FLUIDS-Coagulation Flashcards
(238 cards)
1
Q
Describe the difference in artery and vein anatomy
A
- Tunica media is thicker in arteries
- Tunica externa is the thickest layer in veins
- The tunica externa is thinner than tunica media
2
Q
What are the 3 layers of arteries and veins from outer to inner
A
- Tunica externa (connective tissue)
- Tunica media (smooth muscle layer and elastic tissue)
- Tunica intima (endotherlium)
3
Q
4 factors that contribute to the liquid state of blood
A
- Coagulation proteins circulate in inactive form
- Endothelium is smooth, repelling clotting factors
- Undamaged endothelium prevents activation of platelets
- Activated factors are removed by brisk blood flow
4
Q
What are the 4 steps of hemostasis
A
- Vascular spasm
- Formation of the platelet plug (primary hemostasis)
- Coagulation and fibrin formation (secondary hemostasis)
- Fibrinolysis when clot is no longer needed
5
Q
What can over abundance of procoagulants increase the risk of
A
- Stroke
- MI
- Thrombosis
6
Q
What 2 processes favor clot formation in the body
A
- Procoagulation
2. Antifibrinolysis
7
Q
What 2 factors favor the prevention or destruction of clots
A
- Anticoagulation
2. Fibrinolysis
8
Q
What are 5 procoagulant substances
A
- Coagulation factors
- Collagen
- wVF
- Fibronectin
- Thrombomodulin
9
Q
What are 4 native anticoagulant substances
A
- Protein C
- Protein S
- Antithrombin
- Tissue pathway factor inhibitor
10
Q
What are 3 native fibrinolytic substances
A
- Plasminogen
- tPA
- Urokinase
11
Q
What are 2 native antifibrinolytic substances
A
- Alpha-antiplasmin
2. Plasminogen activator inhibitor
12
Q
What are 2 native vasoconstriction mediators
A
- Thromboxane A2
- ADP
- Serotonin
13
Q
What are 2 native vasodilation mediators
A
- Nitric oxide
2. Prostacyclin
14
Q
What are the functions of the following Coagulation factor= Collagen= wVF= Fibronectin= Thrombomodulin=
A
Procoagulants Coagulation factor= coagulation Collagen= Tensile strength wVF= Plt adhesion Fibronectin= Cell adhesion Thrombomodulin= Regulates naturally occurring anticoags
15
Q
What are the functions of the following Protein C= Protein S= Antithrombin= Tissue pathway factor inhibitor=
A
Anticoagulants
Protein C= degrades factor 5a and 8a
Protein S= Cofactor for protein C
Antithrombin= Degrades factor 9a, 10a, 11a, 12a
Tissue pathway factor inhibitor= inhibits tissue factor
16
Q
What are the functions of the following
Plasminogen=
tPA=
Urokinase=
A
Fibrinolytics
Plasminogen= Precursor to plasmin (breaks down fibrin)
tPA= activates plasmin
Urokinase= activates plasmin
17
Q
What are the functions of the following
Alpha-antiplasmin=
plasminogen activator inhibitor=
A
Antifibrinolytics
Alpha-antiplasmin= inactivates tPA, urokinase
plasminogen activator inhibitor= Inhibits plasmin
18
Q
How are platelets produced
A
Megakaryocytes in the bone marrow
19
Q
Normal platelet level
A
150,000 - 300,000mm^3
20
Q
What is the lifespan of the platelet
A
8-12 days (1-2 weeks)
21
Q
How are platelets cleared
A
By macrophages in the reticuloendothelial system of the spleen
22
Q
How does the spleen affect platelet levels
A
- It clears them via macrophages in the reticuloendothelial system
- Can sequester up to 1/3 of all circulating platelets
23
Q
Where are up to 1/3 of platelets stored
A
Spleen
24
Q
What are 2 essential functions of the platelet
A
- Structural component of the clot
2. Delivery vehicles providing many substates required for clot formation
25
What components are on the external membrane of the platelet
1. Glycoproteins
| Phospholipids
26
What is the function of glycoproteins on the platelet external membrane
1. Repellant of healthy vascular endothelium
| 2. Adheres to injured endothelium, collagen, and fibrinogen
27
What 3 components can the glycoprotein of the platelet membrane adhere
1. Endothelium
2. Collagen
3. Fibrinogen
28
How does the platelet membrane glycoprotein adhere to injured structures
1. GpIb attaches to activated platelet to vWF
| 2. GpIIb-IIIa complex links platelets together to form plug
