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MKSAP: Key Points > Heme key points > Flashcards

Heme key points Flashcards

Complete

1
Q

Tx for aplastic anemia, and what percent of patients will get disease control with this treatment?

A

Cyclosporine and antithymocyte globulin; 70%

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2
Q

Allogenic HSCT is potentially curative for aplastic anemia. Which patients can you consider it in?

A

Younger than 50 w/ compatible donors

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3
Q

Efficacy of hematopoietic GFs in aplastic anemia?

A

Ineffective

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4
Q

Dx of pure red cell aplasia?

A

Bone marrow exam- also helps r/o secondary causes

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5
Q

Tx of idiopathic pure red cell aplasia (2 general options)

A

Prednisone monotherapy

Prednisone + either cyclosporine or cyclophosphamide

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6
Q

How long does it take to see improvement once you start treating idiopathic red cell aplasia with immunosuppression?

A

1-3 months

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7
Q

Dx and Tx of drug-induced neutropenia?

A

Dx: history, timing, and exclusion of other causes
Tx: removal of the offending med

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8
Q

Dx and prognostication of MDS?

A

BM Bx and aspiration w/ cytogenetic studies

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9
Q

What subset of MDS can get away with no Tx at all or infrequent transfusions?

A

Those with low-risk MDS

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10
Q

2 options for Dx of CML?

A

Detect the (9;22) translocation in peripheral blood with either:

  1. RT-PCR
  2. FISH
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11
Q

What class of drug is used as initial and subsequent therapy for CML?

A

TKIs targeting BCR-ABL

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12
Q

What CV ADE is common to all TKIs, and how should you monitor for it?

A

Prolongation of the QT interval; periodic EKG monitoring

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13
Q

4 components of evaluation of erythrocytosis?

A
  1. Pulse ox
  2. Peripheral smear
  3. Measurement of serum epo
  4. Eval for JAK2 mutation
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14
Q

2 components of initial therapy for most patients with P. vera?

A

Low-dose ASA + phlebotomy

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15
Q

Which two subgroups of patients with P. vera can treated with hydroxyurea + phlebotomy?

A
  1. Those older than 60

2. Higher risk of thromboembolism

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16
Q

Tx of essential thrombocythemia in patients with low risk of thromboembolic Cpx?

A

Obs

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17
Q

Tx of essential thrombocythemia in patients with high risk of thromboembolic Cpx?

A

Platelet-lowering therapy

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18
Q

Tx for primary myelofibrosis is primarily palliative except in younger patients, who can get what treatment?

A

Allo HSCT

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19
Q

What drug has a dramatic lytic effect on peripheral and tissue Eos in hypereosinophilic syndrome but is problematic for long-term use?

A

Steroids

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20
Q

Tx of steroid-refractory primary hypereosinophilic syndrome w/ activating mutations of PDGF receptors alpha or beta?

A

Imatinib- leads to durable and dramatic responses

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21
Q

What is the defining clinical clue to APL?

A

DIC

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22
Q

Defining mutation of APL?

A

t(15;17)

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23
Q

What drug leads to prompt resolution of the DIC a/w APL?

A

ATRA

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24
Q

What’s an alternate to chemo used to consolidate remission in otherwise healthy patients with high-risk ALL?

A

Allo HSCT

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25
Q

What drug can be added in treatment of Ph chr + ALL?

A

Dasatinib

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26
Q

3 indications for G-CSF?

A
  1. Stimulate nphil production in autoimmune neutropenia
  2. HSC mobilization
  3. Hasten nphil recovery s/p cytotoxic chemo
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27
Q

3 main indications for epo?

A
  1. Anemia of CKD is iron, B12, and folate levels are okay
  2. Hasten recovery in non-curative chemo-assoc anemia
  3. Reduction of transfusion requirements in MDS
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28
Q

3 clinical scenarios where allo HSCT is most helpful?

A
  1. Aplastic anemia
  2. High-risk MDS
  3. Acute leukemias
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29
Q

Basic pathophys of acute GVHD?

A

Graft T cells recognize pt’s normal guy, skin, and liver sinusoids as foreign

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30
Q

Tx of acute GVHD?

A

High-dose steroids

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31
Q

2 main indications for serum and urine protein electrophoresis for plasma cell dyscrasias?

A

Suspected:

  1. Symptomatic PCD requiring intervention
  2. ASx PCD at high risk of progression to a clinically symptomatic condition
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32
Q

What test can detect monoclonal free light chains before they’re detectable by uPEP?

