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Gen Med Unit 7: Cardio > Arterial Vascular Disease > Flashcards

Arterial Vascular Disease Flashcards

1
Q

What are the steps in atherosclerosis?

A
  1. Endothelial injury occurs
    A. Smoking, ↑ LDL, HTN effect, immune mechanisms
  2. Monocytes & platelets adhere to injured endothelium & cells ∆
  3. Transformed cells (macrophages) oxidize & ingest LDL → foam cells
  4. Foam cells stimulate inflammatory response → endothelial dysfunction
  5. Streaky plaques form between intima & media → lumen narrows
  6. Arterial walls weaken due to plaques
  7. Unstable plaque ruptures & thrombus forms at rupture site→ thrombus or embolus causes ischemic event
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2
Q

What percent of artery stenosis can cause ischemic sxs?

A

In general, asymptomatic until plaque stenosis exceeds 70-80% of luminal diameter which leads to  in blood flow to vital tissues (ischemia)

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3
Q

Define peripheral artery disease

A

any pathologic process causing obstruction to blood flow in the arteries, exclusive of the coronary and cerebral vascular beds

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4
Q

What is the most common artery occluded by atherosclerosis?

A

Superficial femoral artery

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5
Q

What can chronic decreased blood flow to the skin on the lower leg cause?

A
  1. Atrophy
  2. Hair loss
  3. Thinning of skin and SQ tissue
  4. Pale and/or cool skin
  5. Ulcers w/ worsening ischemia –> necrosis, infection, cellulitis
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6
Q

What are the risk factors for PAD?

A
  1. Cigarette smoking
  2. Diabetes
  3. Hyperlipidemia
  4. HTN
  5. Hyperhomocystinemia
  6. Chronic renal insufficiency
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7
Q

What groups are at risk for lower extremity PAD?

A
  1. ≥70 yrs
  2. 50 - 69 yrs w/ Hx of smoking or DM
  3. 40 - 49 yrs w/ DM + 1 other risk factor for atherosclerosis
  4. Leg symptoms suggestive of claudication w/exertion or ischemic pain at rest
  5. Abnormal lower extremity pulse exam
  6. Known atherosclerosis at other sites (coronary, carotid, renal artery disease)
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8
Q

What are the sxs of PAD?

A
  1. Dependent Rubor

2. Claudication

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9
Q

Define Dependent rubor

A
    • foot below heart level turns dusky red
      a. Elevation of foot causes pallor
      b. Foot pain when supine or leg eleved, relieved when dependent
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10
Q

Define claudication

A
  1. severe, cramping pain in calf or thigh while walking
    A. Pain relieved at rest
    B. Blood flow (O2 supply) can’t keep up w/ demand of exercise
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11
Q

What group is tibial and pedal artery occlusion most often seen in? What may be the first sxs?

A

Seen primarily w/ DM

Foot pain at rest or ulceration may be 1st sign of arterial insufficiency

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12
Q

How is tibial/pedal artery occlusion differentiated from diabetic neuropathy?

A

If foot pain relieved by dangling over edge of bed, then the pain is d/t ischemia

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13
Q

Define cellulitis. What are common causative agents?

A
  1. Skin and soft tissue infection
  2. Erythema, warmth, pain, edema
  3. Most common pathogens
    Strep pyogenes, Staph aureus
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14
Q

How is atherosclerosis assessed in heart and lung PE?

A

Auscultate for carotid, clavicle bruits

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15
Q

How is atherosclerosis assessed in abdominal PE?

A
  1. Auscultate for aorta, renal, iliac, femoral bruits

A. R/O pulsatile mass (aortic aneurysm)

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16
Q

How is atherosclerosis assessed in lower extremity PE?

A
  1. Shoes and socks removed
  2. Peripheral pulses
  3. Hair loss
  4. Skin color
  5. Skin changes, sensations
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17
Q

What are the non-invasive tests for PAD?

A
  1. ABI- ankle-brachial index
  2. TBI – toe brachial index
  3. VWF – velocity wave form (Doppler USN)
  4. PVR – pulse volume recording
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18
Q

What is the best initial screening test to perform in a patient with suspected PAD?

