders (Box 5.1): The patho orial and
Table 5.4: Differences between arterial and vene
venou
genesis of acquired thrombophilia is usually multifactorial. thrombus.
Characteristics Arterial thrombus Venous thrombus
Terminology Main cause Injury to Stasis
endothelium
Q Write short note on mural thrombi.
Rate of blood flow Rapid Slow
Mural Thrombus Usual type of Mural Occlusive
thrombus
It is attached to the wall and projects into the lumen,
without complete occlusion of the lumen (refer Fig. 5.8B Common sites Aorta, coronary,
cerebral and
Superficial varicose
veins and deep
andRowchart 5.2). It occurs in heart chambers or in the femoral arteries veins of leg
aortic lumen.
Gross

Occlusive Thrombus Color Gray-white Red-blue

It occludes the lumen of the blood vessel (refer Flowchart

Lines of Zahn More prominent Less prominent
5.2) and prevents the flow of blood. It usually occurs in veins Composition Friable meshwork More trapped RBC
orsmalleror medium sized arteries.
of platelets, andrelatively few
fibrin, RBCs and platelets
Q Write short note on vegetations. degenerating
leukocytes
Vegetation Propogation Retrograde manner In antegrade
from point of manner trom point
Itisathrombus on heart valve (refer Fig. 15.12) and appears attachment of of attachment
aspolypoid mass projecting into the lumen (e.g. infective thrombus(i.e. towards the
endocarditis). towards heart) direction of blood
flow (i.e. towards
Types of Thrombi the heart)

Thrombi may be arterial or venous Effects Ischemia causing

Thromboembolism
type. Differences infarction of area edema and
between arterial and venous thrombus are shown in Table
supplied by the ulceration
5.4 artery containing
thrombus
MORPHOLOGY OF THROMBI Aspirin: Prevents arterial thrombosis.
Layers in Thrombus
First layer of the thrombus on the Heparin and warfarin: Prevents venous thrombosis.
endothelium/endocardium
is a platelet
layer
On top of the platelet layer, fibrin is precipitated to form Site and Types
upstanding laminae which anastomose to form an intricate
Thrombi: Its size and shape depends the site of
structure which resembles coral (coralline
thrombus). In
on
origin and its
between the upstanding laminae and anastomosing fibrin cause. Thrombi can develop anywhere in the cardiovascular
meshwork, the red blood cells get trapped. Retraction system.
of fibrin produces a ribbed appearance on the surface of
thrombus. Heart
O.Write briefly on lines of Zahn. .Cardiac thrombi: Usually develops at sites of
or endocardial injury. turbulence
Lines of Zahn
More common in the atrial
.Both gross and microscopy of thrombus show alternating Can also develop on the
appendages.
light (pale or white) area of platelets held together by fibrin; endocardial surface overtne
site of acute
and dark retracted area of fibrin meshwork with
trapped RBCs. myocardial infarction (refer Fig. 15.105
These alternating laminations of .Valves: Thrombi on heart valves are called
light and dark are known as vegetatoi
lines of Zahn (Figs. 5.8A and B). (refer Fig. 15.12). They are more common on
aortic valves. mitral or
 Q. Differences between postmortem clot and thrombi.
Table 5.5: Differences between antemortem
Dark ares thrombi and postmortem clots.
Light are Characteristics Antemortem Postmortem clots
venous thrombi
Attachment to Focally and firmly Not attached
vessel wall attached

Thrombus: Lines Consistency Dry, granular, firm Gelatinous, soft

and friable and rubbery
of Zahn.
Shape May or may not Have the shape of
fit the vascular the vessel irn which
contours it is found
Appearance Alternate dark and Currant jelly
white areas or chicken fat
appearance
Lines of Zahn Present Absent
Mechanism Changes in blood Occurs in stagnant
flow (stasis) and blood in which
Figs. 5.8A and B: Appearance of thrombus: (A) microscopic and (B) hypercoagulability gravity fractionates
the blood
diagrammatic) showing alternating dark and light areas (lines of Zahn).

