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D&D, BL Unit III > Feb 27, Clotting, Immunohematology > Flashcards

Feb 27, Clotting, Immunohematology Flashcards

1
Q

Platelet growth factor?

A

Thrombopoietin

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2
Q

Three phases in coagulation of an acute injury:

A

Adhesion, Activation, Aggregation

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3
Q

What binds both platelets and factor VIII in acute injury?

A

VWF

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4
Q

What molecule does VWF actually grab onto?

A

Glycoprotein 1B

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5
Q

What does ADP and Ca2+ signalling do within the platelet?

A

Signals for more activation, release of granules, serotonin

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6
Q

What does aspirin inhibit?

A

Arachadonic acid

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7
Q

Arachadonic acid acitivates ________ which activats _____, which induces platelet synthesis/release

A

Prostaglandin H2 (PGH2), Thromboxane (TXA2)

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8
Q

Which three molecules actually build the fibrinogen meshwork?

A

VWF, Platelets, and Fibrin

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9
Q

What is the mechanical cause of EDTA Pseudothrombocytopenia?

A

Clumping of poorly-made platelets. (CBC machine counts clumps as RBC’s)

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10
Q

One disorder you should always keep in mind for pancytopenia/thrombocytopenia?

A

MDS

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11
Q

Toxic Granulation

A

decreased PLT ct, with pinkish WBC cytoplasm, indicates a bacterial or viral infection

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12
Q

Immune Thrombocytopenia Post-Infection

A

Change in immune system leading to low PLT ct. (HIV, HepC, chronic EtOH use)

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13
Q

What do you see on smear with chronic EtOH abuse?

A

decreased PLTs, acanthrocytes, target cells (will also see internal bleeds ex. esophageal varices)

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14
Q

Immune Thrombocytopenia Purpura (ITP)

A

Body makes Ab to PLTs. Pt has easy bleeds/bruising with a decrease in PLTS only - no other WBC disorders

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15
Q

How to treat Immune Thrombocytopenia Purpura (ITP)?

A

Splenecomy, steroids, rituximab, IV IgG

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16
Q

VonWillebrand Disease/Disorder

A

No attachment of Factor VIII to VWF - leads to severe bleeds

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17
Q

Three types of VonWillebrand Disease/Disorder:

A

I: not enough VWF
II: VWF doesn’t fxn properly
III: no VWF at all

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18
Q

What does DDAVP do?

A

Increases the functionality of existing VWF

Tx for type I VW disease

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19
Q

How do you treat type II or III VW disease?

A

Factor VIII replacement therapy

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20
Q

Heparin artificially prolongs PTT or PT?

A

PTT

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21
Q

DDx for a long PTT?

A

x-linked hemophilia, heparin OD, Factor XI deficiency, VW disease, excess fibrinogen

22
Q

DDx if PT is more prolonged that PTT?

A

Liver disease, vit K deficiency, Warfarin OD, factor VII hemophilia

23
Q

DDx if PTT is more prolonged than PT?

A

DIC! sepsis!

24
Q

How does mixing Pt plasma and donor plasma detect inhibitors causing thrombosis?

A

The mixture will not correct the thrombosis

25
Q

What is the Pt prone to with Antiphospholipid Syndrome?

A

Both venous and arterial thromboses (liver disease, migranes)

26
Q

How do you confirm a Lupus Anticoagulant?

A

With RVVT the Russel Viper Venom Test - it activates Factor X

27
Q

What enzyme adds an A or B allele sugar onto RBC antigens?

A

Glycosyl transferase

28
Q

What does the RHD gene do?

A

Makes Rh factor (D/d)

29
Q

What is Hemolytic Disease of the Newborn?

A

When a Rh(-) mom has a Rh(+) firstborn, immunizing her against another Rh(+) baby. Will kill the second fetus

30
Q

What is given to pregnant mothers to disallow Hemolytic Disease of the Newborn?

A

Rhogam! (IgG Ab to Rh(+) from male volunteer donors)

31
Q

What is deficient in Bombay Blood types? What blood type are these Pt’s usually accidentally categorized with?

A

Glycosyl transferase - usually test as blood type O with questionable lab results

32
Q

What happens if you give a patient the wrong blood type in transfusion?

A

Intravascular RBC lysis, causing crystals to form in the glomerulus, leading to acute renal failure

33
Q

What do the Coombs tests actually test for?

A

Antiglobulins (Autoimmune)

34
Q

Direct Coombs procedure?

A

Take washed RBCs from suspect Pt, add the coombs Ab since it will bridge the Pt’s IgG’s that are attached to RBC’s - causes agglutination if +

35
Q

Indirect Coombs procedure?

A

Add susptect Pt’s serum to donor RBCs with needed antigen (ex: Rh- Pt serum with Rh+ RBC’s), add coombs Ab to see if it agglutinates

36
Q

What does a + Direct Coombs test imply?

A

The + agglutination implies that there is an AUTOIMMUNE Ab issue

37
Q

What Ab is present on RBC’s to detect different blood types? Why this kind of Ab?

A

IgM - since the A, B, O sugars are indeed carbohydrates that require the branching IgM Ab for detection

38
Q

What does heparin do?

A

It induces AT3 action - increases natural anti-coagulation

39
Q

What does Warfarin do?

A

It inhibits vit K oxyreductase, disallowing the recycling of vit K to II, VII, IX, XI

40
Q

What is AT3?

A

A serine protease inhibitor that deactivates Factors X and IIa

41
Q

How many saccharides are needed at least to inhibit Factor IIa with AT3? Factor X?

A

18 saccharides - IIa

15 saccharides - X

42
Q

Would you give a pregnant woman Heparin or Warfarin?

A

Heparin

43
Q

Which acts faster, heparin or warfarin?

A

Heparin

44
Q

What do you give if a Pt OD’s on Heparin?

A

Protamine Sulfate (neutralizes the + charge of heparin)

45
Q

Which medical issues indicate a need for daily Warfarin use?

A

PMH of stroke, DVT, recurrent MI’s, etc.

46
Q

Besides warfarin, what are some other noteworthy oral anticoagulant drugs?

A

Pradexa, Eliquis, Xarelto

47
Q

What are some derivatives of heparin?

A

Lovenox (low m.w. heparin)

Fondaparinux (synthetic pentasaccharide heparin)

48
Q

What do fibrinolytic agents do? When do you use them?

A

Lyses clots right after they form - activates tPA’s. Use only in emergency situations only

49
Q

Example of a fibrinolytic agent?

A

Alteplase

50
Q

What do anti-PLT drugs mechanically do?

A

Inhibit PLT production of TXA2 (ASA)
Block the ADP receptor needed to activate PLTs (Plavix/Clopidogril)
Block GPIIb/IIIa to stop fibrinogen cross-linking

51
Q

Examples of anti-PLT drugs?

A

Aspirin, Clopidogril (Plavix)

52
Q

Which two molecules are crucial for successful fibrinogen cross-linking?

A

GPIIb and GPIIIa

D&D, BL Unit III (10 decks)

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