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Disorders that affect Blood Vessels

For year-ii medical students

Debre Tabor university College of

Health sciences
By: Dr.Zemen A.(MD)

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Outline of the presentation
3.normal structure of blood vessels
5.Venous disorders

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By the end of this presentation everyone is expected to
The stracture of blood vessels in normal physiology
and pathology
Risk factors and pathogenesis of atherosclerosis
Common disorders that affect the venous system

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The most clinically significant lesions involve arteries
-venous pathology can also cause clinical disorders

Vascular pathology results in disease via two principal

1. Narrowing or complete obstruction of vessel lumina,
either progressively (e.g., by atherosclerosis) or
precipitously (e.g., by thrombosis or embolism)

2. Weakening of vessel walls, causing dilation and/or

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The general architecture and cellular composition of
blood vessels are the same throughout the
cardiovascular system.
distinct functional requirements in different locations
=>multiple forms of vascular specialization
Why arterial walls are thicker than corresponding
veins at the same level of branching ?

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vessel specialization also means that pathologic
lesions within the vascular tree characteristically affect
only certain parts of the circulation.
atherosclerosis => mainly elastic and muscular
hypertension affects small muscular arteries and
specific types of vasculitis characteristically involve
only vessels of a certain caliber.

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Endothelial cells (ECs) and smooth muscle cells
(SMCs) constitute the bulk of vessel wall cellularity.
remainder of the wall is composed of
extracellular matrix (ECM) including elastin,
collagen, and glycosaminoglycans.
Based on size and stractural features
Arteries:1.large(elastic) arteries
2.medium sized(muscular) arteries
3.small arteries(2 mm in diameter)
&arterioles (20-100 m in diameter)
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Endothelial Cell Properties &FUN-

Vasconstrictors: endothelin, ACE

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Endothelial injury contributes to a host of pathologies
including thrombosis, atherosclerosis, and
hypertensive vascular lesions.
SMCs participate in both normal vascular repair and
pathologic processes such as atherosclerosis.
SMCs are also responsible for the vasoconstriction or
dilation that occurs in response to physiologic or
pharmacologic stimuli.
Intimal Thickening: A Stereotyped Response to
Vascular Injury
Neointimal SMC Vs medial SMC
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ARTERIOSCLEROSIS- literally means "hardening of the
generic term reflecting arterial wall thickening and loss of
Three patterns are recognized, with different clinical and
pathologic consequences:
1. Arteriolosclerosis affects small arteries and arterioles
Two anatomic variants:
Arteriolosclerosis most often associated with DM & HTN.

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2. Mnckeberg medial calcific sclerosis:
characterized by calcific deposits in muscular arteries,
typically in persons older than age 50.
3. Atherosclerosis, from Greek root words for "gruel"
and "hardening," is the most frequent and clinically
important pattern .

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Etiology has multifactorial nature.
Causes are several and expressed as risk factors.
Risk Factors for Atherosclerosis
Two forms of risk factors
1.Nonmodifiable (constitutional )
2.Modifiable(potentially controllable)
two risk factors increase the risk approximately fourfold.
three risk factors are present (e.g., hyperlipidemia,
hypertension, and smoking), the rate of myocardial infarction
is increased seven times.

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Risk Factors for Atherosclerosis
Major Risks Lesser, Uncertain, or Nonquantitated Risks
Nonmodifiable obesity
Increasing age Physical inactivity
Male gender stress("type A personality)
Family history Postmenopausal estrogen deficiency
Genetic abnormalities High carbohydrate intake
Potentially Controllable Hardened (trans)unsaturated fat intake
Hyperlipidemia Chlamydia pneumonia infection
Cigarette smoking
C-reactive protein
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Atherosclerosis affects large&
medium sized arteries
-Coronar y -Carotid
- aorta - Renals
- Femorals

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Atherosclerosis passes through mainly three

1. Fatty streak
2. Plaque(atheroma)
3. Complication of plaque
Understanding of the atherosclerotic process is
based on the knowledge of basic vascular biology.

