CARDIO-VENOUS DZ Flashcards
Pt with PMH of the following: ligamentous laxity, older age, obesity, FH, standing, OCP, estrogens, trauma/surgery, smoking, DVTs or prior h/o ulcers. What are their risk?
Venous DZ
Women who have this are at high risk for benign vein abnormalities.
Reticular veins-Spider veins
Telangiectasis-smaller face legs
A vein abnormality of >3mm defines.
Varicose veins
Clinical classes of Chronic Venous Dz
○ 0 no signs of disease ○ 1 telangiectasias or reticular veins ○ 2 varicose veins ○ 3 edema ○ 4 pigmentation or eczema ○ 5 healed venous ulcer ○ 6 active venous ulcer
Eitology class of Chronic Venous Dz
○ c congenital-
○ p primary-d/t valve degeneration
○ s secondary-post-thrombotic/trauma
Anatomy class of Chronic Venous Dz
○ s superficial veins
○ p perforator veins
○ d deep veins
Pathophysiology class of Chronic Venous Dz
○ r reflux
○ o obstruction
○ b= r, o reflux and obstruction
CEAP= C3EpAdPo
Edema
Primary degeneration
Deep vein
Obstructions
Pt has capillary hemangioma, limb HYPERtrophy, and varicose veins. Wha is the syndrome?
Klippel-Trenauany
Hallmark- PORT WINE STAIN**
Rare- congenital, dfx development of deep vein system
Unilateral
Which are Superficial Venous System in the Lower Extremity?
○ Great saphenous vein
○ small saphenous vein
Which Deep Veins are of Lower Extremity?
○ Post +Ant tibial
○ Peroneal
○ Popliteal vein/femoral
○ Profunda femoris joins femoral vein, to become
common femoral vein in the groinWhat is normal ABI standing pressure?
90-100mmhg systolic
Calf reduces pressure by 70% w/in 10steps
Calf pumps produces 200mmhg to propel blood in one valve veins
How is venous HTN and ulcer developed by REFLUX?
leaky capillaries d/t HTN-inflam response leak into ICF
RBC, matrix metaloproteinase, destroy enzymes- affect Na/K pump= leak
More valves below the knee
Dec up to inguinal lig.
Further away from heart, need help
How is venous HTN and ulcer developed by OBSTRUCTion?
Deep vein obstruction
Pressure may NOT DEC, may INC
L/T ambulatory venous HTN + venous claudication
Which veins DO NOT have valves
common iliac, IVC/SVC, portal venus system
Less muscle to assist
Mrs. Myerss c/o heavy legs, fatigue, pain walking, and itching in Left calf.
PE: bulges in poplietal fossa, mild abrasions, edema, hair loss
PMH- Previous sutures for last abrasion
What other findings?
Venous insufficiency Lipodermatosclerosis Hyperpigmentation (hemosiderin staining) Thickened nails Varicosities Blistering/bullae
Mr. Universe has thigh pain and feeling of tightness
with exercise. What is pathology?
Chronic iliofemoral obstruction can result in venous claudication
What is an inflammatory process that causes a blood clot to form and block one or more veins, and rarely l/t PE?
Superficial thrombophlebitis
common.
painful.
Rarely leads to PE b/c it’s in the superficial system
What is Hypoxia of subcutaneous fat lobules lead to inflammatory response?
Lipodermatosclerosis
● **Hard “woody” induration
●Starts at ankles and progresses proximally- inveterd/ bowling pin appearance
● Avoid biopsy – poor healing of fibrotic tissue
● **Can clinically diagnosis this!
TX- Stanozolol = anabolic steroid with fibrinolytic properties; helps with pain, inflammation and pigmentation
What causes hyperpigmentaion when valves fail → regurgitated blood/venous hypertension, then forces RBC’s to leak from capillaries?
Hemosiderin Staining-brownish-reddish discoloration
● RBC’s degrade and release iron
TX
● irreversible
Differiante btwn hemosiderin and cellulits?
- Hemosiderin does not extend,
- No calor(warm) or dolor(pain)
- doesn’t respond to antibiotics
Mrs. Myers ulcer is irregularly shaped, defined borders, erythematous, hyperpigment induration Exudate- yellow, greenish, gray Her lower ankle has edema PHM varicose veins for years What is her DX?
VENOUS LEG ULCER
1/3 of lower leg MC medial mallelous (Gaiter old term)
RARE above knee or on foot
What is presentation of Venous Leg ULcers that interesting?
Look bad BUT PAINLESS
TX- R.i.C.E, Diuretics prn