A

Ankle Brachial Index (ABI)

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19
Q

Define Ankle Brachial Index (ABI). How is it performed?

A
  1. The ratio of the highest systolic ankle BP to the highest arm BP
  2. Obtained with a hand-held Doppler instrument and a BP cuff
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20
Q

What is an abnormal ABI ratio?

A
  1. A ratio of < 0.90 mmHg
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21
Q

When do you suspect an inaccurate ABI? What groups are susceptible?

A
  1. ABI may be inaccurate in individuals with noncompressible arteries due to medial calcification (suspect when ABI > 1.3mmHg
  2. DM, elderly, end stage renal Dz on dialysis
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22
Q

What is the rationale behind Pulse volume recordings?

A
  1. Based on concept that arterial inflow into the lower extremities is pulsatile leading to measurable changes in the lower-limb volume with each cardiac cycle
  2. Sequential decrease signifies the presence of a flow-limiting lesion in the more proximal arterial segment
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23
Q

How is the doppler US used for pts w/ suspected PVR? When is stenosis suspected?

A
  1. Used in conjunction with the PVR to obtain segmental velocity waveforms & SBP measurements along the UE or LE
  2. ↓ Pulsatility index between the adjacent proximal and the distal arterial segments = significant stenosis
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24
Q

When may a false positive be present on a doppler US?

A

Superficial femoral artery Dz w/out aortoiliac disease → false (+)

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25
Q

How does a duplex US help dx PAD?

A

Provides both vascular imaging and flow velocity info

> 90% accuracy to Dx the location & severity of LE PAD

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26
Q

What are the benefits of CT angiogram to dx PAD?

A
  1. Allows fast imaging of the entire lower extremity and abdomen
  2. Better evaluation (than angiography) of stenoses and visualization of all collateral vessels & surrounding tissues
  3. Safe in patients with pacemakers and defibrillators
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27
Q

What are the drawbacks of using CT angiogram to dx PAD?

A

Contrast has risk of nephrotoxicity

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28
Q

What are the drawbacks of using MRA to dx PAD?

A
  1. Cannot scan pt’s with pacemakers, defibrillators, metal stents, or clips
  2. Gadolinium associated with rare occasions of renal toxicity
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29
Q

What are the benefits of using MRA to dx PAD?

A

High accuracy (90-100%) similar to that of intraoperative catheter angiography

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30
Q

What is the gold standard for diagnosing PAD?

A

Contrast angiography

Provides detailed information about the arterial anatomy and is recommended as the “gold standard”

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31
Q

What are the drawbacks of using Contrast angiography to dx PAD?

A
  1. Invasive procedure
  2. Risk of contrast induced nephropathy in renal dysfunction, DM, low cardiac output, dehydration, advanced age, multiple myeloma
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32
Q

How can the kidney damage from contrast angiography be mitigated?

A
  1. Vigorous IV hydration
  2. Use low-osmolar contrast agents
  3. Minimizing the overall amount of contrast
  4. Pretreatment with N-acetylcysteine (Mucomyst)
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33
Q

How is PAD managed?

A
  1. Risk factor modification: smoking cessation
  2. Exercise program
  3. Pharmacologic treatment
  4. If warranted for symptomatic relief, endovascular or surgical revascularization
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34
Q

What are the sequlae of PAD?

A 
Cellulitis
Osteomyelitis
Gangrene
Limb amputation
Sepsis
Cardiovascular events - major cause of death in patients with PAD
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35
Q

What meds are used for PAD?

A 
1. Cholesterol lowering LDL < 70-100 mg/dL
A. Statin (HMG-CoA reductase inhibitor)
2. HTN Tx BP < 140/90
3. DM management HbA1c < 7.0%
4. Cilostazol (Pletal)
5. Pentoxifylline (Trental)
6. ACE inhibitors
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36
Q

What is the class, moa and contraindications for Cilostazol (Pletal)?

A

Phosphodiesterase inhibitor
Inhibits platelet aggregation
Contraindicated in CHF

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37
Q

What is the moa of Pentoxifylline (Trental)?

A

Inconclusive data on benefit

Lowers blood viscosity  RBC flex

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38
Q

What effect do ACEi have on pts with PAD?

A

ACE inhibitors (ramipril/Altace) reduce the risk of MI, stroke or vascular death by 25% in patients with PAD

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39
Q

What drug should be considered in all pts with symptomatic PAD w/o contraindications?

A

Ramipril

a. has shown improvement in walking distance in stable claudication pts

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40
Q

What are the indications for surgery in pts with PAD?

A

Failed medical management

Limb-threatening ischemia

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41
Q

What are the surgical options for pts w/ PAD? What are the indications for each?

A
  1. Percutaneous revascularization/angioplasty
    A. Less morbidity/mortality. Used for short segments
  2. Surgical revascularization
    A. Indicated for long length occlusion and distal to origin of iliac arteries (i.e. femoropopliteal bypass)
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42
Q

What are PAD emergencies?

A
  1. Acute limb ischemia

2. Thrombus In-Situ

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43
Q

Define acute limb ischemia

A

Sudden occlusion due to 1. Arterial Embolism (30%)
A. Typically from heart
B. Most commonly seen with MI, CHF, A. fib
C. Sudden onset of sx’s w/out pre-existing claudication

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44
Q

Define Thrombus In situ

A
  1. From acute plaque rupture
  2. Longstanding PVD
  3. Hx of claudication w/ recent worsening of sx’s
  4. 60%
45
Q

What are the six p’s (sxs) of acute limb ischemia?

A
  1. Polar (poikithermia)
  2. Pain
  3. Pallor
  4. Pulselessness
    A. Absent peripheral pulse distal to occlusion
  5. Paresthesia
    A. ↓ sensation or absence of light touch
  6. Paralysis
    A. ↓ motor function (cannot wiggle toes or foot)
46
Q

What is the dx study of choice for acute limb ischemia?

A

Doppler (duplex) US

47
Q

How is acute limb ischemia managed?

A
  1. Anticoagulation therapy
  2. Start Heparin IV
  3. Catheter - directed thrombolytic therapy
  4. Percutaneous thrombus extraction
  5. Amputation if irreversible tissue necrosis
48
Q

Define thrombus

A

Stationary blood clot along the wall of a blood vesselnarrows lumen of artery

49
Q

define embolus

A

Detached intravascular mass capable of clogging arterial capillary beds at a site far from its origin

50
Q

What can arterial occlusion result from?

A
  1. Rupture & thrombosis of atherosclerotic plaque
  2. Embolism travels from heart, TAA, AAA
    A. Aortic dissection (active tearing)
51
Q

What are the 6 p’s (sxs ) of arterial thrombosis and embolism?

A
  1. Polar (poikithermia)
  2. Pain
  3. Pallor
  4. Pulselessness
    A. Absent peripheral pulse distal to occlusion
  5. Paresthesia
    A. ↓ sensation or absence of light touch
  6. Paralysis
    A. ↓ motor function (cannot wiggle toes or foot)
52
Q

Where are sxs located with arterial thrombosis and embolism?

A

Symptoms are roughly localized distal to last palpable pulse
Loss of motor function
Muscle tenderness after 6-8hr

53
Q

What dx studies are indicated for arterial thrombosis and embolism?

A

Angiography to confirm location, identify collateral flow and treatment

54
Q

What is the tx for arterial thrombosis and embolism?

A
  1. Based on severity of ischemia
  2. Extent and location of thrombus
  3. General medical condition of patient
    A. Thrombectomy/Embolectomy
    B. Thrombolysis
    C. Bypass surgery
55
Q

Define Thrombectomy/Embolectomy

A

Surgical removal of embolus or thrombus

Usually last resort due to potential complications

56
Q

What surgery is used in arterial thrombosis and embolism?

A
  1. Endovascular surgery
    A. Percutaneous angioplasty with stenting
    2.Bypass surgery.
    A. Use synthetic or vein for vessel graft
57
Q

When is fibrinolytic therapy indicated?

A

Most effective if occlusion < 2 wk old and motor/sensory function intact

58
Q

How is fibrinolytic therapy infused? What are the complications?