29
How are platelets linked to form a plug
GpIIb-IIIa complex links the platelets together
30
What is the function of platelet membrane phopholipids
It's a substrate for prostaglandin synthesis
| -Which produces thromboxane A2
31
What is the function of thromboxane A2
Platelet activation
| A platelet which has synthesized prostaglandin can then activate other platelets
32
What are 7 internal platelet components
1. Actin and myosin
2. Thrombosthenin
3. ADP
4. Calcium
5. Fibrin-stabilizing factor
6. Serotonin
7. Growth factor
33
```
What are the functions or the following internal platelet components
Actin/Myosin=
Thrombosthenin=
ADP=
Calcium=
Fibrin-stabilizing factor=
Serotonin=
Growth factor=
```
Actin/Myosin= plt contraction to form plug
Thrombosthenin= plt contraction assist
ADP= Plt activation and aggregation
Calcium= Coag cascade Fx 4
Fibrin-stabilizing factor= Crosslinks fibrin (Fx 13)
Serotonin= Activates nearby plts
Growth factor= Repair damaged vessel wal
34
What 2 components that are contained inside the plt aid in platelet contraction
1. Actin and myosin
| 2. Thrombosthenin
35
What 2 components that are contained inside the plt aid in plt activation
1. ADP
| 2. Serotonin
36
How does undamaged endothelium prevent platelet function
By secreting
1. Prostaglandin I2
2. Nitric oxide
37
What are 3 functions of prostaglandin I2 and where is it secreted
Secreted by healthy endothelium
Inhibits plt function by
1. preventing vWF adherence
2. TxA2 activation on plt
3. release of storage granules
38
How does nitric oxide prevent platelet function
It inhibits TxA2 receptor on the plt
39
What are 5 platelet surface receptors
1. GPIb
2. ADP
3. TxA2
4. Thrombin
5. GPIIb-IIIa
40
What 3 actions are responsible for the contraction of injured vessels
1. SNS reflex
2. Myogenic response
3. Release of vasoactive substances (TxA2)
41
What is the purpose of vascular spasm following injury
1. reduces blood loss
| 2. Helps procoagulatns remain in affected area
42
What is primary homeostasis, including the 3 step-process
Formation of platelet plug via
1. Adhesion
2. Activation
3. Aggregation
43
What 2 actions occur during primary homeostasis adhesion
1. Collagen is exposed and plts adhere via Gp Ia/IIa and Gp VI receptors
2. vWF is synthesized and released to bind with GpIb receptor
44
What is the function of vWF
ADHESION
| to bind with GpIb receptor on the plt and anchor it to the subendothelium
45
What is Von willebrand disease
A disorder of plt adhesion
46
How are platelets activated during primary homeostasis
Expose collagen and thrombin activate the plts
47
What happens once plts are activated by collagen and thrombin
Plts release ADP and thromboxane A2 which activate nearby plts
48
How are nearby plts activated
The original plt releases ADP and thromboxane A2
49
Which substance released by the plt can aid in vasoconstriction
TxA2
50
What does plt contraction do (3)
1. Promotes plt plug
2. Releases alpha granules (fibrinogen, fibronectin, vWF, plt Fx 4, plt growth factor)
3. Recruits other plts to injured site
51
What are 2 glycoproteins that are expressed on an activated plt
GpIIb and GpIIIa
52
How is plt aggregation accomplished
GpIIb/IIIa receptor complex links activated plt to form plug
53
What factors are required to help configure GpIIb/IIIa to accept fibrinogen
TxA2 and ADP
54
What is the primary purpose of the coagulation cascade
To produce firbin
55
When is the coagulation cascade not necessary
When injury is minimal and only plt plug is needed
56
What is the different events that initiate the extrinsic vs intrinsic pathway
Extrinsic = when coagulation is initiated outside of the intravascular space
Intrinsic = When coagulation is initiated inside the intravascular space
57
What is a mnemonic for coagulation factors
Foolish People Try Climbing Long Slopes After Christmas Some People Have Fallen
58
What are the coagulation factors in order
1. Fibrinogen
2. Prothrombin
3. Tissue factor
4. Calcium ions
5. Labile factor
7. Stable factor
