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Heme > Hemostasis overview/approach to bleeding D/O > Flashcards

Hemostasis overview/approach to bleeding D/O Flashcards

1
Q

What keeps blood flowing w/ hemostasis?

A

Counter regulatory mechanisms to clotting.

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2
Q

Blood vessels damaged internally or externally begins? What phases?

A

Clot formation

  1. Vascular wall
  2. Platelets
  3. Coag cascade
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3
Q

Vascular phase of hemostasis is?

A

The cutting/damage of BVs result in - Vascular spasms (V-con) of smooth muscle.

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4
Q

How long does the vascular response last?

A

Lasts up to 30m

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5
Q

Platelet phase of hemostasis is?

A

Damaged endothelial cells w/in BVs release VWF > makes endothelial surface sticky >
Platelets stick to endothelial (AKA platelet adhesion) >
Adhered PLTs secrete ADP/Thromboxane>
ADP is converted Adenosine (inhibiting activation more)

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6
Q

Thromboxane is?

A

A powerful vasoconstrictor released by PLTs adhered to endothelial surfaces

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7
Q

Purpose of ADP is?

A

ADP causes PLT aggregation by activating Glycoprotein IIb/IIIa receptor to accept fibrinogen > and fibrinogen in turn forms bridges inbetween PLTs >
Forming a PLATELET PLUG

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8
Q

What drugs inhibits P2Y12 ADP receptors?

A

Clopidogrel
Ticagrelor
Prasugrel

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9
Q

P2Y12 ADP receptors inhibitors cause what to happen?

A

Reduces plt activation and aggregation

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10
Q

Glycoprotein IIb/IIIa receptor cause what to happen?

A

Binds fibrinogen > final common location for plt2plt aggregation

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11
Q

Glycoprotein IIb/IIIa inhibitors are useful for? Rx names?

A

ACS - providing anticoagulant effect

    • Abciximab
    • Tirofibran
    • Eptifibatide
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12
Q

Coagulation phase of hemostasis begins when?

A

30seconds to Several minutes after Vascular/plt phases

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13
Q

Coagulation phase overall is?

A

Formation of insoluble protein Fibrin from Fibrinogen through enzyme Thrombin actions.

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14
Q

Fibrins causes?

A

A network of fibers which traps blood cells to form a thrombus (Clot)

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15
Q

Coagulation phase depends on?

A

Coagulation cascade (11 clotting factors(proteins) + calcium (F-4))

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16
Q

Final step of coagulation phase (cascade)?

A

Thrombin generation turns fibrinogen to form fibrin

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17
Q

Intrinsic and extrinsic coag pathway both result in?

A

Prothombin activator (F-X)

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18
Q

Calcium + Factor X causes?

A

Prothrombin > Thrombin

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19
Q

Fibrin clot occurs to the combination of?

A

Fibrinogen + fibrin monomers + calcium + fibrin stablizing factors (F XIII)

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20
Q

Extrinsic pathway is initiated by?

A

Exogenous trigger > Tissue factor (thromboplastin)

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21
Q

Tissue factor timeframe?

A

w/in 12-15s due to chemical shortcut

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22
Q

Extrinsic process 6

A

Damaged tissue >
Tissue factor (thromboplastin) F-3 >
Activates F7 to form F7a >
Activates F10 to form F10a (req calcium) >
FXa + F5a convets prothrombin to thrombin >
Thrombin converts Fibinogen to Fibrin >
Common pathway

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23
Q

Intrinsic pathway is initiated by?

A

Blood contact w/ exposed collagen INSIDE the BV wall

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24
Q

Intrinsic pathway timeframe?

A

Considerably slower (5-10m)

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25
Q

Intrinsic pathway process?

A

Exposed collagen of endothelial wall + F12 = F12a >
F12a activates F11 to make F11a >
F12a + F11a jointly activates F9 to make F9a
F9a + activated F8/F8a + Ca2+ activates F10 = F10a >
F10/F10a + F5a converts prothrombin to thrombin >
Thrombin converts Fibrinogen to fibrin >
Common pathway

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26
Q

Coagulation common pathway process

A

-F10 activation to Fibrin = common pathway-
Enzymatic process w/ F10 activation to F10a >
F10 engages w/ F5, Ca2+, phospholipids from PLTs >
F5 complex > Prothrombin to thrombin conversion
Thombin accelerates Fibrinogen (F1) > fibrin forms

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27
Q

F10 engages w/ what to form what?

A

F10 engages w/ F5 + Ca2+, PLT phospholipids to form a complex called F5 complex AKA prothombinase

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28
Q

3 stages of coagulation are?

A
  1. Extrinsic or intrinsic pathway leads to prothombinase
  2. Prothombinase converts prothrombin > Thombin
  3. Thombin converts Soluble fibrinogen into insoluble fibrin creating a clot
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29
Q

Coagulations factors are produced where? Except?

A

Produved in liver (except vWF)

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30
Q

Which factors are vit-k dependent?

A

F2, F7, F9, F10, Protein C/S

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31
Q

Which coafulation factors are naturally-occuring anti-coagulants?

A

Protein C/S

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32
Q

What is Coumadins MOA?

A

Inhibits Vitamin K dependent factors (transient Protein C deficit occurs faster than coagulation factors deficit = why heparin is req to overlap)

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33
Q

Factor I is?

A

Fibrinogen

34
Q

What happens if Fibrinogen is depleted?

A

Severe bleeding complication esp. in context w/ DIC

35
Q

What produces the majoirty of vWF?

