Peripheral Venous Disease Flashcards

1
Q

What are the five pathophysiology classifications of edema?

A
  • venous hypertension
  • anasarca / decreased oncotic pressure
  • lymphatic dysfunction
  • plain-old fat (not edema)
  • lipedema
    • dysreguation of adipocyts, (not really edema)
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2
Q

What are the major causes of venous hypertension?

A
  • right heart failure
  • venous insufficiency
    • sclerosis from thrombosis, vessicant drugs (chemo, imporoper antibiotics), ideopathic, venous insufficiency begets venous insufficiency elsewhere, venodilating drugs
  • venous thrombosis (acute/chronic)
  • thrombophlebitis
    • inflammatory process that causes a blood clot to form & block one of more veins
  • venous access / infusions
  • arterial / venous fistula / shunting
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3
Q

What is anasarca?

What causes it?

A

Anasarca: loss of oncotic pressure leading to edema

  • cirrhosis / malnutrition
    • decreased protien concentration in blood
  • Mineralocorticoid problems - free water retention / Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
  • Nephrotic syndrome
    • losing protein, decreasing concentration in blood
  • extracorporeal proetin loss (ECMO/dialysis/etc)
  • protein-losing enteropathy
  • myxedema
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4
Q

What are the major causes of lymphatic dysfunction (lymphedema)?

A
  • cancer
    • lymphomas
    • direct tumoral invasion/compresion
    • metastatic infiltration
  • lymphatic damage (surgery, trauma, anatomy)
  • lymphatic filariasis, Hansen’s
    • parasites, leprosy
  • Lymphatic reflux/hypertension
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5
Q

What makes lymphedema different from any other caue of edema?

A

isn’t pitting

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6
Q

What is lipedema?

If often occurs with what comorbid condition?

Most common cause?

Is it pitting?

A
  • lipedema
    • symmetric, painful, dysregulatin of adipoase tissue (weight-loss doesn’t help)
  • frequently with comorbid lymphedema
  • idiopathic
  • non-pitting
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7
Q

What are the common complications of venous hypertension?

A
  • worsening venous hypertension/reflux
  • ulcerations
  • increased infection risk
  • thrombosis risk
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8
Q

What are the 4 categores for classifying peripheral venous disease?

A
  • Clinical classification
  • Etiological classification
  • Anatomic classification
  • pathophysilogic classification
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9
Q

What are vericose veins?

What causes them?

A
  • dialated veins that happen b/c venous reflux and/or venous insufficiency
    • valves break down, cause increasing presure on next segment down (b/c gravity & hydrostatic column)
    • becaue veins are floppy & lack muscular layer found in arteries, they are susceptible to pressure based injury
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10
Q

What is the goal of having areas of venous communication?

How can a pathology of this structure lead to vericose veins?

Treament?

A

to have the superficial veins drain into the deep veins so you can have central return to the circulation

if a perforating vein gets screwed up, you can have blood flow from the deep vein to the superficial vein, and end up creating vericosities

For treatment, you could ablate the perforating veing and keep the hypertension in the depe venous compartment

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11
Q

How do you treat venous hypertension?

A
  • address reversible causes (heart failur, etc.)
  • Compression
    • compression hose
    • ACE wraps
    • Elevate limb
  • venous mapping/perforator vein ablation
  • exercise - THE venous pump of choice
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12
Q

What is Virchow’s Traid?

Why is DVT a concern?

How does it present?

A
  • Virchow’s Triad (elements to form a clot)
    • endothelial injury
    • hypercoagulability
    • stasis
  • risk factor for pulmonary embolism
  • presents with pain, swelling, erythema
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13
Q

How would you diagnose a DVT?

A
  • Pretest probability
    • Well’s criteria (likelyhood it is a clot)
    • D-dimer (very high negative predictive value)
      • extremely non-specific
  • Venogrophy
    • invasive, rarely used, but gold-standard
  • Duplex venous doppler uptrasound
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14
Q

What Well’s test score indicates LOW pretest probability?

MODERATE pretest probability

HIGH pretest probability

A
  • < 0: LOW
  • 1-2: MODERATE
  • > 3: HIGH

** don’t have to memorize but be familiar

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15
Q

What demographics of patients are at high risk of developing DVT?

A
  • hospitalized patients, especially surgical patients
  • cancer patients
  • throbophilia
  • CAPRINI score
    • 0-1 is low risk, anything higher than this would warrent prophylaxis
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16
Q

What strategies can we use to prevent DVT?

A
  • Compresion hose
  • early ambulation
  • pharmacologic prophylaxis
    • warfarin
    • heparin (go to in bad renal disease)
    • enoxaparin
    • fondaparinux (thrombo phrophylaxis)
    • dabigatran/edoxaban/rivaroxiban/etc.
  • Sequential (pneumatic) compression devices
17
Q

What are the treatment strategies for DVT?

A
  • Warfarin
  • Heparin/enoxaparin
  • rivaroxaban/dabigatran/edoxaban/apixaban
  • 6 months for first DVT
  • Lifelong for second DVT, or if thrombophilia identified, thrombolysis, thrombectomy
  • if untreated, 50% risk of PE