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Therapy year 3- sem 2 > Venous Thromboembolism > Flashcards

Venous Thromboembolism Flashcards

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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?

Study These Flashcards
A

aPTT
PT
INR
Anti-Xa levels
CBC
SCR

22
Q

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

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
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
Fondaparineux - MOA - Onset (pharmacokinetics) - Renal - Obese - monitoring - pregnancy? -ADE
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
Warfarin - MOA - Onset (pharmacokinetics) - Dosing - Renal - Obese - monitoring - pregnancy? -interactions
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
DOACs - drug names - MOA - Onset (pharmacokinetics) - Renal - Obese - monitoring - pregnancy? -interactions -ADE
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
Fibrinolytics - drug name - when used - MOA - Onset (pharmacokinetics) - Renal - Obese - monitoring - pregnancy? -interactions -ADE
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
Def bleeding 1. major 2. non- major 3. minor
major - life threamnthing, need blood non-mjor - requires intervention minor - may not need intervention
30
Bleeding in DOACs vs VKA
- more bleeding with VKA - less risk of intracranila bleed with DOACs - same risk of GI bleed
31
bleeding managemnt steps
1. supportive care 2. stop anticoagulants or antiplatelts 3. specific traget agents
32
what are the specific traget agents for bleeding
dabigatran - Idaruciuzumab VKA - vitamin K Apixaban, roveroxiban - PCC LMWH UFH - protamine ( less effctive for LMWH)
33
when to use vit K for warfarin
when INR is above 10 give vit K 4.5-10; omit dose of warfarin
34
TX regiemnes optiosn for first 3-6 months - whne are hese regimens indicated?
- 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
- if PE or extensive proximal DVT
then thromblytics
36
when do we favor single oral agent (DOACs)
- no renal - between weight of 120-140/150 kg - coverge - insurance - no drug interactions - drug adherance - VTE with active malignanacy - oral. drug needed
37
when we favour LMWH with overlap warfarin
- renal dysfunction - drrig interaction with DOACs - weight greater then 140/150 kg - no history of HIT - history of antiphospholip[id syndrome
38
when we favour LMWH alone
- preg - actiove maligamnay and can't have DOAS - high bleeding risk - no history of HIT
39
cancer and VTE?
greater chance of getting one and dying of one
40
if we have cancer what agent should we consider?
LMWH (if interactions) or DOACS (if no interactiosn)
41
why or when would we consider therapy beyong 3 months?
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
course of action for post single un porkoved VTE event
Two clicnial trials showed then a lower dose of apixaban or rivaroxaban after 6 months can be benifial
43
complications of VTE
1. post-thrombotic syndrome 2. Post PE Syndrome/ Chronic thromboembolic pulmonary hypertension (CTEH)
44
post thrombitic syndrome what is it
- occurs in 20-50% - s and S - pain, itching, burning , ambutaory dicomfort , swelling, skin pigmenttayion - venous leg ulceration TX: none, compression sock
45
Post PE Syndrome
decrease pulmonary fucntion, QoL, tolerance - CTEPH - TX: PEA only for severe not established evident for less severe
46
Prevention of VTE non-pharm
ambulate, intermittent penumatic compression (INC), gradual compression stockings )GCS), infereior vena cava filter
47
Prevention of VTE pharm options
low dose: - LMWH - UFH -Fondapurienux - warfarin - not used - DOACs - only used post hip and knee surgeries
48
prophylaix in cancer patients?
DOACS - not widely used
49
how do I choose what agent to use prohpylaix?
1. surgical or medical or cancer 2. risk scoring
50
key education poitn?
no OTC NSAID with anticoagulants

Therapy year 3- sem 2 (9 decks)

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