Hem/Onc Physiology Flashcards

1
Q

What isotype are Anti-A, Anti-B, and Anti-Rh(D)

A

A and B are IgM

Anti-Rh(D) is IgG (can cross placenta and cause erythroblastosis fetalis)

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2
Q

Hemophilia A

A

Factor VIII

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3
Q

Hemophilia B

A

Factor IX

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4
Q

XIIa effects

A

Aside from the intrinsic pathway action of converting XI to XIa. It also turns Prekallikrein to kallikrein which converts plasminogen to plasmin and HMWK to Bradykinin.

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5
Q

What is HMWK

A

High molecular weight kininogen, which activates formation of XIIa

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6
Q

Bradykinin effects

A

Kinin cascade leads to increased vasodilation, permeability, and pain.

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7
Q

Plasmin does what

A

Breaks down fibrin clot and also turns C3 to C3a for complement cascade

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8
Q

How to think about the coagulation cascade

A

Extrinsic is simple: It’s 7 turned to 7a by tissue factor (thromboplastin) which activates 10.
Intrinsic: Collagen, basement membrane, and activated platelets turn 12 to 12a. Which forms 11 a, then 9a. 9a activates 10. You already know that 8 and 5 are components needed for the activation of the other stuff. Finally 10 activates 2 (prothrombin). 13 is at the end of it all and makes the clot super strong.

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9
Q

Difference in factors between PT and PTT

A

PT: 7–10–2–5
PTT: 12, 11, 9, 8, 10, 5, 2 (everything except 7)

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10
Q

Why does heparin only affect PTT

A

Is it that it affects everything in the intrinsic pathway?

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11
Q

ACE affect on bradykinin

A

Inactivates it

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12
Q

Vitamin K pathway

A

Oxidized vitamin K is reduced by Epoxide Reductase which matures II, VII, IX, X, C, and S.

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13
Q

Warfarin MOA

A

inhibits vitamin K epoxide reductase

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14
Q

What does vWF carry

A

VIII

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15
Q

Antithrombin does what

A

Primary targets are thrombin and factor Xa. Inhibits activated forms of factors 2, 7, 9, 10, 11, and 12

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16
Q

Factor V leiden

A

Can’t be inhibited by activated protein C

17
Q

Warfarin necrosis MOA

A

starting warfarin makes you acutely hypercoagulable because protein C has a very short half life, which can lead to the skin necrosis

18
Q

Protein C activation

A

Thrombin-Thrombomodulin complex. The activated protein C uses Protein S as a cofactor to cleave and ianctivate Va and VIIIa.

19
Q

Fibrinolysis does what

A

Destruction of coagulation factors

20
Q

Primary hemostasis pathway

A
  1. vWF binds to exposed collagen upon endothelial damage.
  2. Platelets bind vWF via GpIb receptor and release ADP and Ca2+
  3. ADP helps platelets adhere to endothelium. Also binding to ADp receptor induces GpIIb/IIIa expression at patelet surface.
  4. Fibrinogen binds GpIIb/IIIa receptors and links platelets
  5. Plug stops bleeding
21
Q

Pro-aggregation factors

A

TXA2 (released by platelets)
Decreased blood flow
Inc. platelet aggregation

22
Q

Anti-aggregation factors

A

PGI2 and NO (released by entothelial cells)
Inc. blood flow
Dec. platelet aggregation

23
Q

Aspirin MOA

A

inhibits cyclooxygenase (TXA2 synthesis)

24
Q

Clopidogrel MOA

A

irreversibly blocks ADP receptor. inhibits ADP-induced expression of GpIIb/IIIa

25
Q

Ticlopidine MOA

A

Same as clopidogrel

26
Q

Abciximab MOA

A

inhibits GpIIb/IIIa directly

27
Q

Ristocetin MOA

A

activates vWF to bind to GpIb. Used to diagnose von Willebrand disease. Normal platelet aggregation response not seen in vWD.

28
Q

GpIIb/IIIa MOA

A

It literally crosslinks two platelets together by finding a fibrinogen monomer.

29
Q

Bernard-Soulier syndrome

A

GpIb deficiency

30
Q

Glanzmann thrombasthenia

A

GpIIb/IIIa deficiency

31
Q

COX MOA

A

turns arachidonic acid to TXA2

32
Q

Platelets have what

A

vWF and fibrinogen

33
Q

How does acute phase reactants increase ESR

A

Fibrinogen causes RBC aggregation

34
Q

ESR elevated diseases

A

Infectious, autoimmune, malignant neoplasms, GI disease (ulcerative colitis), pregnancy

35
Q

ESR decreased diseases

A

Polycythemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia