pathology of hаemostasis d.d., professor denefil olha volodymyrivna
TRANSCRIPT
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Pathology of hPathology of hааemostasisemostasis
D.D., ProfessorDenefil Olha Volodymyrivna
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Meaning
• 1. Control of blood fluid condition (is due to adequate correlation between activity of coagulative blood system and anticoagulative one)
• 2. Bleeding stop (is very important for control of the blood circulation index)
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HAEMOSTASIS SYSTEMS COMPONENTS
• * VESSEL’S WALL
• * ТROMBOCYTES
• * SYSTEMS OF THE BLOOD PLASMA:
• - COAGULATIVE
• - ANTICOAGULATIVE • - FIBRINOLYSIS• - KALLIKREIN-KININ
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HAEMOSTASIS SYSTEM
• VESSEL-TROMBOCYTE’S
(PRIMARY HAEMOSTASIS)
- Bleeding stop in micro vessels
• COAGULATIVE (SECONDARY)
FIBRIN CLOTS FORMATION
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НАEMOSTASIS VIOLATION CLASSIFICATION
• BY ETHIOLOGY - HEREDITARY
- ACQUIRED
• BY PATHOGENESIS - VESSEL-PLATELETS НАEMOSTASIS VIOLATION
- COAGULATIVE НАEMOSTASIS VIOLATION
• BY DIRECTION OF THE CHANGES
• - HYPOCOAGULATION
- HYPERCOAGULATION
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HYPOCOAGULATION
• REDUCED PROPERTY OF THE BLOOD TO FORM OF THE BLOOD CLOTS which results in spontaneous bleeding or hemorrhage
• (very often after trivial trauma)
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ETHIOLOGY
• 1. THROMBOCYTOPENIA • 2. THROMBOCYTOPATHY
• 3. VASOPATHY
• 4. CОАGULOPATHY
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THROMBOCYTOPENIA
Pathological condition which is characterized by the decreased amount
of thrombocytes in the blood
(LESS THEN 150·109 /l)
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HEREDITARY THROMBOCYTOPENIA
• As a rule, is accompanied with hereditary thrombocytes defect
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ACQUIRED THROMBOCYTOPENIA
• REASONS• INJURY OF THE THROMBOCYTES - by immune complexes - mechanical trauma (at spleenmegaly, haemangioma)
• THROMBOCYTES MATURATION DEPRESSION
(aplastic anemia, red bone marrow injury by chemical poisons and radiation, tumors in bone marrow – metastasis or primary)
• ACCELERATED USING OF THE THROMBOCYTES
(thrombosis, DIC-syndrome)
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• HETEROIMMUNE Arises most often in children
Reason – change of thrombocyte’s antigen structure (attachment of the viruses at measles, smallpox; attachment of the medicine’s origin haptens; vaccines)
Clinical course is benign (elimination of the reason conduces to absolute recovery)
IMMUNE THROMBOCYTOPENIA
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• AUTOIMMUNE Arises most often in adult
Reason – no immune system tolerance to own thrombocyte’s antigens
Provoked agents: medicines, viruses, bacteria
IMMUNE THROMBOCYTOPENIA
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AUTOIMMUNE THROMBOCYTOPENIA
VERLGOFF’S disease1. Ig G amount on the platelets surface increases in 10 time 2. main place of Ig G synthesis is spleen 3. treatment principles: - spleenectomy - corticosteroids - depression of immune response by medicines * Absolute recovery is not
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THROMBOCYTOPATY
• НАEMOSTASIS VIOLATION AS THE RESULT OF QUOLITATIVE
THROMBOCYTE’S DEFECTS OR THROMBOCYTE’S DYSFUNCTION, WHICH IS CHRACTERISE BY VESSEL-TROMBOCYTE’S НАEMOSTASIS VIOLATION, APPERENCE OF HAEMORHAGIES IN TISSUES AND ORGANS
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HEREDITARY THROMBOCYTOPATY
• WITHOUT VIOLATION OF GRANULES EXCRETION
GLANCMAN’S disease *Type of inheritance - autosomal-recessive *Reason - no glycoproteins 2в and 3а in
thrombocite’s membrane *Pathogenesis – thrombocytes cannot
interact with fibrinogen, so they don’t aggregate
*Signs: skin hemorrhages, nasal bleeding, uterine bleeding (some time deadly!!)
