HAEMORRHAGIA Bleeding
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1 HAEMORRHAGIA Bleeding
2 Cassification Size Location pathomechanism
3 Hematoma: external or may be enclosed within a tissue petechiae : 1-2 mm hemorrhages into skin, mucous membranes, or serosal surfaces increased intravascular pressure thrombocytopenia defective platelet function (as in uremia), clotting factor deficits Purpura: 3 mm same disorders that cause petechiae secondary to trauma, vascular inflammation (vasculitis), increased vascular fragility (amyloidosis)
4 Ecchymoses: >1 to 2 cm after trauma Suffusio: superfitial between tissue layers Apopexie / parenchymal Brain adrenas Meningococcus sepsis
5 Pathomechanism Haemorrhagia per rhexim vessel injury Vasculitis Fragility ATS aneurysm Haemorrhagia per arrosionem Erosive gastritis Ulcus Tu. Haemorrhagia per diapedesim Permeability Patelet
6 Location Hemothorax Hemopericardium Hemascos/hemoperitoneum Hemarthros Metrorrhagia Intracranial Epidural Subdural Subarachnoid Intracerebral/parenchyma
7 Epidural hematoma Temporal bone fracture Middle meningeal artery laceration Lucidum intervallum patients can be lucid for several hours between the moment of trauma and the development of neurologic signs epidural hematoma may expand rapidly and is a neurosurgical emergency requiring prompt drainage
8 Subdural hematoma inner surface of the dura mater and the outer arachnoid layer of the leptomeninges Injury of Bridging veins acute subdural hematoma chronic subdural hematomas
9 Parenchymal Hypertensive intraparenchymal hemorrhage Basal gangia putamen (50% to 60% of cases) thalamus, pons, cerebellar hemispheres Charcot Bouchard microaneurysms Hyaine arteriooscerosis hemangioma AV malformation
10 Lobar hemorrhages: (cerebral hemispheres) hemorrhagic diathesis, DIC neoplasms, drug abuse, infectious and noninfectious vasculitis, cerebral amyloid angiopathy
11 Pathomechanism of bleeding A. thrombocytopenia B. thrombocytopathy C. coagulopathy D. vasculopathy
12 A. Thrombocytopenia: < /mm 3 Normal count /mm 3 < /mm 3 spontaneus bleeding /mm 3 post traumatic bleeding platelet production -bone marrow insuf. - drugs -infection platelet survival - ITP - DIC - giant haemangioma - TTP (thrombotic thrombocytopenic purpura) -HUS sequestration -hypersplenism
13 B. Thrombocytopathia: 1. Congenital: - defects of adhesion - defects of aggregation - defects of release a. Bernard-Soulier (GpIb-vWf) b. Glanzmann thrombasthenia (GpIIb-IIIa. fibrinogen) 2. Acquired - aspirin (cyclooxygenase inhibitor) -uraemia - HIV (CD4, GpIIb-III)
14 C. Coagulopathy 1. Hereditery vonwillebrand disease - bleeding time - platlet count norm. Hemophilia A (f.viii) Hemophilia B (f.ix) - bleeding time norm. - coag. time 2. Acquired - hepatic (K vitamin) f.ii-vii-ix-x, protein C, - DIC
15 D. Vasculopathy 1. Acquired -Infection / Vasculitis Waterhause Fridericksen sy septicemia -Drug reaction/ hypersnsitivity (IC) -Amyloid -steroid /Cushing sy -Henoch-Schönlein (IC) 2. Hereditery -Rendu-Osler Weber (HHT/herediter hemorrhagic teleangiectasis) -Ehlers-Danlos sy
16 PLATELET HEMOSTASIS ENDOTHEL COAGULATION
17 Platelets promote hemostasis by the following interconnected mechanisms adhering to sites of vascular injury or artificial surfaces releasing compounds from their granules aggregating together to form a hemostatic platelet plug providing a procoagulant surface for activated coagulation protein complexes on their phospholipid membranes
18 ENDOTHEL
19 Antithrombotic Prothrombotic Platelet aggregation inhibition PGI2 NO ADPase Thrombin binding and inhibition Heparin like molecules Protein C/S activation Alpha 2-macroglobulin Fibrinolysis Tissue plasminogen activator ( t-pa) Platelet aggregation stimulation Von Willebrand S factor PAF Procoagulant factors Tissue factor Binding factors IXa, Xa Factor V Inhibition of fibrinolysis t-pa inhibitor
20 COAGULATION
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