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SBL - Exam 2 > Bleeding and Clotting > Flashcards

Bleeding and Clotting Flashcards

(68 cards)

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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
the major risk factors for **venous** thrombosis are \_\_\_\_\_\_\_\_.
* immobility * surgery * malignancy * medications * obesity * genetics
26
the most important point in history related to **venous** thrombosis is \_\_\_\_\_\_\_.
whether the event was idiopathic or precipitated * in patients without malignancy, an _**idiopathic** event_ is the _strongest predictor of recurrence of VTE_
27
PFA-100
measures platelet-dependent coagulation * prolonged in patients with some (not all) inherited platelet disorders
28
thromboelastography
useful in guiding intraoperative transfusion * not used in dx of disorders of hemostasis or thrombosis
29
prothrombin time (PT)
measures the **extrinsic** clotting cascade factor **I** (fibrinogen), **II** (prothrombin), **V, VII,** and **X** * sensitivity varies by lab--use INR
30
when testing blood, _________ can give a false value
elevated hematocrit (\> 55%) * this is d/t decreased plasma-to-anticoagulant ratio
31
INR
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
partial thrombin time (aPTT)
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
mixing studies are used for \_\_\_\_\_\_\_\_\_.
distinguishing between factor deficiency and an inhibitor * normal plasma is mixed with the patient's plasma and aPTT or PT are measured
34
if the aPTT corrects in a mixing study:
it indicates and isolated factor deficiency
35
if the aPTT **fails** to correct during a mixing study:
* 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
what is a lupus anticoagulant?
**antibodies** to phospholipids that interfere with phospholipid-dependent coagulation tests
37
lupus anticoagulants can be detected by \_\_\_\_\_\_\_.
dilute Russel viper venom test **(dRVVT)** and tissue thromboplastin inhibition **(TTI)**
38
diagnosis of lupus anticoagulant requires:
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
**thrombin** time measures
**_fibrinogen**_ conversion to _**fibrin_**​
40
thrombin time is prolonged with:
* low fibrinogen levels or **qual**itatively abnormal fibrinogen * the presence of heparin * prsence of dabigatran (direct thrombin inhibitor)
41
measurement of **anti-factor Xa** activity is used to assess:
* LMWH levels * direct measurement of unfractionated (regular) **heparin** activity * activity of direct Xa inhibitors (rivaroxaban, apixaban, edoxaban)
42
anti-thrombin is decreased \_\_\_\_\_\_\_\_\_.
by **heparin** and in the setting of **acute** thrombosis
43
what causes protein C and S levels to increase/decrease?
* increase during **acute** thrombosis * decreased by **warfarin**
44
venous **stasis** (not thrombosis) typically presents with \_\_\_\_\_\_\_.
lower extremity **edema** and achy **pain** in the legs
45
therapy options for venous **stasis** (not thrombosis) include:
* **compression stockings** * unna boots * aspirin
46
what are the underlying risk factors for DVT/PE?
1. venous stasis 2. hypercoagulability 3. endothelial damage
47
the initial and most important step in evaluating possible DVT is \_\_\_\_\_\_\_\_.
**estimating** the clinical **liklihood** of disease
48
D-dimer tests should be performed in patients with \_\_\_\_\_\_\_\_.
**_low_** liklihood of DVT
49
what rules out DVT?
* low clinical probability + * negative D-dimer
50
if D-dimer is positive or clinical likelihood of DVT is high, what should be done?
duplex ultrasonography
51
who should recieve prophylaxis for venous thromboembolism?
* patients with known thromboembolic conditiation and an indication for treatment * hospitalized patients with VTE risk factors
52
symptoms of PE include:
* dyspnea * pleuritic chest pain * cough * hemoptysis * tachypnea * crackles * tachycardia * **accentuated** **pulmonic component of S2**
53
what rules out PE?
* low clinical probability + * negative D-dimer
54
should D-dimer be used in patients with a high liklihood of PE?
**NO**
55
what tests should be done in a patient with a high liklihoood of PE?
* contrast-enhanced CT * V/Q scanning * this is the **only** test that can **rule out** PE
56
Wells criteria for DVT
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
Wells criteria for PE
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
how long should you anticoagulate DVT or PE caused by: * transient risk factor * cancer * unprovoked * recurrent unprovoked * underlying thrombophilia * antiphospholipid Ab
**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
what patients are at **high** risk for DVT/PE _post-op_?
\> 3 intrinsic risk factos * ortho sx, abdominal/pelvic sx, spinal sx, major trauma
60
what patients are at **intermediate** risk for DVT/PE _post-op_?
BMI \> 30, age \> 50 * non-ambulatory, infection, active malignancy, history of VTE
61
what patients are at **low** risk for DVT/PE _post-op_?
minor procedures in healthy patients \< 40 yo * ambulatory, length of stay \< 24 hrs
62
how to _prophylax_ abdominal/pelvic sx patients
enoxaparin for **4 weeks**
63
how to _prohylax_ ortho sx patients
enoxaparin/fondaparinux/DOACs/warfarin for **10 days min** * **35 days** for hip * **12 days** for knee
64
how to _prophylax_ bariatric sx patients
enoxaparin **2 q d**
65
what is the treatment for TTP?
plasmapheresis
66
what is the treatment for VWD?
* cryoprecipitate - replaces VWF * DDAVP - causes release of VWF from endothelium
67
hereditary hemorrhagic telangiectasia | (osler-weber-rendu syndrome)
thinning of vessel walls d/t autosomal dominant mutation in ***endoglin*** * --\> telangiectasias, AVMs, and aneurysmal dilations
68
what is the most common cause of hypercoaguable state in patients with protein C and S deficiency?
warfarin therapy

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