A
  1. Catheter threaded to occluded area
  2. Thrombolytic drug infused
    tPA
    A. Continued 4-24 hr
    B. Lysis confirmed by relief of sx’s and return of pulses and blood flow
  3. Complications
    20-30% require amputation within first 30 days
59
Q

Define Aneurysm

A

Abnormal widening or ballooning of a portion of an artery due to weakness in the wall of the blood vessel
≥ 50% increase in diameter compared to expected normal diameter

60
Q

Where are the most common locations for aneurysms?

A
  1. Cerebral Artery
  2. Abdominal Aorta (75%)
  3. Thoracic Aorta
    A. 50’s-60’s
    B. M>F
61
Q

What are the risk factors for cerebral aneurysms? WHo is more at risk?

A 
Congenital 
Connective tissue disorders 
Polycystic kidney Dz 
AVM 
HTN  
Tumors 
Atherosclerosis 
Smoking
Drug abuse (cocaine)
F>M
30’s-60’s
62
Q

What are the types of cerebral aneurysms?

A
  1. Berry (sacular)
    A.Most common form
  2. Lateral aneurysm
  3. Fusiform aneurysm
63
Q

What are the sxs of cerebral aneurysm?

A 
Usually none
If enlarging:
Pain above & behind the eye
Unlateral facial numbness, weakness, or paralysis 
Dilated pupils 
Vision changes
64
Q

What are the sxs of a cerebral aneurysm rupture?

A 
Thunderclap” headache 
Diplopia 
Nausea 
Vomiting 
Stiff neck
Change in mental status or level of awareness
Ptosis 
Photophobia
65
Q

How are cerebral aneurysms diagnosed?

A

Most go unnoticed until they rupture
Detected by brain imaging obtained for another condition
Noncontrast CT after SAH to confirm aneurysm
MRI/MRA

66
Q

How are unruptured cerebral aneurysms assessed for treatment?

A

Considerations for treatment include:
Type, size (≥ 7-10 mm diam.) & location
Risk of rupture
Pt’s age, PMH, FH
Risk of treatment
Very small aneurysms may be monitored to detect growth or onset of sx’s
Aggressive Tx of comorbidities & risk factors

67
Q

What are the surgical treatment options for unruptured cerebral aneurysms?

A
  1. Preferred in distal arterial segments
  2. Microvascular clipping
  3. Occlusion
  4. Endovascular embolization
68
Q

What is microvascular clipping?

A
  1. Isolate blood vessel feeding the aneurysm and place a metal, clothespin-like clip on the aneurysm’s neck, halting its blood supply
  2. Highly effective
69
Q

What is the occlusion tx for cerebral aneurysms?

A
  1. Clamp off (occlude) the entire artery that leads to the aneurysm
  2. Performed when the aneurysm has damaged the artery
  3. Sometimes accompanied by a bypass
70
Q

What is Endovascular Embolization treatment for cerebral aneurysms?

A
  1. Preferred for posterior circulation aneurysms
  2. Under sedation (GETA)
  3. Femoral artery angiocatheter used to identify aneurysm
  4. Using a guide wire, detachable coils (spirals of platinum wire) are passed thru catheter and released into aneurysm
  5. Coils fill the aneurysm, block it from circulation, and cause the blood to clot, destroying the aneurysm
  6. May require repeat in future
71
Q

What are the most common causes of aortic aneurysm?

A
  1. Atherosclerosis
  2. HTN
  3. Giant cell arteritis
  4. PMR
  5. Marfan syndrome
72
Q

Where is giant cell arteritis usually seen?

A

arteries to head, neck, upper body, arms

73
Q

What does marfan syndrome affect?

A

Genetic connective tissue disorder

Affects heart, blood vessels, eyes, bones, lungs

74
Q

What are the risk factors for AAA?

A
  1. M>F
  2. Age > 60
  3. Caucasian
    • FH (1st degree relative)
  5. Smoking
  6. Presence of other large vessel aneurysms or atherosclerosis
  7. HTN
  8. (↓ risk in DM)
75
Q

What are the characteristics of AAA?