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• BECAUSE EXCRETION OF GRANULESIS VIOLATIED
Type of inheritance - autosomal-recessiveReason – violation of cycleoxigenase
activity, low activity of contractive proteins
Pathogenesis – no thrombocyte’s aggregation at collagen contact, no granules excretion
Signs: skin hemorrhages, nasal bleeding, uterine bleeding (some time deadly!!)
HEREDITARY THROMBOCYTOPATY
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• DEFICIT OF GRANULES AND THEIR CONTENT
• HERDJMANSKY-PUDLAK’S DISEASE (AR)• Reason– deficit of the dense granules
(АDP, аdrenalin, serotonin, Са2+)
• Pathogenesis – no thrombocytes aggregation after contact with collagen, no excretion of the granules substances
• Signs: skin hemorrhages, nasal bleeding, uterine
bleeding
HEREDITARY THROMBOCYTOPATY
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• VIOLATION OF THROMBOCYTE’S ADGESION AND AGGREGATION
• Willebrand-Jurgens syndrome (Аr)• Reason – von Willebrand’s factor deficit• Pathogenesis – violation of thrombocytes adhesion
because activity of c.f.8 is reduced• Bernar-Sulie’s disease (АR)
• Reason – no glycoprotein's 1 in thrombocyte’s membrane
• Pathogenesis – is violated interaction between thrombocytes and f.Willebrand, f. 5, f. 11
• Signs – capillary bleeding (particularly during sex aging and delivery)
HEREDITARY THROMBOCYTOPATY
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THROMBOCYTE’S FACTOR 3 DEFICIT
• BOUE-OWEN’S disease• Reason – f.3 deficit in thrombocytes
• Pathogenesis – no interaction between thrombocytes and coagulative plasma factors
• Signs: skin hemorrhages, nasal bleeding, uterine bleeding
HEREDITARY THROMBOCYTOPATY
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• COMBINATION OF THROMBOCYTOPATIA and OTHER
HEREDITARY ANOMALIES• VISCOTT-ОLDREEG’S syndr.
- Reason – reduced amount in thrombocytes dense granules (АDФ, аdrenalin, serotonin, Са2+) and alpha- granules (beta-thrombglobulin, fibrinogene, fibronectin, growth factor)
- Pathogenesis – weak adhesion and aggregation of the thrombocytes, no granules excretion
- Signs: hemorrhage syndrome appears in childhood (deadly bleeding is possible)
HEREDITARY THROMBOCYTOPATY
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ACQUIRED THROMBOCYTOPATY (ETIOLOGY)
• 1. Leucaemia – granules deficit inside thrombocytes because their maturation is accelerated (reduced adhesion and aggregation)
• 2. Ig М accumulation (causes injury of thrombocyte’s receptors and violation of thrombocytes and coagulative factors interaction (at immune diseases)
• 3. Vitamin В12 deficit (causes violation of granules excretion)
• 4. Medicines
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Medicine’s THROMBOCYTOPATY
* Thromboxan А2 synthesis inhibitors
- antiinflamational steroid medicines
- antiinflamational nonsteroid medicines (aspirin inhibits thrombocytes aggregation, effect last 4-6 days)
* Stimulation of cAMP synthesis
-papaverin
-euphillin
-anabolic steroids
* Са-ions blockers
-verapamil
-corinphar
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VASOPATHY
• Hemorrhage diathesis caused by functional and morphological defect of vessel’s wall
HEREDITARY ACQUIRED
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HEREDITARY VASOPATHY
• RANDIU-ОSLER’S dis., FABRE’S dis. • Reason – violation of connective tisue
development in vessel’s subendothelium - local thickening of the vessels - microvessel’s dilation - little of collagen fibers in subendothelium - vessels are very easy traumatized - weak adhesion end aggregation of the
