Hemostasis I

Question 1

Primary Hemostasis

Answer 1

• Damage to endothelium of blood vessel
• vWF and GP1a released from collagen causing platelets to adhere
• Platelets are stimulated to release ADP, TxA2, vWF recruiting more platelets= platelet plug

Question 2

What factors are involved in the intrinsic pathway of secondary Hemostasis?

Answer 2

XII, XI, IX, VIII

Question 3

Clinical signs of primary Hemostasis vs Secondary Hemostasis?

Answer 3

Primary: Petechia, Echymosis
Oozing from mucosal sites (oral cavity, nose, bladder, GI)

Secondary: bleeding in the body cavity, large sq hematomas

Question 4

How low are plts when we start to worry about spontaneous bleeding/hemorrhage?

Answer 4

10,000

Question 5

Breed differences that can be normal (but look like plt disorders)

Answer 5

CKCS- macro thrombocytopenia

Greyhounds- slightly lower plt counts

Question 6

How low are plts when we start to get concerned?

Answer 6

30,000

Question 7

What tests can we use to Dx to assess Primary Hemostasis? What are the normal values?

Answer 7

BMBT

Dog-

Question 8

Rapid point of care test used to assess secondary Hemostasis? Adv vs Disadvantages?

Answer 8

Activated clotting time (diatomaceous earth or kaolin activates fXII)

Adv: inexpensive and easy
Dis: only assessing intrinsic pathway,

Question 9

Tests available at larger hospitals/commercial labs to assess secondary Hemostasis?

Answer 9

PT, aPTT, fibrinogen, FDPs and D dimers

PT and aPTT asses common pathway

Question 10

What are some reasons for thrombocytopenia (primary Hemostasis disorder)

Answer 10

Bone marrow dz (not generating enough) 
Bleeding/loss
Sequestration- spleen probs 
Consumption- DIC 
Destruction/immune mediated - severe thrombocytopenia

Question 11

Bone marrow Dz causes, dx, tx

Answer 11

Causes: neoplasia, myelosuppressive drugs (chemo), drug rxns (chloramphenicol, estrogen), immune destruction at the level of a precursor
Dx: bone marrow sampling
Tx: eliminate the underlying cause

Question 12

ITP, what is it, plt count, causes

Answer 12

Accelerated destruction of platelets by the immune system

- Platelet count usually

Question 13

Causes of secondary ITP

Answer 13

• Rickettsial Diseases
• Vaccines/Medications – within the past 30 days
• Manifestation of systemic lupus erthematosus
• Secondary to neoplasia (high grade lymphoma, hemangiosarcoma, others

Question 14

Additional diagnostics (other than plt count) for ITP?

Answer 14

-Antiplatelet Antibody Testing (limited availability)
Evaluates for platelet associated Ab’s
Does NOT discern between primary or secondary IMTP
Turn around time: 24-48 hours

-Antinuclear Antibody
One of the tests used to screen for SLE

Question 15

What rickettsial dz’s may play a role in ITP

Answer 15

Ehrlichia canis
Ehrlichia platys
Anaplasma phagocytophilum
Rocky Mountain spotted fever

Question 16

Tx for ITP

Answer 16

Glucocorticoids (cornerstone of therapy)
Vincristine
Human Immunoglobulin
Mycophenolate

Azathrioprine
Cyclosporine
Leflounomide

Question 17

Acute management of ITP if normal PCV

Answer 17

Doxy
Pred
Gastroprotectancts
Cage rest
No jug sticks
Monitor PCV BID and plt count every 1-2 hours
Pt stable/released once unlikely to bleed/need blood production (PCV > 15,000-20,000)

Question 18

Acute management of unstable ITP pt

Answer 18

Marked concurrent anemia 12-15%) while awaiting plt count increase (5-7 days)- multiple transfusions may be needed

Vincristine
Human IVIG

Question 19

How do glucocorticoids help with ITP

Answer 19

At immunosuppressive doses:
-downregulate Fc receptor expression on macs
- decrease Ig affinity for red blood cell
- suppress T cell function
- induce apoptosis of T cells
- B cell Ab production may be inhibited
Results in phagocytosis

Question 20

How does vincristine work for ITP

Answer 20

Premature release of plts from marrow

Question 21

How does human IVIG work for ITP?

Answer 21

Temporary blockade of Fc receptors of phagocytes

Question 22

How does Mycophenolate mofetil work for ITP?

Answer 22

Inhibits inosine-5’-monophosphate
dehydrogenase (enzyme resp for synth of guanosine nucleotides); high levels in activated lymphocytes
-Leads to depletion of guanosine
-Rapid onset of action (2-4 hours for max
enzyme suppression)

Question 23

What does long term monitoring for ITP look like?

Answer 23

Continue prednisone at immunosuppressive dose until platelets are normal for 2 weeks.
-If no response in a stable patient within 7-14 days add another immunosuppressant (mycophenolate, other)

• Taper prednisone over 2-4 months once platelets are normal (25% reduction every 2 weeks)
• Recheck platelet counts while tapering prednisone (ie every 2 weeks)
• If there is a decrease in platelets -> increase prednisone