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PR3154 > DVT > Flashcards

DVT Flashcards

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1
Q

DVT –> PE pathogenesis

A

Blood clot (thrombi) developing in circulation.
Occurs 2nd to stagnation of blood and hyper-coagulable states.
* Thrombus develop in venous circ = DVT
* Thrombus –> emboli
* Right side, pul arteries = pulmonary embolism (PE)

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2
Q

mechanism to control coagulation (hemostasis)

A
  • antithrombin (AT III)
  • heparin
  • thrombomodulin
  • protein C, S
  • tissue factor pathway inhibitor (regulates initiation phase

self-regulatory mechanisms intact so fibrin clot limited to vessel injury zone

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3
Q

mechanism in fibrinolytic system

A

tissue plasminogen activator (tPA) converts
plasminogen –> plasmin

degrades fibrin mesh
produced D-Dimer as by-pdt

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4
Q

Virchow’s triad for VTE

A

1) hypercoagulability (blood)
2) vascular damage (vessel)
3) circulatory stasis (flow)

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5
Q

hypercoagulability

A

BLOOD

major surgery
malignancy
preg (post partum)
thrombophilia
infection, sepsis
IBD
autoimmune conditions

estrogen therapy (COC, tamoxifen, HIT)
inflamm
dehydration

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6
Q

vascular damage

A

VESSEL

thrombophlebitis
cellulitis
atherosclerosis

catheter/ heart valve
venepuncture

physical trauma, strain, injury
microtrauma to vessel wall

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7
Q

thrombo-embolism process

A

calf source: unlikely to embolise

above knee source: more assoc w/ embolism –> Right Heart –> pul arteriole system

  • can lead to PE
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8
Q

criculatory stasis

A

FLOW

immobility
venous obstruction (obesity, tumor, preg)
varicose veins
Afib, LV dysfunciton

congenital abnormalities affect venous anatomy
bradycardia, low BP

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9
Q

DVT clinical presentation

A

sx:
○ Leg swell, pain, warmth
○ Nonspecific. Obj test needed to establish diagnosis
○ unilateral

signs:
○ Superficial vein dilated
§ Palpable cord felt in affected leg
○ Homan’s sign: Pain in back of knee when dorsiflex leg of affected foot

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10
Q

wells score COPSBET3

A

1) active cancer (tx within 6mnths)
1) paralysis, immobilisation of lower extremities
1) bedridden >3days/ major surgery in 4wks
1) localised tenderness along distribution of deep venous system
1) entire leg swollen
1) calf swelling by more than 3cm, when compared to asx leg (below tibial tuberosity)
1) pitting oedema (in sx leg)
1) collateral superficial veins (nonvaricose)

-2) alt diagnosis more likely than DVT

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11
Q

wells scoring

A

=/>3 : high prob
1,2: mod prob
=/>0: low

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12
Q

wells score 0,1,2

A

1) D-dimer
2) positive –> imaging whole leg/ proximal CUS
3) neg –> rule out DVT

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13
Q

wells score >2 pt

A

1) imaging whole leg/ proximal CUS

2) distal DVT –> anticoag/ surveillance

2) proximal DVT –> initiate anticoag
- risk of embolism

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14
Q

D-dimer meaning

A

good negative predictive value
-ve rules out DVT

but +ve does not mean have DVT, plasmin just breaking down fibrin

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15
Q

distal DVT tx

A

high risk recurrence
- tx: 3mnths AC

low risk recurrence
- 4-6wk AC or venous US surveillance

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16
Q

proximal DVT tx

A

tc: at least 3mnths AC (DOAC if no CI)

3mnths: evaluation venous US

stop/ extended AC – yearly evaluation

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17
Q

AC for DVT (PO)

A

apixaban: 10mg BD 7d –> 5mg BD (day 8-90) –> 2.5mg BD (after 6mnths)

rivaroxaban: 15mg BD (21d) –> 20mg OD (day 22-90) –> 10mg OD (after 6mnths)

day 90 or up to 6mnths

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18
Q

renal adj for DOAC

(D,R,A,E)

A

D: <50ml/min + PGPi use (avoid)

R: CrCl < 30ml/min (avoid)

Apix: 15-29ml/min, caution. HD avoid

E: 30-50ml/min or BW <60kg (30mg/day)

avoid if >95ml/min (tx failure)

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19
Q

prophylaxis with DOAC (riva)

Study These Flashcards
A

TKR: 10mg OD x 2wk
THR: 5wk

medically ill for 31-39d

20
Q

switch AC for DVT (SC–>PO)

Study These Flashcards
A

UFH, LMWH sc1mg/kg BD, (SC, 5d) –> dabigatran 150mg BD/ Edoxaban 60mg OD

21
Q

renal dose adj for DOAC (that requires sc doses first )

Study These Flashcards
A

Dabig: crcl <50ml/min + PGPi = VOID

edoxaban: 30mg/day (crcl 30-50ml/min or BW =/< 60kg)

dont use if crcl >95ml/min (tx failure cause renal too good)

22
Q

AC overlap for DVT tx

Study These Flashcards
A

UFH, LMWH, (SC) + warfarin PO daily

(stop sc after =/>5d, INR >2)

23
Q

tx duration for DVT

Study These Flashcards
A

90d, 3mnths (transient risk factor OR 1st unprovoked isolated distal DVT)

180d, 6mnths (1st unprovoked proximal DVT, PE)
- reduce to prophylaxis dose (riva, apix)
- INR 2-3 (warfarin)

