Peripheral arterial occlusive disease PAOD Atherosclerosis (90%). Thromboangiitis

Peripheral arterial occlusive disease PAOD Atherosclerosis (90%). Thromboangiitis

Peripheral arterial occlusive disease PAOD Atherosclerosis (90%). Thromboangiitis

Hambrick, Sharlette, Coordinating Producer has reference to this Academic Journal, PHwiki organized this Journal Peripheral arterial occlusive diseaseUZHHOROD NATIONAL UNIVERSITYSurgical Diseases Chairprof. Roumiantsev K.Ye.PAOD Common Manifestation of Atherosclerosis Prevalence: 12% – 14% of the General Population – Up to 20% of Population > 75 Years Old Increased risk from Cerebrovascular & Coronary DiseaseMAIN CAUSES OF PAODAtherosclerosis (90%). Thromboangiitis obliterans (TAO).Diabetic foot syndrome.

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EPIDEMIOLOGY OF ATHEROSCLEROSIS Incidence Prevalence Mortality (millions) (millions) (%)STROKE .7 4 31MI 1.1 7 33PAD – 22 4 PathophysiologyThe atherosclerotic plaque consists of a core of cholesterol joined to proteins with a fibrous intravascular coveringPlaque gradually progress from narrowing to complete occlusion of medium in addition to large arteries. Also plaque can disrupt with exposing of the core to the vascular lumenPatophysiologyResting blood flow in a person with PAOD is similar to that in a healthy person.Once exercise begins, blood flow increases as much as 10-fold.Blood flow cannot maximally increase in muscle tissue during exercise, because of proximal arterial stenoses.When the metabolic dem in addition to s of the muscle exceed blood flow, claudication symptoms ensue.

Pathophysiology of thrombangiitisgranulomatous inflammation of medial layer with intimal fibrosis;predominant lesion of small, muscle-type arteries – so called distal vasculature;involving into inflammatory process main collateral branches of magistral arteries of lover limbs;subcutaneous veins are often involved;disorders of circulation are more expressed due to primary lesion of collateral vasculature;necrotic changes are more common.PatophysiologyTissue circulation of lower limb is a summary of: level in addition to extension of occlusion, development of collateral vasculature. Levels of occlusion – Aorto-iliac – 24% , – Femoro-popliteal – 50%, – Crural arteries – 17%,V – Combined multilevel – 9%.

HistoryAtherosclerosis is a systemic disease process.Accordingly, patients who present with claudication due to PAOD can be expected to have atherosclerosis elsewhere.A full assessment of the patient’s risk factors as long as vascular disease should there as long as e be per as long as med.Risk factorsDiabetesHypertensionHyperlipidemiaFamily historySedentary lifestyleTobacco use

Clinical PresentationIntermittent Claudication — cramping pain, tiredness, or fatigability of involved muscle groups induced by ambulation in addition to quickly relieved by restThighs, hips, in addition to buttocksCalf pain — rarely alone, more common when combined with femoropopliteal disease Paresthesia is also a pain analogueClinical presentationTrophic changes:Muscle in addition to subcutaneous tissue atrophy;skin pallor, hair loss, shiny skin;dependent rubor of skin or “livedo reticularis”brittle claw nailsulceration, gangreneErectile disfunction ProcedureLower extremity systolic pressureBrachial artery systolic pressure ABI =

Segmental Pressures (mm Hg)150110108620.54150146100840.44ABI150150BrachialPulse Volume Recordings

Exercise ABI TestingConfirms the PAD diagnosisAssesses the functional severity of claudicationMay “unmask” PAD when resting the ABI is normalAids differentiation of intermittent claudication vs. pseudoclaudication diagnosesDuplex ultrasonography combinesgrayscale US – provides a picture of the vessel in direct in addition to transverse projections, assess the condition of the wall in addition to the inner lumen of the vessel;color-doppler US to visualize the bllodflow, its direction or intensity (power-doppler).Triplex ultrasonography combinesduplex US;spectrum of bloodflow evaluation.Ultrasonography – (, )

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