Venous Disorders and DVT Quiz

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Questions and Answers

Which of the following factors can lead to the development of varicose veins?

Excessive hydration

High protein diet

Increased venous flow velocity

Enlarged uterus during pregnancy (correct)

Pregnancy is solely responsible for causing varicose veins.

False

What are some subjective symptoms associated with varicose veins?

Pain, soreness, aching, burning.

Increased venous pressure leads to the distention of capillaries and increased capillary __________.

pressure Signup and view all the answers

Match the following conditions to their associated symptoms:

Varicose Veins = Pain, soreness, aching Venous Stasis Ulcers = Tissue damage and ulceration Superficial Thrombophlebitis = Erythema and inflammation Deep Vein Thrombosis (DVT) = Potentially life-threatening clots Signup and view all the answers

Which of the following is a symptom associated with Deep Vein Thrombosis (DVT)?

Leg discoloration Signup and view all the answers

Venous stasis ulcers are a complication of chronic venous insufficiency.

True Signup and view all the answers

What is one high positive predictive symptom for DVT?

Phlegmasia cerulea dolens Signup and view all the answers

A patient presenting with massive thigh and calf swelling and limb cyanosis is experiencing __________.

Phlegmasia cerulea dolens Signup and view all the answers

Match the following terms with their definitions:

Venous Stasis Ulcers = Chronic wounds caused by venous hypertension Post-thrombotic Syndrome = Long-term complications of DVT Varicose Veins = Enlarged, twisted veins due to valve failure Deep Vein Thrombosis = Formation of a blood clot in a deep vein Signup and view all the answers

What type of DVT has a high risk for embolization?

Obstructive acute DVT Signup and view all the answers

List one risk factor for developing venous disorders.

Prolonged immobility Signup and view all the answers

Venous obstruction can occur due to intraluminal thrombosis.

True Signup and view all the answers

Which of the following is a common risk factor for venous disorders?

Sedentary lifestyle Signup and view all the answers

Deep Vein Thrombosis (DVT) primarily occurs in the upper extremities.

False Signup and view all the answers

What is the primary mechanism of thrombosis related to stasis of blood flow?

Inactivity of calf muscle pump Signup and view all the answers

The presence of a blood clot within a blood vessel is called a ______.

thrombus Signup and view all the answers

Match each term with its definition:

Thrombophlebitis = Formation of a blood clot followed by inflammation of the vessel wall DVT = Presence of thrombus within the peripheral deep venous system Varicose veins = Enlarged, twisted veins often visible under the skin Post-thrombotic syndrome = Long-term complication following DVT characterized by pain and swelling Signup and view all the answers

Which factor increases the effectiveness of antithrombin III?

Heparin Signup and view all the answers

Venous stasis ulcers occur due to increased blood flow.

False Signup and view all the answers

What is the function of plasmin in the body?

To digest fibrin strands and other clotting factors Signup and view all the answers

Common causes of hypercoagulability include pregnancy and ______.

neoplastic disease Signup and view all the answers

What is a common complication of Deep Vein Thrombosis (DVT)?

Post-thrombotic syndrome Signup and view all the answers

Study Notes

Venous Pathophysiology

Venous pathophysiology is the study of the mechanisms involved in the arrest of blood from a damaged blood vessel.
One of the key processes in hemostasis is vasoconstriction.
Vasoconstriction occurs when a blood vessel is injured and smooth muscle cells in the traumatized vessel contract, reducing blood flow.

Hemostasis

Hemostasis is the mechanism involved in the arrest of blood from damaged blood vessels.

Vasoconstriction

When a blood vessel is injured, smooth muscle cells in the vessel contract.
This reduces blood flow through the vessel.
The nerve reflex, myogenic spasm, local humoral factors (like thromboxane A2 and serotonin), initiate these responses.

Formation of Platelet Plug

A platelet plug is formed by normal platelets.
Platelets are cell fragments derived from megakaryoblasts, formed in bone marrow.
Their surface membranes contain glycoproteins making them slippery.
Their cytoplasm contains granules playing a role in the clotting process.

Platelet Reaction

When platelets contact damaged endothelium or collagen fibers, they undergo viscous metamorphosis, swelling and forming irregular shapes.
Platelets become sticky and adhere to rough surfaces and fibers.
They release chemicals, like ADP and thromboxane A2.

