Peripheral vascular dz Flashcards

1
Q

peripheral artery disease (PAD) causes?

A

-atherosclerosis and is a significant independent risk factor for cardiovascular and cerebrovascular morbidity and mortality

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2
Q

what are the sx of PAd?

A
  • initally asx

- can progress to claudication, ischemia, and pain with exercise

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3
Q

what are complications of untreated PAD?

A

critical or acute limb ischemia can lead to pain at rest w/ skin ulceration, gangrene, or loss of limb

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4
Q

what can acute arterial occlusion be caused by?

A

-thrombosis or embolism

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5
Q

what can cause thrombotic dz?

A

trauma, hypovolemia, inflammatory arteritis (takayasu and buerger dz), polycythemia, dehydrations, repeated arterial punctures, and hypercoagulable state

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6
Q

clinical features of PAD

A
  • intermittent claudication, foot or lower leg pain w/ exercise that is relieved by rest
  • may have thigh or butt pain
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7
Q

PE of PAD

A
  • 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
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8
Q

what are sx of severe dz?

A

numbness, tingling, ischemic ulcerations, which may lead to gangrene

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9
Q

what are the 6 P’s of acute aterial occlusion?

A

pain, pallor, pulselessness, paresthesias, poikilothermia, and paralysis

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10
Q

what does acute arterial occlusion threaten

A

limb viabiltiy

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11
Q

how is PAD dx?

A

doppler US flow

ABI: < 0.9 indicates significantdz

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12
Q

what is the gold standard for PAD dx?

A

Angiography

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13
Q

what lab test has a strong association with incidence and progression of PAD?

A

homocysteine

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14
Q

what is Leriche syndrome?

A

iliac artery dz: can lead to Erectile dysfunction

tx w/ sildenafil (adr: priapism)

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15
Q

what does an ABI > 1.4 mean

A

non compressible artery due to calcification

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16
Q

tx of PAD?

A

risk factor modification: stop tobacco, DM, HTN, hyperlipidemia control

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17
Q

what meds can be used to hlep? (reduce sx of claudication)

A

BB, ACEI, statines, progressive exercise

18
Q

what should be used in all pts w/o CI?

A

antiplatelet therapy w. asa or clopidogrel

sx relief w/ cilostazol

19
Q

what is cilostazol?

A

decreases platelet, supresses CAMP degredation, vasodilates

20
Q

what is cilostazol ADR

A

edema, agranulocytosis, MI, bleed, thrombocytopenia

21
Q

what is last line tx for PAD

A

revascularization

22
Q

what is the Brodie-Trendelenburg test?

A

differentiates btw saphenofemoral valve incompetence vs perforator vein incompetence

23
Q

what are vericose veins?

A

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

24
Q

what are vericose veins caused by?

A

superficial venous insufficieny and valvuular incompetence

25
Q

RF for vericose veins

A

prego, obesity, family hx, prolonged sitting/standing, hx of phlebitis

26
Q

what are sx of VV

A

asx

aching, fatigue

27
Q

what are PE finding s of VV

A

chronic distal edema, abnormal pigmentation (brown), fibrosis, atrophy, skin ulcerations that may develop in severe dz

28
Q

dx for VV

A

none, may need dopple to located insufficient vlaves before surgery

29
Q

tx of vv

A

elastic stockings, leg elevation and regular exercise

30
Q

last line tx of vv

A
  • endovenous radiofrequency or laser ablation, compression
    sclerotherapy

-surgical stripping of saphenous tree

31
Q

what is the preferred study for DVT?

A
  • duplex US

- venography is the most accurate method for definitive dx, but is associated with increased risk and rarely needed

32
Q

what does a d-dimer indicate for DVT

A

if < 500, US not needed

33
Q

what is the goldstandard for PE dx?

A

pulmonary angiography, but rarely used. CT angiography is the study of choiice

34
Q

what is the preferre method of anticoag in pts w. DVT

A

enoxaprin (lovenox) or unfractionated heparin followed by warfaring

35
Q

what is chronic venous insuffiency?

A

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

36
Q

how is chronic venou insuff. prevented

A

early aggressive tx of venous reflux states, such as acute thrombophelbiti or vv, compression hose, weight reduction

37
Q

CF or CVI?

A
  • progressive edema starting at the ankle followed by skin and subcutaneous changes
  • itchy, dull pain w/ standing and pain with ucleration
38
Q

what does the skin look like in CVI?

A

shiny, thin, atrophic with dark pigmentary chagnes and subcutaneous iduration

39
Q

where are ulcers most common in CVI?

A

above the ankle- stasis ulcer

40
Q

tx of CVI

A

-genearly therapeutic measures

41
Q

how is stasis dermatitis tx

A

wet compresses and hydrocortisone cream; chronic may need zinc oxide with ichthammol and antifungal cream