8. Antihemophilic factor
9. Christmas factor
10. Stuart-Power factor
11. Plasma thromboplastin antecedent
12. Hageman factor
13. Fibrin stabilizing factor
59
Where are the coagulation factors synthesized
Diet = Fx 4
Vascular wall = Tissue factor (Fx 3)
Liver = all other factors
60
Which factors are vitamin k dependent
Fx 2, 7, 9, 10
61
Which clotting factors are co-factors
5 and 8
62
Which clotting factor begins the common pathway
Fx 10
63
Which clotting factor initiates the extrinsic path
TF (Fx 3)
64
Which clotting factor initiates the intrinsic path
Fx 12
65
What labs measure the intrinsic vs extrinsic path
```
Intrinsic = PTT, ACT
Extrinsic = PT, INR
```
66
Which factors are part of the common pathway
10, (5), 2, 1
67
Which factors are part of the intrinsic pathway
12, 11, 9, (8)
68
Which factors are part of the extrinsic path
TF/Fx3, 7, 4
69
Which anticoagulant inhibits the extrinsic pathway
Warfarin
70
How does Fx 7 activate Fx 10
Requires Fx 4 (calcium)
71
What is the purpose of Fx 5
In the common pathway, it functions in a positive feedback role that accelerates production of prothrombin activator
72
How is Fx 2 (prothrombin to thrombin) activated
By prothrombin activator and plt phospholipids
73
Which clotting factor has the shortest half-life.
| Why is this significant
Fx 7 (4-6 hrs)
Significance = first factor to become deficient in pts with liver failure, vitamin K deficiency, and taking warfarin
74
What is the first factor to be depleted in pts with liver failure, vit K deficiency or taking warfarin
Fx 7
75
What activates Fx 12
Blood trauma, and exposure to collagen
76
What activates Fx 11
Fx 12a
| Requires HMW kininogen and accelerated by prekalikrein
77
What activates Fx 9
Fx 11a
78
What activates Fx 10
Fx 9a and 8
79
What factor is missing with hemophilia A
Fx 8
80
What is the mnemonic for the extrinsic path
For 37 cents, you can purchase the extrinsic pathway
81
What is the mnemonic for the intrinsic path
If you can't buy the intrinsic path for $12, you can buy it for $11.98
82
What is the mnemonic to remember the common pathway
The final common path can be purchased at the five (5) and dime (10) for 1 or 2 dollars on the 13th month
83
What is the primary goal of the extrinsic or intrinsic pathway
To produce prothrombin activator, which initiates the common pathway by activated Fx 2 to 2a (thrombin)
84
What is the function of thrombin (2a)
It's a proteolytic enzyme that changes fibrinogen to fibrinogen monomer
85
How is fibrin incorporated into the plt plug
Activated fibrin-stabilizing factor (13a) facilitates cross-linkage of fibrin fibers and completes the clot
86
What factor is required to complete fibrin activation and cross-link
Fx 13a and Fx 4(Ca++)
87
What are 4 mechanisms the body uses to prevent indefinite clot formation
1. Vasodilation and washout ADP and TxA2
2. Antithrombin inactivates thrombin (2a) and Fx 9a-12a
3. Tissue factor path inhibitor neutralizes tissue factor
4. Protein C and S inhibit Fx 5a and 8a
88
What is the role of antithrombin
Inactivates thrombin 2a and Fx 9a-12a
89
What is the role of tissue factor path inhibitor
Neutralizes tissue factor (3a)
90
What is the role of Protein C and S
Inhibition of Fx 5a and 8a
91
Where is plasminogen synthesized
The liver
92
What is plasmin
A proteolytic enzyme the degrades fibrin into fibrin degradation products
93
What lab measures fibrin degradation
D-Dimer
94
How is plasminogen activated
Injured tissue releases tissue plasminogen activator (tPA)
| Plasminogen is incorporated into the clot and is dormant until it is activated
95
Where are the following released
tPA=
Urokinase=
Streptokinase=
```
tPA= Injured tissue
Urokinase= produced and released by kidneys
Streptokinase= Streptococci secretion
```
96
What is the clinical use of plasmin activators
Dissolve thrombi and restore blood flow
97
How is fibrinolysis terminated when no longer needed
tPA inhibitor = inhibits conversion of plasminogen to plasmin
Alpha-2 antiplasmin = inhibits action of plasmin on fibrin
98
