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SBL - Exam 2 > Bleeding and Clotting > Flashcards

Bleeding and Clotting Flashcards

1
Q

what is the most important predictor of bleeding risk?

A

history of bleeding

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2
Q

spontaneous hemarthroses are a hallmark of _______.

A

moderate and severe factor VIII (hemophilia A) and IX deficiency (hemophilia B)

  • also seen in deficiencies of fibrinogen, prothrombin, and factors V, VII, and X
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3
Q

mucosal bleeding is suggestive of ________.

A

platelet disorders and VWD

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4
Q

what is a bleeding score?

A

used to predict patients more likely to have type I VWD

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5
Q

causes of easy bruising

A

abnormality of blood vessels or their supporting tissues

  • Ehlers-Danlos
  • Cushing’s syndrome
  • chronic steroid use
  • aging
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6
Q

epistaxis is the most common symptom in _______.

A

hereditary hemorrhagic telangiectasia and boys with VWD

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7
Q

bleeding with eruption of primary teeth is characteristic of ___________.

A

moderate and severe hemophilia

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8
Q

heavy menstrual bleeding can result in _______ anemia.

A

iron deficiency

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9
Q

heavy menstrual bleeding is most commonly seen in _________.

A

VWD, factor XI deficiency (hemophilia C), and symptomatic carriers of hemophilia

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10
Q

post-partum hemorrhage is delayed in _________.

A

type I VWD and symptomatic carriers of hemophilia A (factor VIII)

  • VWF and factor VIII usually normalize during pregnancy
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11
Q

angiodysplasia of the bowel is associated with _______.

A

types 2 and 3 VWD

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12
Q

muscle and soft tissue bleeds are commin in _______.

A

factor VIII deficiency (hemophilia A)

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13
Q

________ is the major cause of bleeding-related death in patients with severe hemophilias (factor deficiencies).

A

CNS bleeding

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14
Q

aspirin and NSAIDs that inhibit COX-1 impair _________, and may cause bleeding

A

primary hemostasis

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15
Q

P2Y12 receptor inhibitors (clopidogrel, prasugrel, and ticagrelor) inhibit _________.

A

ADP-mediated platelet aggregation

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16
Q

is the risk of bleeding higher with NSAIDs or with P2Y12 receptor inhibitors?

A

P2Y12 receptor inhibitors

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17
Q

fish oil and omega-3 fatty acids impair _________.

A

platelet function

  • increase expression of PGI3, a potent platelet inhibitor
  • increase expression of TXA3, a weak platelet activator
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18
Q

vitamin E inhibits ________.

A

protein kinase C-mediated platelet aggregation and NO production

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19
Q

liver failure results in _________.

A

combined factor deficiencies

  • because all coagulation factors are made in the liver
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20
Q

defects of platelet adhesion inlcude:

A
  1. VWD
  2. Bernard-Soulier syndrome (lacks GPIb)
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21
Q

defects of platelet aggregation include:

A
  1. Glanzmann thrombasthenia (lacks GPIIb/IIIa)
  2. afibrinogenemia
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22
Q

defects of platelet secretion include:

A
  1. aspirin-like platelet defects
  2. granule storage pool defects
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23
Q

bleeding rarely occurs with platelets at ________.

A

> 50K

  • surgery can be performed as long as the patient has at least 50-80K platelets
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24
Q

the major risk factor for for arterial thrombosis is ________.

A

atherosclerosis

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25
Q

the major risk factors for venous thrombosis are ________.

A
  • immobility
  • surgery
  • malignancy
  • medications
  • obesity
  • genetics
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26
Q

the most important point in history related to venous thrombosis is _______.

A

whether the event was idiopathic or precipitated

  • in patients without malignancy, an idiopathic event is the strongest predictor of recurrence of VTE
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27
Q

PFA-100

A

measures platelet-dependent coagulation

  • prolonged in patients with some (not all) inherited platelet disorders
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28
Q

thromboelastography

A

useful in guiding intraoperative transfusion

  • not used in dx of disorders of hemostasis or thrombosis
29
Q

prothrombin time (PT)

A

measures the extrinsic clotting cascade

factor I (fibrinogen), II (prothrombin), V, VII, and X

  • sensitivity varies by lab–use INR
30
Q

when testing blood, _________ can give a false value

A

elevated hematocrit (> 55%)

  • this is d/t decreased plasma-to-anticoagulant ratio
31
Q

INR

A

standard unit of sensitivity of certain thromboplastins to vitamin K-dependent clotting factors

  • sensitivity of thromboplastin varies by lab, producing different PT times per lab
32
Q

partial thrombin time (aPTT)

A

measures the intrinsic clotting cascade

factor I (fibrinogen), II (prothrombin), V, VIII, IX, X, XI, XII (Haegaman factor), prekallikrein, and high-molecular-weight kininogen

  • sensitivity varies by the phospholipids used in each lab
33
Q

mixing studies are used for _________.

A

distinguishing between factor deficiency and an inhibitor

  • normal plasma is mixed with the patient’s plasma and aPTT or PT are measured
34
Q

if the aPTT corrects in a mixing study:

A

it indicates and isolated factor deficiency

35
Q

if the aPTT fails to correct during a mixing study:

A
  • there is lupus anticoagulant present or
  • there are Abs against certain clotting factors or
  • there are other inhibitors such as heparin, fibrin split products, or paraproteins
36
Q

what is a lupus anticoagulant?

A

antibodies to phospholipids that interfere with phospholipid-dependent coagulation tests

37
Q

lupus anticoagulants can be detected by _______.