Aggregation

ADP and thromboxane A2 activate nearby platelets to undergo adhesion reaction.
Platelets adhere to each other and the original platelets, creating a platelet plug that blocks the wound.
Platelets release factors that are involved in clotting reactions.

Coagulation

Coagulation involves the activation or conversion of soluble factors present in the blood into an insoluble network of fibrin strands that close the wound.
Prothrombin activator (PTA) begins the coagulation process.
PTA forms from the intrinsic or extrinsic pathway, reacting to tissue or endothelial damage.

Coagulation continued

PTA catalyzes the formation of thrombin from prothrombin.
Thrombin catalyzes the conversion of soluble fibrinogen to solid fibrin polymer threads.
Fibrin threads form a mesh, allowing plasma, blood cells, and platelets to aggregate and form the clot.

Clotting Factors

Many substances in the blood play a crucial role in clotting.
These substances are mainly synthesized in the liver.
The factors are present in the blood as inactive agents.

Intrinsic Pathway

The intrinsic pathway is initiated by trauma to blood (platelets).
It's activated when blood contacts damaged endothelial cells or collagen fibers.
Steps involve the activation of factors XII, XI, and IX, leading to the formation of active Factor X.

Intrinsic pathway continued

A complex, including active Factor X, Factor V, platelet factors, and calcium ions, forms the prothrombin activator.
Prothrombin activator converts prothrombin (inactive Factor II) to thrombin.

Extrinsic Pathway

The extrinsic pathway is initiated by trauma to the vessel or external tissues.
Thromboplastin (Factor III) is released from tissues when they're damaged.
Thromboplastin activates and combines with Factor VII, which activates Factor X, leading to the formation of prothrombin activator.

Formation of the Clot

The conversion of soluble fibrinogen into an insoluble fibrin meshwork forms the clot.
Fibrinogen is converted to fibrin monomers by thrombin.
Fibrin monomers polymerize into long fibrin molecules, which are cross-linked to form a mesh.
Fibrin strands stretch across the opening, trapping blood cells to produce a barrier preventing blood loss.

Formation of the Clot continued

The fibrin strands eventually contract, forming an impermeable barrier.

Prevention of Blood Clotting

Endothelial surface factors, such as smoothness, glycocalyx, and thrombomodulin, prevent clotting.
Antithrombin agents (like fibrin and antithrombin III) inhibit thrombin.

Heparin

Heparin, secreted by mast cells, increases the effectiveness of antithrombin.
It decreases Factor XII, XI, IX, and X effectiveness.
Alpha-2 macroglobulin combines with coagulation factors and inactivates them.

Fibrinolysis

Plasminogen is a normal constituent of plasma, but it's inactive.
Plasminogen is trapped in the fibrin clot.
Tissue plasminogen activator (released from damaged tissues) converts plasminogen to plasmin.
Plasmin digests fibrin strands, and other clotting factors. This ultimately dissolves the clot.

DVT Annual Estimates

1-10 million cases of DVT annually.
600,000 cases of pulmonary embolism (PE) annually
200,000 deaths from PE annually.

DVT Incidence

Certain medical procedures increase DVT risk.
- Major GYN surgery (30%)
- Average surgical patients (20-30%)
- Older surgical patients (40-59%)
- Hip fracture (40-50%)
- Hip or knee replacement (50%)
- Myocardial infarction (20-50%)
- Stroke (30-60%)

Thrombus: A blood clot in a blood vessel.
Thrombophlebitis: A blood clot followed by an inflammatory reaction to the vessel wall and surrounding tissue.
Deep Vein Thrombosis (DVT): Thrombus formation within deep peripheral veins.
Superficial Venous Thrombosis/Superficial Thrombophlebitis: Thrombus formation in superficial veins.

Virchow's Triad

Virchow's triad describes three main factors that contribute to DVT formation.
The three factors are: Stasis, Endothelial injury, Hypercoagulability.

Vessel Damage

Direct trauma.
Previous thrombosis.
Inflammation.
Infection.
These can cause activation of clotting factors.
These can inhibit natural fibrinolysis..
These can expose blood to collagen fibers

Stasis of Blood Flow

Bed rest
Immobility
Spinal cord injury
Venous obstruction − Pregnancy are all causes of decreased blood flow, leading to a greater risk of DVT.
Calf muscle inactivity allows clotting factors to accumulate locally.

Hypercoagulability

Pregnancy.
Neoplastic disease/cancer.
Oral contraceptives/estrogen replacement.
Excessive clotting factors.
Absence of normal fibrinolytic factors.

