5. Coag 3 - Case Studies

Front 1

What are some vascular, nonhematologic causes of bleeding?

Back 1

TV SUV PETA
Trauma/surgery, Vasculitis,
Scurvy-Ulcer-Varices,
Polyps, Ehlers-Danlos,
Telangiectasia, Angiodysplasia

Front 2

What are 2 types of inherited coagulopathy?

Back 2

-von Willebrand disease
-Hemophilia

Front 3

What are 4 acquired coagulopathies?

Back 3

DIC
Anticoagulants
Hepatic failure
Vit K deficiency

Front 4

What are 2 causes of acquired thrombocytopathy?

Back 4

-Renal failure
-Drug effects

Front 5

What is an inherited cause of thrombocytopathy?

Back 5

Platelet function defect

Front 6

What is the disease in which there is a defect in the platelet receptor for vWF?

Back 6

Bernard soulier syndrome

Front 7

What is the platelet receptor for vWF?

Back 7

GPIb

Front 8

What is the disease in which there is a defect in the platelet receptor for fibrinogen?

Back 8

Glanzmann thrombasthenia

Front 9

What is the platelet receptor for fibrinogen?

Back 9

GPIIB/IIIa

Front 10

How common are Bernard soulier and glanzmann's thromasthenia?

Back 10

RARE

Front 11

What is a high D-dimer diagnostic for?

Back 11

Clot formation suggestive of deep vein thrombosis.

Front 12

What are the reasons for doing a PTT/PT in a case where thrombosis is suspected?

Back 12

1. PTT will be prolonged due to factor depletion
2. To establish a baseline for anticoagulant therapy

Front 13

What are 3 conditions that contribute to thrombosis?

Back 13

1. Endothelial injury
2. Hypercoagulability
3. Abnormal blood flow

Front 14

What do patients with DVT tend to have?

Back 14

Abnormal bloodflow

Front 15

What are 2 obstructions to bloodflow that predispose a patient to thrombosis?

Back 15

-Pregnancy
-Prior DVT which alters valves and veinous architecture

Front 16

What are 3 examples of hemostatic activation leading to hypercoagulable states?

Back 16

1. Sepsis
2. Neoplasm
3. Foreign bodies not put there by the creator

Front 17

What are 3 examples of damaged endothelium that predispose patients to thrombosis?

Back 17

-Inflammation
-Atherosclerosis
-Trauma

Front 18

What are the 2 categories of secondary hypercoagulable states?

Back 18

1. Disease related factors
2. Circumstantial factors

Front 19

What are the 5 circumstantial factors that cause 2ndary hypercoagulable states?

Back 19

1. Immobilization
2. Pregnancy
3. OCT
4. Obesity
5. AGE

Front 20

What are the 8 disease related factors that lead to 2ndary hypercoagulable states?

Back 20

PIPNMPNH

Front 21

What does PIPNMPNH stand for?

Back 21

Post op state
Immune
Post DVT state
Neoplasm/chemo
Myeloproliferative
PNH
Nephrotic syndrome
Homocysteinemia

Front 22

How does nephrotic syndrome cause a hypercoagulable state?

Back 22

The kidney leaks proteins that are needed for regulating coagulation.

Front 23

What are 3 conditions that are considered Primary Hypercoagulable states?

Back 23

1. Deficiency of Control Proteins (ATIII, Proteins C/S)
2. Factor V Leiden
3. Increased coag factor levels

Front 24

What does heparin work with?

Back 24

Antithrombin III

Front 25

What is the cooperative effect of Heparin/ATIII?

Back 25

Enhanced inhibition of Factors V and X, inhibiting activation of Thrombin.

Front 26

What normally turns on the Protein C/S inhibitory mechanism?

Back 26

Thrombin - it is a negative feedback loop

Front 27

What is the substrate for APC?

Back 27

Factor V - that's what gets inactivated.

Front 28

How do endothelial cells inactivate thrombin?

Back 28

Via Heparin-like molecules on their surface which cooperate with ATIII

Front 29

What is the cofactor necessary for Protein C to work?

Back 29

Thrombomodulin

Front 30

Where is thrombomodulin found?

Back 30

On the surface of endothelial cells

Front 31

What happens when thrombomodulin is bound by Thrombin?