thrombocytes as a result of collagen fibers deficit
Signs: – nasal bleeding, pulmonary-bronchial
bleeding, gastro-intestinal bleeding (some time deadly)
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1. Idiopathial (Caposhi’s sarcoma) - ethiology – unknown2. Stagnantal (Klotc’s dermatitis, Fawr-Rakusho’s
dermatitis) - ethiology – chronic heart failure, local venous
insufficiency3. Distrophial - uprarenal glands hyperfunction, glucocorticoid
therapy (steroid purpura - occurs because collagen fibres synthesis depression)
- vitamin C deficit - vessel’s damage by immune complexex (Shenliayn-Ganouh’s diseas)
Signs: – skin haemorrhagies
ACQUIRED VASOPATHY
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CОАGULOPATHY
• Pathological state which results from deficit of coagulative system activity
HEREDITARY ACQUIRED
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HEREDITARY CОАGULOPATHY
• Group of the diseases caused by hereditary deficit or hereditary molecular anomaly of the substances which control of blood coagulative properties
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• CLASSIFICATION1. Coagulopathy as a result of isolated deficit of internal
mechanism of prothrombinase activation (haemophylia А, В, С, Willebrand’s dis., Hageman’s deficit)
2. Coagulopathy as a result of isolated deficit of external mechanism of prothrombinase activation (hypoproconvertinemia – deficit of VII c. f.)
3. Combined deficit of internal mechanism and external one of prothrombinase activation (parahaemophylia – deficit of V c. f., Stuart-Prauer’s dis. – deficit of X c. f.)
4. Violation of the last stage blood coagulation (afibrinogenemia)
HEREDITARY CОАGULOPATHY
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STATISTIC
• Amount of coagulopathie’s types in general statistic:
Hemophilia А 68 – 78% Willebrand’s disease 9 – 18 % Hemophilia В 6 – 13 % Hemophilia С, parahaemophylia, hypoproconvertinemia 1 – 2 %
Other types are the medical casuistry (occur very rarely)
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Hemophilia А
Haemorrhage syndrome caused by hereditary deficit of VIII f. procoagulative unit
Structure of VIII Factor (high mass protein)1. Procoagulative glucoprotein (VIII:C)2. Glucoprotein, which causes thrombocytes adhesion (VIII:WF)3. Glucoprotein, which causes thrombocytes adhesion due to
ristomicine (VIII:R-cоf.)4. Antigen marker of VIII:C (VIII:C АG)5. Antigen marker of VIII:R-cоf (VIII:R АG)
Activity of factors VIII:K and VШ:W is being decreased at the decrease of complex structure mass.
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• ETHIOLOGY – gene anomaly in X-chromosome which controls synthrsis of procoagulative glucoprotein (VIII:C)
They ill – males (46, XhY ) – females (46, XhXh ), (45, Xh O) Types; - Hemophilia А+ (antigen positive hemophilia is the result of
abnormal VIII:C factor synthesis), they ill 8 –10 % - Hemophilia А- (antigen negative hemophilia – no synthesis of
VIII:C factor), they ill 90 –92 % Clinical signs: hemorrhages in major joints, deep
hematomas of skin, intramuscular hematomas, massive and prolonged posttraumatic bleedings, intra ubdominal bleedings, in side gastro-intestinal tract
Hemophilia А
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• Children of last Russian Car, his sun suffered from hemophilia A.
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• ETHIOLOGY – gene anomaly in X-chromosome which controls synth. of IX coagul. f.
