Thrombocytopenic Disorders Flashcards

1
Q

what are risk factors for thrombosis?

A
  • hereditary or acquired thrombophilic defects
  • malignancy, inflammation, autoimmunde disorders
  • surgery, inactivity, travel,
  • hormonal effects
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2
Q

signs and symptoms of DVT/PE?

A
  • Unilateral extremity swelling, pain, redness, warmth
  • shortness of breath
  • cough
  • hemoptysis
  • chest pain due to lung infarcts
  • may be hypoxic and/or tachycardic
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3
Q

what are tests that can be done for DVT/PE?

A
  • D-dimer: all patients with clinically thrombosis will have D-dimer (very sensitive, but not specific at all)
  • CT angiography: used for people you think has PE; diagnotic test of choice for positive D-dmer and appropriate clinical probabilty
  • ventilation/perfusion (V/Q) scans: sensitive but not specific (anything that alters profusion would affect)
  • venogram is gold standard for DVT but has dye loadn and risk of clot. NOT used in most clinical settings
  • Doppler US
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4
Q

what should you use if someone has a high probability of DVT/PE

A

doppler US
CT angiogram, MR angiogram

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5
Q

what immediate therapy should be considered for a patient with DVT/ PE?

A
  • Consider embolectomy or thrombolytic therapy in unstable patient or cases of RH strain (catheter directed thrombolysis)
  • Vena Cava Filter: PE/proximal DVT in someone who has contraindication to anticoagulation
  • anticoagulation (UFH, LMWH, Fondaparinux, DOAC) should be started immediately (will not breakdown clot but prevent more)
  • DOACS are mainly used
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6
Q

what are examples of provoked DVT? how long would you treat a transient risk factors? persistent risk factors?

A

Provoked: surgeries, long flights, car rides over 4 hours, cancers, inflammatory dieseases pregnancy

transient risk factor: treatment for 3 months
persistent major risk factor: indefinite

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7
Q

unprovoked DVT/PE treatment

A
  • Unprovoked DVT: single episode: at least 3 months, risk benefit discussion re:indefinite
  • Unprovoked PE: indefinite
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8
Q

recommendation for hereditary thrombophilia or APLA with no VTE

A

No medications- doesn’t change anything

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9
Q

What are considered unusual sites for thrombophilia?

A

hepatic, or mesenteric veins, saggital sinus
NOT upper extremities or catheters

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10
Q

what conditions are considered Hereditary thrombophilias?

A
  • Factor V leiden
  • Protrombin Gene mutation
  • Proctein C deficiency
  • Proteins S deficiency
  • antithrombin III deficiency

protein C&S and antithrombin III deficiency highest risk of clots

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11
Q
  • hereditary resistance to activated protein C
  • defect in factor which renders it unable to be degrated by protein C
  • screen with activated protein C resistance test
  • confirm with genetic analysis for factor mutation
  • only associated with venous thrombois
A

Factor V leiden

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12
Q

inhibits clotting factors
* inherited or acquired
* inherited is autosomal dominnat
* deficiency increaes risk of venous thrombosis 30 fold

A

Antithrombin III

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13
Q
  1. what is a strong indepedent predictor of recurrence risk, and so is a potential indication for long term anticoagulation?
  2. the presence of this is not a good predictor of VTE recurrence risk and so chould not generally be used for the basis of proloning therapy?
A

1.) Idipathic VTE
2. the presence of inherited thromobphilia

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14
Q
  • antibodies directed against phospholipid-protein complexes on plasma membranes
  • acquired condition
  • may be primary or secondary
  • associated with: venous thrombosis, stroke, early onset dementia, migraines, fetal loss
A

antiphospholipid antibody syndrome (APLA)

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15
Q

Treatment of APLA

A
  • immunosupression does not decrease risk of thrombosis
  • venous thrombosis: warfarin
  • warfarin refractory: LMWH
  • pregnancy with hx of thrombosis: LMWH
  • Pregnancy w/o thrombosis: prophylactic LMWH +ASA
  • throbocytopenia: steroids, IVIG, anti D
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16
Q
  • incompletely understood but principle mechanism is that patient develops autoantibody against platelet membrane glycoproteins such as GIIb/IIIa
A

Immune thrombocytopenias purpura (ITP)

17
Q
  • Most common in chidhood typically following viral infection
  • self limited, usually mild
  • no systemic illness, well appearing pt
  • mucosal or skin purpura, epistaxis, oral bleeding
  • no spontaneous hemarthroses
  • normal bone marrow biopsy or megakaryocytic hyperplasia
    *also common in women
A

ITP

18
Q

treatment of ITP

A
  • In children with no bleeding or mild bleeding not at risk: observation
  • in adults: corticosteroids (prednisone, dexmethasone) 1st line- IVIG second line and (rituximab &splenectomy if refractory)
19
Q
  • flu-like illness as predrome
  • age 20-40, female> male
  • pentad (FAT RN): Fever, anemia (microangiopathic hemolytic anemia) thrombocytopenia, renal insufficiency, Neurologic status changes
A

TTP

20
Q

cause and treatment of TTP?

A

acquired- antibody that attack proteases ADAMTS13
hereditary- deficiency of proteases ADAMTS13

Treatment
* untreated is rapidly fatal
* steroids
* FFP replenishes ADAMTS13 for hereditary;
* plasma exchange
* rituximab

21
Q
  • triad of renal failure, microangiopathic hemolytic anemia and thrombocytopenia

typical
* seen in children after prodrome of diarrhea (certain strains of E.coli infection with shiga toxin which is reportable)
* 40% will have neuro involvement, often seizures
* many will have long term renal damage, but most recover some renal function
* treated with conservative measures (steroids, FFP)

A

Hemolytic Uremic Syndrome (HUS)

22
Q
  • inappropriate activation of thrombin (factor IIa)
  • leads to activation of clotting system which depletes clotting factors and platelets (dysregulation)
  • can be acute or chronic

caused by
* sepsis
* severe trauma/burns
* pregnancy complication (retained placenta)
* cancer
* liver disease

A

Disseminated intravascular coagulation (DIC)

23
Q

what labs would you expect to see in DIC?

A

prolonged PT, PTT
decreased platelets
low fibrinogen