Peripheral vascular dz Flashcards

(41 cards)

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
RF for vericose veins
prego, obesity, family hx, prolonged sitting/standing, hx of phlebitis
26
what are sx of VV
asx aching, fatigue
27
what are PE finding s of VV
chronic distal edema, abnormal pigmentation (brown), fibrosis, atrophy, skin ulcerations that may develop in severe dz
28
dx for VV
none, may need dopple to located insufficient vlaves before surgery
29
tx of vv
elastic stockings, leg elevation and regular exercise
30
last line tx of vv
- endovenous radiofrequency or laser ablation, compression sclerotherapy -surgical stripping of saphenous tree
31
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
32
what does a d-dimer indicate for DVT
if < 500, US not needed
33
what is the goldstandard for PE dx?
pulmonary angiography, but rarely used. CT angiography is the study of choiice
34
what is the preferre method of anticoag in pts w. DVT
enoxaprin (lovenox) or unfractionated heparin followed by warfaring
35
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
36
how is chronic venou insuff. prevented
early aggressive tx of venous reflux states, such as acute thrombophelbiti or vv, compression hose, weight reduction
37
CF or CVI?
- progressive edema starting at the ankle followed by skin and subcutaneous changes - itchy, dull pain w/ standing and pain with ucleration
38
what does the skin look like in CVI?
shiny, thin, atrophic with dark pigmentary chagnes and subcutaneous iduration
39
where are ulcers most common in CVI?
above the ankle- stasis ulcer
40
tx of CVI
-genearly therapeutic measures
41
how is stasis dermatitis tx
wet compresses and hydrocortisone cream; chronic may need zinc oxide with ichthammol and antifungal cream