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SBL > Diagnosis and Management of Bleeding and Clotting Disorders > Flashcards

Diagnosis and Management of Bleeding and Clotting Disorders Flashcards

1
Q

history of epistaxis and gingival bleeding should make you think of what?

A

mucosal bleeding–> platelet disorder until proven otherwise

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2
Q

if you see spontaneous hemarthrosis in a question stem, what is the diagnosis until proven otherwise?

A

hemophilia (factor VIII or factor IX deficiency)

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3
Q

what does a primary hemostatic deficiency consist of?

A

platelet disorders

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4
Q

what does a secondary hemostatic deficit consist of?

A

coagulation factor deficiency or inhibitor

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5
Q

what are the three main components to hemostasis?

A

platelets, plasma proteins, and the vessel wall

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6
Q

testing for vWF, how do you test to see if there is enough?

A

test for the antigen

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7
Q

testing for vWF, how do you test to see if it binds to platelets?

A

test for cofactor

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8
Q

testing for vWF, how do you test to see if it protects/enables FVIII?

A

test for FVIII

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9
Q

what defines a Type 1 vWD? (vWF antigen level, vWF activity, vWF antigen/activity ratio, and Factor VIII levels)

A

vWF antigen: decreased, vWF activity: decreased, vWF antigen/activity ratio: normal, and factor VIII: normal

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10
Q

how do you treat Type 1 vWD? with minor bleeding

A

desmopression (temporarily)- it allows release of vWF from endothelial cells/platelets

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11
Q

what are the side effects of desmopressin?

A

flushing, hypotension, HYPONATREMIA

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12
Q

how do you treat type 1 vWD with major bleeding?

A

plasma derived or recombinant vWF

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13
Q

what disease types of vWD are autosomal dominant?

A

type 1, type 2A and type 2B- so it is the most common types you’ll see

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14
Q

what is a heavy menstrual bleeding defined as?

A

by a change of pad/tampon every hour and clots >1 cm

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15
Q

When trying to diagnose hemophilia, why do we get a genetic test?

A

it can help predict disease severity (certain mutations are associated with more significant bleeding) and it eliminates other diseases in the differential

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16
Q

what is something that could help you distinguish between vWD and hemophilia A?

A

a normal bleeding time in hemophilia versus von willebrand disease (vWD typically has an increased bleeding time because it is a platelet disorder)

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17
Q

which types of von willebrand disease have significantly decreased FVIII levels?

A

type 2N and type 3

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18
Q

what is the inheritance pattern of hemophilia A?

A

x-linked recessive (can hide in family members (aka they are carriers without knowing))

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19
Q

What is the management of hemophilia: prevention?

A

prevention: avoid bleeding in acute and chronic situations, set a baseline activity

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20
Q

what is the treatment of hemophilia?

A

goal isn’t to cure the disease, but to increase factor activity to achieve hemostasis–> most standard therapy is recombinant FVIII

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21
Q

what is an example of recombinant FVIII and what is the downfall to this medication?

A

Emicizumab: binds to FIXa and X- it is an effective prophylactic drug, but it is so costly

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22
Q

what is likely if the mixing study shows failure to correct?

A

an inhibitory antibody is likely and it is unlikely to be a deficiency in a clotting factor

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23
Q

How do you treat acquired hemophilia A?

A

if they have low titers–> you administer FVIII to get that up to allow the common pathway to occur; if they have high titers–> you given them Factor VII- you just bypass the entire intrinsic pathway until you can address the inhibition with immunosuppression

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24
Q

what is the key to treating acquired hemophilia?

A

address the inhibition with immunosuppression

25
Q

what are the characteristics of acquired hemophilia A?

A

often seen in older adults, can occur postpartum (or even during pregnancy), often associated with autoimmune disease (RA/ SLE), and may be seen in malignancy

26
Q

What components make up virchow’s triad?

A

venous stasis, endothelial injury, and hypercoaguability

27
Q

what contributes to venous stasis?

A

intra-operative period, post-operative period, travel

28
Q

what contributes to endothelial injury?