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Fatty streak formation
EC senses changes in hemodynamic force and
blood borne signals.
Endothelium reacts to those changes by
synthesizing and releasing vasoactive substances.
Atherosclerosis arises from disruption of the
normal homeostasis.
Injury to the endothelial cells by traditional risk
factors and newer risk factors(like CRP) causes
diminished production and availability of NO
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Imbalance between NO and contracting factors
(endothelin-1, angiotensin, oxidants)
Expression of adhesion and chemoattractant
molecules on EC.
Results increased leukocyte EC adherence and
migration into the intima

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Fatty streaks

Fatty streak-a collection of foam cells in the intima

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Atheroma(Plaque formation)

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Evolution from fatty streak to plaque results from
Proliferation, migration of SMC to intima and
collagen synthesis and deposition
Continued release of cytokines by activated EC,
T cells, and foam cells influences SMC activity
Growth of the plaque results from
1. Expansion of the lipid core
2. SMC proliferation and fibrosis
3. Neovascularization of the plaque and rupture
of the new fragile vessels
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Components of plaques
Atherosclerotic plaques have three principal
1 . cells, including SMCs, macrophages, and T
2. ECM, including collagen, elastic fibers, and
proteoglycans and
3 .intracellular and extracellular lipid

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Consequences of plaque growth
1.lumen obstruction that can present with angina.

2. atherosclerotic plaques weaken the underlying media and can themselves

rupture, causing acute catastrophic vessel thrombosis.
Complicated plaque and clinical consequences
Plaque expansion
Weakening of the fibrous cap
Proinflammatory cytokines and Ox-LDL causes SMC death
reducing collagen synthesis promoting fibrous cap thinning
Further thinning of fibrous cap is caused by several proteinases,
collagenases, and gelatinases that degrade collagen tissue
Weak fibrous cap is vulnerable to rupture precipitating acute
thrombotic complication

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Plaque disruption
Disruption of the plaque may be caused by
1. Hemodynamic stress
2. Erosion of the endothelial surface
3. Rupture of the cap and spilling of its content

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Clinical consequence of
complicated plaque
When this occurs in different organs it has different
clinical manifestation and different names
Sudden death
Renal artery stenosis- hypertension, renal failure
Atherosclerotic aortic disease
Peripheral vascular disease(PVD/PAD)
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Existence of atherosclerosis is as old as recorded

human history.
Globally it remained rare prior to the 19th century.
In the 20th century it attained an epidemic
proportion in the industrialized countries being a
leading cause of death.
In these countries life time risk at age of 40 is 49%
& 32% for males and females.

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Increase in its incidence paralleled economic
development and improving life expectancy
. From control of infectious diseases
. Malnutrition
. Adoption of life style that promoted atherosclerosis
Currently similar trend is seen in developing countries.
It has become already a leading cause of death in
several developing countries.
The increased incidence/prevalence parallels increase
in distribution of its risk factors.

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Even in Ethiopia it increased in frequency from
being completely absent in the earlier hospital
reviews to being one of the leading causes of
emergency admissions in major cities.

Living long enough with wrong habits and

taking excess calories

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Prevention of Atherosclerotic Vascular Disease

1.Primary prevention aimed at either delaying

atheroma formation or encouraging regression of
established lesions in persons who have not yet
suffered a serious complication of atherosclerosis.
risk factor identification and modification of those
that are amenable to intervention
-cessation of cigarette smoking
-control of hypertension, weight loss, exercise, and
-lowering total and LDL blood cholesterol levels while
increasing HDL (e.g., by diet or through statins)

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Secondary prevention programs intended to prevent
recurrence of events such as myocardial infarction or
stroke in symptomatic patients .
-judicious use of aspirin (anti-platelet agent), statins,
and beta blockers (to limit cardiac demand), as well as
surgical interventions (e.g., coronary artery bypass
surgery, carotid endarterectomy).

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venous thromboembolism

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THROMBUS-the formation of solid or semisolid mass
from the constituents of the blood in blood vessels.
Embolism-the migration of thrombus from its site of
formation to other site.
Dysregulation of normal homeostasis.

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Pathogenesis of TE
There are three primary influences on thrombus
formation :
Virchow's triad:

(1) endothelial injury

(2) stasis or turbulence of blood flow, and
(3) blood hypercoagulability

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Virchow's triad in thrombosis. Integrity of endothelium is the most important
factor. Injury to endothelial cells can also alter local blood flow and affect
coagulability. Abnormal blood flow (stasis or turbulence), in turn, can cause
endothelial injury. The factors may act independently or may combine to promote
thrombus formation.
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Endothelial Injury
This is a dominant influence, since endothelial loss by
itself can lead to thrombosis.
particularly important for thrombus formation
occurring in the heart or in the arterial circulation.
physical loss of endothelium leads to exposure of
subendothelial ECM, adhesion of platelets, release of
tissue factor, and local depletion of PGI2 and
plasminogen activators.

