1
Q
normal hemostasis includes
A
- platelets
- endothelium
- plasma clotting factors
2
Q
function of platelets
A
- maintenance of vascular integrity
- platelet plug formation
- platelet phospholipid complex expression (leads to promotion of coagulation cascade)
- promotion of endothelial repair
3
Q
name 2 platelet inhibitors
A
- cyclooxygenase inhibitors (aspirin)
2. ADP receptor antagonists (ticlopidine and clopidogrel)
4
Q
what are other platelet inhibitors
A
- phosphodiesterase inhibitors (dipyridamole)
2. glycoprotein (GP) IIB/IIIa receptor antagoinsts
5
Q
mechanism of phophodiesterase inhibitors
A
increases [ ] of cAMP and cGMP
6
Q
function of endothelium
A
- metabolic transfer
- barrier functions
- synthesis of mediators of interactions between endothelium and blood components
- thomboresistance - prevents clotting
- mediation of vascular repair
7
Q
examples of endothelial thromboresistance
A
- heparin-like molecules
- PGI2 and nitric oxide (NO) synthesis
- plasminogen activation
- ADP degradation
- thrombin inactivation
- thrombomodulin production
- protein S synthesis
8
Q
where do heparin-like molecules act at
A
at interface of endothelial cells and plasma
9
Q
function of heparin-like molecules
A
activate antithrombin III
10
Q
activated antithrombin II cleaves
A
thrombin, factors Xa and IXa
11
Q
what is thrombomodulin
A
endothelial surface protein
12
Q
thrombomodulin is a receptor for
A
thrombin
13
Q
thrombomodulin binds thrombin and coverts it to an
A
activator of protein C
14
Q
activated protein C (APC) cleaves factors
A
VA and VIIIa
15
Q
protein S is a cofactor for
A
activated protein C
16
Q
other functions of activated protein C
A
- contributes to significant reduction of mortality in patients with severe sepsis
- attenuates various deleterious events induced by lipopolysaccharide (LPS)
17
Q
activated protein C has associated —- and — effects
A
anti-inflammatory
profibrinolytic
18
Q
activated protein C inhibits
A
tumor necrosis factor-alpha (TNF-alpha) production
19
Q
events initiated by endothelial disruption
A
- vasoconstriction (neurogenic, endothelin)
- platelet adhesion and aggression
- release of TxA2
- initiation of coagulation
- fibrinolysis
20
Q
what are the 3 distinct phases of the newest representation
A
- initiation
- propagation
- termination
21
Q
what are initiation
A
-chemical or mechanical damage to tissue
22
Q
function of initiation
A
- exposes tissue factor (TF) to the plasma circulation
- induces TF expression by monocytes, activated endothelium
23
Q
Tissue factors interacts with a small amount of
A
preexistant factor VIIa in the plasma
24
Q
interaction of TF and preexistant factor VIIa form
A
extrinsic tenase (TF/VIIa/IX/X) on a phospholipid surface
25
rapid inactivation of the extrinsic tenase by
tissue factor pathway inhibitor (TFPI)
26
extrinsic tenase generates small amounts of factors
IXa and Xa
27
Xa cleaves
prothrombin (II) to form small amounts of thrombin (IIa)
28
initial small amounts of thrombin activates
cofactor proteins
factors V and VIII to VA and VIIIa
platelets
29
cofactor activation initiates assembly on
platelet phospholipid surface of intrinsic tenase (VIIIa/IX/X) which leads to Xa activation
30
function of prothrominase (Va/Xa/II/Ca++)
accelerates thrombin formation (IIa)
31
thrombin and fibrinogen form
fibrin
32
function of fibrin
- removal of fibrinopeptide A and B
| - cross-linking
33
termination
formation of thrombin/thrombomodulin complex activates protein C which inactivates Va and VIIIa
34
how is extrinsic tense inactivated
spontaneous decay of TFPI
35
inactivation of Xa and thrombin (IIa) by
antithrombin III
36
prothrombin time (PT) is a measure of
extrinsic pathway of coagulation
37
Prothrombin Time measures factors
VII, X, V, II and fibrinogen
38
prothrombin time is a mixture of
thromboplastin (tissue factor) plasma, calcium ion
39
expect a clot to form in ---s when using PT
12 seconds
40
partial thromboplastin time is a measure of
intrinsic pathway of coagulation
41
PTT measures factors
XII, XI, IX, VIII, X, V, II, fibrinogen
42
PTT is a mixture of
phospholipid platelet substitude (partial thromboplastin), plasma, calcium ions
43
a clot form in ---s with PTT
25 seconds
44
name 2 disorder of hemostasis
1. antithrombotic (hemorrhagic) disorder
| 2. prothrombotic (hypercoaguable) states
45
what are the antithrombotic (hemorrhagic) disorders
- classic hemophilia
- Christmas disease
- von Willebrand's disease
- disseminated intravascular coagulation with consumption coagulopathy etc.