They ill – males (46, XhY ) – females (46, XhXh ), (45, Xh O) Types; - Hemophilia B+ (antigen positive hemophilia is the
result of abnormal IX factor synthesis) - Hemophilia B- (antigen negative hemophilia – no
synthesis of IX factor) Clinical signs: hemorrhages in major joints, deep
hematomas of skin, intramuscular hematomas, massive and prolonged posttraumatic bleedings, intra ubdominal bleedings, in side gastro-intestinal tract
Hemophilia B
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Hemophilia in newborn
(subcutaneous hematoma)
Subcutaneous hematoma in childe
after injection
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Acquired coagulopathy • Character – polydeficit
• ETHIOLOGY 1. immune inhibition of coagulative factor (antigenic
noncompatibility of the mother and the fetus)
2. K-vitamin dependent coagulative factors deficit (VII, X, IX, II) а) poor vitamin K synthesis (dysbacteriosis, profusal diarrhea,
enteropathies ) б) violation of vitamin K absorbtion (obturative icterus) в) damage of the liver
3. heparin or herudin overdose
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Hypercoagulation
• Pathological property of the blood which is characterised by trombuses formation inside the
vessels
trombosis
DIC-syndrome
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DIC-syndromedisseminated intravascular blood coagulation syndrome
• CLASSIFICATION
• By clinical course 1) acquired
2) chronic
1) local
2) diffuse
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ETHIOLOGY
1. Infection , sepsis (bacteriemia, virusemia)2. Chok - traumatic, hemorrhagical, anaphylactic,
cardiogenic, septic (at septic shock death occurs in 100 % cases)
3. Surgical operation4. Thermal burns and chemical ones5. Terminal states (stages of the dying), heart stop6. Acute intravessels hemolysis of the RBC’s 7. Obstetrics pathology (20-25 %)8. Leukemia (33-45 %)9. Immune diseases 10. Allergy reactions
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DIC-syndrome stages
• 1) Hypercoagulation (numerous thrombus's formation because hyperactivity of coagulative system)
• 2) Coagulopathy of using (exhaustion of coagulative system, overusing of the thrombocytes for thrombus's formation)
• 3) Hypocoagulation (decrease of coagulative system activity, activation of anticoagulative system and fibrinolysis)
• 4) Finishing (recovery, complications, death)
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1) Hyperthrombinemia
(thromboplastin from injured tissues and blood cells comes in to the bloob and conduces thrombin formatting)
DIC-syndrome pathogenesis
At infection active monocytes start to produce such coagulative factors as
VII, X, IX, II
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2) Thrombocytes aggregation
(it causes thrombocytopenia of using which results in bleeding)
3) Erythrocyte’s damage and hemolysis
(couses АDP excretion, thrombocyte’s adhesion and aggregation)
DIC-syndrome pathogenesis
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4) “Humoral protease detonating ” (activation of coagulative factors,
anticoagulative factors, fibrinolytics, proteins of kallikrein-kinin system, proteins of complement system causes accumulation of great amount of proteins disintegration metabolites in the blood. They are very toxic and damage a vascular wall and tissues)
DIC-syndrome pathogenesis
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5) Blood coagulative factors exhaustion (causes bleeding)
6) Exhaustion of coagulative system (results in thrombosis)
DIC-syndrome pathogenesis
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1. Hemocoagulative shock (at acute DIC-syndrome)
reason microcirculation violations (causes tissue’s hypoxia) accumulation of proteolysis toxic substances
signs * decrease of arterial pressure * decrease of central venous pressure * development of profusal bleeding (promotes the
transformation of hemocoagulative shock into the hemorrhagic one )
DIC-syndrome clinical signs
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2. Нaemostasis violation
1. Hypercoagulation
Main sign – thrombosis
Blood is clotted in test-tube
2. Hypocoagulation
Main sign – bleeding
At the same time exhaustion of fibrinolysis system occurs)
DIC-syndrome clinical signs
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3. Thrombocytopenia
results from thrombuses great amount formation in vessels
(Thrombocytopenia of using)
DIC-syndrome clinical signs
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4. Block of microcirculation(causes damage of the organ-targets)
- in lungs (thrombuses come from venous system) – results in acute respiratory failure
- in kidneys - acute renal failure- in ventricle and intestine - results in mucous
membrane dystrophy and profusal bleedings, intoxication, chok (high morbidity percentage)
- in suprarenal glands- in liver- in pituitary gland
DIC-syndrome clinical signs
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Thank you for attention !