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endothelium need not be denuded or physically
disrupted to contribute to the development of
any perturbation in the dynamic balance of the
prothrombotic and antithrombotic activities of
endothelium can influence local clotting events.
Significant endothelial dysfunction (in the absence of
endothelial cell loss) may occur with hypertension,
turbulent flow over scarred valves, or by the action of
bacterial endotoxins.

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homocystinuria, hypercholesterolemia, radiation, or
products absorbed from cigarette smoke, may be
sources of endothelial dysfunction.

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Alterations in Normal Blood Flow
Turbulence: contributes to arterial and cardiac
thrombosis by causing endothelial injury or
stasis is a major contributor to the development of
venous thrombi.
Normal blood flow is laminar, such that platelets flow
centrally in the vessel lumen, separated from the
endothelium by a slower moving clear zone of plasma.

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Stasis and turbulence :
-Disrupt laminar flow and bring platelets into contact
with the endothelium
-Prevent dilution of activated clotting factors by fresh
flowing blood
-Retard the inflow of clotting factor inhibitors and
permit the build up of thrombi
- Promote endothelial cell activation, resulting in local
thrombosis, leukocyte adhesion, etc.
-Hyperviscosity syndromes (such as polycythemia)
increase resistance to flow and cause small vessel

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Hypercoagulability generally contributes less
frequently to thrombotic states but is nevertheless an
important component in the equation.
divided into:
-primary (genetic) and
-secondary (acquired) disorders
Of the inherited causes of hypercoagulability,
mutations in the factor V gene and the prothrombin
gene are the most common.

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Secondary (acquired) hypercoagulable states
Unlike the hereditary disorders, the pathogenesis of
acquired thrombotic diatheses is frequently
multifactorial and is therefore more complicated .
oral contraceptive use
hyperestrogenic state of pregnancy

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Hypercoagulable States
Primary (Genetic)
Mutation in factor V gene( factor V leiden)
Mutation in prothrombin gene
Mutation in methyltetrahydrofolate gene
Antithrombin III deficiency
Protein c & s deficiency
very rare
Fibrinolysis defects

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Secondary (Acquired)
High risk for thrombosis:
- Prolonged bedrest or immobilization
-Myocardial infarction
- Atrial fibrillation
- Tissue damage (surgery, fracture, burns)
- Cancer
-Prosthetic cardiac valves
-Disseminated intravascular coagulation(DIC)
-Heparin-induced thrombocytopenia(HIT)
-Antiphospholipid antibody syndrome (lupus anticoagulant
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Lower risk for thrombosis:
- Cardiomyopathy
-Nephrotic syndrome
-Hyperestrogenic states (pregnancy)
- Oral contraceptive use
-Sickle cell anemia
- Smoking

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acquired causes
Among the acquired causes of thrombotic diathesis, the
heparin-induced thrombocytopenia (HIT) syndrome and
antiphospholipid antibody syndrome (previously called the
lupus anticoagulant syndrome) deserve special mention).
HIT syndrome occurs when administration of
unfractionated heparin (for therapeutic anticoagulation):
-induces autoantibodies to complexes of heparin and a
platelet membrane protein (platelet factor 4).
-This antibody binds to similar complexes present on
platelet and endothelial surfaces, resulting in platelet
activation and endothelial cell injury, and a net
prothrombotic state.

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Antiphospholipid antibody syndrome
The antiphospholipid antibody syndrome (APS) is
defined by the presence of two major components:
1.Presence in the plasma of at least one type of
autoantibody known as an antiphospholipid antibody
2.The occurrence of at least one of the following
clinical manifestations: venous or arterial thromboses,
or pregnancy morbidity(miscarriage).