A

Serum free light chain assay

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33
Q

What’s the most sensitive test for detecting monoclonal free light chain gammopathies?

A

Serum free light chain assay

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34
Q

A combo of what 3 tests will detect almost all plasma cell dyscrasias?

A
  1. sPEP
  2. Serum immunofixation
  3. Serum free light chain assay
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35
Q

Definition of MGUS? (3 components)

A
  1. M protein level less than 3 g/dL (or less than 500 mg/24 hr of urinary monoclonal free light chains)
  2. Clonal plasma cells comprising less than 10% of the bone marrow cellularity
  3. Absence of plasma cell dyscrasia-related signs or symptoms
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36
Q

Definition of smoldering multiple myeloma? (3 components?

A
  1. No evidence of myeloma-related signs or symptoms requiring therapy
    Plus either:
    -Serum M protein level of 3 g/dL or greater (or more than 500 mg/24 hr of urinary monoclonal free light chains)
    -Clonal plasma cells comprising 10% or more of the bone marrow cellularity
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37
Q

Define symptomatic multiple myeloma. (3 components)

A
  1. Presence of serum M protein
  2. Bone marrow plasma clonal cells of 10% or greater
  3. End-organ damage (CRAB)
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38
Q

Management of smoldering multiple myeoma? Give freq of checkups and 4 labs to be done at each.

A

q3-6 mo. Get CBC, creatinine, serum Ca, repeat M protein

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39
Q

Tx of choice for smoldering multiple myeloma at low risk of progression?

A

Expectant Mx w/ monitoring q3-6 mo

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40
Q

What treatment for eligible multiple myeloma patients is a/w improved PFS and sometimes OS?

A

Auto HSCT w/ high-dose mephalan after initial induction therapy

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41
Q

3 components of Dx of AL amyloidosis?

A
  1. Presence of amyloid deposits in the tissue Bx sample (from abd fat pad, marrow, or organ Bx)
  2. Proof that amyloid deposits are monoclonal free light chains
  3. Confirmation to clonal plasma cell disorder
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42
Q

Efficacy of auto HSCT in AL amlyoidosis

A

In select patients, it’s shown

  • high hematologic response rates
  • improved organ fxn
  • durable PFS and OS
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43
Q

What percent of patients with Waldenstroms have Sx of hyperviscosity?

A

31%

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44
Q

Symptomatic hyperviscosity is a medical emergency, requiring what Tx?

A

Plasmapheresis

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45
Q

7 Sx of hyperviscosity (as seen in Waldenstroms, etc)

A
  1. HA
  2. Blurred vision
  3. Hearing loss
  4. Tinnitus
  5. Dizziness
  6. AMS
  7. Nasal and oropharyngeal bleeding
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46
Q

What are 3 hyperviscosity-related findings you may see on fundoscopic exam of a Waldenstroms patient?

A
  1. Dilated retinal veins
  2. Papilledema
  3. Flame hemorrhages
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47
Q

MC disease a/w mixed cryoglobulinemia?

A

Hep C

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48
Q

Management of type 1 cryoglobulinemia with hyperviscosity?

A

Plasmapheresis + treatment of the underlying disorder

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49
Q

Tx of mixed cryoglobulinemia?

A

Treatment of the underlying disease. Add immunosuppressive therapy for pts w/ more severe manifestations of vasculitis

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50
Q

How can you use retic count to Ddx btwn rbc underproduction vs destruction in determining cause of anemia?

A

Retic count is low in underproduction and high in destruction

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51
Q

Hematopathologic hallmark of iron deficiency anemia?

A

Microcytic hypochromic anemia

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52
Q

In iron-deficiency anemia, what’s the sequence of anemia, morphologic changes in the cells, and changes in the iron studies.

A

Changes in iron studies -> anemia -> morphologic cell changes

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53
Q

Describe transferrin sat and serum ferritin level in iron deficiency anemia

A

Transferrin sat: less than 15%

Ferritin level: less than or equal to 12 ng/mL

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54
Q

What iron replacement is the cheapest option and also just as effective as any of the more expensive PO options?

A

Ferrous sulfate

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55
Q

Inflammatory anemia: describe MCV, serum iron level, and TIBC

A

Normocytic
Low serum iron
Low TIBC

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56
Q

Management of inflammatory anemia?

