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Block 3b1 PHM > DVT/PE > Flashcards

Flashcards in DVT/PE Deck (51)
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1
Q

Prophylaxis & acute mgt of DVT (2)

A

UFH/LMWH

2
Q

Category & ex’s (2) of drugs for long-term DVT prevention

A

Oral anticoagulants: Warfarin & Rivaroxaban

3
Q

Virchow’s Triad

A

“SHE”
Stasis: post-op/long drive or flight

Hyper coagulability: coagulation cascade problem
(ie: Factor V Leiden mutation)

Endothelial damage (i.e.: exposed collagen that triggers clotting cascade)

4
Q

Imaging test of choice for DVT

A

Compression ultrasound w/ Doppler

5
Q

Imaging test of choice for PE

A

CT pulmonary angiography

6
Q

Factor Xa Anticoagulant w/ greatest efficacy & 2 examples

A

LMWH (dalteparin, enoxaparin)

7
Q

Direct Xa Inhibitors (2)

A

Apixaban, Rivaroxaban

8
Q

Factor IIa (Thrombin) Anticoagulant w/ greatest efficacy

A

Heparin

9
Q

Direct Thrombin Inhibitors (3)

A

Argatroban, Dabigatran, Bivalirudin,

10
Q

Prophylaxis and Acute Mgmt of DVT

A

UFH or LMWH (eg: enoxaparin)

11
Q

Tx & Long term prevention of DVT

A

Oral anticoagulants (eg: warfarin, rivaroxaban)

12
Q

Indirectly lowers activity of thrombin and factor Xa w/ short T1/2

A

UFH

13
Q

Clinical Use of Heparin

A

Immediate anticoagulation for pulmonary embolism

acute coronary syndrome, MI, DVT

14
Q

Anticoagulant that doesn’t cross placenta & monitored via PTT

A

Heparin

15
Q

AE of Heparin

A

Bleeding, Thrombocytopenia (HIT), osteoporosis, hypoaldosteronism, hyperkalemia, drug-drug interactions

16
Q

Rapid reversal agt vs. Heparin

A

Protamine Sulfate: (+) charged molecule that binds (-) charged Heparin

17
Q

Heparin class that acts predominantly on Factor Xa (#1-w/ 2ex’s) and only on Factor Xa(#2)

A

1) LMWH (eg: enoxaparin, dalteparin)

2) Fondaparinux

18
Q

MOA of Heparin-induced Thrombocytopenia (HIT)

A

dev of IgG ab’s vs. heparin bound PT factor 4 (PF4)

ab-Hep-PF4 complex activates PT’s->Thrombosis & Thrombocytopenia

19
Q

Only PO direct thrombin inhibitor

A

Dabigatran

20
Q

Clinical use of direct thrombin inhibitor

A

VTE, a fib, HIT

doesn’t require lab monitoring

21
Q

What can reverse dabigatran (direct thrombin inhibitor)?

A

idarucizumab

22
Q

MOA of Warfarin

What is its metabolism affected by?

A

interferes w/ Y-carboxylation of vit K dep clotting factors (II, VII, IX, X) and proteins C & S

metabolism influenced by polymorphisms in gene for vit k epoxide reductase complex (VKORC1)

23
Q

What is the effect of warfarin in a laboratory assay?

A

effect on extrinsic pathway, ↑ PT and w/ long T1/2

24
Q

Clinical Uses of Warfarin (2)

A

Chronic anticoagulation (eg: VTE prophylaxis) & stroke prevention in a fib

25
Q

CI of Warfarin

A

Pregnant women bc crosses placenta; follow PT/INR

26
Q

AE of Warfarin

A

Bleeding, teratogenic,
skin/tissue necrosis*
(due to small vessel micro thrombosis*)

27
Q

Explain the early transient hyper coagulability w/ warfarin use

A

Factors C & S with shorter T1/2 than clotting factors II, VII, IX, X

28
Q

Warfarin reversal (a) & rapid reversal (b)

A

Vit K (a)/FFP or PCC (b)

29
Q

What is heparin “bridging” & why is it imp?

A

Heparin frequently used when starting warfarin
Heparin’s activation of antithrombin enables anticoagulation during initial transient hyper coagulable state caused by warfarin

Initial heparin Tx ↓ risk of recurrent VTE & skin/tissue necrosis

30
Q

Compare route of admin, site of action & onset of action in Heparin vs. Warfarin

A

Heparin:
Parenteral (IV, SC)
Blood
Rapid (secs)

Warfarin:
PO
Liver
Slow, limited by half lives of normal clotting factors

31
Q

Direct Factor Xa Inhibitors (2)

A

Apixaban, Rivaroxaban

32
Q

Clinical use of direct Factor Xa inhibitors (2)

A

Tx and prophylaxis of DVT & PE , stroke paralysis in patients w/ a fib

33
Q

+ of oral anticoagulant agents?

A

Don’t usually require monitoring

34
Q

AE & limitation of direct factor Xa inhibitors

A

Bleeding; not easily reversible

35
Q

Grade the reversibility of the heparin classes

A

UFH: Robust
LMWH: Moderate
FPX: Little, if any

36
Q

What are HIT paradoxes?

A
Anticoagulant-induced thrombosis
Clotting, not bleeding disorder
PT transfusions can ↑ thrombosis risk
Simply stopping heparin may not prevent thrombosis
Warfarin CI as acute monotherapy
37
Q

How might HIT present clinically?

A

Drop in PT count & or new thrombosis

38
Q

Describe the nature of heparin exposure in HIT in terms of

a) Heparin Class
b) Dose/Duration
c) Route of admin
d) Clinical Setting

A

a) UFH>LMWH
b) High>Low dose
c) Long term>Short term
IV>SC, flushes, heparin coated devices
d) cardiac, orthopedic or ICU

39
Q

Derivation & action of Argatroban

A

L arginine; Univalent inhibitor of thrombin, inhibiting clot bound & soluble thrombin

40
Q

Indication of Argatroban

A

Anticoagulant for prophylaxis/Tx of thrombosis, or PCI in patients w/ HIT*

41
Q

Anticoagulant w/o cross-reactivity w/ heparin induced antibodies

A

Argatroban

42
Q

Limitation of Argatroban

A

No known antidote

43
Q

Therapeutic Effect of Argatroban

A

Rapid, ~30 mins (IV but no bolus)

44
Q

Argatroban Elimination

A

Hepatic metabolism; T1/2 ↑ in patients w/ mild hepatic impairment

45
Q

Given the challenging transition from Argatroban, what other drug may be beneficial?

A

Direct Factor Xa Inhibitors

46
Q

What are 2 imp points to remember during Argatroban therapy transition?

A

1) Don’t rely on warfarin alone until HIT is adequately controlled
2) Give several days for warfarin to attain its therapeutic effect

47
Q

What are some criteria that have to be met before Argatroban is discontinued? (5)

A
  • INR>4.0^2
  • Obtain INR 4-6 hours after Argatroban discontinued
  • Absence of new TEC’s
  • PT recovery
  • Restart Argatroban Tx if INR falls below therapeutic range
48
Q

What are 2 anticoagulants that are CI in acute HIT?

A

a) Warfarin

b) LMWH: cross-reactive w/ heparin antibodies

49
Q

What is one + of Fondaparinux?

A

Rarely cross reacts w/ heparin ab’s

No EBM but anecdotal support

50
Q

3 +/- of Oral Xa Inhibitors

A

+:
PO
Easy dosing
No routine monitoring

-:
$
No antidote
Renal clearance

51
Q

Why is warfarin not used in acute thrombotic settings?

A

Bc it requires 3-4 days to have anticoagulant effects