What are 2 enzymes that convert plasminogen to plasmin
tPA
| Urokinase
99
What are the 3 phases of the cell-based coagulation cascade
1. Initiation
2. Amplification
3. Propagation
100
What is the initiation phase of the cell-based coagulation cascade
When TF is expressed, the TF/7a reaction activates factor 10 (common path) making a small amount of thrombin (2a)
101
What is the amplification phase of the cell-based coagulation cascade
Plt and cofactors amplify large-scale thrombin production
| Activation of plts, Fx 5, and 11
102
What is the propagation phase of the cell-based coagulation cascade
Large quantities of thrombin are produced on the surfaces of plts
103
How does the propagation phase begin
When Fx 10 is activated by Fx 4 (Ca++), 8, and 9 on the surface of the plt
104
What is the end-result of the propagation phase
The phase produces a positive feedback mechanism the produces enough thrombin to activate fibrin
105
Why do thrombin levels remain low in the initiation phase of the cell-based coagulation cascade
Tissue factor pathway inhibitor (TFPI) limits the amount of tissue factor released
106
What phase are plts activated in the contemporary coagulation model
The amplification phase
107
What does aPTT measure
activated partial thromboplastin time
Intrinsic and final common pathways
The time it takes to form a clot using phospholipid and cCa++
108
Normal PTT value
25-32 seconds
109
How reduced are clotting factors before a change is seen with aPTT
by more than 30%
110
What does PT measure
Prothrombin time
Measures the extrinsic and final common pathway
Time it take to form a clot using tissue factor and Ca++
111
What does INR measure
Calculation that standardizes PT results
| Ratio between pts PT and standard mean PT
112
What is the normal INR and goal for pt s on warfarin
Normal = 1
| On warfarin = 2-3
113
What does the ACT measure and its purpose
Activated clotting time
| Purpose = to guide heparin dosing
114
What is normal ACT level
90-120 seconds
115
What does a plt count NOT measure
The function of the plt, only the amount of plt
116
What does bleeding time measure
Plt function
| Evaluates the ability to form a plt plug
117
What is a normal bleeding time
2-10 minutes
118
What does a D-Dimer measure
Fibrinolysis
| Elevated D-dimer = likely a thrombus somewhere in the body
119
What are the 5 components of a TEG
```
R time
K Time
alpha angle
Max amplitude
Amplitude at minutes after MA
```
120
```
R Time:
Definition=
Normal value=
Problem area=
Treatment=
```
Definition= Time to begin forming clot
Normal value= 6-8 min
Problem area= coagulation factors
Treatment= FFP
121
```
K Time:
Definition=
Normal value=
Problem area=
Treatment=
```
Definition= Time until clot achieves fixed strength
Normal value= 3 - 7 min
Problem area= Fibrinogen
Treatment= Cryo
122
```
Alpha angle:
Definition=
Normal value=
Problem area=
Treatment=
```
Definition= Speed of fibrin accumulation
Normal value= 50-60 sec
Problem area= Fibrinogen
Treatment= Cryo
123
```
Max amplitude (MA):
Definition=
Normal value=
Problem area=
Treatment=
```
Definition= Measures clot strength
Normal value= 50-60 mm
Problem area= Platelets
Treatment= Plts, DDAVP
124
```
Amplitude at min after MA:
Definition=
Normal value=
Problem area=
Treatment=
```
Definition= Height of amplitude after 60 min
Normal value= MA - 5
Problem area= Excess fibrinolysis
Treatment= TXA, aminocaproic acid
125
How is a prolonged TEG R time treated
FFP
126
How is a prolonged K time treated
Cryo
127
How is a low alpha angle treated
cryo
128
How is a low MA treated
Platelets
129
What 3 locations produce endogenous heparin
Basophils
Mast cells
Liver
130
What pathway of coagulation cascade is affected by heparin
Intrinsic and final common pathway
131
Heparin MOA
Binds to antithrombin forming a heparin-AT complex. This accelerates ATs anticoagulant ability
132
What is the function of the heparin-AT complex
To neutralize thrombin (2a), and activated Fx 9-12
Inhibits plt function
133
If heparinization has failed, what should be considered
AT deficiency
134
Describe the properties of the heparin compound
Large, negatively charged, water-soluble compounds
| Small Vd
135
How is heparin metabolized
Heparinase
136
How is heparin eliminated
Degradation by macrophages
| Renal excretion
137
What is the aPTT when heparin is therapeutic
1.5-2.5 normal ( 50-88 sec)
138
When is ACT measured in conjunction with surgical heparin administration
Baseline (before heparin)
3 min post administration
Then q30 min
139
What 3 physiologic factors affect ACT
1. Hypothermia
2. Thrombocytopenia
3. Deficient fibrinogen, Fx 7 or Fx 12
140
What are 5 side effects of heparin
1. Hemorrhage
2. HIT
3. Allergic reaction
4. HoTN
5. Decreased AT concentration
141
What are 3 contraindications for heparin use
1. Neurosurgical procedures
2. HIT
3. Regional anesthesia (neuraxial)
142
Describe the protamine compound
Highly alkaline
| Strong positive charge
143
What is the MOA of protamine
The positive charge of protamine and negative charge of heparin create a neutralization reaction that stops heparins activity
144
Protamine dosing
1 mg for every 100 units of heparin in circulation
145
How is the heparin-protamine complex cleared
Via the reticuloendothelial system
146
What is unique about protamine administration alone
It is an anticoagulant
147
What are 3 important side effects of protamine
1. HoTN
2. Pulmonary HTN
3. Allergic reaction
148
Why does HoTN occur with protamine administration and how is this attenuated
Histamine release
| Give over >5 min
149
Why can pulmonary HTN occur with protamine administration
TxA2 and serotonin release
150
What can indicate a possible allergic reaction to protamine
1. Fish allergy
| 2. Previous sensitization to NPH insulin
151
What is warfarin MOA
Inhibition of the enzyme vitamin K epoxide complex. This complex converts inactive vit K to active vit K
152
Which clotting factors are inhibited by warfarin and why
Fx 2, 7, 9, 10 b/c they are vit K dependent
| Protein C and S
153
Describe the protein binding ability of warfarin
Highly protein-bound
154
What lab values monitor warfarin therapeutic concentrations
PT/INR
155
What are the antidotes for warfarin
Vit K
| FFP
156
What are 2 treatment for warfarin reversal
Recombinant fx 7a
| Prothrombin complex concentrate (PCC)
157
Describe the vitamin K compound
Fat-soluble vitamin
| Requires fat and bile for absorption
158
What are 5 risk factors for vitamin k deficiency
1. Poor dietary intake
2. Abx therapy killing off gut flora
3. Malabsorption d/t obstructive biliary tract
4. Hepatocellular dx
5. Neonates
159
What organ is Vit K function dependent on
Liver
160
How long does vitamin k take to restore concentration of dependent clotting factors
4-8 hrs
161
Why can't vitamin K be given IV
It can cause life-threatening anaphylaxis
162
What are 4 classes of antiplatelet drugs
1. ADP receptor inhibitors
2. GpIIb/GpIIIa Receptor antagonists
3. COX inhibitors
4. Cox-2 inhibitors
163
What are 4 examples of ADP receptor inhibitors
Have -CLO- or -GREL- in the name
1. CLOpidoGREL
2. TiCLOpidine
3. PrasuGREL
4. TicaGRELor
164
What are 3 examples of GpIIb/IIIa receptor antagonists
With an AB or BA (for GpIIB/IIIA
1. AbciximAB
2. EptifiBAtide
3. TirofiBAn
165
What are 2 examples of non-specific COX inhibitors
Aspirin
| NSAIDs
166
What are 2 examples of COX-2 inhibitors
Rofecoxib
| Celecoxib
167
What are 4 classes of anticoagulant drugs
1. Heparins
2. Thrombin inhibitors
3. Fx 10 inhibitors
4. Vit K antagonists
168
What are 4 examples of heparin anticoagulants
```
Unfractionated
1. Heparin
LMWH
2. Enoxaparin
3. Dalteparin
4. Tinzaparin
```
169
What are 2 examples of thrombin inhibitors
1. Argatroban
| 2. Bivalirudin
170
What is an example of a Fx 10 inhibitor
FondaparinuX
171
How many days before a procedure should ADP receptor inhibitors be stopped
```
Clopidogrel = 7 days
Ticlopidine = 14 days
Prasugrel = 2-3 days
Ticagrelor = 1-2 days
```
172
How many days before a procedure should GpIIb/IIIa receptor antagonists be stopped
```
Abciximab = 3 d