A

Treat the underlying disease

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57
Q

In CKD, underproduction anemia affects what percent of those with a GFR less than 25 to 30?

A

90%

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58
Q

Underproduction anemia in CKD is usually _____chromic and _____cytic with what sort of retic count?

A

Normochromic, normocytic with low retic

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59
Q

Use of epo levels in Dx of anemia of CKD?

A

Not helpful

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60
Q

How can you use MMA and homocysteine levels to Ddx btwn B12 and folate deficiency?

A

B12 deficiency: both are high

Folate deficiency: MMA normal, homocysteine high

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61
Q

Initial therapy in most patients w/ B12 deficiency?

A

High-dose PO B12 supplementation of 1000-2000 micrograms/d. This is usually as effective as parenteral admin in most pts, even in those w/ intrinsic factor deficiency.

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62
Q

Tx of folate deficiency?

A

PO folate, 1-5 mg/d until complete hematologic recovery

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63
Q

Can you use PO folate to treat folate deficiency in malabsorption conditions?

A

Yup

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64
Q

What should you check for B12 deficiency before treating folate deficiency?

A

Large doses of folic acid can lead to improved hematopoiesis but won’t fix the CNS/PNS injuries a/w B12 deficiency

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65
Q

Patients with chronic hemolytic anemia require what supplement?

A

Folic acid

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66
Q

4 vaccines that pts w/ chronic hemolytic anemia must get?

A

Pneumococcal, HIB, flu, meningococcal

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67
Q

Peripheral smear findings in acute hemolysis 2/2 G6PD deficiency (2)?

A

Bite cells, Heinz bodies

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68
Q

Describe the following findings in the thalassemias:

  1. MCV
  2. Special cells on smear
  3. Erythrocyte count
  4. Iron studies
A
  1. Microcytic
  2. Target cells
  3. Elevated or normal
  4. Normal
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69
Q

Electrophoresis findings in beta-thal?

A

Slightly increased A2 and fetal Hb

70
Q

Electrophoresis findings in alpha-thal?

A

Normal, unless they have 3 deletions- then some HbH

71
Q

3 common disease-altering strategies in congenital hemolytic anemias?

A

HSCT
Prophylactic transfusions
Hydroxyurea therapy

72
Q

Describe 5 benefits of hydroxyurea therapy in sickle cell disease?

A
  1. Decrease vaso-occlusive epidoes
  2. Decrease acute chest syndrome
  3. Decrease trasfusion requirements
  4. Decrease hospitalization
  5. Prolong OS
73
Q

Sickle cell patients shouldn’t get TFNs unless they’re in one of these 2 situations?

A

Symptomatic anemia

Signs of end-organ damage

74
Q

3 physical findings in warm AIHA?

A

Pallor, jaundice, splenomegaly

75
Q

6 lab findings in warm AIHA?

A 
Increased retics
Elevated bili
Decreased/absent haptoglobin
Increased LDH
Positive antiglobulin (Coombs)
Spherocytes
76
Q

Mainstay treatment for warm AIHA?

A

Steroids

77
Q

Mainstay treatment for cold agglutinin disease?

A

Cold avoidance

78
Q

3 causes of macroangiopathic hemolytic anemia

A

Heart valve disorders (esp mechanical heart valves)
Intracardiac tumors
Rupture of chordae tendineae

79
Q

What causes march hemoglobinuria?

A

Repetitive trauma to the soles of feet or palms of hands, like with marching or running

80
Q

4 infectious causes of hemolytic anemia

A

Plasmodium species
Babesia microti
C. perfringens
Bartonella bacilliformis

81
Q

What’s the most sensitive and cost-effective initial screening test for hemochromatosis?

A

Elevated transferrin sat

82
Q

What 3 groups of patients should be screened for hereditary hemochromatosis?

A

Active liver disease
First degree relatives of pts w/ classic HFE-related hemochromatosis
Abnormal iron studies

83
Q

What’s the best way to prevent morbidity/mortality in hemochromatosis patients?

A

Prompt and aggressive phlebotomy treatments before end-organ complications occur

84
Q

How do you treat patients with secondary iron overload w/ ongoing anemia?

A

Iron chelation

85
Q

Describe clinical diagnosis of TTP

A

Presence of thrombocytopenia and microangiopathic hemolytic anemia in the absence of other causes of these findings, and may include neuro Sx, abdominal pain, renal disease, and fever.

