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Clin Path > Sample study guide > Flashcards

Sample study guide Flashcards

1
Q

What is the major regulatory enzyme thrombopoeiesis?

A

thrombopoietin (TPO)

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2
Q

Where does TPO come from and how does it work?

A

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.

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3
Q

What role do platelets play in hemostasis?

A

They are responsible for forming the platelet plug in primary hemostasis plug will support secondary hemostasis.

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4
Q

How is the primary hemostatic plug formed?

A

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

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5
Q

What laboratory tests do we use to access platelet concentration?C

A

A blood smear or a hematology analyzer.

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6
Q

When does spontaneous hemorrhage occur?

A

Less than 20,000ul of platelets.

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7
Q

When do you get possibly decreased platelet concentration on the analyzer (2 instances)?

A

When your platelets are too big or are clumped.

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8
Q

What laboratory tests do we use to access platelet morphology?

A

A blood smear or a hematology analyzer. (Blood is actual morphology, hematology analyzer does MPV

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9
Q

What does an increased MPV mean?

A

It is typical of thrombopoiesis.

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10
Q

What does the presence of macrothrombocytes suggest?S

A

Increase in platelet production

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11
Q

What are the tests used in the clinical setting to evaluate platelet function?

A

Leading tests (buccal mucosal bleeding time (BMBT) or cuticle (toenail) bleeding time)

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12
Q

What test do we use to access platelet production?

A

Bone marrow aspirate (BMA)

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13
Q

In a thrombocytopenic patient, how should healthy bone marrow respond?

A

It would respond by making more platelets.

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14
Q

What are your major mechanisms for thrombocytopenia? List 1 – 2 differentials for each mechanism.

  • Thrombocytopenia: (production, destruction, sequestration and loss or consumption = causes of)
A

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)

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15
Q

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?

A

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.

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16
Q

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?

A

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)

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17
Q

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

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.

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18
Q

What is the platelet with associated bleeding pattern?W

A

platelet bleeding vs coagulopathy bledding. plts are mucosal petechiations/hemorrhages and coagulopathies are widespread hemorrhages into body cavities etc etc.

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19
Q

Expression of which cofactor initiates coagulation?

A

Tissue factor

20
Q

Which factor drives amplification?

And which form factors does it affect?

A

Thrombin.

Effects factors Va, VII, VIIIa, XI

21
Q

What are the four vitamin K dependent factors?

A

II, VII, IX, X

22
Q

Which coagulation factor has the shortest half-life?

A

Factor VIII

23
Q

What are the three components that contribute to coagulation efficiency?

A

Calcium, platelet membrane, factor V.

24
Q

What cofactor is required for anti-thrombin to inactivate thrombin?

A

Heparin

25
Q

What are the two major end the products of fibrinolysis?

A

Fibrin degradation products (FDPs) and D-dimers

26
Q

How do you collect a sample for coagulation tests?

What tube do you use?D

A

Use a clean stick (?)

Use a sodium citrate tube.

27
Q

What are the two test that access the intrinsic/common pathway?
Which is more sensitive?
How do you interpret these tests (e.g. when is it abnormal)?

A

aPTT, ACT

aPTT is more sensitive (also more expensive)

it is abnormal when you have an extended/prolonged clotting time (70% deficient in factor XII, XI, IX, VIII)

*(ACT = 95% deficient)

28
Q

What is the one test that accesses the extrinsic/common pathway?
How do you interpret this test?

A

PT

It is abnormal when you have extended/prolonged clotting time (happens when you’re 70% deficient in factor VII)

29
Q

What 2 test do you use to access fibrinolytic activity?

How do you interpret this test?

A

quantitative kits for FDPs and D-dimers.

If you see FDPs that means you should look for DIC (pathologically increased) (see for both: increased fibrinolysis, severe internal hemorrhage with fibrinolysis, decreased clearance of FDP by liver). If you see an increase D-Dimers clot was broken down.

30
Q

What is the mechanism of warfarin toxicosis?
What type of bleeding pattern you expect?
How does the coagulation panel appear? (PLTs, BMBT, PT, PTT, FDPs)

A

Warfarin binds and prevents you 2 vitamin K enzymes from working which prevents your vitamin K dependent cofactors from being activated.

They are very easy to bleed. (Slide 39)

PT prolonged, aPTT/ACT prolonged, PIVKA positive, platelet count: usually normal

31
Q

What is the mechanism of DIC?
What type of bleeding patterns do you expect?
How does the coagulation panel appeared in the consumptive phase? (PLTs, BMBT, PT, PTT, FDPs)

A

Two phases: hypercoaguable phase (1st) (thrombosis, ischemic necrosis and organ dysfunction), consumptive phase (2nd) (consumption of platelets/coagulation factors/anti-thrombin, BLEEDING)

petechiation, ecchymosis, hematuria, G.I. bleeding, epistaxis, massive bleeding (platelet associated)

Thrombocytopenia (usually mild to moderate), prolonged PT/aPTT, decreased fibrinogen concentration, increased at FDP and D-Dimers, decreased anti-thrombin (AT). *(hemorrhagic anemia, schistocytes)

32
Q

Why might you get a coagulopathy in a patient with liver disease?
What 2 tests would you run prior to doing a liver biopsy?

A

The liver is responsible for making the coagulation factors and metabolism of dysfunctional factors. Therefore you will see a decrease in the synthesis of coagulation factors, and production of dysfunctional factors (failure to metabolize/reduce vitamin K).

The 2 tests are PT and aPTT

33
Q

What are the major blood systems in the dog?

A

DEA and Dal

34
Q

What are the most antigenic blood types in the dog?

A

DEA 1.1 and 1.2

35
Q

The dogs have naturally occurring isoantibodies?

A

No

36
Q

What blood type is not always expressed in Dalmatians?

A

Dal

37
Q

What are the major blood systems in the cat?

A

AB group system and Mik

38
Q

The cats have naturally occurring isoantibodies?

A

Yes

39
Q

Which feline blood type is associated with strong isoantibodies?

A

Type B (British hate Americans, but Americans don’t hate British (that much))

40
Q

What are the two most antigenic blood types in the horse?

A

Aa and Qa

41
Q

In a major cross match, what is tested in the recipient? The donor?

A

The recipient/patient has its serum tested with the donor’s blood.

42
Q

How do you interpret a cross match?

A

Interpreted by checking for hemolysis, and by checking for the agglutination.(Slide 69 – 72 for more information)

43
Q

What is a positive cross match? A negative cross match?

A

Negative: no agglutination or hemolysis = they are compatible and you can do a transfusion.

Positive: agglutination or hemolysis are detected = they are not compatible and you can’t do the transfusion.

44
Q

What is the general mechanism of the neonatal isoerythrolysis?

A

Mother after her first pregnancy will form anti-bodies to baby’s blood type. During second pregnancy anti-bodies from first pregnancy can end up in the colostrum of the mother’s milk if the baby at the same blood type as the first pregnancy. When the baby drinks the colostrum the anti-bodies attack the babies blood causing it to die.

45
Q

What is the general mechanism of acute hemolytic transfusion reactions?

A

Intravascular Hemolysis (blood cells are lysed) (slide 86 – 89)

46
Q

What is the general mechanism of delayed hemolytic transfusion reactions?

A

Extra vascular hemolysis (delayed) (slide 90)

Clin Path (4 decks)

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