Coagulation Studies Flashcards

1
Q

What test evaluates the INTRINSIC and COMMON pathways?

A

PTT or aPTT

Used to monitor unfractionated heparin

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2
Q

Test that evaluates the EXTRINSIC and COMMON pathway

A

PT

Used to monitor warfarin (Coumadin) therapy

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3
Q

What is INR

A

International Normalized Ratio

More accurate reflection of PT, calculated as a ratio of the patient’s PT to the control PT

Results are independent of reagents used

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4
Q

Goal INR is dependent on the …

A

Underlying need for anticoagulation

Examples:
Mechanical heart valves
Atrial fibrillation
VTE

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5
Q

What is considered the normal INR?

A

1

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6
Q

Target INR for prophylaxis

A

1.5-2.0

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7
Q

Target INR for VTE (DVT or PE)

A

2.0-3.0

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8
Q

Target INR in atrial fibrillation

A

2.0-3.0

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9
Q

Target INR for mechanical MITRAL valve

A

2.5-3.5

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10
Q

Target INR for mechanical AORTIC valve

A

2.0-3.0

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11
Q

What is the inhibitor screen

A

Aka mixing test

Coagulation factor deficiency vs inhibitor problem

Not as commonly used

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12
Q

What is the Thrombin Time test?

A

Measures the final step of coagulation, the conversion of fibrinogen to fibrin

Not used as an initial screen

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13
Q

Why would you measure Fibrinogen?

A

Low levels can result in impaired clot formation and increased bleeding risk

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14
Q

What is the D-Dimer test?

A

To RULE OUT a VTE

Lots of false positives so use for rule out only

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15
Q

When might you order a hypercoagulable panel

A

Umm, mostly never. It’s expensive. Use for looking for underlying disease, mostly genetic.

Components:
Antithrombin
Factor V-Leiden
Protein C
Protein S
Prothrombin gene mutation
Lupus anticoagulant (Anti-phospholipid antibodies)
MTHFR gene
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16
Q

Part of the hypercoagulable panel that might be positive in recurrent miscarriages

A

MTHFR gene - 5,10-methylenetetrahydrofolate reductase

Basically the motherfucker gene

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17
Q

Congenital coagulation disorders

A
Hemophilia A (Factor VIII deficiency)
Hemophilia B (Factor IX deficiency)
von Willebrand disease
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18
Q

Primary hypercoagulable disorders

A
Antithrombin deficiency
Protein C deficiency
Protein S deficiency
Factor V Leiden mutation
Prothrombin gene mutation
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19
Q

Examples of acquired platelet dysfunction

A

Drugs (chemo, abx), uremia, liver disease (cirrhosis), von Willebrand disease, Myeloproliferative disease

20
Q

How do you manage a patient with platelet dysfunction?

A

Treat the underlying cause!

Maybe a platelet transfusion

21
Q

What the heck is splenic sequestration?

A

Splenomegaly (hypersplenism) can lead to thrombocytopenia

For example, vascular congestion in cirrhosis

22
Q

Diseases that lead to destruction of platelets

A

Immune thrombocytopenia (ITP)

Disseminated intravascular coagulation (DIC)

Heparin-induced thrombocytopenia (HIT)

Thrombotic microangiopathies
• Thrombotic thrombocytopenic purpura
• Hemolytic Uremic Syndrome

23
Q

What is Heparin-Induced Thrombocytopenia?

A

New onset (acquired) thrombocytopenia/thrombus while on heparin

Anti-platelet antibodies cause platelet activation —> increased risk of venous and arterial thrombosis —> eventually leading to thrombocytopenia and prothrombotic states

24
Q

TTP and HUS are characterized by:

A

Thrombocytopenia due to the incorporation of platelets into thrombi in the microvasculature and microangiopathic hemolytic anemia (mechanical shearing of RBCs as they pass through platelet rich micro thrombi in the microvasculature)

25
Q

What is TTP

A

Thrombotic Thrombocytopenic Purpura

Medical emergency

F>M, more common in African Americans

Can be acquired or hereditary (ADAMTS-13 gene)

Causes microthrombi to form throughout body —> purpura/petechiae, pallor, jaundice, etc

26
Q

Pentad for TTP

A

Microangiopathic hemolytic ANEMIA

Thrombocytopenia

Acute kidney Injury (AKI) - uncommon

Neurological deficits

Fever

27
Q

Classic Hemolytic Uremic Syndrome

A

AKA: Shiga toxin-mediated HUS

Predominately occurs in children infected with Shiga-toxin producing E.coli O157:H7

