TEST 3- HEMOSTASIS/COAG Flashcards
(122 cards)
1
Q
Trapped plts, rbc and fibrin; forms clot.
A
Fibrin network
2
Q
First cell belonging to the plt lineage
A
Megakaryoblast
3
Q
Megakaryoblast formation into plt sequence..
A
Megakaryoblast
Megakaryocyte
Megakaryocyte breakup (into fragments)
Platelets
4
Q
Platelets are anuclear. TRUE/FALSE
A
TRUE
5
Q
Normal circulating conc of plts
A
150,000-450,000 plt/microliter
6
Q
Halflife of plt
A
8-12 days
7
Q
Contractile proteins found in the cytoplasm of plts
A
Actin
Myosin
Thrombosthenin
8
Q
Purpose of ER and Golgi apparatus in cytoplasm of plt
A
ER: Ca++ storage
GA: enzyme synthesis
9
Q
Plts contain mitochondria for ADP/ATP synthesis. TRUE/FALSE
A
TRUE
10
Q
These two things are in the cytoplasm of plts and play a role in plt aggregation, plt antiaggregation and some vasoconstriction
A
PGs
TxA2 synthesis
11
Q
Stabilizes fibrin threads and the clot; located in cytoplasm of plt.
A
Fibrin-stabilizing factor synthesis
12
Q
Used to repair damaged tissue; promote healing; in cytoplasm of plt.
A
Growth factors
13
Q
3 components of the cell membrane of plt
A
Glycoproteins coating
Phospholipids
Receptors
14
Q
Part of the cell membrane that prevents plts from adhering to normal vascular endothelium
A
Glycoprotein coating
15
Q
Part of cell membrane that plays a role in coagulation cascade
A
Phospholipids
16
Q
Part of cell membrane that allows plts to become activated
A
Receptors
17
Q
Prevention of blood loss
A
Hemostasis
18
Q
How hemostasis is achieved (in order)
A
Vascular constriction Plt plug formation Blood coag/clot Fibrin formation and repair of vessel Clot lysis
19
Q
4 Things that cause vascular constriction
A
Trauma
Vascular smooth muscle Spasm
Pain/SNS reflexes (NE/epi released when cut, etc.)
Plts–TxA2–vasoconstriction
20
Q
The greater the trauma, the greater the amount of constriction, TRUE/FALSE
A
TRUE
21
Q
Plts are activated when they contact _______ vascular endothelium and collagen in BV wall.
A
Damaged
22
Q
When plts contact damaged vessel, they swell and exude _______, or “false feet” projections
A
Pseudopods
23
Q
After exuding pseudopods, these contract and release clotting factors
A
Actin
Myosin
Thrombosthenin
24
Q
After actin/myosin/thrombosthenin contract, plts get sticky and aggregate; adhere to _______ and ________ factor in BV wall
A
Collagen
Von willebrand factor
25
This activates other plts after plts start adhereing to BV wall
ADp and TxA2 secretion
26
Plts express ______ receptors to form platelet plug
Receptors
27
Fibrinogen receptors form fibrinogen _______, converted eventually to mesh/clot
Fibers
28
After fibrin threads form in plt plug, this may seal what type of injury?
Small BV injury
29
Larger injury requires what beyond plt plug formation?
Blood coagulation or blood clot
30
VWF deficiency can lead to major bleeding issues; how can we treat this?
Give VWF conc
DDAVP (desmopressin)
Cryoprecipitate
31
Blood coag/clot begins _____ min for minor injury; and ______ sec for major trauma
1-2 min minor
15-20 sec major trauma
32
In ______ min tear in vessel is filled with clot
3-6 min
33
Clot retracts in _______ min; closes tear more
20-60 min
34
Balance between procoagulants and anticoagulants
Normally anticoagulants predominate
After injury: procoagulants predominate
35
Procoagulants should only predominate ________, if not you can have coagulopathies.
Locally (to injury)
36
3 essential steps of coagulation
Activation of blood coag factors and formation of prothrombinase (prothrombin activator)
Prothrombinase converts prothrombin to thrombin
Thrombin converts fibrinogen to fibrin fibers = enmesh plts, blood cells, and plasma to form clot
37
2 pathways for prothrombinase formation
Extrinsic (tissue factor) pathway
Intrinsic (contact activation) pathway
38
Beginning with activation of Factor ____, both become a common pathway
X
39
If blood vessel ruptures, both pathways are activated simultaneously. TRUE/FALSE.