46
what are the prothombotic (hypercoaguable) states
- hereditary thrombophilia
- lupus anticoagulant
- HIT syndrome (heparin induced thrombocytopenia and thrombosis syndrome)
- disseminated intravascular coagulation (DIC)
47
hereditary thrombophilia is most often present in
adolescents or young women
48
hereditary thrombophilia presents with
- venous thrombosis
| - recurrent thromboembolism
49
name 2 hereditary thrombophilia
Factor V Leiden
Prothrombin 20210A transition
Methylene Tetrahydrofolate Reductase Mutation
50
Factor V Leiden has a mutation in
factor V
| causes resistance to activated protein C
51
what are the 3 Hereditary THrombophilia deficiencies
1. antithrombin III deficiency
2. protein C deficiency
3. protein S deficiency
52
Genes implicated in hereditary thrombophilia
- factor V Leiden and other factor V variants
- prothrombin 20210G-A polymorphism
- hyperhomocysteinemia and homocystinuria
- antithrombin 3
- protein C
- protein S
- numerous others
53
lupus anticoagulant has a prolonged --- test
partial thromboplastin time
54
in lupus anticoagulant what interfers with PTT test
antiphopholipid antibodies
55
symptoms of Lupus Anticoagulant
- increased venous and arterial thrombosis
| - sometimes associated with autoimmune diseases such as SLE
56
what is HIT syndrome
heparin-induced thrombocytopenia (and thrombosis)
57
HIT syndrome is caused by
antibodies to the complex of heparin and platelet factor 4 (PF4)
58
HIT syndrome is related to what kind of therapy
therapy with high molecular weight heparin (avoided by using low molecular weight heparin)
59
HIT syndrome is clinically characterized by
heparin induced thrombocytopenia followed by thrombotic complications (cause too much clotting)
60
disseminated intravascular coagulation (DIC) is caused by
- an obstetric complication caused be:
- retained dead fetus
- premature separation of placenta (abruptio placentae)
61
DIC is gram ---- species
negative
62
DIC can lead to what type of trauma
- leg surgery
| - hemolytic transfusion rxns
63
DIC can cause what type of malignancy
lung, pancrease, other
64
what is DIC
widespread deposition of fibrin in microvasculature
65
what factors are involved with DIC
factor VII, V, II and fibrinogen
66
what is consumption of coagulopathy
- depletion of platelets and coagulation factors
| - associated with DIC
67
DIC has prolongation of
- prothrombin time (V,II, fibrinogen)
- PTT (VIII, V, II, fibrinogen)
- thrombin time (fibrinogen)
68
DIC has presence of
fibrin-fibrinogen degradation (split) products (FDP)
Pathology
flashcards
Decks in class (18)
# Cards
-
Introduction to Pathology57
-
Cellular Reaction to Injury Overview and Adaptations52
-
Cellular Reaction to Injury Necrosis: Mechanisms and Morphologic Changes90
-
Cellular Reactions to Injury: Apoptosis and Adaptations102
-
Inflammation 190
-
Inflammation 287
-
Regeneration and Repair Part I85
-
Regeneration and Repair Part II85
-
Hemodynamic Disorders: Hemostasis68
-
Thrombosis, Embolism and Infarction115
-
Edema, Hemorrhage, Congestion and Shock105
-
Genetic Disorders Part 1134
-
Genetic Disorders Part 256
-
Hypersensitivity, Autoimmunity and Immunodeficiency Part 156
-
Hypersensitivity, Autoimmunity and Immunodeficiency Part 288
-
Hypersensitivity, Autoimmunity and Immunodeficiency Part 365
-
Hypersensitivity, Autoimmunity and Immunodeficiency Part 475
-
Neoplasia Part 166