Triad:
Microangiopathic hemolytic anemia
Thrombocytopenia
Acute Kidney Injury

28
Q

Lab findings in TTP and HUS

A

Microangiopathic hemolytic anemia
• Fragmented RBCs (Schistocytes - helmet cells)
• Increased LDH, Increased indirect bilirubin
• Low serum haptoglobin
• Negative Coombs test

Thrombocytopenia

PT and aPTT are normal

Acute kidney injury

29
Q

Treatment for TTP and HUS

A

Plasma exchange and supportive care

30
Q

Differentiating TTP and HUS

A

Both have microangiopathic hemolytic anemia (schistocytes etc) and thrombocytopenia

HUS is more likely to AKI but TTP can have it too

TTP has NEURO deficits, FEVER< and ADAMTS-13 link

HUS linked to E.coli O157:H7 infection

31
Q

Conditions in which there is an impaired production of platelets

A

Congenital bone marrow failure
Acquired bone marrow failure
Exposure to chemotherapy, radiation
Bone marrow infiltration (neoplastic, infectious)
Nutritional (Vit B12/folate/iron deficiency, alcoholism)

32
Q

Different anticoagulants

A

Unfractionated heparin (UFH) - IV
Low-molecular weight heparin (LMWH) - aka Lovenox, IM
Warfarin (Coumadin) - oral

Factor Xa Inhibitors (Arixtra, Xarelto, Eliquis, Savaysa, Lixiana)

Oral direct thrombin inhibitors (Pradaxa)

Direct oral anticoagulants (Rivaroxaban, Apixaban, Edoxaban, Dabigatran)

33
Q

Considerations when putting a patient on anticoagulation

A
Select of both INITIAL and LONG-TERM agent
Route
Renal function (no LMWH for CKD)
Antidote (easier with older drugs)
Contraindications (no UFH in pregnancy)

Others:
Cost, duration, compliance, guidelines, doing, follow up…

34
Q

Baseline labs to get before starting a patient on UFH?

A

aPTT, PT/INR
CBC

Maybe pregnancy test? UFH contraindicated in pregnancy

35
Q

Labs for monitoring a patient on UFH

A

aPTT or Factor Xa (newer method)

36
Q

Baseline labs for LMWH?

A

aPTT
PT/INR
CBC
Serum creatinine (to test kidneys - LMWH contraindicated in CKD)

37
Q

Labs for monitoring while on LMWH

A

Generally, none - it’s weight based dosage, so 1mg/kg 2x/day

If required, anti-factor Xa activity testing

38
Q

Recommended long-term anticoagulant for patients with DVT of the leg or PE and NO cancer:

A

DOACs are recommended over warfarin, warfarin is recommended over LMWH

39
Q

Warfarin inhibits the conversion of ____________ to active form.

A

Vitamin K

Depletion of vitamin K dependent clotting factors, along with inhibition of Protein C

40
Q

When do we use warfarin?

A

Prophylaxis and/or treatment of VTE

Inherited thrombophilia

Atrial fibrillation

Prosthetic heart valve

Stroke

41
Q

How do you START warfarin

A

Don’t need a “loading” dose - may increase hemorrhagic complications. And doesn’t offer more rapid protection

For most patients, warfarin should be initiated on day 1 or 2 of heparin (UFH or LMWH) at an initial dose of 5mg/day

Parental therapy should overlap with warfarin for AT LEAST 5 days and until INR is therapeutic for a minimum of 24 hours or 2 consecutive days

42
Q

How often to monitor INR for warfarin patients

A

Daily when starting, then weekly

Once stabilized at desired INR, every 2-4 weeks

Adjust warfarin dose as necessary

43
Q

Major meds that interfere with warfarin

A
Increased effect:
Acetaminophen
Aspirin
Cephalosporins
Ciprofloxacin
Diclofenac
Macrolide abx
Bactria

Decreased effect:
ORAL BIRTH CONTROL

44
Q

How to you manage a patient with supratherapeutic INR?

A

Reversal agents

Vitamin K (oral, SC, or IV)

Fresh frozen plasma (FFP)

Prothrombin complex concentrate (PCC)

45
Q

If INR is 4.5-10 and no evidence of bleeding?

A

Vitamin K not suggested. Just hold the warfarin.

46
Q

If INR >10 and no evidence of bleeding?

A

PO vitamin K

47
Q

Warfarin-associated major bleeding calls for…

A

Rapid reversal of AC with PCC as suggested rather than fresh frozen plasma

Vitamin K 5-10 mg IV should also be given