DVT Flashcards

1
Q

List some DDx for leg swelling?

A

Exudate (inflammation -> vasodilation and proteinaceous exudate)

  • cellulitis
  • septic arthritis

Transudate (disturbed hydrostatic or colloid osmotic pressure, low protein -> clearer)

  • RHF
  • liver cirrhosis
  • nephrotic syndrome
  • leg abscess -> obstructing venous outflow

Other: haematoma, Baker’s cyst rupture, lymphoedema

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2
Q

List some DDx for leg pain?

A

Venous: DVT, ulcer, leg wound
Muscular: muscle pain, compartment syndrome
Skeletal: fracture
Infectious: septic arthritis, osteomyelitis, cellulitis, wound infection

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3
Q

What is the Well’s score for probability calculation of DVT/PE?

A
  1. active cancer (+1)
  2. calf swelling >3cm (+1)
  3. swollen unilateral superficial veins (+1)
  4. unilateral pitting oedema (+1)
  5. previous DVT (+1)
  6. swelling of entire leg (+1)
  7. localised tenderness along deep venous system (+1)
  8. paralysis, paresis, recent cast immobilisation of LL (+1)
  9. Bedridden (>3 days) or major surgery (past 12 weeks) (+1)
  10. alternative diagnosis (-2)

Scoring:
Likely: >2 -> Ix doppler US
Unlikely: <2 (DVT prevalence 5%) -> iX D-dimer testing

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4
Q

What risk factors could effect Virchow’s triad?

A

Virchow’s triad:

  1. Endothelial injury: smoking, surgery
  2. Abnormal blood flow: dehydration, immobility, surgery
  3. Hypercoagulability: surgery, malignancy, pregnancy, thrombophilia, drugs (OCP, HRT)
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5
Q

How is a Duplex US used?

A

Duplex US procedure:
• Pass transducer over skin above BV
• Transducer sends and receives sound waves (amplified by microphone) -> sound waves bounce of solid objects (e.g. RBCs) -> movement of RBCs reflected as change in pitch of reflected sound waves
No blood flow -> no pitch change
• Reflected sound waves process though computer -> provide info about speed and direction of flow

Looking for:

  • reduced blood flow in the deep venous system (DVT)
  • echogenic band inside vein (thrombus)
  • venous diameter (decreased in acute, increased in chronic)
  • non-compressible venous segment (thrombus)
  • absent colour flow (completely occlusive thrombus)
  • lack of flow augmentation of calf squeeze (DVT)
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6
Q

What is an ABI and how does it work?

A

Ankle brachial index (ABI): a measure of the ratio of systolic blood pressure at the ankle to the blood pressure in the upper arm

  • Inflate cuff proximal to artery and continue inflation until pulse in the artery ceases
  • Deflate cuff slowly, when artery pulse is re-detected through the probe, that is SBP
  • Dorsal pedis and posterior tibial in each foot (take the larger value)
  • Left and right brachial arteries (take the larger value)

Results:
<0.9 = narrowing/blockage of arteries in legs (arterial disease)
>1.2 = abnormal vessel hardening/calcification from peripheral vascular disease

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7
Q

How would you manage a DVT?

A

Non-pharmacological:
o Encourage exercise
o Compression stockings

Pharmacological:
o LMWH (e.g. Enoxaparin 1.5mg/kg SC, daily)- potentiates ATIII to bind and inhibit Xa -> reduce clot formation -> reduce thrombosis
o Unfractionated heparin if pt high bleeding risk (easier to reverse)
o Bridge to Warfarin (INR 2-3)- inhibits epoxide reductase -> prevent activation of vit K dependent clotting factors (2, 7, 9, 10)
- Started same day as LMWH and continued indefinitely.
- Monitored with monthly blood tests (INR, extrinsic pathway)
o IVC filter if pt actively bleeding -> prevent PE

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8
Q

Describe the MAO of Warfarin?

A

Warfarin MA:
inhibits epoxide reductase
-> preventing activation of vit K dependent clotting factors (2, 7, 9, 10) and anticoag proteins C and S

Note: initial prothrombotic effect (couple days): anticoag factors proteins C and S destroyed first (shorter half lives)
-> need to bridge with unfractionated heparin or LMWH

Note: teratogenic
Reversal: Vit K (rapid reversal with FFP)
Monitor: PT and INR (extrinsic)

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9
Q

List some SE of Warfarin?

A

SE:

  • bleeding
  • teratogenic
  • skin/tissue necrosis (small BV microthrombi in first few days of hypercoagulability)
  • drug-drug interactions: other palsma protein-bound drugs may displace warfarin causing more free fraction -> bleeding (e.g. Sulphonamides, Sulphonyureas, NSAIDs)
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10
Q

Describe the MAO of unfractionated heparin and LMWH?

A

Heparin MA: lowers activity of thrombin and factor Xa

Unfractionated heparin MA: increases antithrombin III activation -> inhibits factors IIa, Xa and other proteases
- used in renal impairment

LMWH MA (e.g. Clexane, Enoxaparin): potentiated antithrombin III action -> inactivate factor Xa only
- better bioavailability, x2 longer half life, subcut, no lab monitoring (APTT/intrinsic), reversal difficult 

Heparin reversal: protamine sulfate (positively charged moleculer binds negatively charged heparin)

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11
Q

Compare the monitoring of warfarin and unfractionated heparin?

A

Warfarin: monitor INR monthly

  • extrinsic path
  • international normalised ratio (INR) expresses PT in standardised way
  • INR = (prothrombin time patient/ prothrombin time observer) x ISI
  • Results: INR 1 is normal, INR 2-3 therapeutic ratio (longer to clot)

UFH: APTT daily
- intrinsic path

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12
Q

List some SE of heparin Rx?

A

Common (>1%):

  • haemorrhage
  • bruising at injection site
  • hyperkalaemia
  • non-immune thrombocytopenia

Uncommon (<1%):

  • elevated liver enzymes
  • anaphylaxis
  • heparin-induced thrombocytopenia (HIT): delayed thrombocytopenia to day 5, more common in UFH, (IgG antibodies complex with heparin-PF4 -> platelet activation and lysis -> contents trigger coag cascade -> thromboses), Rx cease heparin

LTM SE: alopecia, osteoporosis

Drug interactions: azole antifungals, HIV protease inhibitors

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