This document summarizes varicose veins, including their definition, causes, symptoms, and treatment options. Varicose veins are distended and tortuous veins, usually in the legs, caused by valve incompetence and blood pooling. They are often due to genetic factors but can be caused by activities that increase abdominal or leg pressure like pregnancy, obesity, or standing. Common symptoms include aching, swelling, and unsightly leg appearance. Treatment may involve support stockings, surgical procedures, and addressing underlying risk factors. More severe cases can lead to chronic venous insufficiency with skin changes, ulceration and impaired healing if not properly managed.

1. Dr: Wael H.Mansy, MDDr: Wael H.Mansy, MD
Assistant ProfessorAssistant Professor
College of PharmacyCollege of Pharmacy
King Saud UniversityKing Saud University
Disease of the veins
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2. Definition:
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
extremities.
Varicose Veins
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3. 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 one-
way 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
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4. (From Marieb, E.N.,Human Anatomy and Physiology, 3rd
ed., Benjamin Cummings, Glenview, IL, 1995.
Varicose Veins
Valve (open)
Skeletal
muscle
Direction of
blood flow
Valve (closed)
VeinVenous valves
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5. Varicose Veins
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6. CausesCauses
PrimaryPrimary
 Congenital abnormality, most common cause (weakCongenital abnormality, most common cause (weak
mesenchymal tissue)mesenchymal tissue)
SecondarySecondary
 Anything that raises intra-abdominal pressure or raisesAnything that raises intra-abdominal pressure or raises
pressure in superficial/deep venous systempressure in superficial/deep venous system
 soso……::
 PregnancyPregnancy
 Abdominal/pelvic massAbdominal/pelvic mass
 AscitesAscites
 obesityobesity
 constipationconstipation
 thrombosis of leg veinsthrombosis of leg veins
 spend long periods of time standing (barbers, for example)
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7. The most common manifestations
are :
1. Aching and edema
2. Their appearance through the skin is unsightly.
3. May be associated with varicocele or inguinal hernia.
Treatment often involves:
1. The use of support stockings to prevent venous
pooling.
2. Surgical interventions may also be used to improve
appearance and reduce discomfort.
Varicose Veins
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8. Chronic venous
insufficiencyThe 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.
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9.  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.
Chronic venous
insufficiency
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10. Venous ThrombosisA 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
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11.  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
asymptomatic.
 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.
Venous Thrombosis
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12. 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.
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13. Embolism 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.
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14. 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 blood-
clotting 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.
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15. Aspirin
 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
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16. Anticoagulant and thrombolytic drug
therapy Thrombolytic drugs are also known as fibrinolytic or clot-dissolving drugs.
 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.
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