HEMOSTASIS. By Prof\ Sameh Shamaa Prof Of medical Oncology and Internal medicine Mansoura Faculty Of Medicine. HEMOSTASIS. HEMOSTASIS. Def:- stoppage of bleeding from the blood vessels Mechanisms v.c of blood vessels platelet plug formation Blood coagulation (fibrinogen fibrin)
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By Prof\ Sameh Shamaa
Prof Of medical Oncology and Internal medicine
Mansoura Faculty Of Medicine
Def:- stoppage of bleeding from the blood vessels
includes the processes that result in the formation of the platelet plug.
-The blood vessels : the vessel walls esp. the subendothelial layer.
- The platelets
- 2 plasma glycoproteins:
-Willebrand factor ,which also presents inside the platelets
1-v.c of the bl. vessel.
2- Platelets adhesion to subendothelial layer, ( Willebrand factor is necessary for this stage)
adhesion of platelets-3- platelets secretion:
their activation and secretion of ADP,adrenaline, noradrenaline –> aggregation & activation of other platelets.
4- Aggregation of platelets.
5- Formation of capillary plug.
(spontaneous, after trauma, or surgery)
(capillary or platelets defect not characteristic of hemophilia)
suggests hemophilia (coagulation defect)
suggests acquired fibrinogen defect
time needed for the platelet plug formation
If . N. ------ Normal 1ry homeostasis .
↑ ------ platelet or vascular defect.
sphygmomanometer cuff above the cubital fossa and raise the pressure to 100 mm Hg (or midway between systolic & diastolic if systolic pressure <100) for 5 - 7' minutes- deflation '3 minutes later count the number of petichea in area of 3 cm diameter, 1 cm below the cubital fossa Normally up 10 if more than 20, means platelets or capillary wall defect
only done if there is a prolonged bleeding time with normal platelet count
Def :- represent the conversion of fibrinogen (soluble protein) to fibrin (insoluble) meshwork which occludes the point or vessel rupture.
BY One of 2 systems:
I-urgent system II-delayed system
(Extrinsic system.) (Intrinsic system.)
I-urgent system. II-delayed system
Extrinsic system. Intrinsic system.
12-20'' (seconds) 4-8' (minutes)
In vivo only. In vivo & in vitro
Due to tissue damage. due to contact with foreign surface
Tissue factor activation of contact system
X < ------------------------------------IX a < ---------------- IX
2- prothrombin thrombin
FACTORS NICESSORY ARE:
Tissue factor and Factor VII
Necessary factors: -
XII (Hageman factor)
- Contact system XI
- F. IX
- F. VIII
- F. X
- Ca. ++
- phospholipids of the platelet’s membrane
|--------------------------------------------------| Kalierne XII kininogene
Rest of intrinsic pathway
Thrombin Formation: (IIa)
- prothrombin (II) Ca++ platelets
- Xa IIVCa++
- V (acceleririe) Xa
- Ca + + IIa
(Fibrinogen) -------------------- Ia
is the process wherein a fibrinclot, the product of coagulation, is broken down.Its main enzymeplasmin cuts the fibrin mesh at various places, leading to the production of circulating fragments that are cleared by other proteases or by the kidney and liver
When plasmin breaks down fibrin, a number of soluble parts are produced. These are called fibrin degradation products (FDPs). FDPs compete with thrombin, and so slow down the conversion of fibrinogen to fibrin (and thus slows down clot formation).
Normally 4-10 minutes
Generally ---> N. in platelets defects.
↑ = coagulation defect
But not very sensitive: - only +ve when blood coagulation is very defective
HEMOSTA fibrinolysis (Hyperfibrinolysis), SIS
general exploration or the extrinsic pathway (Quick time)
N : 16-18 sec.
or CKT(cephaline koalin time)
General exploration of the intrinsic pathway
clotting time of recalcified plasma in the presence of phospholipid (cephaline), while koalin powder for activation of Hageman factor'. Affected by factors XII, XI, IX, VIII, X, II
detect the defects in the conversion of fibrinogen ---> fibrin
Measured by addition of thrombin to citrated patients plasma
(hypo or hyper or dysfibrinogenemia)
(5)Deficiency of F XIII (fibrin stabilizing factor ) detected by noting the solubility of fibrin in 5M urea or 1% monochloroacetic acid (can't dissolve fibrin in the presence of factor XIII).In congenital defect of f. XIII ---> dissolution of the clot in <10.
(6) Assay for each cogulation factor is available
1-Inhibitors for a specific factor (especially F. VIII)
usually ---> severe hemorrhage
2- Inhibitors against platelets or tissue phospholipids ---> prolongation of tests of coagulation (Quick or CKT) e.g L.E
but usually no hemorrhagic manifestations
3- if there is ↑of Quick test or CKT or thrombine:-
50% of normal plasma + 50% of patient plasma
(incubation at 370c for I hour) repeat the test
If become normal ---> factor defect
if no correction ---> presence of inhibitors.
Dosage of fibrinogen
I- B.T↑, platelets ↓( ↓80.000; mm3)
2- B.T↑, platelets normal
Qualitative platelets abnormalities Willebrand disease
congenital or acquired
platelet factor tests dosage of factor VIII
3- ↑Quick + ↑CKT Other tests are N
Acquired defect of several defect of factor common for
factors (II, VII, X,V) 2 pathways ex. X or V or II
4- Quick N., ↑ CKT: either:
I- Hemophilia Aor B.
2- Rarely ---> defect of one factor of the contact system (XII, or XI or others)
5- Quick ↑, CKT N
isolated defect of factor VII
in 3, 4..5 dosage of the factors with suspected deficiency, also search for inhibitors. Ex:
- ↑ Quick, normal dosage of factors---> hyperfibriongenemia which inhibit the test
- ↑Quick +↑CKT + no F. defect --->? Inhibitors, e.g. antiphospholipides.
* heparine in the blood or in the tube. Here T.T can be corrected by adding either
a- toluidine blue
b-Reptilase time (incomplete thrombin not sensitive to heparin and not inhibited by antithrombin III).
* If (a-b also defective) ---> troubles of fibrin polymerisation :either due to abnormal fibrin (dysfibrinogenimia) or inhibition e.g by ---> myeloma protein or F.D.P.
* congenital afibrinogenimia or hypofibrinogenimia
8-All tests ate Normal:
* Capillary fragility (usually only ecchymoses ) ---> measurement of cap.fragility.
* deficient factor XIII
* no hemostatic troubles.