Module 2 Exam 1 lecture 5 Flashcards

1
Q

VTEs are formed where?

A

In areas of slow distributed flow

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2
Q

T/F stasis blood promotes thrombus

A

true

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3
Q

what are venous thrombi composed of?

A

RBC, Fibrin and platelets

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4
Q

how do symptoms of VTE occur?

A

Flow is obstructed
vascular tissue becomes inflamed
thrombus occurs and affects venous blood flow
Emboli occur and enter pulmonary circulation

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5
Q

Do all DVTs lead to PEs? Do all PEs come from DVTs?

A

Not all DVTs lead to PEs, but all PEs come from DVTs

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6
Q

What is the virchous triad

A

3 main things that could cintribute to blood clot development

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7
Q

Name the virchous triad

A
  1. Hypercoagulable state- pregnancy, cancer
  2. Endothelial injury- abnormalities of surface of contact with blood
  3. Circulatory stasis- abnormalities in blood flow (long periods of immobility)
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8
Q

pathway for the development of VTE

A

Vessel wall injury (exposure of endothelium)
This triggers platelet adhesion and aggregation
and coagulation cascade is activated
This produces thrombin, triggering fibrin formation

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9
Q

What activates degradation of clot

A

Tissue plasminogen activator (TPA)

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10
Q

Which factors are procoagulant

A

VWF, Factor Xa, Factor II (thrombin), factor XIIIa, TF, XIIa

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11
Q

Which factors are anticoag

A

Heparin, antithrombin, proteins C and S, thrombomodulin

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12
Q

3 phases of coagulation cascade?

A

Initiation phase
Amplification phase
propagation phase

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13
Q

How is the initiation phase started?

A

Tissue factor bearing cell is exposed to BV after injury

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14
Q

How is amplification phase started?

A

BV damage leads to trace amounts of THROMBIN, leading to amplification phase

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15
Q

What is the amplification phase?

A

Clotting factors become activated developing fibrin clot.

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16
Q

What is the propagation phase? key part in propagation phase?

A

Propagation phase leads to development of fibrin clot. A key part is the development of large amounts of thrombin

17
Q

How is fibrinogen turned into fibrin

A

By thrombin

18
Q

prothrombin and thrombin othe rnames

A

Prothrombin-factor 2
thrombin-factor 2a

19
Q

rivaroxaban is what type of drug

A

factor Xa inhibitor

20
Q

Argatroban is what type of drug

A

DTI

21
Q

Name NOAC/DOAC drugs

A

DTI- Dabigatran
Factor Xa inhibitors-
rivaroxaban
apixaban
Edoxaban

22
Q

Which NOAC/DOAC is only used for hip surgery

A

Dabigatran

23
Q

Which NOAC/DOAC is approved for Knee and hip surgery

A

Rivaroxaban/apixaban

24
Q

Which NOAC/DOAC uses renal adjustments in Scr not CRCL

A

Apixaban

25
Q

Which NOAC/DOAC is the only one that needs dosage adjustments for older/frail patients

A

apixaban

26
Q

Which NOAC/DOAC is not used if a patients CrCL is above 95

A

edoxaban

27
Q

WHen dosing Dabigatran and edoxaban, how is it different from dosing rivaroxaban and apixaban

A

Dabigatran and edoxaban require 5-10 days of parenteral injectable anticoagulation then switched to oral

Rivaroxaban and apixaban- Both PO at higher or more frequent doses for 7 days, then lower doses PO for 6 months plus

28
Q

T/F we can use rivaroxaban/apixaban after the 6 months regardless of what drug pt was on 0-6 months

A

True

29
Q

How is warfarin given?

A

UFH/LMWH/fondaparinux 5 days, overlap with warfarin AND INR >2

30
Q

When should we use UFH with warfarin?

A

When CRCL<30

31
Q

What is INR? What is a normal INR?

A

INR is a number that represents how long it takes for blood to clot. Normal INR =1
hugher number =higher bleeding risk

32
Q

counseling factors about warfarin

A

Drugs- Gs make u bleed (ginseng, garlic, ginko), aspirin and NSAIDs increase bleeding risk
Diseases- any changes in medical condition since last time I saw you?
Doses- any missed doses
Diet- any changes in VIT K intake?
drink- any ETOH consumption

Bruises bleeding

33
Q
A