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Year 3 - Clinical > 17 - PAD > Flashcards

17 - PAD Flashcards

1
Q

What is involved in the pathophysiology of atherosclerosis?

A
  • Endothelial damage/dysfunction
  • Local inflammation
  • Accumulation & oxidation of lipids
  • Smooth muscle cell proliferation
  • Cellular apoptosis, necrosis, fibrosis
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2
Q

When does a person start forming plaques in their arteries?

A

Entire life

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3
Q

Histologic classification & progression of atherosclerotic plaques

A

Early (childhood & early adulthood; usually clinically silent)
- Stage 1 = initial lesion; small amounts of intracellular lipid deposits
- Stage 2 = fatty streak; larger amounts of intracellular lipid deposits
- Stage 3 = intermediate lesion; small extracellular lipid pools
Late (middle age & later; may be clinically silent or overt)
- Stage 4 = atheroma (lipid core); extracellular lipid core
- Stage 5 = fibroatheroma; lipid core & fibrotic changes
- Stage 6 = complex plaque; surface defects (ulcerations, hemorrhage, thrombosis)

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4
Q

Atherosclerosis in pt-friendly language

A
  • Many people build “plaques” in the arteries
  • Plaques are like a layer of wax on inside of blood vessels
  • Many reasons for building plaques, like genetics & aging (not just how much cholesterol is in your blood)
  • Blood contains something that acts like glue (is naturally sticky) & sticks to anything that doesn’t look like the normal inside of a blood vessel
  • Sometimes plaque can form something like a pimple, & sometimes these plaques can burst, causing blood to stick to that area & the blood vessel can become blocked
  • Everything that gets blood from that blocked vessel becomes starved for blood & oxygen & starts to die
  • Sometimes this happens more slowly & can lead to stable narrowings in an artery that can limit blood flow & cause problems
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5
Q

Manifestations of atherosclerotic cardiovascular disease (ASCVD)

A
  • Cerebrovascular disease (carotid artery stenosis, transient ischemic attacks, ischemic stroke)
  • Coronary artery disease (stable and/or unstable)
  • Aortic atherosclerosis (thromboembolism, cholesterol embolization, aortic aneurism)
  • Renovascular disease (“renal artery stenosis” – chronic kidney disease, hypertension)
  • Peripheral artery disease (intermittent claudication, acute & critical limb ischemia)
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6
Q

Risk factors for ASCVD (non-modifiable)

A
  • Age (incidence of clinical disease rises sharply w/ increasing age, especially following middle age)
  • Sex (men > women b/c of hormonal effects in women)
  • Genetics/hereditary
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7
Q

Risk factors for ASCVD (modifiable)

A
  • Smoking (single most significant modifiable risk factor; accelerates all stages of atherosclerosis)
  • Dyslipidemia (linear correlation w/ CV risk)
  • Insulin resistance, diabetes (advanced glycation end products, inflammation)
  • Hypertension (arterial stress, especially impactful in heart & brain)
  • Chronic kidney disease (specifically progression of CKD)
  • Diet (prefer controlled caloric intake – whole grains, nuts & seeds, vegetables & fruits, fatty fish, etc.)
  • Inactivity
  • Adiposity (especially visceral fat; apples vs. pears)
  • Inflammation
  • Depression (80% increased risk of CVD & CV death w/ depression; relationship is bi-direction)
  • Drugs (various mechanisms; ex: chronic NSAID use)
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8
Q

Peripheral artery disease

A
  • Atherosclerotic disease leading to partial or complete obstruction of one or more peripheral arteries
  • May affect arms, pelvis, or legs
  • Signs & sx vary from none to severe
  • Incidence increases sharply w/ age
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9
Q

Manifestations of PAD

A
  • Asymptomatic (most patients)
  • Atypical leg sx
  • Intermittent claudication (IC)
  • Acute limb ischemia (ALI)
  • Critical limb ischemia (CLI)
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10
Q

Atypical leg sx of PAD

A
  • May include non-joint-related pain or discomfort that:
    • Doesn’t stop an individual from walking
    • Begins w/ exertion but is not alleviated w/in 10 minutes of rest
    • Begins at rest but worsens w/ exertion
  • Px w/ atypical sx, or who are asymptomatic, have functional impairment comparable to px w/ claudication
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11
Q

