Peripheral vascular dz Flashcards
peripheral artery disease (PAD) causes?
-atherosclerosis and is a significant independent risk factor for cardiovascular and cerebrovascular morbidity and mortality
what are the sx of PAd?
- initally asx
- can progress to claudication, ischemia, and pain with exercise
what are complications of untreated PAD?
critical or acute limb ischemia can lead to pain at rest w/ skin ulceration, gangrene, or loss of limb
what can acute arterial occlusion be caused by?
-thrombosis or embolism
what can cause thrombotic dz?
trauma, hypovolemia, inflammatory arteritis (takayasu and buerger dz), polycythemia, dehydrations, repeated arterial punctures, and hypercoagulable state
clinical features of PAD
- intermittent claudication, foot or lower leg pain w/ exercise that is relieved by rest
- may have thigh or butt pain
PE of PAD
- femoral and distal pulses will be weak or absent; aortic, iliac, or femoral bruit may be present
- skin changes in lower extremity: loss of hair, shiny atrophic skin, pallor with depending rubor
what are sx of severe dz?
numbness, tingling, ischemic ulcerations, which may lead to gangrene
what are the 6 P’s of acute aterial occlusion?
pain, pallor, pulselessness, paresthesias, poikilothermia, and paralysis
what does acute arterial occlusion threaten
limb viabiltiy
how is PAD dx?
doppler US flow
ABI: < 0.9 indicates significantdz
what is the gold standard for PAD dx?
Angiography
what lab test has a strong association with incidence and progression of PAD?
homocysteine
what is Leriche syndrome?
iliac artery dz: can lead to Erectile dysfunction
tx w/ sildenafil (adr: priapism)
what does an ABI > 1.4 mean
non compressible artery due to calcification
tx of PAD?
risk factor modification: stop tobacco, DM, HTN, hyperlipidemia control
what meds can be used to hlep? (reduce sx of claudication)
BB, ACEI, statines, progressive exercise
what should be used in all pts w/o CI?
antiplatelet therapy w. asa or clopidogrel
sx relief w/ cilostazol
what is cilostazol?
decreases platelet, supresses CAMP degredation, vasodilates
what is cilostazol ADR
edema, agranulocytosis, MI, bleed, thrombocytopenia
what is last line tx for PAD
revascularization
what is the Brodie-Trendelenburg test?
differentiates btw saphenofemoral valve incompetence vs perforator vein incompetence
what are vericose veins?
dilated, torturous veins that develope superficially in the lower extremeiteis, particularly in the distribution of the great saphenous vein
-smaller blue-green, flate reticular veins, telangiectasias, and spider veins are further evidence of venous dysfunction
what are vericose veins caused by?
superficial venous insufficieny and valvuular incompetence
RF for vericose veins
prego, obesity, family hx, prolonged sitting/standing, hx of phlebitis
what are sx of VV
asx
aching, fatigue
what are PE finding s of VV
chronic distal edema, abnormal pigmentation (brown), fibrosis, atrophy, skin ulcerations that may develop in severe dz
dx for VV
none, may need dopple to located insufficient vlaves before surgery
tx of vv
elastic stockings, leg elevation and regular exercise
last line tx of vv
- endovenous radiofrequency or laser ablation, compression
sclerotherapy
-surgical stripping of saphenous tree
what is the preferred study for DVT?
- duplex US
- venography is the most accurate method for definitive dx, but is associated with increased risk and rarely needed
what does a d-dimer indicate for DVT
if < 500, US not needed
what is the goldstandard for PE dx?
pulmonary angiography, but rarely used. CT angiography is the study of choiice
what is the preferre method of anticoag in pts w. DVT
enoxaprin (lovenox) or unfractionated heparin followed by warfaring
what is chronic venous insuffiency?
characterized by loss of wall tension in veins, which results in states of venous blood and often is associated w/ a hx of DVT, leg injury, or varicose veinss
how is chronic venou insuff. prevented
early aggressive tx of venous reflux states, such as acute thrombophelbiti or vv, compression hose, weight reduction
CF or CVI?
- progressive edema starting at the ankle followed by skin and subcutaneous changes
- itchy, dull pain w/ standing and pain with ucleration
what does the skin look like in CVI?
shiny, thin, atrophic with dark pigmentary chagnes and subcutaneous iduration
where are ulcers most common in CVI?
above the ankle- stasis ulcer
tx of CVI
-genearly therapeutic measures
how is stasis dermatitis tx
wet compresses and hydrocortisone cream; chronic may need zinc oxide with ichthammol and antifungal cream