extended duration
- yearly evaluation
** bleeding risk acceptable

24
Q

risk factor for VTE

Study These Flashcards
A
  • to consider need for VTE prophylaxis
    age, prior VTE hist
    blood stasis
    vascular injury
    hypercoagulability
25
VTE prophylaxis for specific grp of pts
1) medically ill -- Padua risk score 2) surgical pt -- Caprini risk score 3) cancer pt -- Khorona risk score
26
PE effect
RV failure systemic congestion and low LV preload reduced CO overt RV failure circulatory collapse + shock occlude blood flow to lungs (alveolar haemorrhage) less gas exchange necrosis impaired O2 delivery to organs fatal circ collapse
27
PE clinical presentation
sx: ○ Cough, chest pain, chest tight, SOB, palpitation § Diff dx: myocardial infarction ○ Hemopytsis (cough blood) ○ Massive clot: dizzy, light headed § Poor perfusion signs: ○ Tachypnea, tachycardia, diaphoretic (sweat, look unwell) ○ Neck vein distended ○ Massive clot: cyanotic, hypotensive § Hypoxic, cardiogenic shock. Die in mins
28
PE diagnosis modified wells criteria HIPOD HM HM DO 100IP
3) clinical sx of DVT (leg swell, pain w/ palpation) 3) other diagnosis less likely than PE 1.5) HR > 100 1.5) immobilisation (=/>3days) or surgery in last 4wks 1.5) previous DVT/ PE 1) hemoptysis 1) malignancy
29
PE scoring modified wells criteria
> 6: high prob 2-6: mod prob <2: low prob
30
PE severity and risk assessment -- determines drug choice high, intermediate low parameters
high: haem instable, clinical parameters, RV dysfunction (TTE) , elevated troponin intermediate:clinical parameters, TTE/ troponin lvls low: all neg
31
high risk PE tx
1) systemic thrombolytic therapy - mortality > risk of bleeding - followed by anticoag UFH, LMWH 2) anticaog + UFH (weight adj bolus) - impt UFH is reversible esp for heam unstable
32
thrombolytics used in PE
1) rTPA 100mg over 2h/ 0.6mg/kg over 15mins max 50mg 2) streptokinase (not in SG) 3) urokinase (expensive, local catheter clot) tenecteplase for MI, not for VTE
33
CI for fibrinolysis
absolute: - hist of haemorrhagic stroke/ stroke of unknown origin - ischaemic stroke previous 6mnths - CNS tumour - major trauma, surgery, head injury (past 3wks) - bleeding diathesis (susp to bleed) - active bleed relative - preg, post partum - TIA in last 6mnths - OAC - liver disease - PUD - endocarditis
34
alteplase tenecteplase: AMI, IV bolus (BW)
dosed by BW, infusion FU and monitor for bleed, BP --> intracranial haemorrhage alteplase dose: 100mg over 2h/ 0.6mg/kg over 15mins (max 50mg)
35
thrombolysis protocol
inclusion - acute ischemic stroke - within 4.5hr of onset - CT scan consistent with acute ischemic stroke exclusion hx of ICH, IS (3mnths), subarachnoid/ intracranial haemorrhage - endocardities, aortic arch dissection - active internal bleeds, GI haemorrhage - major surgery/ serious trauma in last 14d - Lumbar puncture in last 7d - preg BP > 185/110 counts: INR > 1.7, PLT <100,000, glucose < 2.7 use of DTI, Xa inhibitor in last 48hr use of warfarin in last 48hr unless INR < 1.7 LMWH in last 24hr
36
intermediate - low risk PE tx
1) initiate anticoag (if IV: LMWH > UFH) (if PO: DOAC > VKA) unless = VKA + LMWH (INR 2-3) - renal impaired (<30ml.min) - preg, lactation - antiphospholipid Ab syndrome
37
why LMWH > UFH
less inhibitory activity against thrombin than UFH. both binds to antithrombin, cause conformational change to inactivate factor Xa UFH has 18 saccharide units long, catalyse antithrombin-mediated inactivation of thrombin (antithrombin-thrombin complex) LMWH: more specific for Xa UFH: more specific to thrombin (PTT)
38
reperfusion in PE
* rescue thrombolytic therapy recc in haem deterioration on anticaog tx
39
duration of anticaog PE
therapeutic anticaog for =/> 3mnths for all pt with PE - discontinue after 3mnth if reversible risk factors - extension beyond 3mnths if APS, recurrent VTE (not transient risk factor) consider: 1st PE no identifiable risk factor * FU: drug tolerance, adherence, hepatic, renal function, bleeding risk at regular intervals
40
VTE in preg risk factors
higher risk in preg > non-preg women (incr during preg, peaks at post partum) risk factors: - prior VTE - obesity - medical comorbidities - stillbirth - pre-eclampsia - post partum hemorrhage - Caesarean section
41
challenges of VTE in preg
D-Dimer rises in preg differential diagnosis (oedema from preg)
42
diagnosis of PE during preg
compression proximal US chest x-ray
43
tx of VTE in preg
LMWH, weight base dosing sc enoxaparin 1mg/kg BD APS +ve, switch to warfarin during breastfeeding
44
fun facts of DOAC and LMWH
rivaroxaban 10mg (prophy) non-MAF enoxaparin 60, 80mL is graduated at 10mL increments
45
UFH VTE dose
tx: 80 units/kg --> 18units/kg/hr infusion prophylaxis: 5000units Q8-12h PCI: 2000-5000 units for ACT of 250-300s (repeat bolus to maintain ACT) monitor: aPTT, ACT (for PCI)
46
why UFH is preferred in PE
UFH is easily reversal when stopped - Used in high risk pt for PE - If pt starts to bleed, able to reverse easily (shorter half-life 1hr) - To start on thrombolytics (if vv unstable, would have started this)
47
enoxaparin VTE doses
tx: 1mg/kg Q12H or 1.5mg/kg OD renal <30ml/min, preg, cancer = 1mg/kg OD prophy: 40mg OD until ambulatory or 30mg BD PCI: 0.3mg/kg bolus monitor: anti-Xa lvls when renally impaired, preg

PR3154 (11 decks)

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