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

Hemostasis overview/approach to bleeding D/O Flashcards

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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
Intrinsic pathway process?
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
26
Coagulation common pathway process
-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
27
F10 engages w/ what to form what?
F10 engages w/ F5 + Ca2+, PLT phospholipids to form a complex called F5 complex AKA prothombinase
28
3 stages of coagulation are?
1. Extrinsic or intrinsic pathway leads to prothombinase 2. Prothombinase converts prothrombin > Thombin 3. Thombin converts Soluble fibrinogen into insoluble fibrin creating a clot
29
Coagulations factors are produced where? Except?
Produved in liver (except vWF)
30
Which factors are vit-k dependent?
F2, F7, F9, F10, Protein C/S
31
Which coafulation factors are naturally-occuring anti-coagulants?
Protein C/S
32
What is Coumadins MOA?
Inhibits Vitamin K dependent factors (transient Protein C deficit occurs faster than coagulation factors deficit = why heparin is req to overlap)
33
Factor I is?
Fibrinogen
34
What happens if Fibrinogen is depleted?
Severe bleeding complication esp. in context w/ DIC
35
What produces the majoirty of vWF?
Blood vessel endothelium
36
BV endothelium provides what?
A surface which to bind to
37
vWF fx?
Binds to stabilize F8 | Mediates PLT aggregation
38
What factors exists as a complex w/in the plasma?
vWF and F8
39
a vWF deficit (Von Willibrands Dz) can lead to?
A defect involving both... 1. PLT dysfx - (Unable to form plug) 2. Coag Dysfx - (Unable to stabilize F8)
40
What is a F8 deficit known as?
Hemophilia A
41
What is F4?
Ca2+
42
Antithrombin III is a?
Normal circulating plasma protease inhibitor
43
Purpose of ATIII?
Inhibits thrombin activity (PVT excessive thrombosis)
44
How is AT III activated?
Binds heparin to cause conformation change leading to increased inhibition of thrombin
45
PT lab test measures?
Activity of proteins w/in extrinsic pathway
46
How is PT coag test performed?
adding thromboplastin to plasma and waiting for fibrin formation.
47
PT coag test detects what deficiencies?
F2, F5, F7, F10 and fibrinogen
48
NL value of PT coag test?
10-14 seconds
49
PT and PTT stands for?
``` PT = Prothrombin time PTT = Partial Thromboplastin Time ```
50
PTT measures?
The activity of proteins w/in the intrinsic pathway
51
How is PTT performed?
By artifical stimulation of F12
52
PTT test will detect deficiencies in?
F2, F5, F8, F9, F10, F11, F12 and fibrinogen
53
NL PTT lab value is?
25-40 seconds
54
INR stands for?
International normalized ratio
55
INR is a?
calculation based on pt's PT used to assess extrinsic pathway
56
What type of correlation does INR have w/ PT?
Direct correlation
57
NL INR value?
0.8-1.2
58
NL PLT value?
100-450k
59
PLT may be falsely low due to?
Clumping - typically mediated by immunologic sensitivity to EDTA (pseudothrombocytopenia)
60
Falsely low PLT count per CBC can be confirmed and evaluated w/?
Blood smear
61
Mixing study is?
1:1 mix of ABNL serum w/ NL serum to determine the possibility of a Factor deficits VS presence of an inhbitor (antibody)
62
If PT/PTT is corrected w/ mixing study then?
Factor deficiency is present
63
If PT/PTT is not corrected w/ mixing study then?
Likely inhibitor to one of the coag factors that affects plasma and pts blood. (classicly Lupus Anticoagulant)
64
Bleeding time is a measurementt of?
Platelet fx after a cut w/ needle/lancet (difficult/unreliable)
65
NL bleeding time is?
1-8m
66
Determining if a bleeding D/O is from more than one sit helps by?
Bleeding from >1 site = more likely a True bld D/O
67
Asking if patient has had a bleed D/O there whole life vs recently helps by?
Inherited VS acquired bleeding D/O
68
A -PLUG- issue implies?
A platelet issue Ass/w capillary bleeding (oozing blood) -mucous membrane bleeding usually (nose, oral, GI)
69
Pts w/ <10k PLT are at risk for
Spontaneous LRG-volume bleeds -PLUG D/O-
70
A -reinforcement- issue implies?
Coagulation factor problem Ass/w large vessel bleeding (gushing blood) - Hemathrosis, (LRG - hematomas, ecchymosis, trauma)
71
Petechiae can be ass/w what type of Hemostasis issue?
Platelet issue
72
Hemathrosis can be ass/w what type of Hemostasis issue?
Coagulation issue
73
Questions to be aware of when considering Bleed D/O?
Quantitative vs Qualitative Reduced survival vs reduced production Issue w/ PLTs vs Factors
74
DDx of isolated elevated PTT?
``` (Intrinsic pathway) Von willebrands disease Hemophilia A/B Other factor deficits besides hemophilia Inhibitors Liver disease ```
75
DDX of isolated elevated PT?
(extrinsic pathway) F7 deficit or inhibitor Liver disease
76
DDX of elevated PT and PTT
Excess heparin and coumadin DIC Severe liver disease Vit K deficit
77
Thrombocytopenia QUAN defects reducing SURVIVAL?
Immune Thrombocytopenia HIT Thrombotic Thrombocytopenia purpura/HUS Hypersplenism
78
Thrombocytopenia QUAN defects reducing PRODUCTION?
BM D/O Infection (sepsis) Rx - chemotherapy, ETOH
79
Thrombocytopenia QUAL defects of CONGENITAL causes
vWF Dz Bernard-Soulier Dz Glanzmann's thrombasthenia
80
Thrombocytopenia QUAL defects of Acquired causes
Rx - Chemo, ETOH, Heparin) | ESRD (uremia)
81
Bernard-Soulier Dz is
deficiency in PLT (GP Ib-IX-V) receptor which binds vWF = defective PLT adhesion
82
Glanzmann's thrombasthenia is due to
PLTs lacking GP IIb/IIIa

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