Blood Vessels Upper layer: It is poor in cells and is yellow-white. It is

Arteries: Arterial thrombi tend to be white. firm representing coagulated plasma without red blood
Aorta or larger arteries usually develop mural thrombi. cells. It is called chicken fat because of its color and
Thrombi developing in the medium or smaller arteries consistency.
are frequentty occlusive. They
develop (in decreasing
order of frequency) in the coronary, cerebral and Fate of the Thrombus (Flowchart 5.2)
femoral arteries.
. Describe fate of a thrombus.
Veins:
Venous thrombosis (phlebothrombosis) are
Dissolution/lysis of thrombi without any consequences.
usually
-

Recent thrombi may totally disappear due to

oclusive, and form a long cast of the lumen. They
tion of fibrinolysis.
activa
occur usually at sites of stasis, and contain more
-

0ld thrombi are more resistant to

trapped RBCs (and relatively few platelets). They are lysis.
therefore known as red, or stasis thrombi. Propagation of thrombi: It is the process in which
thrombigrow and increase in size. The thrombus which
was initially mural,
Postmortem Clots may become occlusive thrombus.
The propagating portion of a thrombus is
0.Describe the appearance of postmortem dot. poorly attached
to the wall and therefore,
Determination of whether a clot is formed during life
prone to
fragmentation and
embolization.
antemortem thrombi) or after death (postmortem clot) is Arterial thrombi grow
important in a medical autopsy and in forensic pathology.
retrograde from the point of
attachment
Diferences between antemortem thrombi and
venous Venous thrombi extend in the direction of blood
postmortem clots are listed in Table 5.5. After death, the red flow.
blood cells settle and
produce two layers. Embolization: Thrombi may get detached from its site
Lower layer: It contains many RBCs, which have settled of origin and form emboli. These emboli can travel to
by gravity forms a dark red lower portion. This has a other sites through the circulation and lodge in a blood
reddish and gelatinous appearance which resembles vessel away from the site of thrombus formation. The
currant jelly.
consequences depend on the site of lodgment. Large
108 Exam Preparatory Manual for Undergraduates-Pathology

Flowchart 5.2:Fate of thrombus

Dissolution/lysis Thrombi: Treatment with fibrinolytic

acgents
iseffective only when it is administered in
Mural thrombus
Propagatlon Kidney the first few hours of a thrombotic
episode
Embolus Fate of thrombus:
Dissolution Propagation
Embolization Organization
Arterial
Infarct
Fate of Embolism emboli
Recanalization Mycotic aneurysm
thrombus
Embolization to Thrombosis: Formation of
solida mass from
Occluslve
Venous lungs the constituents of flowing blood.
thrombus Thrombus Embolus emboli
Virchow's triad:
Organization 1. Endothelial injury
2. Abnormal blood flow
tt
3. Hypercoagulability
Recanalization Thrombosis: Can develop with physical injury
to endothelium or endothelial dysfunction
Longitudinal view Cross view without physical injury.

