HEMOSTASIS
Stanislav Nepomnyashchikh
212 group, medical faculty
HEMO
= blood
STASIS
= remain
CLOT REMOVAL
VASOCONSTRICTION
PLUG FORMATION
CLOTTING OF BLOOD
VASOCONSTRICTION
INJURY
LOCAL CONTROLS
Thromboxane A2
Thx A2
INJURY
SYSTEMIC CONTROL
Epinephrine
Thx A2
INJURY
INJURY
Epinephrine
Thx A2
PLUG FORMATION
CLOTTING OF BLOOD
VII + Tissue factor
IX + VIII
X + V
II
Fibrin clot
Antithrombin
TFP
inhibitor
Protein S and
protein C
Fibrinolysis
INHIBITION OF EXCESSIVE
CLOTTINGDavid Lillicrap; Nigel Key; Michael Makris; Denise O'Shaughnessy (2009). Practical Hemostasis and Thrombosis. Wiley-
Blackwell. pp. 1–5
CLOT REMOVAL
tPA
tPA
Plasmin Plasmin
Plasmin
inhibitor
tPA
PAI
FDPs
Cesarman-Maus G, Hajjar KA (May 2005). "Molecular mechanisms of fibrinolysis".
British journal of haematology 129 (3): 307–21
…A LITTLE MORE
TPA
Pros: no immune
reaction
Cons: 2000$ 50 mg
Streptokinase
Pros: 2$ 136 mg
Cons: immune
reaction
Zivin JA. Ischemic cerebrovascular disease. In: Goldman L, Schafer AI, eds. Goldman's Cecil
Medicine. 24th ed. Philadelphia, PA: Elsevier Saunders; 2011: chap 414
FIBRINOLYTICS
Mari G, Abuhamad A, Cosmi E, Segata M, Altaye M, Akiyama M. Middle cerebral artery peak
systolic velocity: technique and variability. J Ultrasound Med. 2005 Apr;24(4):425-30.
Hatton, Chris (2008). Haematology (Lecture Notes). Cambridge, MA: Blackwell
Publishers. pp. 145–166
ANTICOAGULANTS
A NEW ERA IN ANTICOAGULANTS
Jessica L. Mega, M.D., M.P.H.; N Engl J Med 2011; 365:1052-1054
Wynbrandt, James; Ludman, Mark D. (1 January 2009)
BLOOD CLOTTING
DISORDERS
Thank you

Hemostasis