A
  1. Most often affects aortic segment below renal arteries (infrarenal aorta)
  2. Maximal diameter >3.0 cm considered aneurysmal in most adult pts
  3. Aneurysmal diameter- strongest predictor of rupture, Also, rate of aneurysm expansion
  4. Uncommon for AAA < 5cm to rupture
76
Q

What are the sxs of AAA?

A
  1. Usually asymptomatic
  2. May be nonspecific symptoms
  3. Patient may be aware of abnormally pronounced pulsation
  4. Systolic bruit over aneurysm
  5. Expansion/dissection can cause pain
    A. Steady
    B. Deep
    C. Boring
    D. Usually LS region
77
Q

What are the sxs of a AAA rupture?

A
  1. Occurs in about 50% of patients
    A. Severe pain
    B. Hypotension
    C. Pulsatile abdominal mass
78
Q

What are the complications of AAA?

A 
1. Rupture (Life threatening)
A. 50% of ruptured AAA pts that reach hospital for Tx; of them, 30-50% die 
B. Untreated mortality = 100%
C. May present with
-Abdominal pain-acute
-Back pain-acute
-Hypotension
-Tachycardia
D. Recent Hx minor abdominal trauma
E. Recent Hx isometric straining
2. Thrombus/Embolus
A. Extremity pain
3. DIC
A. Abnormal endothelium triggers thrombosis and consumption of coag factors
79
Q

How is AAA diagnosed?

A
  1. Often Incidental
    A. Seen on CT or X-ray obtained for another reason
  2. Confirmed by ultrasound or CT
  3. Always consider in elderly who present with acute abdominal or back pain!
80
Q

Ate what age are pts screened for AAA?

A

≥ 65 yr

81
Q

What is the clinical course of AAA?

A
  1. Varies
    A. Enlarge at steady rate 1-4 mm yr
    B. 20% remain unchanged
    C. Monitor with U/S q 6-12 months
82
Q

How is tx for AAA determined?

A

Determined by size and symptomatology

83
Q

What are the medical management options for AAA?

A
  1. Smoking cessation
  2. Tight BP control
  3. Cholesterol reduction
84
Q

What are the indications for surgical tx of AAA?

A
  1. If asymptomatic, elective repair not recommended until risk of rupture > risk of repair
  2. Recommended intervention when aneurysm > 5.5 cm
    A. Risk of rupture >5-10% per year
  3. Aneurysm ↑ in size >0.5 cm in 6 mos. regardless of size
  4. Thromboembolic complications
    A. Aggressive medical management of CAD prior reduces risk of cardiovascular event
85
Q

What are the surgical management options for AAA?

A
  1. Replacement of aneurysmal portion with synthetic (Dacron) graft
  2. Placement of endovascular stent graft within aneurysm
    A. Less invasive
    B. Can be used if operative risk too great for open procedure
    C. Frequent f/u required due to stent graft complications
86
Q

How is an AAA treated in the emergent situation?

A
  1. Pt presents in hypovolemic shock due to massive hemorrhage
    A. ABC’s
    B. Fluid resuscitation
    C. Blood transfusion
    D. Control HTN
    E. Keep MAP ≈ 70-80 mmHg
  2. CBC, CMP, PT/PTT, blood type and cross match for transfusion
  3. Open resection or endovascular stent grafting
  4. Many patients have multiple comorbidities affecting overall mortality
87
Q

What are the risk factors for thoracic aortic aneurysms?

A
  1. Atherosclerosis
  2. Prolonged HTN
  3. Smoking
  4. Older age
  5. Other aneurysms: 25% of TAA pts have AAA too
  6. Congenital connective tissue disorders
    A. Marfan syndrome,
    B. Ehlars-Danlos syndrome
  7. Blunt trauma
  8. known aortic valve disease
  9. Recent aortic manipulation
    10 Family history
88
Q

What are the symptoms of TAA?

A
  1. Chest pain
    A. Severe tearing (dissecting) acute pain that radiates to back between scapulae
  2. Severe HTN
    A. 25% w/hypotension (bleed, tamponade)
  3. Differing P & BP due to subclavian artery compression
  4. Stroke, abdominal pain, extremity pain
    A. Thromboembolism
89
Q

What are the symptoms of TAA caused by?