Eptifibatide = 1 d
Tirofiban = 1 d
```
173
How long before a procedure should thrombin inhibitors be stopped
```
Argatroban = 4-6 hrs
Bivalirudin = 2-3 hrs
```
174
How many days before a procedure should warfarin be stopped
2-4 days
175
How do cox inhibitors prevent plt aggregation
By blocking COX-1 and stopping conversion of arachidonic acid to PG and ultimately TxA2
176
What is the MOA of aminocaproic acid and TXA
Plasminogen activation inhibitor; prevents conversion of plasminogen to plasmin
177
What is the MOA of aprotinin
Inhibits plasmin, kallikrein, thrombin, protein C
178
What is the MOA of DDAVP
Stimulates factor 8 and vWF factor release
179
What is von Willebrand disease
Disorder of plt function
| Plt count is normal but do not function properly
180
What are 2 key function of vWF
1. Anchors plt to vessel wall at site of injury (adhesion)
| 2. Carries inactivated factor 8 in the plasma
181
What are the 3 classifications of von Willebrand disease
Type 1 = mild reduction in vWF production
Type 2 = The vWF produced doesn't work well
Typw 3 = Sever reduction in amount of vWF produced
182
What labs will be altered in a pt with von Willebrand dz
PTT = increased
Bleeding time = increased
No changes in PT/INR, Plt count or fibrinogen
183
How does DDAVP aid in procoagulation
It stimulates the release of endogenous vWF
| Increases Fx 8 activity
184
What coagulopathic disease is DDAVP best suited.
Von Willebrand dz type 1
185
DDAVP is a synthetic analog of which hormone
ADH
186
Which von Willebrand dz type is DDAVP not appropriate
Type 3 dz does not respond to desmopressin
187
Dose for DDAVP
0.3 mcg/kg IV
188
Following DDAVP administration, how long before bleeding time improves
12-24 hrs
189
2 Side effects of desmopressin
1. Vasodilation (esp w/ rapid administration)
| 2. Hyponatremia (d/t free water retention)
190
What What is the first-line agent for patients with Type 3 von willebrand disease
Purified 8-vWF concentrate
| The risk of transfusion related issues is decreased
191
What blood products are indicated for treatment of pts with von Willebrand disease
```
Cryo = has fx 8, 13, fibrinogen, and vWF
FFP = contains all clotting factors
```
192
What coagulating factors are in cryoprecipitate
Fx 8, 13, vWF
| Also has fibrinogen
193
What factor is deficient in Hemophilia A
Factor 8
194
What are signs of severe hemophilia A
Spontaneous bleeding into joints, muscles, and vital organ
195
Which labs will be altered in pts with hemophilia A and why
PTT will be prolonged
B/c fx 8 is part of the intrinsic pathway (PT is not affected)
All other labs are normal
196
What should the pt with hemophilia A receive before surgery
Factor 8 concentrate
197
What is the half-life of factor 8 concentrated
8-12 hrs
198
What other treatment options are available for pts with hemophilia A undergoing surgery
FFP
Cryo
DDAVP
TXA (dental procedures)
199
What should always be available for pts with hemophilia A undergoing surgery
Type and crossmatch
200
What is hemophilia B
Factor 9 deficiency
201
What treatment can be given prior to surgery in pts with hemophilia B
Factor 9-prothrombin complex concentrate
202
What is the dose for recombinant factor 7
90-120 mcg/kg
203
In which pts can recombinant factor 7 be useful
Hemophilia A or B pts that develop inhibitor that prevent exogenous Fx 8 or 9 from achieving therapeutic goals
204
What are the risks of giving recombinant factor 7 in hemophilia pts
It can increase the risk of arterial thrombosis (MI or embolic stroke) or venous thrombosis
205
What is DIC
disseminated intravascular coagulation
| It is characterized by simultaneous hemorrhage and systemic thrombosis
206
What become deficient with DIC and why
Plt, fibrinogen, and clotting factors
| Because they are consumed from being used to stop bleeding while forming microvascular thrombi
207
What labs are altered in DIC
```
PT/PTT = increased
D-Dimer = increased
Plt = decreased
Fibrinogen = decreased
```
208
What causes tissue hypoxia and acidosis in DIC
