W3 Venous Disease (Quiz 2. See Study Guide) Flashcards
What are the three types of venous disease?
—venous insufficiency
—varicose veins
—venous thrombosis
Veins
Anatomy just for review
Venous insufficiency
Etiology
Primary
Secondary
Familiarise yourself with anatomy
primary
—dysfunction of valve
secondary
—DVT
—trauma
—pregnancy
—obesity
—prolonged standing
—venous outflow obstruction
Venous insufficiency
What is the Pathophysiology?
—congenital weak vein walls become dilated under normal pressure
—congenitally abnormal valves
—valve failure d/t direct injury
diseases veins + venous hypertension = chronic venous insufficiency
—inc venous pressure impedes blood flow
—leukocytes are trapped
—damage to capillary basement layer
—proteins leak out to tissue
—dec O2 delivery to tissues = hypoxia
Venous insufficiency [know]
Presentation/ exam findings
Work up
Treatment
pain → burning, swelling, throbbing, cramping, aching, heaviness, restless leg, leg fatigue
skin changes → edema, itchy, dry, flakey, non-healing ulcers
Work Up
—labs: D-dimer to r/o venous thrombosis
—duplex u/s
magnetic resonance venography → most sensitive and specific test
—venous plethysmograpy
—physiologic venous function test
—ambulatory venous pressure test
Treatment
—compression stocking
—leg elevation
—unna boot
—venoablation procedures
—ligation with stripping
—sclerotherpay
—radio frequency ablation
—common in post menopausal women
Varicose veins — what are they?
Etiology
More common in
What is the associated syndrome?
Which most common vein/location?
—dilated and tortuous superficial veins
—LE
—F>M
—family history ++
Klippel-Trenaunay Weber syndrome
—most common vein → saphenous
—also snore tail area, esophageal, spermatic cord
—spider telectangasia
Varicose veins
Symptoms
Treatment
—most asymptomatic
—dull ache or pressure sensation
—possible swelling and skin ulceration
—common in ankle area
Treatment
—treated for cosmetic reasons
—laser
—endogenous laser therapy
—radiogrequency ablation
—surgical vein ligation and removal
Venous thrombosis [know]
What is it?
Pathophysiology?
aka VTE, DVT and PE
—commonly silent, picked up on autopsy
—DVT accounts for most cases of PE
— >40y/o
Virchow’s Triad [know]
1. Stasis of blood flow/venous stasis
2. Hypercoagulability
3. Endothelial injury
Endothelial injury → vasoconstriction → activation of platelets → platelet plug at injury site → 3 phases of plug formation (primary hemostasis) → platelet adhesion, activation and aggregation → coagulation cascade → clot formation → clotting factors → fibrin mesh + platelets → form clot (secondary hemostasis) → results in hard clot at site of endothelial injury
DVT
Review of coagulation cascade, clot formation and fibrinolysis
DVT [know]
Risk factors: primary genetic (4) and secondary acquired?
Where do they occur?
Primary — genetic
—Factor V Leiden
—prothrombin mutation
—antithrombin deficiency
—protein C or S deficiency
Secondary — acquired
—immobilisation
—afib
—tissue injury
—cancer
—DIC
—HITT
—oral contraceptives
—smoking
—obesity
Occur in DEEP veins — typically between muscles
—common sites [know]: calves, popliteal, femoral and iliac veins as well as arms, cerebral, mesenteric
DVT
Symptoms and PE
Labs and diagnostics
Symptoms
—unilateral leg pain worse when standing/walking
—leg swelling/edema
—warmth/erythema
—tenderness
—palpable cord/vein
—positive Homan’s sign
—colour changes of skin
Labs/Diagnostics
—D-dimer (95% sensitive but not specific. Helpful to rule out thrombus but can be elevated for other reasons)
—duplex u/s 95% sensitive
—CT venography
—MR venography
[SKILLS OSCE]
What is this?
Acute DVT
DVT
Treatment [know for length unprovoked]
—3 months
—UFH/LMWH
—or DOAC (apixaban, rivaroxaban, dabigatran)
—or warfarin (Coumadin)
DTV
Prophylaxis
—hospitalised patients
—heparin/LMWH
