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
2
Q
When does a person start forming plaques in their arteries?
A
Entire life
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)
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
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)
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
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)
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
9
Q
Manifestations of PAD
A
- Asymptomatic (most patients)
- Atypical leg sx
- Intermittent claudication (IC)
- Acute limb ischemia (ALI)
- Critical limb ischemia (CLI)
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
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)
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
13
Q
Stage 1 of ALI
A
- Limb viable
- No sensory loss or muscle weakness
- Venous & arterial audible on Doppler
14
Q
Stage 2a of ALI
A
- Limb marginally threatened
- Minimal (toes) sensory loss
- No muscle weakness
- Venous audible & arterial inaudible on Doppler
15
Q
Stage 2b of ALI
A
- Limb immediately threatened
- Sensory loss, worse distally
- Mild-moderate muscle weakness
- Venous audible & arterial inaudible on Doppler
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
