Arterial

Thrombosis
PRESENTED TO: MR. ALI TAHIR
Arterial Thrombosis

 A blood clot within an artery is known as an arterial thrombosis.

 Arterial thrombosis denies oxygen and nutrition to an area of the

body.
 Arterial thrombosis are responsible for heart attacks,
strokes and peripheral vascular disease (thrombosis in leg
arteries).
Causes of Arterial Thrombosis

 Thrombosis of an artery leading to the heart causes a myocardial

infarction.
 Thrombosis of an artery leading to the brain causes a stroke.
 Arterial thrombosis usually affects people who already have
atherosclerosis or narrowing of the arteries.
 Atherosclerosis causes the walls of the arteries to ‘fur up’ with
deposits of atheroma, a fatty porridge-like substance.
 Atherosclerosis tends to develop in areas where the blood flow is
more turbulent.
Risk Factors for Arterial Thrombosis

The risk factors for arterial thrombosis include:

▪ Smoking.
▪ High blood pressure.
▪ Increased levels of cholesterol.
▪ Diabetes.
▪ Getting older.
▪ Family history.
▪ Poor diet.
▪ Physical inactivity.
Symptoms of Arterial Thrombosis

 The build-up of atheroma causes the arteries to narrow, which

can lead to heart disease and heart attacks, strokes or peripheral
vascular disease.
Symptoms of heart disease
▪ Atheromatous heart disease is caused by ‘furring up’ of the
arteries surrounding the heart. It can lead to a condition known as
angina.
▪ The symptoms of angina include chest pain during exercise or
when feeling emotionally stressed. The pain usually goes away
when you stop exercising.
Symptoms of Arterial Thrombosis

▪ A heart attack, or myocardial infarction, occurs when a clot blocks

one of the arteries supplying blood to the heart. This is nearly
always due to narrowing on the artery by atherosclerosis.
▪ A stroke occurs either when an artery supplying part of the brain is
blocked (ischaemic stroke) or when it ruptures and bleeds into the
brain (haemorrhagic stroke).
Venous Thrombosis
Venous thrombosis

▪ A venous thrombus is a blood clot (thrombus) that forms within a

vein. Thrombosis is a term for a blood clot occurring inside a blood
vessel.
▪ Venous thrombosis blocks return of deoxygenated blood to the
heart.
▪ The clot, or "thrombus," blocks or impairs blood flow in the vein,
leading to symptoms and secondary complications.
Types

▪ There are two types:

▪ Deep vein thrombosis (DVT): is a clot in a deep vein, usually in the
leg, but sometimes in the arm or other veins.
▪ Pulmonary embolism (PE): occurs when a DVT clot breaks free
from a vein wall, travels to the lungs and blocks some or all of the
blood supply. Blood clots in the thigh are more likely to break off
and travel to the lungs than blood clots in the lower leg or other
parts of the body.
▪ This combination is called venous thromboembolism.
Causes

▪ Venous thrombosis is quite common in the lower extremities, but

can also occur in the upper extremities.
▪ Venous thrombus are caused mainly by a combination of venous
stasis and hypercoagulability but to a lesser extent endothelial
damage and activation.
▪ The three factors of stasis, hyper-coagulability, and alterations in
the blood vessel wall represent Virchow's triad, and changes to the
vessel wall are the least understood.
Risk factors

▪ Older age.
▪ Major surgery, orthopedic surgery, neurosurgery.
▪ Cancers, most particularly pancreatic, but not cancers of the lip,
oral cavity, and pharynx.
▪ Immobilization, as in orthopedic casts the sitting position, and
travel, particularly by air.
▪ Pregnancy and the postpartum period.
▪ Antiphospholipid syndrome (such as lupus anticoagulant).
▪ Trauma and minor leg injury.
Symptoms

 DVT symptoms include:

▪ Pain or tenderness in your arm or leg, usually in the thigh or calf
▪ Swollen leg or arm
▪ Skin that’s red or warm to the touch
▪ Red streaks on the skin
 Pulmonary Embolism include:
▪ Shortness of breath
▪ Fast breathing
▪ Chest pain under your rib cage
▪ Rapid heart rate
Sequel of Thrombosis

Fibrinolysis: Many small thrombi are completely removed by

fibrinolytic system.
Organization: Capillary grow into the point of thrombus attachment
within a day or two.
Calcification: In diseased vessel organization note may take place.
The thrombus shrinks, calcium salts are deposited and covert into
phlebolith.
Embolism part of thrombus may be detached and carried along in
the blood stream to impact in a distant vessel.
Sequel of Thrombosis
Sequel of Thrombosis

• Thromboembolism is multifactorial, and risk factors accumulate

(or even multiply) • Thromboembolism can affect any organ or
tissue.

▪ Many aspects of modern lifestyle promote thrombosis and

atherosclerotic vascular disease
Progression of Atherosclerosis

▪ Atherosclerosis develops progressively through continuous

evolution of arterial wall lesions centered on the accumulation of
cholesterol-rich lipids and the accompanying inflammatory
response.
▪ These changes have been described in the histopathology of
human plaques and the plaques of experimental animals. These
systematically observed changes are closely similar in the
coronary arteries, the carotid arteries, and the aorta, and they form
a strong description of the total cumulative development of
atherosclerosis.
Progression of
Atherosclerosis
▪ As development progresses with lipid accumulation and inflammation,
the processes and histologic changes become increasingly complex
and can vary considerably among individuals and within any given
individual. In the natural course of atherosclerosis, spontaneous
regression of early-stage lesions may occur, but the intermediate and
advanced stages appear to be continuously progressive.

▪ This concept of a developmental continuum of plaque changes is

useful as an aid to understanding the potential steps of atherosclerosis
development. Although our current molecular understanding of these
steps and their integration is fragmentary, their general outline
supports crucial interplay among lipid accumulation, lipid oxidation,
and inflammation.
▪ The continuous development of atherosclerosis usually is
described in 2 ways that are different but complementary: as an
extended series of histologic processes and changes, and as a
shorter series of different classes of lesions that are grossly visible
to the unaided eye.

▪ Together, these approaches enhance our understanding of

atherosclerosis. Both are clinically useful when combined with
clinical imaging of plaques for diagnosing each individual patient's
stage of atherosclerosis and risks, and for selecting appropriate
therapy.