A

trauma, implanted devices, catheters

29
Q

what contributes to hypercoagulability?

A

genetic mutations, nephrotic syndrome, hyper-viscosity due to malignancy, autoimmune/ inflammatory disease, contraceptives, and cigarette smoking

30
Q

what are sites for proximal DVTs?

A

iliac, femoral , and popliteal veins

31
Q

what are the sites for distal DVTs?

A

below the knee, popliteal vein is not involved!

32
Q

what are the reasons for a provoked DVT?

A

surgery, hospital admission, malignancy, auto-immune disease, estrogen therapy

33
Q

what are the reasons for an unprovoked DVT?

A

there are no identifiable environmental events

34
Q

a saddle PE leads to heart failure because why?

A

you have increased pressure on the right ventricle, you get right ventricular strain and ballooning into the left ventricle and you get hypotension

35
Q

how do you diagnose a thromboembolism?

A

Lab test: d-dimer; radiography: ultrasound for DVT and CT angiogram for PE

36
Q

you do not order a d-dimer on everybody. So when do you order one?

A

if the patient’s history is not super convincing, but you still need to rule out a VTE- you only order it on people with low probability

37
Q

what is d-dimer?

A

the degradation of products of cross-linked fibrin

38
Q

d-dimer has a high negative predictive value. What does this mean?

A

if D-dimer is negative, you are not dealing with a thromboembolic phenomenon

39
Q

what is the gold standard test for a DVT?

A

compression ultrasound

40
Q

what is the gold standard for imagining for a PE?

A

CT angiogram

41
Q

if for some reason a patient cannot tolerate a CT angiogram, which imaging modality should be ordered?

A

ventilation/perfusion (V/Q) scan

42
Q

what is the downfall of a V/Q scan?

A

you can’t 100% diagnose a blood clot- it is just going to look for a mismatch between ventilation and perfusion

43
Q

What does a protein C deficiency highlight?

A

a hypercoagulable state

44
Q

mesenteric vein thrombosis should make you think what?

A

hypercoagulable state

45
Q

what is the role of Proteins C and S?

A

they block the sites at VIII and V to inhibit the clotting cascade

46
Q

where are proteins c and s synthesized?

A

in the liver

47
Q

what does deficiency of proteins c or s cause?

A

thrombophilia (the inhibition is removed, so you just keep having this viscous cycle of clotting, which promotes thrombophilia)

48
Q

what is a paradoxical embolism?

A

passage of an embolus from the venous circulation to the arterial circulation

49
Q

how do you diagnose a paradoxical embolism?

A

with a transesophageal echocardiography (TEE) with bubble study

50
Q

what allows for a paradoxical embolism to occur?

A

a patent foramen ovale (PFO)

51
Q

what is the most common cause of strokes in patients under the age of 55?

A

a patent foramen ovale

52
Q

How does heparin work?

A

it inhibits factors II, IX, X, and XI

53
Q

what are 3 examples of Factor Xa inhibitors?

A

rivaroxaban, apixaban, and endoxaban

54
Q

what is an example of a direct thrombin inhibitor?

A

dabigatran

55
Q

how does warfarin work?

A

it inhibits vitamin K dependent factors ( II, VII, IX, X)

56
Q

which drugs are now considered safer and better than warfarin?

A

rivaroxaban and apixaban

57
Q

how long do you need to be anticoagulated?

A

it depends- provoked thromboembolism with no underlying conditions or enduring risk factors: anticoagulate for 3-6 months; however, if you have more than 2 spontaneous thromboses, you are going to have indefinite or lifelong anticoagulation

58
Q

how long do you anticoagulate if you have a patient that has 1 spontaneous thrombosis at an unusual site (such as the mesentery or cerebral venous)?

A

indefinite or lifelong anticoagulation is required

59
Q

when might anticoagulation be contraindicated? and what is the treatment options for these patients?

A

metastatic brain cancer with a high risk of bleeding or intracranial hemorrhage or they have a thrombocytopenia with high risk of bleeding; an inferior vena cava filter would be the least evil of all options

SBL (14 decks)

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