A
  1. Most asymptomatic until complications develop

2. Due to compression of adjacent structures

90
Q

What are the CXR findings that indicate a TAA?

A

Widened mediastinum or enlarged aortic knob

91
Q

What is the gold standard for daignosing TAA? What other imaging tools are used?

A
  1. MRI( gold standard),

2. TEE (unstable, rupture or dissection suspected), Angiography

92
Q

Define aortic dissection

A

Tearing of the aortic intimal layer

Blood dissects into the aortic media through the tear, creating a false lumen

93
Q

What is the difference between type A and Type B aortic dissections?

A
  1. Type A = Ascending aorta. Highest mortality 7-36% at experienced centers esp in first 24-48 hrs
    Type B = Distal aorta
94
Q

What PE findings may indicate TAA?

A
  1. Pulse deficit
  2. SBP limb differential > 20 mm Hg
    A. Subclavian artery compression
  3. Focal neurologic deficit
  4. Murmur of aortic regurgitation (new)
95
Q

What is the prognosis of TAA?

A
  1. 85% mortality w/in 2 weeks if untreated
96
Q

How is TAA treated?

A
  1. Proximal dissection-surgical emergency
  2. Post repair, f/u with freq MRI
    A. Recurrent TAA or dissection common in 1st 2 yrs
97
Q

What diagnostic studies are used to diagnose aortic dissection?

A
  1. EKG
    A. May show LVH or may be normal
  2. CXR
    A. Widened mediastinum or abnormal aortic contour
  3. CT Chest & Abd
    A. Imaging modality of choice in acute scenario due to less imaging time
98
Q

How is aortic dissection treated medically?

A
  1. ↓ Aortic wall stress by controlling BP & HR
    A. SBP to 100-120 mmHg
    B. HR < 60 bpm
99
Q

What agents are used to control HR and BP in aortic dissection?

A
  1. Labetolol/Trandate IV (propranolol /Inderal, metoprolol/Lopressor)
    A. Alpha & Beta blocker
    B. In asthma/COPD/CHF- use CCB (diltiazem/Cardizem or verapamil/Calan)
  2. Nitroprusside added as adjunctive therapy once SBP 100-120 mmHg and good renal function (arterial line)
    A. Arteriolar and venous vasodilator
    B. Never use w/out Beta blocker
100
Q

What surgical treatments are used for type A aortic dissection?

A
  1. Surgery for all Type A aneurysms

A. Grafting and replacement of diseased portion of arch

101
Q

What surgical treatments are used for type B aortic dissection?

A
  1. Surgery for Type B aneurysms if dissection is continuing

2. Type B uncomplicated- medical management

102
Q

How often do aortic dissection pts need CT scans?

A
  1. Baseline CT before hospital discharge, then 3,6,12 mos
  2. Patients w/ uncomplicated Type B dissections whose BP is controlled and who survive acute episode w/o complications require tight BP control and annual CT scans
103
Q

What are the symptoms and complications of a ruptured unstable TAA?

A

Many die immediately
May present w/ severe chest or back pain, hypotension, shock
Patients exsanguinate into pleural or pericardial space

104
Q

What are the complications of TAA dissection?

A

Compression of or erosion into adjacent structures

105
Q

How is an unstable TAA treated surgically?

A

Endovascular stent grafting vs. open surgical synthetic graft

106
Q

When is surgery indicated for unstable TAA?

A
  1. Elective surgery
    A. > 5-6 cm ascending aorta and > 6-7 cm descending aorta
  2. Other surgical indications
    A. Symptomatic
    B. Traumatic
    C. Genetic connective tissue disease (Marfan, etc.)
107
Q

How is stable TAA medically managed? What lifestyle changes need to occur?

A 
1. Aggressive treatment
A. SBP 100-120 mmHg
-Beta blocker (or CCB)
B. HR<60 bpm
2. Smoking cessation
108
Q

How often should pts with a stable TAA have CT scans?

A

Serial CT’s q 6-12mos

Frequent f/u to check sx’s

Gen Med Unit 7: Cardio (13 decks)

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