Formation of Venous Thrombus (Location)

90% of DVTs occur in the legs.
Acute DVT usually begins with platelet and fibrin deposits accumulating behind venous valve cusps.
Usual site in muscular veins of the calf.

Formation of Venous Thrombus (Propagation)

Thrombus grows and may form a free-flowing clot loosely attached to the venous wall.
It may fill the vein and occlude it, partially or completely obstructing venous return.
A thrombus may spontaneously dissolve or lyse.

Formation of Venous Thrombus (Fate)

Thrombus organization.
Clot contraction pulls vein walls together.
New channels are formed in the vessel lumen
Vein valves may be destroyed.

Symptoms (clinical manifestations) (clinical diagnosis)

Silent DVT: no symptoms initially or pain/swelling and tenderness.
Increased venous resistance, pressure, edema, extravasation of blood.
Symptoms include persistent leg pain with acute onset, persistent leg swelling, calf pain/tenderness, leg discoloration.
DVTs are often clinically asymptomatic or have vague symptoms.

Complications

Embolization
Phlegmasia cerulea dolens: severe DVT with pain, swelling, cyanosis
Unnecessary treatment
Post-phlebitic syndrome
Chronic venous insufficiency
Venous stasis ulcer

Venous vs. Arterial Symptoms

Venous symptoms tend to be acute onset, with swelling, calf/thigh pain, and local tenderness, but pallor is different.
Arterial symptoms are more progressive, with intermittent pain when walking, coolness of the foot/limb, pallor, and eventual gangrene.

Deep Vein Thrombosis (Obstructive vs. Non-Obstructive)

Acute DVT is characterized by distended veins, a new propagating clot that isn't tightly attached to the vein wall, and high risk of embolization; larger lumen with thrombus.
Chronic DVT is characterized by a smaller vein lumen with a consolidated clot, tight attachment to the vein wall, and low risk of embolization.
Non-obstructive chronic DVT presents with a thrombus that's eccentric, may have a free-floating tail, normal flow around the clot, and adheres to the vein wall.

Deep Vein Thrombosis (Fate of thrombus)

Lysis of thrombus: rate of lysis depends on its size and the flow in the channels of the vein.
Neointimal thickening: thrombus adheres to, and fibroelastic tissue incorporates into the vein wall.
Restoration of flow: partial reopening of native or formation of collateral channels.
Post-thrombotic syndrome (PTS)/Post-phlebitic syndrome: Chronic deep vein obstruction, chronic deep valve incompetence, and symptoms like progressive leg pain and swelling.

Varicose Veins

Primary varicose veins: dilated, elongated, and tortuous superficial veins, especially in the legs, due to incompetent valves in superficial veins.
Secondary varicose veins: valve damage from DVT causes retrograde flow in perforators and deep veins, resulting in increased venous pressure and complete flow disruption

Pregnancy and Varicose Veins

Pregnancy may exacerbate varicose veins.
Enlarged uterus compresses the inferior vena cava (IVC) and iliac veins.
Hormonal changes make veins more compliant.
Reduced venous flow velocity may increase venous distention making it more likely.

Risk Factors

Family history
Increasing age
Female gender
Pregnancy
Obesity
Standing occupations
History of previous DVT is common

Clinical Manifestations (Varicose Veins)

Cosmetic disturbance, pain, soreness, aching, burning, throbbing, and cramping are common complaints.
Other symptoms include muscle fatigue, restless legs, swelling, discoloration, inflammatory dermatitis, recurrent/chronic cellulitis, cutaneous infarction, or ulcerations, malignant degeneration.

Venous Stasis Ulcers

Increased venous pressure causes capillary distention and increased capillary pressure, opening junctions between endothelial cells, and causing proteins and fluid to seep into the tissues.
Reduced oxygen transfer leads to ischemia and ulceration.

Superficial Thrombophlebitis

Thrombosis of superficial veins.
Not as serious as DVT.
Risk factors can be IV infusions and IV drug abuse..
Symptoms include erythema, inflammation, local tenderness, and a palpable cord or mass. Superficial thrombophlebitis generally causes more pain than DVT.

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Description

Test your knowledge on the factors leading to varicose veins and deep vein thrombosis (DVT). This quiz covers symptoms, risks, and complications associated with venous disorders, aiding in your understanding of vascular health. Perfect for medical students and health professionals!