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Flashcards in Vascular Disease CC - Lohr Deck (28)

What is Intermittent Claudication (IC)?

What disease is IC often seen with and what is its prevalence in pts with that disease?


Cramping, thightness, and fatigue in the buttock, hip, thigh, calf, and foot. Typically excercise-induced, does not occur with standing. Relieved with rest (typically <5min).

Seen in ~1/3 cases of PAD.


What is a current problem in the treatment of PAD as compared to CAD?

Atherosclerotic risk factors are treated less intensively in PAD patients than CAD patients (lipid lowering therapies, diet, and exercise are all stressed less for PAD pts.)


What is the 10-year mortality of PAD?


(for reference, breast cancer's is 23%)


The CV Physical Exam for a pt suspected of having PAD shound include what elements?

1) Inspection of feet for ulcers, fissures, calluses, tinea, xanthomas, and overall skin health

2) Ausculation of abdomen & femoral arteries for presence of bruits

3) Palpation to feel for abdominal aortic aneurysm

4) Palpation of the femoral, popliteal, posterial tibial, and dorsalis pedis pulses


What pulses can be congenitally absent?

Ankle pulses:

Posterial Tibial (PT) - 0.2%

Dorsalis Pedis (DP) - 8.7-12% 

N.B. DP absence occurs 3x> in whites than blacks


What is the grading scale for pulses?

Normal: 2

Diminshed: 1

Absent: 0


What non CV findings may be found upon inspection of a pt with PAD?

  • Hair loss
  • Thick, brittle toenails
  • Smooth, shiny skin
  • SubQ fat atrophy
  • Muscle atrophy
  • Skin fissures
  • Ulceration
  • Gangrene


Describe the differences between venous and arterial ulcers in terms of location, appearance, and pain.


Venous: Lower 1/3 of leg

Arterial: Varies, but most commonly on the foot or toes


Venous: Uneven edges, ruddy granulation tissue, no necrosis. Hemosiderin deposits in leg, leg may be warm, leg & foot have normal pulses.

Arterial: Deep pale base with even edges & necrosis. Leg may be cool. Diminished or absent leg & foot pulses. 


Venous: No pain to moderate pain. Relieved by elevation.

Arterial: Very painful. Relieved by placing in dependent position (down.)


What are some general physical findings in the foot in a pt with PAD?


Pallor - supine position or elevated.

Dependent rubor - dependent (lowered) position. Dilated skin capillaries fill with doexygenated blood.


What are the most common "first screening" noninvasive evaluations for PAD?

What about some good second evaluations?

Other noninvasive options?


Most common, first: Ankle-Brachial Index and Ankle-Toe Index

Next steps: Exercise treadmill testing, Segmental limb pressures

Others: Pulse volume recording, Arterial duplex ultrasonography, CT angio, MRI


How is the Ankle-Brachial Index (ABI) defined?

How is the test performed?

If the ABI appears normal but you suspect PAD, what should you try next?


ABI = (Ankle Systolic Pressure (DP or PT) / (Brachial a. Systolic Pressure)

Subject in resting position. Measurements taking using a hand-held Doppler. Divide the higher of either the DP or PT by the higher of the brachial measurements.

If ABI is normal at rest, repeat w/ pt on treadmill - may reveal the pathology.


What range is desirable for the ABI?

Under what ABI value is 95% sensitive and specific for arterial disease?

What does an ABI above the normal range indicate?

What does ABI predict?


Normal: 0.90-1.30

Arterial Disease: <0.90

ABI >1.30: Abnormal - indicates noncompressible vessels (seen with diabetes and diffuse vessel calcification)

ABI is an independent predictor of mortality in PAD. Degree of ABI reduction correlated with severity of disease.


Arterial Duplex Ultrasonography combines which two types of ultrasonography (hence duplex)?

What does each of the two types visualize?

What is PSV and what does it have to do with this imaging technique?



1) Grey scale (B-mode) Ultrasound: Visualizes the architecture of a blood vessel so lumen narrowing can be seen directly.

2) Color-Doppler Ultrasound: Visualizes the blood flow within a vessel, with color proportional to the velocity of flow.

PSV = Peak Systolic Velocity. The peak blood flow speed through a vessel during systole is also an indication of vessel stenosis or narrowing. The greater the speed, the worse the stenosis (think of a finger over a garden hose).

2x increase in PSV = >50% stenosis

3x increase in PSV = >75% stenosis


How does cigarette smoking complicate and act as a risk factor for PAD?

  • Increased PAD risk 2x-5x
  • ~90% of pts w/ claudication are current or ex-smokers
  • Smoking increases PAD risk >> CAD risk
  • PVD Dx made ~10 yrs earlier in smokers
  • Level of tobacco use = rate of PAD progression
    • More progression to limb ischemia and loss


What comorbidity:

  • Increases risk of PAD 2-4x?
  • Results in more extensive disease?
  • Results in greater vascular calcification?
  • Increases odds of needign amputation?

What benefits accrue from managing this comorbidity well?


Diabetes Mellitus

Benefits of controlling DM in PAD:

For every 1% reduction in HgA1c, substantial decreases in risk for:

  • amputation
  • death from PAD
  • MI
  • Stroke
  • HF


Describe two drugs used for the treatment of Intermittent Claudication in PAD, including their:

1) Names

2) Biochemical Mechanism

3) Physiological Effects

A1) Pentoxifylline

A2) Nonspecific PDE inhibitor

A3) Improves RBC deformability (hemorrheologic agent), weak antiplatelet activity, some vasodilation

B1) Cilostazol

B2) PDE3 inhibitor, focus on increasing cAMP

B3) Platelet aggregation inhibitor, vasodilation, increases HDL-C and lowers TGs


What non-pharmaceutical is also very effective in improving claudication over time?