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Although the clinical manifestations of APS occur in
other disease populations, in the APS they occur by
definition in the context of aPL.
aPL, which are directed against plasma proteins bound
to anionic phospholipids, may be detected as:
-Lupus anticoagulants
-Anticardiolipin antibodies
-Antibodies to 2 glycoprotein-I

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-In vivo these antibodies induce a hypercoagulable state, by
inducing direct platelet activation or by interfering with
endothelial cell production of PGI2.
- APS occurs either as a primary condition or in the setting of
an underlying disease, particularly systemic lupus
erythematosus (SLE).
-Although antiphospholipid antibodies are associated with
thrombotic diatheses, they have also been identified in 5%
to 15% of apparently normal individuals, implying that they
may be necessary but not sufficient to cause full-blown
antiphospholipid antibody syndrome

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Thrombi can develop anywhere in the cardiovascular
system (e.g., in cardiac chambers, on valves, or in
arteries, veins, or capillaries).
-The size and shape of a thrombus depend on the site
of origin and the cause.
Arterial or cardiac thrombi typically begin at sites of
endothelial injury or turbulence.
venous thrombi characteristically occur at sites of

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Thrombi are focally attached to the underlying
vascular surface.
arterial thrombi tend to grow in a retrograde direction
from the point of attachment, while venous thrombi
extend in the direction of blood flow (thus both tend
to propagate toward the heart).
The propagating portion of a thrombus tends to be
poorly attached and therefore prone to fragmentation,
generating an embolus.

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Thrombi can have grossly (and microscopically)
apparent laminations called lines of Zahn:
these represent pale platelet and fibrin layers
alternating with darker erythrocyte-rich layers.
distinguish antemortem thrombosis from the bland
nonlaminated clots that occur in the postmortem state
thrombi formed in sluggish venous flow usually
resemble statically coagulated blood
-careful evaluation generally reveals ill-defined
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Arterial thrombi :
-frequently occlusive
-produced by platelet and coagulation activation
-they are typically a friable meshwork of platelets,
fibrin, erythrocytes, and degenerating leukocytes.
-Although arterial thrombi are usually superimposed
on an atherosclerotic plaque, other vascular injury
(vasculitis, trauma) can be involved.

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Venous thrombosis (phlebothrombosis):
-almost invariably occlusive
-the thrombus can create a long cast of the lumen;
venous thrombosis is largely the result of activation of
the coagulation cascade, and platelets play a secondary
thrombi form in the sluggish venous circulation &
tend to contain more enmeshed erythrocytes and are
therefore called red, or stasis, thrombi.

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venous thrombosis cont...
-The veins of the lower extremities are most commonly
affected (90% of venous thromboses); however, venous
thrombi can occur in the upper extremities,
periprostatic plexus, or ovarian and periuterine veins;
under special circumstances they may be found in the
dural sinuses, portal vein, or hepatic vein.

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Thrombi occurring in heart chambers or in the aortic
lumen are designated mural thrombi.
Thrombi on heart valves are called vegetations.
postmortem clots Vs venous thrombosis
-gelatinous -firmer & focally attached
-red dark dependant - sectioning reveals
Portion strands of gray fibrin
-yellow, "chicken fat" supernatant
-not attached to underlying wall
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Fate of Thrombus
If a patient survives the initial thrombosis, in the ensuing
days or weeks thrombi undergo some combination of the
following four events:
1. Propagation: Thrombi accumulate additional platelets
and fibrin=>vessel obstruction
2. Embolization: Thrombi dislodge or fragment and are
transported elsewhere in the vasculature.
3. Dissolution: Thrombi are removed by fibrinolytic
4. Organization and recanalization:
Thrombi induce inflammation and fibrosis (organization)

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Low-power view of an artery with an old thrombus. A, H&E-stained section. B,

Stain for elastic tissue. The original lumen is delineated by the internal elastic
lamina (arrows) and is totally filled with organized thrombus, now punctuated by a
number of recanalized channels (white spaces)

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Venous thrombi can cause
congestion and edema in vascular beds distal to an
most worrisome for their capacity to embolize to the
lungs and cause death.

arterial thrombi can embolize and even cause

downstream tissue infarction.

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Venous Thrombosis
Superficial venous thrombosis
- occur in the saphenous system
- particularly when there are varicosities
- cause local congestion, swelling, pain, and
tenderness along the course of the involved vein
- rarely embolize
Deep vein thrombosis(DVT):
- thrombi in the larger leg veins at or above the knee
joint (e.g., popliteal, femoral, and iliac veins) are more
serious because they may embolize.