venous thrombi may get detached and travel to the Lines of Zahn: They help to distinguish antemortem thrombus
pulmonary circulation to the lungs as pulmonary emboli.
from postmortem clot
Organization: If thrombi are not dissolved (either
spontaneously or by therapy), these older thrombi Rarely, a large round thrombus may form on the mitral valve and
become organized by the ingrowth of endothelial cells, obstruct the lumen of the valve.
smooth muscle cells, and fibroblasts. Small,
organized
thrombi may be incorporated into the vessel wall. Agonal thrombi: Thrombi developing on one or both ventricles
Canalization/recanalization: New lumen/channels shortly before death.
linedby endotheliat cetts rmay form in an organized
thrombus. These capillary channels may form thorough- Venous thrombus: Deep ein of the lower extremity (90% of cases)
fare channels and can re-establish the continuity of the is the most common site.
original lumen.
Mycotic aneurysm(refer pages 116 and 401): Rarely, the Attachment: Thrombi are focally attached to the underlying
central region of the thrombi may undergo enzymatic surface
digestion due to lysosomal enzymes released from
Postmortem clot: Currant jelly and chicken fat appearance.
trapped leukocytes and platelets. If bacteremia develops,
these thrombi may become infected and produce an
inflammatory mass. This region of the vessel becomes VENOUS THROMBosIs
weak and can produce mycotic aneurysm.
(PHLEBOTHROMBOSIS)
Venous thrombosis: Stasis is the major cause.
Q.Write short note on phlebothrombosis and discuss the causesan
Antiphospholipid syndrome: Associated with
pathogenesis of venous thrombosis.
Venous thrombosis
Recurrent abortion Veins Involved
Antibody to lupus
Most commonly superficial or deep veins of the leg are
Mural thrombus: Occurs in heart chambers or in the aortic lumen. involved.
 Hemodynamic Disorders,

GDerficial Venous Thrombi

Site: They develop in the varicosities involving Vein
saphenous veins. Direction of Endothelial cells
blood flow
Efects: It can cause local congestion, swelling (edema),
nain, and tenderness. The local edema and impaired Primary platelet thrombus
venous drainage predispose the overlying skin to
infections from slight trauma and to the development
ofvaricose ulcers. Embolization is very rare.

Deep Venous Thrombosis (DVT) Coralline thrombus

Lower extremity DVTs are found in association with
venous stasis and hypercoagulable states.
Sites: Larger veins in the leg at or above the knee (e.g.
popliteal, femoral, and iliac veins).
Effects:
Even though DVTs can cause local pain and edema, Occluding thrombus
the venous block produced by themis usually rapidly
1696
balanced by the development of collateral channels.
- More prone to embolization into the lungs and
produce pulmonary infarction. About 50% of DVTs are
asymptomatic and are detected after embolization.
Consecutive clot

Pathogenesis of DVT Fig.5.9: Various stages the pathogenesis

(Phlebothrombosis)
. Discuss the causes and pathogenesis of venous thrombosis/
phlebothrombosis
Deep venous thrombosis is caused bythe same etiological
factors that favor arterial and cardiac thrombosis. These
include endothelial injury, stasis, and a hypercoagulable
state.
Different stages in the development of DVTS (Fig. 5.9) are:
Primary plateletthrombus:
-
in
ofphlebothrombosis.
Occuding thrombus: Further growth of thrombus
progressively occludes the lumen of the vein and forms
occluding thrombus.
Consecutive clot: Occlusive thrombus stops the blood
flow. Since, thrombi can develop only in the streaming
blood, the blood column beyond the occluding
thrombus clots to form a consecutive clot. Thereafter,
the consecutive clot may be halted and endothelialized
or it can spread (propagate).

Damage to the intimaofthe vein causesadhesion ofPropagated clot:B):There

(Figs. 5.10A and
are two methods
ofpropagation
platelets at damaged site> platelets aggregate toform
pale platelet thrombus. Thrombus formation in each tributary: The con-
-

