Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

R9 > Chapter 38 - Hypercoagulable states > Flashcards

Chapter 38 - Hypercoagulable states Flashcards

1
Q

Virchow’s triad

A

1) endothelial injury 2) stasis of blood 3) hypercoagulability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Congenital hypercoagulable defects that increase both arterial and venous thrombosis

A

1) Hyperhomocysteinemia 2) increased lipoprotein A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Patient risk factors for thrombosis

A

1) age 2) OC use 3) hormone replacement therapy 4) pregnancy 5) cancer 6) infection 7) trauma 8) surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Two groups of congenital hypercoagulable states associated with VTE

A

1) reduced natural anticoagulants: antithrombin, protein C, protein S 2) defects resulting in gain of procoagulant function: factor V leiden, prothrombin G20210 mutation, increase coag factors 8, 9, 11 and dysfibrinogenemia group 2 less thrombogenic but more common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Venous thromboembolism and inherited thrombophilias

A

TABLE 38.1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Prevalence of protein C or S deficiency

A

< 1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Percentage of group 1 thrombophilia that will have symptomatic thrombotic event before 60 yo

A

30-50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Antithrombin deficiency prevalence

A

0.02% of population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Three types of antithrombin deficiency

A

TYPE 1 = decrease antithrombin functional activity and antigen TYPE 2 = reduced activity but normal antigen levels; mutation in active inhibitory site TYPE 3 = moderate decreased activity due to impaired interaction with heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Deficiency of protein C prevalence

A

0.2% 2.5-6% in people with VTE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Action of activated protein C

A

Cleaves coagulant cofactor 8a and 5a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Types of protein C deficiency

A

TYPE 1: reduced function and antigen protein level TYPE 2: reduced function but preserved antigen level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment of protein C deficiency

A

If VTE then consider lifelong anticoagulation especially if < 40 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Homozygous protein C deficiency get this neonatal disorder

A

Purpura fulminans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment of warfarin necrosis

A

1) FFP 2) vitamin K 3) heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Protein S action

A

vitamin K-dependent cofactor for inactivation of factor 5a and 8a by activated protein C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Types of protein S deficiency

A

TYPE 1: reduced function and antigen level TYPE 2: reduced function but normal antigen TYPE 3: reduced free protein S due to enhanced C4b binding but normal antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Protein S forms in blood

A

20-40% free floating = active 60-80% bound to complement binding protein C4b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Protein S level in pregnancy

A

Falls in 2nd and 3rd trimester

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Protein S level reduction associated with

A

1) cancer 2) lupus 3) antiphospholipid antibody syndrome (APLAS) 4) sepsis 5) chronic inflammatory disorder 6) advanced HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Factor V leiden molecule pathology

A

1) mutation in 506 position 2) glycine for arginine 3) cleavage site to APC resistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Factor V Leiden epidemiology

A

2-7% European 10% of VTE patients 30-50% of patients being worked up for thrombophilia

23
Q

Other rare cleavage mutation of factor Va

A

Arg306Thr

24
Q

Prothrombin gene mutation G20210A key points

A

1) increased plasma level of prothrombin 2) increased prothrombin mRNA stability 3) most common in European population 1-4%; 5-10% of VTE patients, 15% of thrombophilia patients

25
Q

Ethnicity with highest factor 8 level

A

African american > white and asian

26
Q

Measuring factor 8 activity key points

A

1) has to measure with ESR or CRP 2) each lab should define 90th percentile for population individually

27
Q

Factor 8 level significance

A

increases in inflammation infection, IBD, cancer

28
Q

Two metabolic pathways of homocysteine

A

1) vitamin B6 pathway = cystathionine beta synthase 2) folate, B12 pathway = 5,10-methylenetetrahydrofolatate reductase (MTHFR) and methionine synthase

29
Q

Effect of homocysteine on thrombosis

A

1) toxic effect on endothelium 2) enhanced platelet acdtivation 3) oxidation of LDL-C 4) inflammatory decrease in endothelial TM 5) increase in vWF and factor 8

30
Q

Lipoprotein A action

A

competes with tPA, plasminogen and plasmin for binding fibrin and endothelial annexin INHIBITS FIBRINOLYSIS

31
Q

Sticky platelet syndrome key points

A

1) autosomal dominant disorder 2) early onset MI and PAD 3) hyperactivity to epinephrine and ADP 4) normal response to thrombin, collagen and arachdonic acid

32
Q

Three types of platelet response in sticky platelet syndrome

A

TYPE 1: hyperactive to both ADP and epinephrine TYPE 2: hyperactive to epinephrine TYPE 3: hyperactive to ADP

33
Q

Treatment of sticky platelet syndrome

A

ASA

34
Q

Recurrence of VTE in unprovoked VTE

A

5-10% per year 50% develop by 10 years

35
Q

Acquired hypercoagulable states

A

1) APLAS 2) cancer 3) HIT 4) chronic inflammation (IBD, Behcet’s, SLE) 5) surgery 6) pregnancy, estrogen 7) infection

36
Q

APLAS key points

A

1) can co-exist with SLE but 50% do not 2) antibodies against lupus anticoagulant 3) antibodies bind anticardiolipin and beta 2 glycoprotein

37
Q

Lupus anticoagulant and anti cardiolipin antibody effect

A

10x increase in VTE

38
Q

APLAS on coagulation test

A

prolonged aPTT

39
Q

Characteristic of APLAS

A

thrombosis at unusual sites recurrence 50% high mortality variant = CAPS

40
Q

Cancer on coagulation

A

increase fibrinogen, factor 8 and platelet VTE 1-43% risk of VTE 7-20x increase

41
Q

Nonbacterial thrombotic endocarditis

A

cardiac manifestation of systemic hemostatic activation in cancer patients = platelet and fibrin vegetation on cardiac valves 30-70% have lab evidence of overt DIC

42
Q

Pregnancy on coagulation factor changes

A

1) increase fibrinogen, factor 8 2) reduce protein S

43
Q

VTE risk in pregnancy

A

4-6x higher

44
Q

Rate of left sided VTE in pregnancy

A

90%

45
Q

Pregnant patients with these deficiency should get anticoag prophylaxis

A

1) antithrombin deficiency 2) protein C deficiency 3) protein S deficiency 4) antiphospholipid syndrome 5) factor V leiden

46
Q

Treatment of pregnant patient with active thrombosis

A

LMWH full dose

47
Q

HIT pathophysiology

A

Antibody against neoantigen on platelet factor 4 (PF4) after binding to heparin

48
Q

Thrombotic rate in HIT patients

A

30-70%

49
Q

Rate of thrombotic death in HIT

A

4-5%

50
Q

Monitoring platelets in HIT

A

1) 5 days after starting heparin 2) 50% decrease triggers investigation 3) serologic screening for HIT-associated heparin/PF4 antibody

51
Q

Algorithm to decide on testing or just treating new VTE patients

A

FIGURE 38.1

52
Q

Laboratory tests to order depending on family history

A

FIGURE 38.2

53
Q

Thrombophilic defects and tests available for testing

A

TABLE 38.2

R9 (200 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions