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22 Cards in this Set

  • Front
  • Back

Venous Pathophysiology

Deep venous thrombosis (DVT)


superficial venous thrombosis (SVT)


varicose veins


post-phlebitic syndrome


Pulmonary Embolism (PE)

Untreated manifestation of DVT

Pulmonary Embolism (PE)


collateral formation (active remodeling of non-functional or smaller secondary veins)


damaged venous valves


tissue damage complete occlusion

Clinical Manifestation of DVT

Leg swelling


dilated superficial veins


calf and thigh tenderness


stasis dermatitis


venous ulceration


can be complicated by PE

Clinical Diagnosis of DVT

often difficult


Dvt can be entirely asymptomatic


the primary indications of DVT can have multiple other causes


cellulitis


lymphangitis


bakers cyst


underlying arterial disease

Deep venous thrombosis

involves the formation and propagation of thrombus within the lumen of the deep veins.


increased venous resistance increases venous pressure.


the usual decrease in venous pressure with exercise is absent in acute DVT.


Venous thrombosis

occurs when blood elements become solidifies and held in place by a fibrin (protein involved in clotting) net.


Differs from arterial thrombosis.


venous - RBC and fibrin (coagulation thrombi)


Arterial - Platelet aggregates and fibrin

Resolution of thrombus

Thrombus may recanalize allowing flow to be reestablished.


Permanent damage may result.


Residual webs and bands may remain.


Partial obstruction/damage to venous valves ofter results.

Virchow's Triad

has 3 primary risk factors for venous disease


Stasis


Endothelial injury


Hypercoagulability



consider patient history

Stasis

Non moving blood tends to clot


-immobility


-polycythemia (high circulating RBC count)

Endothelial and

damage to the vein wall can form a nidus for the formation of clot.


blood will try to repair rough surfaces


-dysfunction- smoking and hypertension


-damage- surgery, catheter and trauma

Hypercoagulability

various conditions, inherited or acquired, and increase the tendency for blood to clot.


-Hereditary- factor V leiden, prothrombin G2021OA, protein C and S deficiency.


-Acquired-cancer, chemotherapy, OCT/HRT, pregnancy, obesity and hit

Deep venous thrombosis

in deep veins


forms anywhere that blood flow slows down


valve pockets/cusps


soleal sinus


left common illac vein (anatomically)

Typical DVT progression

starts as small nidus (formed) clot


some spontaneously lyse (death of cells)


others propagate (both directions)


occupies small area initially


as clot grows vein enlarges


veins can dilate to 7 times normal size

Occlusive DVT

initially dilates vein


contracts and pulls vessel walls with it over time


vein shrinks with age


collaterals (active remodeling of smaller secondary veins) form.

Non occlusive DVT

only attaches to part of the vein wall


Thrombus will contract and get smaller


recanalization


less valvular damage

venous pressure in DVT

due to high venous pressure, collateral (smaller secondary) veins become engorged


swelling from edema


can lead to ulceration and stasis changes.

Pulmonary Embolism (PE)

part of the thrombus breaks off


travels through right heart to the PA


lodges in lung (shortness of breath-dyspenea and chest or back pain


can cause death

Superficial Venous Thrombosis (SVT)

superficial veins of the lower extremity


rarely progresses into deep vein


rarely results in PE


clinical presentation


tenderness over affected area


palpable cord


warmth


local inflammation



Varicose veins

elongated, dilated, tortuous superficial veins that are usually incompetent


deep veins are surrounded and supported by muscle

varicose veins (primary)

congenital, inherent weakness of walls


May become prominent following pregnancy


no abnormality of deep veins

varicose veins (secondary)

DVT


absence of deep venous valves


congenital absence or atresia of deep veins

Post phlebitis syndrome (AKA post thrombotic syndrome)

following a DVT, the collaterals that bypassed the venous obstruction are damaged due to the inflammatory process.


valves no longer work properly


results in chronic edema, stasis changes and ulceration.