86
Q

How can you treat atypical HUS?

A

Infusions of eculizumab

87
Q

Why shouldn’t you use antiplatelet antibody testing recommended for immune-mediated thrombocytopenia?

A

It has such low sensitivity and specificity. In fact, no diagnostic test can ID immune-mediated thrombocytopenia.

88
Q

When may pts w/ ITP require therapy (2)?

A

Platelet count

89
Q

Diagnosis of HIT requires what two tests?

A

Serologic testing w/ ELISA

Functional testing w/ serotonin-release assay

90
Q

What should you expect in a pt w/ clinical bleeding but a normal platelet count, PT, and aPTT?

A

Qualitative platelet defect

91
Q

Bleeding into muscles or joints in characteristic of what type of disorder?

A

Humoral clotting factors

92
Q

Mucosal bleeding is characteristic of what type of disorder?

A

Primary hemostasis

93
Q

4 features correlated with a higher likelihood of an underlying bleeding disorder in women being evaluated for menorrhagia

A
  1. Nighttime “flooding”
  2. Passing clots larger than a quarter
  3. Duration longer than 8 days
  4. Development of iron deficiency
94
Q

Describe the aPTT, PT, and aPTT mixing study in hemophilia A and B

A

Long aPTT, normal PT, and aPTT mixing study will fully correct

95
Q

What test is diagnostic of hemophilia A or B?

A

Measurement of baseline factor activity (8 for A, 9 for B)

96
Q

Describe general Tx of hemophilia

A

Factor concentrates, given prophylactically or in response to bleeding

97
Q

5 tests (and their results) in diagnosing vWD

A
  1. vWf antigen and activity levels of 30% or less
  2. Factor VIII levels normal or low
  3. Platelet function analyzer-100: prolonged
  4. PT normal
  5. aPTT: normal or slightly prolonged
98
Q

2 drugs you can use to treat menstrual or other minor bleeding or for surgical Ppx in vWd?

A

Estrogen-containing OCPs

Desmopressin

99
Q

Describe the following labs in coagulopathy of liver disease:

  1. PT
  2. aPTT
  3. Fibrinogen levels
  4. Fibrinogen function
  5. Factor VIII levels
A
  1. PT: long
  2. aPTT: long
  3. Fibrinogen levels: low
  4. Fibrinogen function: possibly dysfunctional
  5. Factor VIII levels: supranormal
100
Q

Why can fibrinogen possibly be dysfunctional in coagulopathy of liver disease?

A

Abnormal glycosylation

101
Q

Patients with coagulopathy of liver disease may be deficient in what vitamin, further exacerbating their coag probs?

A

Vitamin K- so replete if you suspect a deficiency

102
Q

How do you treat significant bleeding in coagulopathy of liver disease (3)?

A

Cryoprecipitate, FFP, and platelets

103
Q

Two components of treatment of acquired factor VIII inhibitor?

A

Treat bleeding episodes w/ recombinant activated factor VIII. Immunosuppression to eradicate the inhibitor.

104
Q

Core focus of management of DIC?

A

Treatment of the underlying cause

105
Q

You have a patient w/ a history of alloimmunization who now has repeat alloantibody screening that’s negative. Can they get RBCs containing antigens to which they’re alloimmunized? Why or why not?

A

Nope! Anamnestic responses can occur, resulting in delayed hemolytic transfusion reactions

106
Q

Transfusion threshold for hemodynamically stable, hospitalized medical and post-surgical pts?

A

Less than 7-8

107
Q

If you have to give Rh(D)-positive platelets to an Rh(D)-negative woman of childbearing potential, what should you do to decrease the risk of alloimmunization?

A

Coadminister anti-D immune globin

108
Q

Definition of platelet transfusion refractoriness?

A

Increase in platelet count less than 10,000 when measured within 1 hr after transfusion

109
Q

2 general causes of platelet transfusion refractoriness?

A

Alloimmunization vs non-immune factors

110
Q

Name some non-immune factors that can cause platelet transfusion refractoriness (4)

A

Sepsis
Hypersplenism
DIC
Meds (including ampho B)

111
Q

In pts w/ heme malignancies undergoing chemo or HSCT, what’s your platelet transfusion threshold?

A

Less than 10,000

112
Q

Efficacy of FFP in treatment of mild coagulopathies (INR 1.85 or less)?

A

Ineffective

113
Q

What 4 factors does inactivated 4-factor prothrombin complex concentrate contain?

A

II, VII, IX, and X

114
Q

Combo of what 2 things is used in treatment of major warfarin-associated bleeding?

A

Vitamin K + inactivated 4-factor prothrombin complex concentrate

115
Q

8 s/s of acute hemolytic transfusion reaction?

A 
Fever
Chills
Dyspnea
Red urine
Flank pain
Kidney injury
DIC
HypoTN/shock
116
Q

3 components of therapy for acute hemolytic TFN reaction?

A
  1. TFN discontinuation
  2. IV hydration
  3. Appropriate CV support
117
Q

When do delayed hemolytic TFN reactions present, and what are the 3 main Sx?

A

2-10 days after TFN, p/w fever, jaundice, and worsening anemia

118
Q

Are delayed hemolytic TFN reactions primarily intravascular or extravascular?

A

Extravascular

119
Q

6 s/s a/w TFN-associated circulatory overload?

A

Dyspnea, hypoxia, tachycardia, HA, HTN, and findings of volume overload

120
Q

When does TRALI occur and how does it present?

A

W/in 6 hr of TFN of rbcs, platelets or FFP. P/w acute lung injury that escalates quickly and includes dyspnea, hypoxia, fever, chills, and hypoTN.

121
Q

2 primary interventions for all non-hemolytic transfusion reactions?

A

TFN discontinuation + supportive care

122
Q

What type of transfusion reaction are patients with IgA deficiency at particularly high risk for?

A

Anaphylactic TFN rxn

123
Q

3 components of Tx of transfusion anaphylactic rxn?

A
  1. DC TFN
  2. Exclude other transfusion rxns
  3. Appropriate anaphylaxis Mx
124
Q

2 components of Mx of allergic rxn during TFN?

A
  1. DC TFN to r/o a more severe allergic rxn

2. Antihistamines

125
Q

When does TFN-associated GVHD present?

A

Several days to one month after TFN

126
Q

7 s/s of transfusion-associated GVHD?

A
  1. Diffuse maculopapular rash
  2. Jaundice
  3. Abdominal pain
  4. n/v
  5. Diarrhea
  6. Severe pancytopenia
  7. Abnormal LFTs
127
Q

Basis of Mx of a suspected TFN-associated bacterial infection?

A

Abx therapy w/ gram +/- coverage

128
Q

3 advantages of erythrocyte exchange over rbc TFN in sickle cell disease?

A
  1. Doesn’t increase blood viscosity
  2. Avoids iron overload
  3. More effectively decreases the concentration of HbS
129
Q

2 reasons EBM recommends against routine thrombophilia testing?

A

ID of inherited abnormalities doesn’t:

  • alter duration of recommended anticoagulation
  • reliably predict the risk of recurrence
130
Q

MC inherited thrombophilia?

A

Factor V Leiden

131
Q

Testing for factor V leiden: screening and confirmatory tests?

A

Screen w/ activated protein C resistance assay

Confirm w/ PCR testing for the factor V leiden

132
Q

How does heterozygous prothrombin G20210A mutation change risk of initial VTE and recurrence of VTE?

A

Increases risk of initial VTE 3x, but no increased risk of recurrence

133
Q

Do you routinely screen for cancer in all pts w/ unprovoked VTE?

A

Nope

134
Q

How long should patients with anti-phospholipid antibody syndrome and Hx of unprovoked VTE undergo anticoagulation?

A

Indefinitely- there’s a high rate of recurrent VTE

135
Q

What 3 groups of contraceptive present the greatest risk of VTE?

A

4th gen estrogen-progesterone contraceptives, and contraceptive rings and patches

136
Q

How do progestin-releasing IUDs change risk of VTE?

A

They don’t

137
Q

Name 3 strong RFs for arterial and venous thrombosis

A

Polycythemia vera, essential thrombocythemia, and myelofibrosis

138
Q

VTE Ppx should be considered for every hospitalized patients based on risk assessment for what two things?

A

VTE and bleeding

139
Q

A low probability Wells score plus what else rules out VTE?

A

Negative D dimer

140
Q

General Tx of proximal DVT?

A

Anticoagulant therapy

141
Q

2 components of Tx of PE w/ hypoTN?

A

Thrombolytic therapy + anticoagulation

142
Q

Duration of anticoagulation for provoked VTE?