TRUE
40
Which pathway can become out of control or explosive?
Extrinsic pathway
41
What starts the extrinsic clotting pathway
Tissue damage
42
What starts the intrinsic clotting pathway
Contact with collagen of damaged blood vessel
43
Final outcome of both extrinsic/intrinsic pathway Stage 1.
Prothrombinase
44
______ pathway can feed into the ________ pathway; which part feeds in to the other?
Extrinsic can feed into intrinsic pathway
Thromboplastin/factor VII complex
45
This electrolyte plays major role in both clotting pathways; necessary
Ca++
46
Coagulation factors are synthesized where?
The liver
Abnormal liver fxn can lead to abnormal coag.
47
Prothrombinase converts prothrombin into ______; final outcome of stage ____.
Thrombin
Stage 2
48
Vitamin K dependent clotting factor
Prothrombin
49
Where do we get vitamin K?
Green leafy veggies
E.coli in bowel synthesizes vit K
50
What are a couple of ways that we can cause deficits in vit K in our pts; possible causing decreased clotting ability?
Abx destroy normal flora of bowel
Enemas prior to sx, esp bowel sx
51
Other vit K depending clotting factors besides prothrombin
Facet VII, IX, and X
52
Vit K is fat soluble so have to have adequate _____ in GI tract to absorb it.
Bile
53
Thrombin, along with _____ converts fibrinogen into _____, which forms final fibrin clot in stage 3.
Ca++
Fibrin
54
2 ways production of thrombin enhances clotting
Feeds back into intrinsic pathway
Activates factor XIII which plays role in fibrin clot
55
Prothrombin is an ______ globulin (plasma protein)
Alpha-2
56
Thrombin converts fibrinogen to ______ mnomers, which polymerize to form fibrin and fibrin fibers.
Fibrin
57
Thrombin further activates these factors, ending in more formation of prothrombinase.
Factor V, VIII, XI, XIII
58
Thrombin activates _______; which strengthens bonds between fibrin fibers
Fibrin-stabilizing factor
59
Meshwork of fibrin fibers entrapping plts, blood cells, plasma.
Clot
60
Expresses most fluid (serum) from clot; type of drainage?
Clot retraction; Actin, myosin, thrombosthenin, and Ca++ in plts
Purulent drainage
61
Pulls edges of blood vessel closer together; aids hemostasis and healing
Clot retraction
62
Clot invaded by fibroblasts to form connective tissue in clot, lot changed to fibrous tissue and eventual repair, ________ enhance repair
Plt growth factors
63
When is tissue restored to pretty much original form and fxn after injury?
If injury small
64
What happens to repaired tissue after major injury?
Tissue not like former/original state = scar tissue. Will not fxn as before.
65
Good example for tissue repair, but fxn not restored to original quality.
Heart tissue after MI; will not contract the same
66
Inactive protein in clot until tPA released
Plasminogen
67
What happens when tissue plasminogen activator (tPA) is released ?
Converts plasminogen to plasmin
68
Proteolytic enzyme; digests fibrin fibers and procoagulants; lyses clot.
Plasmin
69
4 things that prevent coagulation of normal BV
Vascular endothelium
Fibrin fibers absorb thrombin to prevent clot spread
Antithrombin III
Endogenous heparin
70
4 Components to vascular endothelium that prevent coagulation.
Smooth
Mucopolysaccharide glycocalyx repels plts and clotting factors
Thrombomodulin binds thrombin (prevents clots)
Endothelial damage: activation of factor XII and plts
71
Endogenous substance that combines and inactivates thrombin
Antithrombin III
72
Endogenous heparin synthesized and secreted by what cells?
Mast cells
Basophils
73
Synthesizes heparin in tissue spaces
Mast cells
74
Synthesized heparin in the blood
Basophils
75
Heparin combines with __________ III and increases effect by 100-1000 X's
Antithrombin III
76
Antithrombin III also combines with and removes what factors?
Factors VII, IX, X, XI, XII
77
Clotting factors effected by heparin
Activated Factor VII, IX, X
Factor XI, XII
Thrombin
78
Lovenox inhibits this as well as heparin
Activated factor X
79
Clotting factors effected by warfarin
Factor VII, IX, X
Prothrombin
80
How long it takes to convert prothrombin into thrombin; assesses extrinsic and common pathway.
Prothrombin time PT
81
Normal PT level
11-16 sec
82
Drug monitored when getting PT levels a lot of the time.
Coumadin
83
This value standardizes the PT, so we can compare values.
INR
84
Translate INR: 1
Prothrombin time is = international standard for normal
85
Are there times you would be okay with a higher INR?
Yes. Ex: mechanical valve replacement
86
Measures intrinsic and common pathway; monitors heparin therapy.
Activated partial thromboplastin time (aPTT)
87
Normal PTT
26-42 sec
88
Assesses the plasma level of the precursor of fibrin; need adequate amount to form fibers
Plasma fibrinogen
89
Assesses for degradation products/breakdown of clots.
D-dimer test
90
Condition where D-diner is extremely high.
DIC
91
DIC is initially characterized by widespread __________, then _______ are used up faster than liver can produce them and _________ will predominate with extensive bleeding resulting.
Coagulation
Procoagulants
Anticoagulants
92
Conditions that are at risk for developing DIC
Obstetric conditions
Burns
Infection, especially gram (-) septicemia
93
Common to all pts with DIC
Hypotension
Hypoxemia
Acidosis
Stasis of capillary blood flow
94
S/S of DIC
Hemorrhage everywhere !
95
DIC will eventually lead to what?
Multisystem organ dysfunction and death
96
Treatment/management of DIC
Blood product
Remove cause
Heparin or antithrombin III
Maintain organ viability
97
What is the logic behind the controversial therapy of giving heparin etc during DIC?
If stop excessive procoagulation initially, then will stop the whole process
98
How do we maintain organ viability when treating DIC ?
Mechanically ventilate
Vasopressors
Normal fluid balance
99
Increased or decreased during DIC?
Bleeding time
Increased
100
Increased or decreased during DIC?
Plt count
Decreased
101
Increased or decreased during DIC?
Plasma fibrinogen
Decreased
102
Increased or decreased during DIC?
Fibrin degradation products
Increased
103
Increased or decreased during DIC?
D-dimer test
Increased
104
Increased or decreased during DIC?
PT/INR
Increased
105
Increased or decreased during DIC?
APTT
Increased
106
Increased or decreased during DIC?
Clotting factors II, V, VII, X
Decreased
107
Does not have to be ABO compatible, transfuse SLOW!!
PLATELETS
108
Plt transfusion depends on both quantitative and qualitative measures, explain.
Some ppl may have dysfunctional plts, even if the level present is accurate
109
When should you transfuse plts to stable pts w/o evidence of bleeding?
<10,000/uL
110
Prophylaxis for invasive procedures such as LP, spinal/epidural, central line, liver biopsy or major sx
<50,000/ uL
111
For massive transfusions (>1 or 2? Blood volume) of prbc's, when should you transfuse plts?
<75,000/uL
112
Plt transfusion level when pts having surgery on the eye or in the central nervous system
<100,000/uL
113
Contains all the factor involved in coagulation; must be ABO compatible
FFP
114
Why does FFP have to be ABO compatible
Contains antibodies that can respond to a recipients RBC antigens
115
Indications for FFP
Correction of inherited factor deficiencies when there is not specific factor concentrate
PT or aPTT > 1.5 times normal
Correction of acquired factor deficiencies with clinical evidence of bleeding
Reversal of vit K antagonists (warfarin)
116
Example of acquired factor deficiencies that may require FFP transfusion
Liver disease
DIC
Massive transfusion
117
Used to reverse Coumadin
Vit K
118
Used to reverse heparin
Protamine
119
Contained in cryoprecipitate
Fibrinogen
VWF
Factor VIII
Factor XIII
120
Indication for cryoprecipitate is DIC with fibrinogen
<80-100
121
Indication for cryo during massive transfusion with fibrinogen
<100-150
122
Cryo given for prophylaxis for what pts?
Hemophilia A
vWD
Congenital dysfibrinogenemias
