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Therapy year 3- sem 2 > Venous Thromboembolism > Flashcards

Venous Thromboembolism Flashcards

1
Q

what is a thrombus

A

stationary blood clot at point of origin

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2
Q

what is thrombosis

A

the production of a thrombus

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3
Q

what is an embolus

A

a blood clot that has moved and occlueds a vessel

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4
Q

what is embolism

A

the obstruction of occulsion of a vessel due to a embolus

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5
Q

what are antithrombotic agents? examples?

A

affect the process of thrombosis

include anticoagulants and antiplatetst

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6
Q

what is a thrombus composed of?

A

fibrin (string)
platets (timbits)
red blood cells (donuts)

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7
Q

how does a clot form

A

prothrombin becomes thrombin - whihc allows fro fibrinogen to become fibrin

then as plasminogen becomes plasmin it propagtes this porcess

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8
Q

how do levels of fibrin, plasminogen, and rbc differ between arteries and veins?

A

arteries -White
- fibrin (3), plasmin (4), RBC (1)

Mixed
- fibrin (2), plasmin (3), RBC (2)

veins - red
- fibrins (4), plasmin (1), RBC (4)

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9
Q

what is VTE? most common ones?

A
  • umbrella term for a VTE in venous vasculature
  • DVT and PE
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10
Q

Superficial Vein Thrombosis location

A

superfical veins of upper or lower

  • often linked to varicsoe veins
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11
Q

DVT location

A

-deep in veins of leg, in upper extremity of DVT

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12
Q

distal and proximal facts DVT

A

distal - most common spot

proximal - bigger risk for embolism

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13
Q

where do PE form?

A

not lungs and get stuck in lung

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14
Q

what are the risk factors of Virchow’s Triad for DVT ?

A
  1. hypercoagulability
    - preg
    - malignancy
    -drugs (SERM, Estrogen0
    - genetic abnormalioties
  2. statis
  3. Vascular injury
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15
Q

S and S of DVT

A
  • pain, swelling, erythema
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16
Q

clinical tool to knonw DVT

A

D-Dimer

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17
Q

Disgnostic test for DVT

A

doppler ultrasound

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18
Q

S and s of PE

A
  • couhg, tourble breathing
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19
Q

presence of D -dimer

A

has clot need to treat

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20
Q

VTE tx guidline

A

0-3: initial mananment

3-6: primary Tx

6- onwards: secondary tx - at this point we decide if we stop anticoagulants or continue indefintiely

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21
Q

Labs values for VTE monitoring?

A

aPTT
PT
INR
Anti-Xa levels
CBC
SCR

22
Q

what drug classes do we have for the tx of VTE?

A
  1. UFH
  2. LMWH
  3. Vit K antagonist
  4. Anti- factor 10 A (Xa) inhibitors
  5. Direct Thrombin inhibitors
  6. fibrinolytics
23
Q

UFH
- MOA
- Onset
- Renal
- monitoring
- pregnancy?
-ADE?

A

unfractionated heparin
MOA: inactiavtes thrombin by petentiating action of antithrombin III

Onset of effect: IV (minutes) or SC (1-2 hours)

Renal: no adjustment

Monitoring: aPTT and CBC (every 2-3 days)

Pregenancy: can be used

ADE: Thrombocytopenia

Early- 25%
- transiset and rebound with cntinues therpay

LAte - heparin induced thrombocytopenis (HIT)
- immun mediatied
- occurs in 7-14 days
- longer therpay or IV use more at risk

24
Q

LMWH
- name of drugs
- MOA
- Onset (pharmacokinetics)
- Renal
- Obese
- monitoring
- pregnancy?
-ADE?

A

low Moleccular weight heparin

Drug names: edns in parin
MOA: inhibit Xa

Onset: Sc - 3-5 hours for peak affect - longer plasma half life, more predictable

Renal: if less then 30 mL/min then once daily only enoxaparin

Obese: avoid capping consider BID

Moniotring: CBC and Scr, Anti- Xa factor is preg, obes eor renal

preg: yes

ADE: Same as UFH, less chance of HIT

25
Q

Fondaparineux
- MOA
- Onset (pharmacokinetics)
- Renal
- Obese
- monitoring
- pregnancy?
-ADE

A

MOA: syntheic inhibitor of Xa however has alot of the same side chains as UFH

Onset: Sc 1-3 hours

Renal” reducde dose in modertate 30-50, avoid less then 30

Obese: no dose capping consider 10 mg

  • moniotring: s and s make take days to resolve
  • CbC and SCr periodcially

pregenancy: yes

ADE: other then bleeding uncommon

26
Q

Warfarin
- MOA
- Onset (pharmacokinetics)
- Dosing
- Renal
- Obese
- monitoring
- pregnancy?
-interactions

A

MOA: depletes Vit A dependent factors and depectlest pretin C and S (these are good for anticoagulation so my depelting them we could be put into a state of procoagulation)

Onset: oral - 100% bioavvailoity, hepatic metabolism

Dosing: can take a while to act so should start on a short term agent like LMWH, UFH or fondapurineux, for first 5 days - once two INR in range can stop short term agent

Renal: no dose adjustement
Obese; no

Monioring: s and s relife
chcek INR should be in range 2-3, for 2-3 readings, chcek INR at day 3 and then once stable can chcek once a week, once every two weeks, once every three weeks with minimum of once a month chcek
- if dose adjustment need to hcek with in 1- 2 weeks

pregenancy: avoid

Interaticions: has alot
genrela
- antibiotics consider within 3 days
amiodarone - will increase INR with first week
always chcke interactions with natural helath porducts