Exercise! Especially walking.

  • At least 30min sessions
  • At least 3x a week
  • At least for 6 months


1) What class of drug is considered Class I (clearly indicated) for reducing the risk of MI, stoke, and vascular death associated with symptomatic PAD?

2) What two drugs in specific are commonly used?

3) What drug is not indicated this scenario?

1) Antiplatelet Agents

2a) Aspirin (75-325mg/day)

2b) Clopidogrel (75mg/day) as an alternative to aspirin

3) Warfarin is NOT INDICATED. Not shown to be of benefit as an addition to antiplatelet therapy in PAD, and increases risk of major bleeding.


A) When should a revascularization procedure be considered for treating PAD?

B) What 3 types of revascularization procedures are available?



  • Lifestyle-limiting symptoms
  • Disability despite appropriate non-surgical management
  • Favorable risk/benefit ratio expected


  • Percutaneous
  • Surgical
  • Combined



You are evaluating a patient who is presenting with shortness of breath and substernal chest pain. What "High Risk" findings in the categories below would make you concerned about the possibility of acute Aortic Dissection (AoD)?

1) Underlying Conditions

2) High Risk Pain Features

3) High Risk Exam Features


1) Conditions:

  • Marfan syndrome
  • Connective tissue diseases
  • Family or prior individual Hx of aorta or aortic valve disease

2) Pain: Chest, back, or abd pain described as:

  • Abrupt and severe
  • Ripping, tearing, sharp, or stabbing quality

3) Exam:

  • Perfusion deficit (pulse deficit, SBP differences, focal neuro defecit)
  • Aortic insufficiency murmur (new or not previously painful)
  • Hypotension or shock state


You determine a patient has acute aortic dissection and needs surgery quickly. What should you do to stabilize the patient prior to surgery?


Reduce the wall stress on the aorta!

  • IV Metoprolol to lower BP and HR
    • CCB (diltiazem) can be given if pt cannot tolerate beta-blocker
    • Do NOT lower HR is severe aortic insufficiency is present!
  • Once HR and BP are controlled, IV ACEIs or vasodilators (hydralazine) can be given
    • Do NOT give vasodilators before the beta-blocker. Reflex tachy will increase wall stress!


What is GPA?


Granulomatosis with Polyangiitis

(aka Wegener's Granulomatosis)

A systemic vasculitis that includes granuloma formation and inflammation of small and medium blood vessels. Involves autoimmunity with ANCAs (anti-neutrophil cytoplasmic antibodies).

Lung and kidney damage from GPA can be fatal. The disease requires long-term immunosupression.


As a systemic vasculitis, GPA has MANY possible symptoms. Name some possible symptoms in the following areas:

  • ENT
  • Eye
  • Nervous System
  • Skin
  • CV


  • ENT
    • Chronic sinusitis
    • Rhinitis
    • Epistaxis
    • Saddle nose deformity
    • Conductive & Sensorineural hearing loss
    • Tracheal/Subglottic granulomatous masses
  • Eyes
    • Conjunctivits/Episcleritis/Uveitis    
    • Optic nerve vasculitis
    • Retinal artery occlusion
    • Proptosis (forward displacment of eye
  • Nervous System
    • Mononeuritis multiplex (multiple, random neuropathies throughout body due to vasculitis and granulomatous masses)
      • Affects CNS (palsies) and PNS (sensorimotor issues)
  • Skin
    • Palpaple purpure or skin ulcers
  • CV
    • Pericarditis & coronary arteritis (leads to sudden death, seen post-mortem)
    • Hypercoaguability (PEs, etc.)
  • Other
    • Arthralgias
    • Other organs (GI, GU, thyroid, liver, breast, parotid gland)


What are the five categories of GPA?


  1. Localized: Upper and/or lower respiratory tract disease, no systemic symptoms
  2. Early systemic: Any systemix symptoms, without organ- or life-threatening disease
  3. Generalized: Renal or other organ threatening disease.
  4. Severe: Renal or other vital organ failure.
  5. Refractory: Progressive & unresponsive to pharmaceutical treatment


How is a diagnosis of GPA made?


  • Clinical symptoms
  • Presence of ANCAs
  • Biopsy shows necrotizing granulomas in:
    • Lung
    • Kidney
    • Sinus


What is the current two-drug regimen for GPA?

How fatal is GPA without treatment?


Cylcophosphamide (alkylating agent) and Glucocorticoids

Mean survival is 5 months without treatment, 12.5 months with glucocorticoids alone. Steroids + Cyclo can cause disease remission but only for a mean of 48 months. 5-year survival is around 80%. Nasty business.


What are the largest morbidity issues with GPA?

What are the largest morbidity issues with immunosuppresive treatment for GPA?



  • Chronic renal insufficiency
  • Hearing loss
  • Cosmetic & functional nasal deformities
  • Chronic sinus dysfunction
  • Pulmonary insufficiency


  • Fertility issues
  • Cyclophosphamide cystitis
  • Increased malignancy risk
  • Serious infections


Because GPA is thought to be mediated by the production of ANCAs by autoreactive B-cells, what other drug that we've learned would make sense to use in GPA?

How is this drug incorportated into GPA treatment today?


Rituximab - CD20-mediated B-cell apoptosis

The RAVE study demonstrated the Rituximab is an effective alternative to cyclophosphamide in inducing disease remission and may be better in treating relapses than cyclophosphamide.

Can use either steroids + cyclophosphamide or steroids + rituximab to induce disease remission.