Venous stasis favors accumulation of coagulation
factors, which is activated to form fibrin.
Coralline thrombus: The fibrin and thrombin formed
encourages further accumulation of platelets. The
platelets along with fibrin form upright laminae growing
across the stream. Between the laminae,
stasis promotes
further deposition of fibrin with trapped RBC nd WBCs.
This produces alternate layers fuised
of patelets and
fibrin with trapped blood cells. The
contraction offibrin
produces a charaçteristic ribbed (ripple) appearance
on the surface of thrombus. These
raised platelet ridges
are known as lines of Zahn.
secutive clot when reaches the entrance of venous
tributary may form another coralline thrombus
over the clot. This causes occlusion of opening of
tributary. A consecutive clot will again form up to
the opening of next venous tributary. Thus, several
thrombi with associated consecutive clot may be
formed.
Clotting en mass beyond the thrombus: Another
method of propagation is formation of long column
of consecutive clot attached to only one thrombus.
These consecutive clots may break and produce fatal
massive pulmonary embolism.
Complications of arterial and cardiac thromb: .Write short note on retrograde embolism.
.Fragmentation and embolization
.
Common sites of embolization: Retrograde emboli: Emboli, which travel against
Organs with rich blood supply, the flow of blood are known as retrograde emboli.
ie.brain, kidneys, and spleen.
Example, prostatic carcinoma metastasis to the spine.
It occurs through retrograde spread via intraspinal veins
EMBOLISM which carry the emboli from large thoracic ducts and
abdominal veins due to increased pressure in the body
gDefine embolism. Mention the different types of embolism/embolus
cavities (e.g. during coughing or straining).
with examples. Add a note on air embolism and fat embolism.
QDefine embolism. Embolus: Detached intravascular mass transported to a site
distant from its point of origin.
Definition: An embolus is a detached intravascular solid, liquid,
or gaseous mass that is
transported in the blood to asite distant Unless otherwise specifhed, emboli should be considered throm
from its point of origin. botic in origin and the process is known as thromboembolism.

Types of Emboli PULMONARY EMBOLISM

QMention different types of emboli. Q.Write short note on pulmonary embolism.
Classification: Depending on:
Definition: Pulmonary embolism (PE) is defined as an embolism
1. Physical nature of the emboli:
which emboli occlude pulmonary arterial tree.
.Solid: Thromboemboli, atheromatous material, in
tumor emboli, tissue fragments, bacterial clumps or
parasites, foreign bodies.
.Liquid: Fat, bone marrow and amnioticfluid.
Siteof Origin of Emboli (Fig. 5.11)
Deep leg veins: DVTs are the source in more than 95%
Gaseous: Air or other gases. of cases of pulmonary emboli. Deep leg veins include
2. Whether infected or not
popliteal, femoral or iliac veins.
Bland: Sterile. Other sites: Pelvic veins, vena cava.
Septic: Infected. Risk of pulmonary embolism: Major risk factor is after
be endogenous
3. Source (Fig. 5.13): The emboli may increases with advancing age, obesity,
from surgery. The risk
form within the body) or exogenous (introduced prolonged operative procedure, postoperative
infection,
outside). cancer, and pre-existing
venous disease.
.Cardiacemboli: Usually they arise from left side ofthe these throm-
atrial appendage, (2) Mechanism: DVTs undergo fragmentation >
heart. Example, emboli from: (1)
boemboli are carried through progressively larger vascular
left ventricle in myocardial infarction, (3) vegetations heart > right ventricle
endocarditis. channels-> into the right side ofthe
on the valves in infective arterial vasculature.
> enter into the pulmonary
they
.Vascular emboli:
(e.g. atheromatous plaque,
-
Arterial emboli
Embolism
aneurysms).
vein thrombus, tumor Fate of Pulmonary
Venous emboli (e.g. deep
Fate depends on the size of the embolus.
emboli). pulmonary emboli
emboli). organization: Small
Lymphatic emboli (eg.
tumor
1. Resolution or
of pulmonary
branches
into the smaller
4. Flow of emboli. may travel Most (60-809%)
resolve completely.
embolism. arteries and may
of time they
Write short note on paradoxical and the emboli of them are clinically silent. With passage
They are rare the wall
Paradoxical emboli: the incorporated into
circulation and bypass become organized and are

originate in the
venous
such
right-to-left shunt
a
of pulmonary vessel.
through obstruct
lungs by traveling (incomnpletely
closed/patent
Massive pulmonary
embolism: When emboli
septal defect 2. it is known
as an atrial defect. Then, they circulation,
interventricular
60% or m o r e of the pulmonary
foramen ovale) or block the blood
flow embolism.
heart and pulmonary
enter the left side of the as massive

arteries (refer page 439).

to the systemic