27
Q

DOACs
- drug names
- MOA
- Onset (pharmacokinetics)
- Renal
- Obese
- monitoring
- pregnancy?
-interactions
-ADE

A

MOA ;
Dabigatran - direct thrombin inhibtors
Apixaban, riveroxaban, edoxaban - Xa inhibtors

Onset: Oral (low bioavailiailty), 3-4 hours - take 24 hiurs to clear system

renal:
apixaban - avoid less then 15
riveroxaban - avoid less then 15
dabigatran - avoid less then 30
edoxoaban

Obese: limited data

Monitoring:
s and s may take days to weeks to stabilize
CBC, Scr, a[tt every 3-6 months
- lab test. not reliable

Pregenancy: no

interactions: strong P-gp inducers or inhibtors - lots of drugs

ADE:
- well tolerates
- dyspepsia or gastritiswith dibigartan

28
Q

Fibrinolytics
- drug name
- when used
- MOA
- Onset (pharmacokinetics)
- Renal
- Obese
- monitoring
- pregnancy?
-interactions
-ADE

A

drug name: alteplase

when used: in emergency when patient has no bleeding contraindications. consider case by case. in frequent use in DVT

MOA: breaks clots - plasmin breaks fibrin

Onset: Iv (immedaite)

renal : none

Obese: none

Pregency: ???

Interactions: ???

ADE: bleeding
1. major
2. non- major
3. minor

29
Q

Def bleeding
1. major
2. non- major
3. minor

A

major - life threamnthing, need blood

non-mjor - requires intervention

minor - may not need intervention

30
Q

Bleeding in DOACs vs VKA

A
  • more bleeding with VKA
  • less risk of intracranila bleed with DOACs
  • same risk of GI bleed
31
Q

bleeding managemnt steps

A
  1. supportive care
  2. stop anticoagulants or antiplatelts
  3. specific traget agents
32
Q

what are the specific traget agents for bleeding

A

dabigatran - Idaruciuzumab
VKA - vitamin K
Apixaban, roveroxiban - PCC
LMWH UFH - protamine ( less effctive for LMWH)

33
Q

when to use vit K for warfarin

A

when INR is above 10 give vit K

4.5-10; omit dose of warfarin

34
Q

TX regiemnes optiosn for first 3-6 months - whne are hese regimens indicated?

A
  • if no PE and not extensive proximal DVT
    1. Apixaban ingle drug
    2. riveroxaban single durg
    3. LMWH single drug
    4. Warfarin with overlap of UFH or LMWH
    5. LMWH for 5-10 days then dabigatran (no overlap)
    6/ LMWH for 5-10 daus then edoxaban (no overlap)
35
Q
  • if PE or extensive proximal DVT
A

then thromblytics

36
Q

when do we favor single oral agent (DOACs)

A
  • no renal
  • between weight of 120-140/150 kg
  • coverge - insurance
  • no drug interactions
  • drug adherance
  • VTE with active malignanacy
  • oral. drug needed
37
Q

when we favour LMWH with overlap warfarin

A
  • renal dysfunction
  • drrig interaction with DOACs
  • weight greater then 140/150 kg
  • no history of HIT
  • history of antiphospholip[id syndrome
38
Q

when we favour LMWH alone

A
  • preg
  • actiove maligamnay and can’t have DOAS
  • high bleeding risk
  • no history of HIT
39
Q

cancer and VTE?

A

greater chance of getting one and dying of one

40
Q

if we have cancer what agent should we consider?

A

LMWH (if interactions) or DOACS (if no interactiosn)

41
Q

why or when would we consider therapy beyong 3 months?

A

3 months is the intital therlya

beyonf 3 month therpay is needed to prevent subsequent episodes - if we can identy the precipating factor and know it’s constant then we continue therpay, similary if we don’t know the cause we conitnue therpay. we only stop when we kno wthe cause but it is not something that will occur again - unporvoked

42
Q

course of action for post single un porkoved VTE event

A

Two clicnial trials showed then a lower dose of apixaban or rivaroxaban after 6 months can be benifial

43
Q

complications of VTE

A
  1. post-thrombotic syndrome
  2. Post PE Syndrome/ Chronic thromboembolic pulmonary hypertension (CTEH)
44
Q

post thrombitic syndrome what is it

A
  • occurs in 20-50%
  • s and S - pain, itching, burning , ambutaory dicomfort , swelling, skin pigmenttayion - venous leg ulceration

TX: none, compression sock

45
Q

Post PE Syndrome

A

decrease pulmonary fucntion, QoL, tolerance
- CTEPH - TX: PEA only for severe not established evident for less severe

46
Q

Prevention of VTE non-pharm

A

ambulate, intermittent penumatic compression (INC), gradual compression stockings )GCS), infereior vena cava filter

47
Q

Prevention of VTE pharm options

A

low dose:
- LMWH
- UFH
-Fondapurienux
- warfarin - not used
- DOACs - only used post hip and knee surgeries

48
Q

prophylaix in cancer patients?

A

DOACS - not widely used

49
Q

how do I choose what agent to use prohpylaix?

A
  1. surgical or medical or cancer
  2. risk scoring
50
Q

key education poitn?

A

no OTC NSAID with anticoagulants

Therapy year 3- sem 2 (9 decks)

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