Back 31

It activates Protein C which then proteolyses factors V and 8

Front 32

So what is APC resistance?

Back 32

Factor V leiden - it is mutated and so resistant to APC.

Front 33

What is the cofactor for APC?

Back 33

Protein S

Front 34

Why is the Lupus Anticoagulant a misnomer?

Back 34

Because when present it is actually in a HYPERcoagulative state.

Front 35

What is the lupus anticoagulant?

Back 35

An Antiphospholipid Antibody

Front 36

Is Antiphospholipid Antibody syndrome acquired or inherited?

Back 36

Acquired

Front 37

What are 2 clinical symptoms of Antiphospholipid Antibody syndrome?

Back 37

-Venous and/or arterial thrombosis
-Recurrent fetal wastage

Front 38

What does the Antiphospholipid antibody bind?

Back 38

Phospholipid binding proteins - the vit K dependent factors.

Front 39

What will be falsely positive in antiphospholipid syndrome?

Back 39

Syphilis test for anticardiolipin

Front 40

What is the serologic test that you order to detect Antiphospholipid antibody?

Back 40

Anti-beta2GP1

Front 41

What are the lupus anticoagulant test?

Back 41

Doing the PT/PTT to test for the inhibitor.

Front 42

What is the diagnostic result that will show a lupus anticoagulant?

Back 42

Failure of the mixing study to correct, but correction when lots of phospholipid is added to the test.

Front 43

Why doesn't the antiphospholipid antibody result in a anticoagulant state in the body?

Back 43

Because there are loads of phospholipid in the body, and it overwhelms the antibody so it has no effect physiologically.

Front 44

Why is the patient often hypercoagulable in antiphospholipid syndrome?

Back 44

Because it is an autoimmune disease.

Front 45

What is the more specific mixing test to detect lupus anticoagulant?

Back 45

dRVVT

Front 46

What is dRVVT?

Back 46

dilute Russel Viper Venom test

Front 47

Why is dRVVT used for lupus anticoagulant?

Back 47

Because the viper venom activates factor 10 and only the common cascade, more specific.

Front 48

What are 2 conditions that are associated with both arterial and venous thrombosis?

Back 48

-Homocysteine
-APLA syndrome

Front 49

What is the clinical manifestation of APCR?

Back 49

Venous thrombosis

Front 50

What is Prothrombin Gene?

Back 50

A mutation that results in increased levels of prothrombin

Front 51

What is the clinical manifestation of Prothrombin Gene mutation? Why?

Back 51

Venous thrombosis - because there's more thrombin activated by normal clotting cascades.

Front 52

Why does homocysteinuria cause arterial and venous thrombosis?

Back 52

Because elevated levels of homocysteine makes EC's unhappy.

Front 53

What does arterial thrombosis normally show up as?

Back 53

Myocardial infarction.

Front 54

What is DIC akin to?

Back 54

Running your car in neutral - you chew up a lot of gas (fibrinogen) and produce a lot of exhaust (d-dimers)

Front 55

So what tests will be abnormal in DIC?

Back 55

-Platelets low
-PT and PTT prolonged
-Fibrinogen low
-Ddimer pos

Front 56

What will DIC present as?

Back 56

EITHER
-Bleeding
or
-Clotting

Front 57

What is the typical setting in which bleeding will be seen?

Back 57

IV's

Front 58

What is the typical setting in which clotting will be seen?

Back 58

Meningococcal meningitis

Front 59

What are the consequences of DIC?

Back 59

-Disturbed hepatic function
-Release of cardiac enzymes due to ischemia
-Altered mentation
-Renal insufficiency
-ARDS, Adrenal infarct, GI bleeds, and skin symptoms

Front 60

How is DIC treated?

Back 60

TREAT THE UNDERYLING CAUSE!!!

Front 61

What is the replacement therapy for decreased fibrinogen?

Back 61

Cryo

Front 62

What is the replacement therapy for decreased coag proteins and anticoag proteins?

Back 62

FFP

Front 63

What is the replacement therapy for thrombocytopenia?

Back 63

Platelet concentrates

Front 64

What is the treatment for patients in thrombosis?

Back 64

Anticoagulant