Disease of the veins Dr: Wael H.Mansy, MD Assistant Professor College of Pharmacy King Saud University.

Disease of the veins
Dr: Wael H.Mansy, MD
Assistant Professor
College of Pharmacy
King Saud University
Varicose Veins
Varicose veins are veins that have become distended over
time. Long, tortuous and dilated veins of the superficial
varicose system due to the pooling of blood in the lower
Varicose Veins
Pathophysiology of Varicose Veins:
Veins are thin-walled vessels that are easily distended by
the chronic pooling of blood in the lower extremities.
Chronic distention of veins can reduce effectiveness of oneway venous valves that are present in the lumen to prevent
the back flow of blood and lead to a condition termed
valvular incompetence.
These venous valves work in conjunction with skeletal
muscle pumps in the legs to move blood back to the heart
from the extremities.
Varicose Veins
Valve (open)
Valve (closed)
Venous valves
Direction of
blood flow
(From Marieb, E.N.,Human Anatomy and Physiology, 3rd ed., Benjamin Cummings, Glenview, IL, 1995.
Varicose Veins
 Congenital abnormality, most common cause (weak
mesenchymal tissue)
 Anything that raises intra-abdominal pressure or raises
pressure in superficial/deep venous system
 so…:
Abdominal/pelvic mass
thrombosis of leg veins
spend long periods of time standing (barbers, for example)
Varicose Veins
The most common manifestations are :
Aching and edema
Their appearance through the skin is unsightly.
May be associated with varicocele or inguinal hernia.
Treatment often involves:
The use of support stockings to prevent venous pooling.
Surgical interventions may also be used to improve
appearance and reduce discomfort.
Chronic venous insufficiency
The presence of varicose veins and valvular incompetence can lead to
a condition called chronic venous insufficiency.
As a result of chronically impaired blood flow, congestion,
edema and poor tissue nutrition, pathologic changes may
eventually occur in the lower extremities.
Chronic venous insufficiency
Manifestations may include:
skin atrophy, dermatitis, ulceration and tissue necrosis.
Infection or trauma of the lower extremities that occurs in a
patient with chronic venous insufficiency may have serious
consequences because poor blood flow reduces delivery of
immune cells and impairs wound healing.
Treatment involves:
interventions similar to those for varicose veins.
Venous Thrombosis
A thrombus is
A blood clot that forms in the lumen of a blood vessel. A thrombus may
form in an artery, but it is more common in veins due to the lower
pressure and reduced blood flow found in the venous circulation.
Factors that may contribute to the formation of a
thrombus include the following:
1. Stasis of blood due to poor blood flow, immobility, heart failure,
myocardial infarction and hypotension
2. Damage to blood vessels from trauma, surgery, IV drugs, catheters
or immune response
3. Hypercoagulability of blood resulting from pregnancy, malignancies,
coagulation disorders, dehydration or use of oral contraceptives
Venous Thrombosis
Thrombi may form in superficial vessels of the skin and extremities or
in deep veins of circulation or tissues. Most superficial thrombi are
benign and self-limiting, but deep vein thrombus (DVT) can be much
more dangerous.
Although a thrombus may present with pain, tenderness and swelling,
it is estimated that nearly half of all deep vein thrombi are
As most deep vein thrombi occur in the lower extremities, painful
compression or tenderness and swelling of the calf or thigh region
might be used to diagnose a DVT in these areas.
DVT are associated with significant mortality and morbidity and require
intensive treatment.
Treatment and prevention
of venous thrombus
 Prevent
blood stasis in susceptible patients
through ambulation, use of elastic stockings,
exercise or elevation of legs
 Anticoagulation therapy (warfarin, heparin)
Thrombolytic therapy to dissolve clots
(streptokinase, TPA).
 Surgical removal of clots.
Unfortunately, for many patients with DVT the first manifestation of the
thrombus is a pulmonary embolism.
An embolism is a thrombus that breaks loose and travels through circulation.
Common sites for lodging of emboliare the small pulmonary blood vessels of
the lungs. Emboli that lodge in cerebral or coronary blood vessels may be
rapidly fatal. A bolus of fat released by the breakage of long bones or an
injection of air o foreign matter into the bloodstream through intravenous or
intra-arterial lines can also act as an embolism. Ischemia and possible death of
tissues may occur when blood flow is blocked by an embolus.
Anticoagulant and thrombolytic drug therapy
Anticoagulant drugs prevent the formation of blood clots by interfering with
distinct steps in the blood-clotting cascade (see Chapter 3). Two of the
most commonly used anticoagulants are warfarin (administered orally) and
heparin (administered intravenously). Warfarin prevents the reduction of
vitamin K, which is a cofactor necessary for activity of a key carboxylase in
the clotting cascade. Heparin acts via an effect on antithrombin III. As a
result of its mechanism of action, warfarin does not exert an anticoagulant
effect in vitro (i.e., blood in test tube) whereas Anticoagulant drugs prevent
the formation of blood clots by interfering with distinct steps in the bloodclotting cascade . Two of the most commonly used anticoagulants heparin
does. Neither warfarin nor heparin has any action against clots that have
already formed. Both drugs are bound to a significant extent to circulating
plasma proteins that can alter their bioavailability. A main potential adverse
effect of both warfarin and heparin is unwanted bleeding and hemorrhage.
Drugs that inhibit microsomal metabolism, inhibit platelet aggregation or
displace oral anticoagulants from plasma proteins can enhance the action
of anticoagulants and increase the risk of unwanted bleeding.
Anticoagulant and thrombolytic drug therapy
is a potent inhibitor of platelet aggregation through its
inhibition of the enzyme cyclo-oxygenase.
Inhibition of the cyclo-oxygenase enzyme reduces the
formation of thromboxane A2 , a substance that stimulates
platelet aggregation . Since platelet aggregation and
activation appear to play a major role in thrombus formation,
drugs like aspirin may be of significant therapeutic value in
preventing their occurrence. A number of clinical trials have
demonstrated the effectiveness of aspirin in preventing the
tissue damage that accompanies blood vessel occlusion in
arteriosclerosis and myocardial infarction.
Anticoagulant and thrombolytic drug therapy
Thrombolytic drugs are also known as fibrinolytic or clot-dissolving
Unlike anticoagulants that prevent the formation of blood clots,
thrombolytic drugs cannot prevent their formation. A number of
thrombolytic drugs are now available for clinical use, including
streptokinase, anistreplase, alteplase (tissue plasminogen activator)
and urokinase.
These agents promote the formation of plasmin (from plasminogen),
an enzyme that degrades the fibrin proteins that make up the
framework of a thrombus. The most common unwanted effects of
these thrombolytic agents are unwanted bleeding and hemorrhage.
Thrombolytic drugs have proved to be of clinical benefit in reducing
mortality in patients experiencing myocardial infarction.

similar documents