Generalized thrombin formation that creates microvascular clots impairing tissue perfusion. Leads to organ failure
209
Why is hemorrhage a problem in DIC
Due to widespread fibrin deposition, fibrinogen, coag factors, and plts are consumed. There is nothing left for hemostasis where it is needed
210
Are fibrinolytics part of DIC
Yes, Release of tPA and urokinase-type plasminogen activator occurs
211
What are 7 signs of DIC
1. Ecchymosis
2. Petechiae
3. Mucosal bleeding
4. Bleeding at IV puncture sites
5. Prolonged PT/PTT
6. Increased D Dimer
7. Decreased fibrinogen and AT
212
What 3 conditions are associated with high risk for developing DIC
1. Sepsis (gram-neg bacilli)
2. Obstetric complications (pre-E, placental abruption, AFE)
3. Malignancy (adenocarcinoma, leukemia, lymphoma)
213
What is affected by AT deficiency
The ability to inactivate Fx 9, 10, 11, and 12 leading to thrombin (2a) inhibition
Heparin responsiveness
214
What are pts with AT deficiency at risk for
VTE
215
Treatment for AT deficiency
AT concentrate
| FFP
216
What is the etiology of heparin-induced thrombocytopenia
The body initiates an immune response against heparin after it binds to plt factor 4
IgG antibodies activate platelets resulting in uncontrolled clot formation
217
Why is the plt count low during HIT
Because the plt have been activated by IgG antibodies and used to form widespread clots
218
What is the difference in pathology between HIT type 1 and 2
Type 1 = heparin induced plt aggregation
Type 2 = Antiplatelet antibody IgG attack factor 4 immune complex causing plt aggregation
219
What is the precipitating event of HIT type 1 vs type 2
Type 1 = large heparin doses
Type 2 = any heparin dose
220
What is a typical plt count in HIT type 1 vs type 2
Type 1 < 100,000
Type 2 < 50,000
221
What is the onset of HIT type 1 vs type 2
Type 1 = 1-4 days post heparin
Type 2 = 5-14 days post heparin
222
What is the coagulation status in HIT type 1 vs type 2
Type 1 = minimal
Type 2 = hypercoagulable
223
What is the treatment for HIT type 2
Direct thrombin inhibitors:
Bivalirudin
Hirudin
Argatroban
224
What is the function of protein C
Anticoagulant effect by inhibiting Fx 5a and 8a
225
What is protein S
a co-factor of protein C
226
What is the result of protein C or S deficiency
Hypercoagulable state
| Increased risk of thrombosis
227
What is the treatment of protein C or S deficiency
Initial thromboembolic event is treated with heparin, then pt transitioned to warfarin
228
What is Factor 5 Leiden mutation
Resistance to anticoagulant effect of protein C
229
What are 4 thrombotic disorders
1. AT deficiency
2. HIT
3. Protein C or S deficiency
4. Factor 5 Leiden mutation
230
3 ways the RBC function is affected by sickle cell disease
1. Deoxygenation of hgbS leads to sickling
2. Sickling causes RBCs to clump and cause obstruction in microvasculature, impairing tissue perfusion
3. Sickle cells are more prone to hemolysis and removal by spleen (shorter life-span)
231
What does anesthetic management of the pt with sickle cell disease focus on
Preventing the following:
1. Pain
2. Hypothermia
3. Hypoxemia
4. Acidosis
5. Dehydration
232
How is a sickle cell vaso-occlusive crisis treated
Analgesia
| IV hydration
233
What is the result of a vaso-occlusive crisis
Impaired tissue perfusion
| Ischemic injury
234
What causes acute chest syndrome in pts with sickle cell disease
```
Thrombosis
Embolism
Infection
Hypoventilation
Narcotics
Splinting
Pain
```
235
Diagnosis parameters for acute chest syndrome in sickle cell disease
CXR with new lung infiltrates
| One of the following symptoms: chest pain, dyspnea, cough, wheezing
236
When is acute chest syndrome most likely to occur
in the postoperative period
237
What is a sequestration crisis
When the spleen removes RBCs from circulation at a faster rate than the bone marrow produces them leading to anemia and hemodynamic instability
238
What can cause an aplastic crisis and how is it manifested
Causes = viral infection (parvovirus B19)
Manifestation = Bone marrow suppression can cause anemia
