Sample study guide Flashcards
What is the major regulatory enzyme thrombopoeiesis?
thrombopoietin (TPO)
Where does TPO come from and how does it work?
It comes from the liver, bone marrow, and endothelium. It is caused by a decrease in platelet number and will cause the bone marrow to make more platelets.
What role do platelets play in hemostasis?
They are responsible for forming the platelet plug in primary hemostasis plug will support secondary hemostasis.
How is the primary hemostatic plug formed?
Platelets adhered to sub endothelium, then undergo activation (which includes shape change), then secrete their granules, and aggregate to form the platelet plug. (Look at slides 25, 27 – 28, 30 – 31 for more info on each step)F
What laboratory tests do we use to access platelet concentration?C
A blood smear or a hematology analyzer.
When does spontaneous hemorrhage occur?
Less than 20,000ul of platelets.
When do you get possibly decreased platelet concentration on the analyzer (2 instances)?
When your platelets are too big or are clumped.
What laboratory tests do we use to access platelet morphology?
A blood smear or a hematology analyzer. (Blood is actual morphology, hematology analyzer does MPV
What does an increased MPV mean?
It is typical of thrombopoiesis.
What does the presence of macrothrombocytes suggest?S
Increase in platelet production
What are the tests used in the clinical setting to evaluate platelet function?
Leading tests (buccal mucosal bleeding time (BMBT) or cuticle (toenail) bleeding time)
What test do we use to access platelet production?
Bone marrow aspirate (BMA)
In a thrombocytopenic patient, how should healthy bone marrow respond?
It would respond by making more platelets.
What are your major mechanisms for thrombocytopenia? List 1 – 2 differentials for each mechanism.
- Thrombocytopenia: (production, destruction, sequestration and loss or consumption = causes of)
loss/hemorrhage (acute severe hemorrhage = mild thrombocytopenia), consumption (DIC, vasculitis, viral infection), destruction (primary/idiopathic, secondary (drugs, viruses, sepsis, neoplasia)), decreased production (bone marrow hypoplasia, neoplasia, myelonecrosis or myelofibrosis), abnormal distribution (splenomegaly, hepatomegaly), pseudo-thrombocytopenia (Too big or clumped)
What are your two differentials for severe thrombocytopenia?
How do you differentiate between them on the CBC? hat lab test would you run to differentiate between them?
Destruction or decreased production.
Destruction will have a normal function test (you can’t tell the difference by a CBC.).
I would run a bone marrow aspirate (BMA), antiplatelet anti-body test.
What are the two major mechanisms of thrombocytosis?
What are the three diseases that may cause a reactive thrombocytosis?
What are three situations that may cause a reactive thrombocytosis?
Increased production or increased distribution in plasma.
Chronic inflammatory disease, IMHA,
rebounded from thrombocytopenia, post splenectomy, response to some drugs, excitement and exercise (splenic contraction)
What is the mechanism involved in von Willebrand disease (vWD)?
What changes would you see on a CBC?
Would you see a change in the bleeding time?
What test would you run to confirm vWD?
A defect in the adhesion molecule causing platelets not to adhere and float away (von Willebrand factor).
An increase in mature platelets (?).
You would see a prolonged bleeding time.
You would analyze the plasma for von Willebrand factor.
What is the platelet with associated bleeding pattern?W
platelet bleeding vs coagulopathy bledding. plts are mucosal petechiations/hemorrhages and coagulopathies are widespread hemorrhages into body cavities etc etc.