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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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hemostasis

HEMOSTASIS

By Prof\ Sameh Shamaa

Prof Of medical Oncology and Internal medicine

Mansoura Faculty Of Medicine

HEMOSTASIS

hemostasis1
HEMOSTASIS

Def:- stoppage of bleeding from the blood vessels

Mechanisms

  • v.c of blood vessels
  • platelet plug formation
  • Blood coagulation (fibrinogen fibrin)
  • Clot retraction
  • fibrinolysis to dissolve the clot

HEMOSTASIS

primary hemostasis
PRIMARY HEMOSTASIS

includes the processes that result in the formation of the platelet plug.

Necessary factors-:

-The blood vessels : the vessel walls esp. the subendothelial layer.

- The platelets

- 2 plasma glycoproteins:

- fibrinogen

-Willebrand factor ,which also presents inside the platelets

mechanisms
Mechanisms:

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.

HEMOSTASIS

exploration of the 1ry homeostasis
Exploration of the 1ry homeostasis
  • Important points in the history of any bleeding patients :

HEMOSTASIS

slide6

Family history

  • Duration (recent onset or since childhood)
  • Duration of the bleeding episode.
  • Circumstance of bleeding

(spontaneous, after trauma, or surgery)

HEMOSTASIS

type and character of bleeding
Type and character of bleeding: -
  • Purpuric spots

(capillary or platelets defect not characteristic of hemophilia)

  • Hematoma, hemarthrosis or large ecchymoses at the site of trauma :

suggests hemophilia (coagulation defect)

  • Sudden severe bleeding from multiple sites after prolonged surgery or during obstetric procedures

suggests acquired fibrinogen defect

HEMOSTASIS

slide9

Capillary resistance test of Hess

  • Platelets count
  • Bleeding time

time needed for the platelet plug formation

If . N. ------ Normal 1ry homeostasis .

↑ ------ platelet or vascular defect.

HEMOSTASIS

capillary resistance test of hess
Capillary resistance test of Hess:

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

HEMOSTASIS

slide11

Other tests

only done if there is a prolonged bleeding time with normal platelet count

  • Measurement of capillary resistance
  • Measurement of Willebrand factor
  • Platelets function tests (Adhesiveness, Aggregation)
  • other tests for platelets (clot retraction, ↓ prothrombin consumption).

HEMOSTASIS

coagulation of blood
Coagulation of Blood

Def :- represent the conversion of fibrinogen (soluble protein) to fibrin (insoluble) meshwork which occludes the point or vessel rupture.

HEMOSTASIS

first step activation of factor x
First Step :Activation of factor X

BY One of 2 systems:

I-urgent system II-delayed system

(Extrinsic system.) (Intrinsic system.)

HEMOSTASIS

systems of coagulation
systems of coagulation

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

Xa

2- prothrombin thrombin

3-fibrinogen Fibrin

HEMOSTASIS

extrinsic system
EXTRINSIC SYSTEM

FACTORS NICESSORY ARE:

Factor X

Tissue factor and Factor VII

Tissue F.

VIIa VII

Xa X

Blood vessel

HEMOSTASIS

intrinsic system
INTRINSIC SYSTEM

Necessary factors: -

XII (Hageman factor)

- Contact system XI

Kallikrene

kininogene

- F. IX

- F. VIII

- F. X

- Ca. ++

- phospholipids of the platelet’s membrane

HEMOSTASIS

slide17

Contact System:

Foreign surface

|--------------------------------------------------| Kalierne XII kininogene

Fragmentation

XIIa

XI XIa

Rest of intrinsic pathway

IX

HEMOSTASIS

slide18

Rest of intrinsic pathway

IX

Platelets

Ca ++

IXa

X VIIIa

VIII

Xa

II IIa

HEMOSTASIS

second step of coagulation
Second Step: of Coagulation

Thrombin Formation: (IIa)

Factors needed:

- prothrombin (II) Ca++ platelets

- Xa IIVCa++

- V (acceleririe) Xa

- phospholipids

- Ca + + IIa

HEMOSTASIS

3 rd step fibrin formation
3rd Step :Fibrin Formation

Fibrin Formation:-

------------------------

IIa

XIII XIIIa

(Fibrinogen) -------------------- Ia

(Soluble fibrin)

Insoluble Fibrin

HEMOSTASIS

physiological anticoagulants
Physiological anticoagulants
  • 1- Serine protease inhibitors :inhibit the coagulation cascade.
  • 2-Neutralizers of activated coagulation factors (components of protein C system)

HEMOSTASIS

1 serine protease inhibitors
1-Serine protease inhibitors:
  • 1-Antithrombin (III).
  • 2-Heparin and heparin like substance.
  • 3-Alpha 1 antitypsin.
  • 4-Alpha 2 macroglobulin

HEMOSTASIS

2 neutralizers of activated coagulation factors components of protein c system
2-Neutralizers of activated coagulation factors:(components of protein C system)
  • 1-Protein C: synthesized in the liver, vit. K dependant, activated by thrombin.
  • 2-Thrombomodulin.
  • 3-Protein S and C4b-binding protein.

HEMOSTASIS

fibrinolysis
Fibrinolysis

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

HEMOSTASIS

measurement
Measurement

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).

exploration of the coagulation
Exploration of the coagulation
  • whole blood clotting time

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

HEMOSTASIS

slide28

(2) One stage prothrombin time:

general exploration or the extrinsic pathway (Quick time)

N : 16-18 sec.

  • addition of tissue thromboplastin +
  • ca++ to decalcified plasma ---> measure the time till coagulation occur.
  • Affected by factors VII,X, V, II & fiboinogen (only severe defect)

HEMOSTASIS

slide29

(3) partial thromboplastin time (PTT)

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

HEMOSTASIS

slide30

Thrombin time

detect the defects in the conversion of fibrinogen ---> fibrin

Measured by addition of thrombin to citrated patients plasma

If polonged

  • Abnormalities of fibornogen

(hypo or hyper or dysfibrinogenemia)

  • Heparin
  • Presence of some abnormal proteinswhich inhibits the polymerisation of monomers of fibrin. (e.g myeloma protein

HEMOSTASIS

slide31

(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

HEMOSTASIS

slide32

(7) Detection of coagulation inhibitors:

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.

HEMOSTASIS

practical investigation of hemostatic trouble
PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE

B.T

Platelets count

Quick test

CKT

Thrombin time

Dosage of fibrinogen

HEMOSTASIS

practical investigation of hemostatic trouble1
PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE

I- B.T↑, platelets ↓( ↓80.000; mm3)

Thrombocytopenia

2- B.T↑, platelets normal

Qualitative platelets abnormalities Willebrand disease

congenital or acquired

platelet factor tests dosage of factor VIII

HEMOSTASIS

practical investigation of hemostatic trouble2
PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE

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)

HEMOSTASIS

practical investigation of hemostatic trouble3
PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE

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.

HEMOSTASIS

practical investigation of hemostatic trouble4
PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE

6-↑T.T either:

* 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.

HEMOSTASIS

practical investigation of hemostatic trouble5
PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE

7- ↓fibrinogen

* congenital afibrinogenimia or hypofibrinogenimia

  • Acquired hypofibrinogenimia e.g.liver cirrhosis.
  • consumption of fibrinogen: e.g.D.I.V.C, fibrinolysis

HEMOSTASIS

slide39

PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE

8-All tests ate Normal:

* Capillary fragility (usually only ecchymoses ) ---> measurement of cap.fragility.

* deficient factor XIII

* no hemostatic troubles.

HEMOSTASIS

thank you

Thank You

HEMOSTASIS