Intermittent claudication

A
  • Fatigue, discomfort, cramping, and/or pain of vascular origin in muscles of lower extremities
  • Consistently induced by exercise
  • Consistently relieved by rest (w/in 10 min)
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12
Q

Acute limb ischemia (ALI)

A
  • Acute (< 2-week duration), severe hypoperfusion of a limb, characterized the 6 P’s
    • Pain (at rest; will diminish over time as nerves die)
    • Pallor
    • Pulselessness
    • Poikilothermia (“perishing cold”; limb will be cool to the touch)
    • Paresthesias (tingling or pricking)
    • Paralysis
  • Skeletal muscle may tolerate severe ischemia for only 4-6 hours before muscle necrosis
  • May be related to underlying PAD or may be related to other conditions that can result in ALI through either thrombotic or embolic mechanisms
  • Medical emergency
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13
Q

Stage 1 of ALI

A
  • Limb viable
  • No sensory loss or muscle weakness
  • Venous & arterial audible on Doppler
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14
Q

Stage 2a of ALI

A
  • Limb marginally threatened
  • Minimal (toes) sensory loss
  • No muscle weakness
  • Venous audible & arterial inaudible on Doppler
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15
Q

Stage 2b of ALI

A
  • Limb immediately threatened
  • Sensory loss, worse distally
  • Mild-moderate muscle weakness
  • Venous audible & arterial inaudible on Doppler
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16
Q

Stage 3 of ALI

A
  • Limb irreversibly damaged
  • Profound sensory loss (anesthetic)
  • Profound muscle weakness (paralysis)
  • Venous & arterial inaudible on Doppler
17
Q

Critical limb ischemia (CLI)

A
  • Chronic (>/ 2-week duration) ischemic rest pain, non-healing wounds/ulcers (hasn’t healed in 1-3 months), or gangrene in one or both legs (may be in digits) attributable to objectively proven arterial occlusive disease
  • Up to 15% of px w/ claudication will progress to CLI over approx. 5 years
  • Diagnosis through signs & sx
18
Q

Who to screen for PAD

A
  • > / 65 y/o
  • 50-64 + family history of PAD
  • 50-64 + risk factor(s) for PAD – diabetes, history of smoking, hyperlipidemia, hypertension
  • < 50 y/o + diabetes + another risk factor
  • Known atherosclerotic disease in another vascular bed (ex: coronary/
    carotid/
    subclavian/
    renal/
    mesenteric artery stenosis or abdominal aortic aneurism)
19
Q

Describe how medical history and physical exam are used to diagnose PAD

A
  • Px known to be at risk of PAD should be screened w/ comprehensive medical history & assessed for:
    • Exertional leg sx (including claudication or other walking impairment)
    • Ischemic rest pain
    • Non-healing wounds or gangrene
    • Elevated pallor; dependent rubor
  • Px at risk for PAD should also undergo vascular exam including:
    • Palpation of lower extremity pulses
    • Auscultation for femoral bruits
    • Inspection of legs & feet
  • BP measurement of both arms
  • Abnormal physical exam findings must be confirmed w/ diagnostic testing
20
Q

What type of diagnostic tests are done for PAD?

A
  • Resting ankle-brachial index (ABI) = initial test, often all that’s required
  • Depending on presentation & ABI results, further tests may be required, including:
    • Exercise treadmill ABI testing (if resting ABI normal or borderline)
    • Toe-brachial index
    • Additional perfusion assessment measures (ex: transcutaneous oxygen pressure or skin perfusion pressure)
  • Anatomic imaging reserved for px being assessed for revascularization
21
Q

Describe ankle brachial index (ABI)

A
  • Resting ABI = non-invasive test obtained by measuring ratio of SBP at ankle to SBP in upper arm in supine position
  • SBP checked 4 times in each ankle (twice for each dorsalis pedis artery & posterior tibial artery) & twice in each arm; average of 2 values is used
  • Lower BP in leg vs. arm suggests stenosis due to PAD
  • ABI of each leg is calculated by dividing the higher ankle pressure by the higher of the right OR left arm BP
  • Resting ABI results – severe < 0.5; abnormal 0.5-0.9; borderline 0.91-0.99
22
Q

What additional screening is done for diagnosis of PAD?