A

Blood vessel endothelium

36
Q

BV endothelium provides what?

A

A surface which to bind to

37
Q

vWF fx?

A

Binds to stabilize F8

Mediates PLT aggregation

38
Q

What factors exists as a complex w/in the plasma?

A

vWF and F8

39
Q

a vWF deficit (Von Willibrands Dz) can lead to?

A

A defect involving both…

  1. PLT dysfx - (Unable to form plug)
  2. Coag Dysfx - (Unable to stabilize F8)
40
Q

What is a F8 deficit known as?

A

Hemophilia A

41
Q

What is F4?

42
Q

Antithrombin III is a?

A

Normal circulating plasma protease inhibitor

43
Q

Purpose of ATIII?

A

Inhibits thrombin activity (PVT excessive thrombosis)

44
Q

How is AT III activated?

A

Binds heparin to cause conformation change leading to increased inhibition of thrombin

45
Q

PT lab test measures?

A

Activity of proteins w/in extrinsic pathway

46
Q

How is PT coag test performed?

A

adding thromboplastin to plasma and waiting for fibrin formation.

47
Q

PT coag test detects what deficiencies?

A

F2, F5, F7, F10 and fibrinogen

48
Q

NL value of PT coag test?

A

10-14 seconds

49
Q

PT and PTT stands for?

A 
PT = Prothrombin time
PTT = Partial Thromboplastin Time
50
Q

PTT measures?

A

The activity of proteins w/in the intrinsic pathway

51
Q

How is PTT performed?

A

By artifical stimulation of F12

52
Q

PTT test will detect deficiencies in?

A

F2, F5, F8, F9, F10, F11, F12 and fibrinogen

53
Q

NL PTT lab value is?

A

25-40 seconds

54
Q

INR stands for?

A

International normalized ratio

55
Q

INR is a?

A

calculation based on pt’s PT used to assess extrinsic pathway

56
Q

What type of correlation does INR have w/ PT?

A

Direct correlation

57
Q

NL INR value?

58
Q

NL PLT value?

59
Q

PLT may be falsely low due to?

A

Clumping - typically mediated by immunologic sensitivity to EDTA (pseudothrombocytopenia)

60
Q

Falsely low PLT count per CBC can be confirmed and evaluated w/?

A

Blood smear

61
Q

Mixing study is?

A

1:1 mix of ABNL serum w/ NL serum to determine the possibility of a Factor deficits VS presence of an inhbitor (antibody)

62
Q

If PT/PTT is corrected w/ mixing study then?

A

Factor deficiency is present

63
Q

If PT/PTT is not corrected w/ mixing study then?

A

Likely inhibitor to one of the coag factors that affects plasma and pts blood. (classicly Lupus Anticoagulant)

64
Q

Bleeding time is a measurementt of?

A

Platelet fx after a cut w/ needle/lancet (difficult/unreliable)

65
Q

NL bleeding time is?

66
Q

Determining if a bleeding D/O is from more than one sit helps by?

A

Bleeding from >1 site = more likely a True bld D/O

67
Q

Asking if patient has had a bleed D/O there whole life vs recently helps by?

A

Inherited VS acquired bleeding D/O

68
Q

A -PLUG- issue implies?

A

A platelet issue
Ass/w capillary bleeding (oozing blood)
-mucous membrane bleeding usually (nose, oral, GI)

69
Q

Pts w/ <10k PLT are at risk for

A

Spontaneous LRG-volume bleeds -PLUG D/O-

70
Q

A -reinforcement- issue implies?

A

Coagulation factor problem
Ass/w large vessel bleeding (gushing blood)
- Hemathrosis, (LRG - hematomas, ecchymosis, trauma)

71
Q

Petechiae can be ass/w what type of Hemostasis issue?

A

Platelet issue

72
Q

Hemathrosis can be ass/w what type of Hemostasis issue?

A

Coagulation issue

73
Q

Questions to be aware of when considering Bleed D/O?

A

Quantitative vs Qualitative
Reduced survival vs reduced production
Issue w/ PLTs vs Factors

74
Q

DDx of isolated elevated PTT?

A 
(Intrinsic pathway)
Von willebrands disease
Hemophilia A/B
Other factor deficits besides hemophilia
Inhibitors
Liver disease
75
Q

DDX of isolated elevated PT?

A

(extrinsic pathway)
F7 deficit or inhibitor
Liver disease

76
Q

DDX of elevated PT and PTT

A

Excess heparin and coumadin
DIC
Severe liver disease
Vit K deficit

77
Q

Thrombocytopenia QUAN defects reducing SURVIVAL?

A

Immune Thrombocytopenia
HIT
Thrombotic Thrombocytopenia purpura/HUS
Hypersplenism

78
Q

Thrombocytopenia QUAN defects reducing PRODUCTION?

A

BM D/O
Infection (sepsis)
Rx - chemotherapy, ETOH

79
Q

Thrombocytopenia QUAL defects of CONGENITAL causes

A

vWF Dz
Bernard-Soulier Dz
Glanzmann’s thrombasthenia

80
Q

Thrombocytopenia QUAL defects of Acquired causes

A

Rx - Chemo, ETOH, Heparin)

ESRD (uremia)

81
Q

Bernard-Soulier Dz is

A

deficiency in PLT (GP Ib-IX-V) receptor which binds vWF = defective PLT adhesion

82
Q

Glanzmann’s thrombasthenia is due to

A

PLTs lacking GP IIb/IIIa

Heme (8 decks)

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