A

3 months

143
Q

What is the only clear indication for an IVC filter?

A

Acute pelvic or proximal leg DVT who can’t be anticoagulated bc of active bleeding or a very high risk of bleeding

144
Q

Treatment of non-extensive superficial venous thrombophlebitis?

A

Symptomatic therapy w/ analgesics, anti-inflammatories, and warm or cold compresses

145
Q

What percent of upper extremity DVTs are primary vs secondary?

A

20% primary, 80% secondary

146
Q

80% of upper extremity DVTs are 2/2 one of which two causes?

A

Central venous catheters or cancer

147
Q

MC RF for Budd-Chiari?

A

A myeloproliferative neoplasm (ex- polycythemia vera, ET, and primary myelofibrosis)

148
Q

Duration of anticoagulation for acute portal or mesenteric vein thrombosis?

A

At least 3 mo

149
Q

What are the two diagnostic tests of choice for cerebral and sinus vein thrombosis?

A

CT venography and MR venography

150
Q

Duration of anticoagulation for cerebral and sinus vein thrombosis a/w a transient RF?

A

3-6 mo

151
Q

Duration of anticoagulation for unexplained cerebral and sinus vein thrombosis in which no higher risk thrombophilia has been detected?

A

6-12 mo

152
Q

Duration of anticoagulation for cerebral and sinus vein thrombosis a/w a higher risk thrombophilia?

A

Long term

153
Q

Duration of anticoagulation for recurrent cerebral and sinus vein thrombosis?

A

Long term

154
Q

What dosing strategy will allow you to achieve therapeutic aPTTs most quickly when selecting an unfractionated heparin dose?

A

Weight-based heparin dosing normograms

155
Q

What agent reverses warfarin anticoagulation?

A

Protamine

156
Q

What feature of LMWH allows weight-based dosing w/o lab monitoring?

A

Predictable pharmacokinetics

157
Q

Which patients should only get LMWH with extreme caution or not at all?

A

Severe renal disease (CrCl less than 30)

158
Q

Why can fondaparinux be dosed once daily? And why can is be given w/o lab monitoring?

A

It has a half-life of approx 17 hr.

It doesn’t bind significantly to plasma proteins

159
Q

Describe admin of fondaparinux in patients with poor kidney function

A

Use w/ caution in CrCl of 30-50

CI w/ CrCl less than 30

160
Q

What else can you give a patient who is taking daily warfarin but has fluctuating INRs?

A

100-150 microg/d of vitamin K

161
Q

Describe efficacy of 4 factor prothrombin complex concentrate vs 3 factor prothrombin complex concentrate in restoration of individual clotting factor activity.

A

4 factor can do it in close to 100% of pts. 3 factor must be supplemented w/ FFP or low dose of recombinant activated VIIa.

162
Q

6 features common to apixaban, dabigatran, edoxaban, and riveroxaban?

A
  1. Rapid onset of action
  2. No need for routine monitoring
  3. No dietary restrictions
  4. Short half-lives
  5. CI or dose adjustment needed in moderate to severe CKD
  6. Lack of reversal agents
163
Q

Pregnant women with Hb values below what should prompt a search for anemia other than gestational? Give value for 1st tri and different value for 2nd/3rd tri

A

Less than 11 in first tri, less than 10 in second and third tri

164
Q

How does prophylactic transfusion (exchange or normal) affect number of pain crises and pregnancy-related M/M in pregnant sickle cell pts?

A

Reduces number of pain crises but doesn’t affect M/M

165
Q

What two lab abnormalities are a clue to something other than gestational thrombocytopenia?

A

Platelets less than 50k or schistocytes

166
Q

In pregnant pts w/ ITP, you don’t need to treat it unless platelets drop below what? How does this change in the final month?

A

Less than 30k

Platelet count of 50k or greater is desired in the final month in case of CS

167
Q

What’s the most effective therapy for HELLP, preE, and acute fatty liver of pregnancy?

A

Emergent delivery of the fetus

168
Q

Pregnancy is a/w how much of an increased risk of thromboembolism? When is the greatest risk of VTE?

A

5x increased risk. First 6 wk post-partum

169
Q

Tx of choice for VTE in pregnancy?

A

Weight-based LMWH

170
Q

Duration of anticoagulation therapy for VTE during pregnancy?

A

At least 6 wk postpartum for a therapy duration of at least 3 mo

MKSAP: Key Points (6 decks)

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