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may cause local pain and edema
-the venous obstruction may be rapidly offset by
collateral bypass channels.
-Consequently, deep venous thromboses are entirely
asymptomatic in approximately 50% of patients and
are recognized in retrospect only after they have

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An embolus is a detached intravascular solid, liquid, or
gaseous mass that is carried by the blood to a site
distant from its point of origin.
Virtually 99% of all emboli represent some part of a
dislodged thrombus, hence the term
Rare forms of emboli include:
fat droplets, bubbles of air or nitrogen, atherosclerotic
debris (cholesterol emboli), tumor fragments, bits of
bone marrow, or foreign bodies such as bullets

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Pulmonary Thromboembolism (PTE)
The consequences of thromboembolism include
ischemic necrosis (infarction) of downstream tissue
Depending on the site of origin, emboli may lodge
anywhere in the vascular tree:

-The clinical outcomes are best understood from the

standpoint of whether emboli lodge in the pulmonary
or systemic circulations.

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Embolus derived from a lower extremity deep venous thrombosis and
now impacted in a pulmonary artery branch

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Pulmonary embolism has an incidence of 20 to 25 per
100,000 hospitalized patients.
In more than 95% of cases, venous emboli originate
from deep leg vein thrombi above the level of the knee.
an embolus can pass through an interatrial or
interventricular defect, thereby entering the systemic
circulation (paradoxical embolism)

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PTE cont...
Most pulmonary emboli (60% to 80%) are clinically
silent because they are small.
Sudden death, right ventricular failure (cor
pulmonale), or cardiovascular collapse occurs when
60% or more of the pulmonary circulation is
obstructed with emboli.
.Embolic obstruction of medium-sized arteries can
cause pulmonary hemorrhage but usually not
pulmonary infarction because the lung has a dual
blood supply and the intact bronchial arterial
circulation continues to supply blood to the area.

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PTE cont...
left-sided cardiac failure (and resultant sluggish
bronchial artery blood flow) may result in a large
Embolic obstruction of small end-arteriolar
pulmonary branches usually does result in associated
infarction.Many emboli occurring over a period of
time may cause pulmonary hypertension with right
ventricular failure.

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Systemic Thromboembolism
Systemic thromboembolism refers to emboli in the
arterial circulation.
Most (80%) arise from intracardiac mural thrombi,
two-thirds of which are associated with left ventricular
wall infarcts and another quarter with dilated left atria
(e.g., secondary to mitral valve disease).
The remainder originate from aortic aneurysms,
thrombi on ulcerated atherosclerotic plaques, or
fragmentation of valvular vegetations.

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STE cont...
The major sites for arteriolar embolization are the
lower extremities (75%) and the brain (10%), with the
intestines, kidneys, and spleen affected to a lesser
The consequences of embolization in a tissue depend
-vulnerability to ischemia
-caliber of the occluded vessel, and
-the collateral blood supply
-in general, arterial embolization causes infarction of
the affected tissues.

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Fat Embolism
after fractures of long bones (which contain fatty
marrow) or after soft-tissue trauma.
fat and marrow embolism occurs in some 90% of
individuals with severe skeletal injuries .
fewer than 10% of such patients show any clinical
Fat embolism syndrome is characterized by:
-pulmonary insufficiency, neurologic symptoms,
anemia, and thrombocytopenia.
Affected patients develop a classic triad hypoxemia,
neurologic abnormalities, and a petechial rash.
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fatal in about 10% of cases.
Typically, the symptoms appear 1 to 3 days after injury,
with sudden onset of tachypnea, dyspnea, and

Neurologic symptoms include irritability and

restlessness, with progression to delirium or coma.
Pathogenesis of FES:
"Mechanical" fat embolism
Production of toxic intermediaries

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Air Embolism
Gas bubbles within the circulation can obstruct
vascular flow (and cause distal ischemic injury) almost
as readily as thrombotic masses can.
Air may enter the circulation during obstetric
procedures or as a consequence of chest wall injury.
Generally, more than 100 mL of air are required to
produce a clinical effect.
-bubbles can coalesce to form frothy masses
sufficiently large to occlude major vessels.

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decompression sickness:
occurs when individuals are exposed to sudden
changes in atmospheric pressure.
-Scuba and deep-sea divers, and underwater
construction workers are at risk.
- bends: The rapid formation of gas bubbles within
skeletal muscles and supporting tissues in and about
joints is responsible for the painful condition called
the bends.

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chokes :In the lungs, gas bubbles in the vasculature
cause edema, hemorrhages, and focal atelectasis or
emphysema, leading to respiratory distress, called the
caisson disease:
- chronic form of decompression sickness
- persistence of gas emboli in the bones leads to
multiple foci of ischemic necrosis.
- The heads of the femurs, tibias, and humeri are most
commonly affected.
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Rx of Decompression sickness
Treating acute decompression sickness :
-placing the affected individual in a compression
chamber to increase barometric pressure and force the
gas bubbles back into solution.

-Subsequent slow decompression theoretically permits
gradual resorption and exhalation of the gases so that
obstructive bubbles do not re-form.

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Amniotic Fluid Embolism
a grave but fortunately uncommon complication of
labor and the immediate postpartum period (1 in
50,000 deliveries)
mortality rate in excess of 20% to 40%.
The onset is characterized by sudden severe dyspnea,
cyanosis, and hypotensive shock, followed by seizures
and coma.
If the patient survives the initial crisis, pulmonary
edema typically develops, along with (1/2 of the
patients) DIC, due to release of thrombogenic
substances from amniotic fluid.

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Pathogenesis of AFE
underlying cause is entry of amniotic fluid (and its
contents) into the maternal circulation via a tear in the
placental membranes and rupture of uterine veins.
Classically, there is marked pulmonary edema and
diffuse alveolar damage , with the pulmonary
microcirculation containing squamous cells shed from
fetal skin, lanugo hair, fat from vernix caseosa, and
mucin derived from the fetal respiratory or
gastrointestinal tracts.
Systemic fibrin thrombi indicate the onset of DIC.

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Varicose Veins
Varicose veins & phlebothrombosis/thrombophlebitis
together account for at least 90% of clinical disease
associated with veins.

Varicose veins are abnormally dilated, tortuous veins

produced by prolonged increase in intraluminal
pressure and loss of vessel wall support.

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Pathogenesis of vv
If the valves in the perforating veins become
incompetent, blood can be forced from the deep to the
superficial venous plexuses; this is a major factor in the
development of varicosities.

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Some 10% to 20% of adult males and 25% to 33% of
adult females develop lower extremity varicose veins
obesity increases the risk, and the higher incidence in
women is a reflection of the elevated venous pressure
in lower legs caused by pregnancy.
A familial tendency toward premature varicosities
results from imperfect venous wall development.

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Clinical Course
Varicose dilation renders the venous valves incompetent
and leads to stasis, congestion, edema, pain, and
The most disabling sequelae include persistent edema in
the extremity and secondary ischemic skin changes
including stasis dermatitis and ulcerations; poor wound
healing and superimposed infections can become chronic
varicose ulcers.
embolism from these superficial veins is very rare.
This is in sharp contrast to the relatively frequent
thromboembolism that arises from thrombosed deep veins.
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Venous ulceration of the ankle

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Thrombophlebitis and Phlebothrombosis
The deep leg veins account for more than 90% of cases
of thrombophlebitis and phlebothrombosis
-interchangeable designations for venous thrombosis
and inflammation.

-the periprostatic venous plexus in males and the

pelvic venous plexus in females are additional sites, as
are the large veins in the skull and the dural sinuses
(especially in the setting of infection or

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Peritoneal infections (e.g., peritonitis, appendicitis,
salpingitis, and pelvic abscesses) can lead to portal
vein thrombosis.
For deep venous thrombosis (DVT) of legs, congestive
heart failure, neoplasia , pregnancy, obesity, the
postoperative state, and prolonged bed rest or
immobilization are the most important clinical
Genetic hypercoagulability syndromes can also be
associated with venous thrombosis.

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In patients with cancer, particularly adenocarcinomas,
hypercoagulability occurs as a paraneoplastic
syndrome related to tumor elaboration of
procoagulant factors .
In this setting, venous thromboses classically appear
in one site, disappear, and then reoccur in other veins,
so-called migratory thrombophlebitis (Trousseau sign)

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Reading assignment
- Benign tumours : -Haemangiomas
- glomus tumour
- Malignant tumours : -Angiosarcoma
- Kaposi's sarcoma

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