Chapter 4: hemodynamic disorders, thrombus, shock Flashcards
What is the difference in an edema and an effusion?
Edema = fluid in tissues Effusion = fluid in interstitial space
Name the causes of edema:
1) Increased cappilary hydrostatic pressure (often venous return)
2) Decreased plasma somotic pressure (often albumin)
3) Sodium and water retention (causes the two mentioned above)
4) Lymphatic obstruction
What is hyperemia and congestion?
An increase in the blood supply to an organ and reduced outflow of blood from an organ respectively.
What is a hemostasis?
The bodys creation of a clot in response to tissue or endothelial injury.
Hemorhagic vs thrombotic
“bleeder” vs abnormal creation of clots.
What is the typical stages in hemostatic response?
1) Vasoconstriction of the arteriole.
2) primary hemostasis - the formation of platelet plug. exposure of sybendothelial von WF and collagen which promote platelet adherence and activation.
3) secondary hemostasis - deposition of fibrin. Subendothelial cells expose Tissue factor which activates factor VII.
4) Clot stabilization and resorption. t-PA release (tissue plasminogen activator) fibrinolysis and thrombomodulin (inhibits cascade).
check page 117.
Platelet role:
1) they have granules: alpha granules have p-selectin and contains vWF, fibrinogen, factor V, PDGF and TGF beta. Delta granules have ADP, ATP etc.
undergoes changes when activated:
1) adhesion through collagen and glycoprotein Ib (there has the be vWF.
2) change of shape - amongst other glycoprotein IIb - binds fibrinogen.
3) secretion of granules - ADP activates more.
2+3 = activation - often through thrombin (binds to PAR - protease activated receptor) and ADP.
4) platelet aggregation - Gp-IIb forms complex with Gp-IIIa and binds fibrinogen which has numerous binding sites.
Clotting in vivo:
VII -> VII-TF when contacted by TF
VII-TF -> IX -> IXa
IXa -> X -> Xa-Va
Xa-Va -> prothrombin -> thrombin
thrombin -> fibrinogen -> fibrin.
Look at page 118
Limiters of coagulation:
1) plasmin - made from plasminogen cleaves fibrin. Possibly XII started. Also t-PA activated.
2) Healthy endothelium produces a lot of anticoagulants.
- Platelet inhibitors: Prostacyclin (PGI2), NO, ADPase, binds thrombin.
- antiocoagulants: protein c receptor and thrombomodulin bind thrombolin and protein c. Which activates protein C - protease of clotting factors. Heparin like molecules - binds antithrombin III which inactivates thrombotic factors.
- fibrinolytic - produces t-PA.
Name the triade of Virchow:
1) Endothelial injury or stress
2) Hypercoagulability
3) Abnormal blood flow
What is thrombomodulin?
A protein expressed by the endothel which stops the activity of thrombin - upon injury the expression of this is downregulated in the endothelial cells.
What are PAIs?
Plasminogen activator inhibitors - limit fibrinolysis and downregulates t-PA.
What constitutes abnormal blood flow?
1) turbulence
2) stasis
Why does stasis promote thrombosis?
1) Activates platelets
2) disrupts laminar flow making the endothelial cells comen in contact with the platelets and activating
3) prothrombotic factors won´t get washed away.
What is hypercoaguability?
1) primary (genetic) eg. factor V Leiden - usually if people younger than 50.
2) secondary (acquired) Eg. smoking, fat, HIT (heparin induced thrombocytopenia - antibodies against heparin makes complexes which activates platelets)
