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PATH 310- Midterm Exam Guide - Comprehensive Notes for the exam ( 26 pages long!)


Department
Pathology and Molecular Medicine
Course Code
PATH 310
Professor
Christine Hough
Study Guide
Midterm

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Queen's
PATH 310
MIDTERM EXAM
STUDY GUIDE

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Hemophilia
Etiology: cause, or set of causes, of a disease or condition
Pathogenesis: mechanism for development of a disease
Coagulopathy: oditio here lood’s aility to for lots (or
coagulate) is impaired
Thrombosis: pathological process with formation of blood clot
(thrombus) in an uninjured vessel (cause of sudden death)
Occlusion: blockage or closing of vessel
Erythrocytes: red blood cells
Leukocytes: white blood cells
Bleeding diathesis: tendency towards prolonged or excessive bleeding
Fibrinolysis: enzymatic break down of fibrin, or fibrin clot
Pro-coagulant: activators of coagulation promote conversion of
prothrombin to thrombin, i.e. platelet activation and endothelial
damage
Anticoagulant: inhibitors of coagulation fibrinolytic factors,
anticoagulant factors, and the endothelium itself
Hemostasis: normal process that stops bleeding after vessel injury with
formation of a hemostatic plug (rapid and controlled)
Primary hemostasis: vasoconstriction and platelet plug formation
(damaged endothelial cells, vasoconstriction to reduce blood
loss, platelets express receptors that interact with sticky
vWF causing it to roll slowly, other receptors activated to
make firm adhesion, conformational change, platelets
release granules of ADP and thromboxane which recruits
more platelets to the site of injury, aggregation and cross
linking with fibrinogen, vWF and collagen to form
hemostatic plug)
Secondary hemostasis: with larger damage, plug is not strong
enough, so fibrin clot formation occurs
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(amplification of the initial response, clotting factors
circulate as zymogens and are activated by proteolysis,
soluble fibrinogen is transformed into insoluble fibrin)
Thrombolysis: breakdown of a thrombus (blood clot)
Tissue factor: exposure of TF protein on SMCs is the initiation of
coagulation, as it causes factor 7 to come and interact with it forming a
complex that will go on to activate factor 10
Von Willebrand factor: interacts with platelets after endothelial
damage, crosslinking with fibrinogen and collagen to make plug
Thrombin: key player in the coagulation cascade, activates many
factors like 10, 8, and 5 (in the intrinsic pathway), also helps to convert
fibrinogen into fibrin
Prothrombin: converted to thrombin by activated F10 and F5
Factor 5: active form helps F10 convert prothrombin to thrombin (part
of common pathway)
Factor 7: makes activated complex with TF when it is exposed, activates
F10 (extrinsic pathway)
Factor 8: complex with F9a to activate F10 (deficiency is hemophilia A),
synthesized in extrahepatic sources, scaffold protein that brings F9 and
F10 together in optimal way (could maybe mimic with antibody?)
Factor 9: activated by F11 or F7a-TF complex, makes complex with F8a
to activate F10 (deficiency is hemophilia B), synthesized in hepatocytes
Factor 10: activated by TF-F7 complex, along with F5 it begins to create
small amounts of thrombin from prothrombin at the phospholipid
surface (part of common pathway)
Tenase complex: both intrinsic (F8a is cofactor, F9a is enzyme, and F10
is substrate) and extrinsic (TF, F7a, and F10). Complex is critical for
coagulation, if any component is missing, coagulopathy can result
Endothelial cells: at rest prevent platelet aggregation, and produce
thrombomodulin (inhibits thrombin), inhibition of coagulation, and
produce factors that are important in activating fibrinolysis
Hemophilia: monogenic X-linked disorder, bleeding diathesis and
coagulopathy, a for a platelet plug ut a’t hold it together
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