A
  • Px w/ PAD at risk for additional ASCVD manifestations & may be screened for abdominal aortic aneurysm (AAA) via ultrasound
  • Further screening not routinely done in absence of clinical signs/sx as risk reduction strategies for PAD reduce risk for other manifestations of ASCVD
23
Q

Goals of therapy for PAD

A
  • Reduce sx, improve functional status, & QOL

- Reduce risk of CV ischemic events (& resultant limb loss, acute coronary syndrome, stroke, or death)

24
Q

Overview of non-pharms and pharm therapy for PAD

A
  • Non-pharms = supervised/structured exercise program; lifestyle modification; smoking cessation; pt education; revascularization (some px)
  • Pharm (all px) = antiplatelet (single agent); statin; hypertension management; blood glucose management
  • Pharm (some px) = rivaroxaban + ASA; dual antiplatelet therapy (DAPT) after revascularization; ACE inhibitor/ARB
25
Q

List some non-invasive non-pharms for PAD

A
  • Exercise programs demonstrate significant & persistent benefits for IC/leg sx, functional status, & QOL
    • First line for ALL symptomatic patients
    • Unstructured programs are not efficacious
  • Lifestyle modification (optimize diet for ASCVD reduction)
  • Smoking cessation
  • Pt education (daily foot inspections, avoiding barefoot walking, selecting appropriate footwear)
26
Q

Difference between structured vs. supervised exercise programs

A
  • Supervised = in hospital/facility; directly supervised intermittent walking; 30-45 min/session; moderate-maximum claudication, alternating w/ periods of rest
  • Structured = community- or home-based; pt self-directed w/ HCP advice; pt counselled on how to begin & progress; should be similar to supervised program
27
Q

List some invasive non-pharms for PAD

A
  • Revascularization

- Amputation (for ischemia w/ non-salvageable limb; ALI, CLI)

28
Q

What type of revascularization should be done for certain sx?

A
  • For severe/debilitating claudication/leg sx – ballon angioplasty, stenting, or bypass
  • For limb-threatening ischemia & salvageable limb (ALI) – anticoagulation (heparin), surgical embolectomy
  • For limb-threatening ischemia & salvageable limb (CLI) – balloon angioplasty or drug-coated balloon angioplasty; stenting +/- atherectomy; surgical revascularization (bypass)
29
Q

Describe antiplatelet therapy for PAD

A
  • Single agent, ASA (81-325 mg daily) or clopidogrel (75 daily)
    • Indicated for all px w/ ABI < 0.90
    • Usefulness unclear w/ borderline ABI (0.91-0.99)
  • DAPT (ASA 81 mg + clopidogrel 75 mg daily) may be indicated post-revascularization
30
Q

Describe anticoagulant therapy for PAD

A
  • Px w/ ALI should be fully anti-coagulated w/ unfractionated heparin pending revascularization
  • ASA 81 mg + rivaroxaban 2.5 mg BID may be used for prevention of stroke, MI, CV death, acute limb ischemia & mortality in px w/ CAD and/or PAD
  • COMPASS trial proved rivaroxaban + ASA reduced risk of CV death, stroke, or non-fatal MI vs. ASA alone or rivaroxaban alone
31
Q

Describe statin therapy for PAD

A
  • Indicated for all px w/ PAD
  • Higher potency & dose corresponds to greater reduction in ASCVD events (atorvastatin 40-80 mg or rosuvastatin 20-40 mg)
    • Don’t titrate up; start at maximum dose & decrease if needed
32
Q

Describe ACE inhibitor/ARB therapy for PAD

A
  • Indicated for hypertensive px w/ PAD

- May be used in all px w/ PAD to reduce long-term risk of CV ischemic events

33
Q

What other agents may be used for PAD?

A
  • Cilostazol – not available in Canada; selective phosphodiesterase-3 inhibitor
  • Pentoxyphylline – not recommended for tx of claudication b/c no benefit
  • All px should receive annual flu shot

Year 3 - Clinical (30 decks)

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