A

dilute Russel viper venom test (dRVVT) and tissue thromboplastin inhibition (TTI)

38
Q

diagnosis of lupus anticoagulant requires:

A
  1. prolongation of a phospholipid-dependent coagulation test (LA-PTT, dRVVT, or TTI)
  2. lack of correction when mixed with normal plasma, and correction with the addition of activated platelet membranes or certain phospholipids
39
Q

thrombin time measures

A

fibrinogen** conversion to **fibrin​

40
Q

thrombin time is prolonged with:

A
  • low fibrinogen levels or qualitatively abnormal fibrinogen
  • the presence of heparin
  • prsence of dabigatran (direct thrombin inhibitor)
41
Q

measurement of anti-factor Xa activity is used to assess:

A
  • LMWH levels
  • direct measurement of unfractionated (regular) heparin activity
  • activity of direct Xa inhibitors (rivaroxaban, apixaban, edoxaban)
42
Q

anti-thrombin is decreased _________.

A

by heparin and in the setting of acute thrombosis

43
Q

what causes protein C and S levels to increase/decrease?

A
  • increase during acute thrombosis
  • decreased by warfarin
44
Q

venous stasis (not thrombosis) typically presents with _______.

A

lower extremity edema and achy pain in the legs

45
Q

therapy options for venous stasis (not thrombosis) include:

A
  • compression stockings
  • unna boots
  • aspirin
46
Q

what are the underlying risk factors for DVT/PE?

A
  1. venous stasis
  2. hypercoagulability
  3. endothelial damage
47
Q

the initial and most important step in evaluating possible DVT is ________.

A

estimating the clinical liklihood of disease

48
Q

D-dimer tests should be performed in patients with ________.

A

low liklihood of DVT

49
Q

what rules out DVT?

A
  • low clinical probability +
  • negative D-dimer
50
Q

if D-dimer is positive or clinical likelihood of DVT is high, what should be done?

A

duplex ultrasonography

51
Q

who should recieve prophylaxis for venous thromboembolism?

A
  • patients with known thromboembolic conditiation and an indication for treatment
  • hospitalized patients with VTE risk factors
52
Q

symptoms of PE include:

A
  • dyspnea
  • pleuritic chest pain
  • cough
  • hemoptysis
  • tachypnea
  • crackles
  • tachycardia
  • accentuated pulmonic component of S2
53
Q

what rules out PE?

A
  • low clinical probability +
  • negative D-dimer
54
Q

should D-dimer be used in patients with a high liklihood of PE?

A

NO

55
Q

what tests should be done in a patient with a high liklihoood of PE?

A
  • contrast-enhanced CT
  • V/Q scanning
    • this is the only test that can rule out PE
56
Q

Wells criteria for DVT

A

high (> 3), moderate (1-2), low (0)

  • active cancer - 1
  • paralysis/immobilization - 1
  • bedridden for >3 d or majory surgry within 4 w - 1
  • entire leg swollen - 1
  • tenderness along deep vein - 1
  • calf swelling > 3 cm - 1
  • unilateral pitting edema - 1
  • collateral superficial veins - 1
  • alternative dx more likely thanPE - (-)
57
Q

Wells criteria for PE

A

high (> 6), moderate (2-6), low (< 2)

  • clinical evidence of DVT - 3
  • PE is most likely dx - 3
  • HR > 100 - 1.5
  • immobile > 3 d or surgery within 4 w - 1.5
  • previous DVT/PE - 1.5
  • hemoptysis - 1
  • malignancy - 1
58
Q

how long should you anticoagulate DVT or PE caused by:

  • transient risk factor
  • cancer
  • unprovoked
  • recurrent unprovoked
  • underlying thrombophilia
  • antiphospholipid Ab
A

3 months, then

  • transient risk factor - 3 months
  • cancer - as long as cancer is active (enoxaparin)
  • unprovoked - indefinite (w ASA) if necessry
  • recurrent unprovoked - indefinite
  • underlying thrombophilia - indefinite
  • antiphospholipid Ab - indefinite
59
Q

what patients are at high risk for DVT/PE post-op?

A

> 3 intrinsic risk factos

  • ortho sx, abdominal/pelvic sx, spinal sx, major trauma
60
Q

what patients are at intermediate risk for DVT/PE post-op?

A

BMI > 30, age > 50

  • non-ambulatory, infection, active malignancy, history of VTE
61
Q

what patients are at low risk for DVT/PE post-op?

A

minor procedures in healthy patients < 40 yo

  • ambulatory, length of stay < 24 hrs
62
Q

how to prophylax abdominal/pelvic sx patients

A

enoxaparin for 4 weeks

63
Q

how to prohylax ortho sx patients

A

enoxaparin/fondaparinux/DOACs/warfarin for 10 days min

  • 35 days for hip
  • 12 days for knee
64
Q

how to prophylax bariatric sx patients

A

enoxaparin 2 q d

65
Q

what is the treatment for TTP?

A

plasmapheresis

66
Q

what is the treatment for VWD?

A
  • cryoprecipitate - replaces VWF
  • DDAVP - causes release of VWF from endothelium
67
Q

hereditary hemorrhagic telangiectasia

(osler-weber-rendu syndrome)

A

thinning of vessel walls d/t autosomal dominant mutation in endoglin

  • –> telangiectasias, AVMs, and aneurysmal dilations
68
Q

what is the most common cause of hypercoaguable state in patients with protein C and S deficiency?

A

warfarin therapy

SBL - Exam 2 (5 decks)

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