CVD.pptx

CVD -: PRESENTED BY D. ABRAR AL MUBARK MBBS (OIU ) MD (U O K )  When say CVD or CVA * We mean pathological process involving blood. vessel The most common cause of death in the*. developed world Most prevalent cause of neurological *.morbidity -: The main pathogenic mechanism are...

CVD -: PRESENTED BY D. ABRAR AL MUBARK MBBS (OIU ) MD (U O K )  When say CVD or CVA * We mean pathological process involving blood. vessel The most common cause of death in the*. developed world Most prevalent cause of neurological *.morbidity -: The main pathogenic mechanism are. Thrombotic occlusion -1. Emboli occlusion -2. Vascular rupture -3 -: Stroke Is clinical designation applied to all of these. condition when symptom being acutely Thrombosis |embolism have similar consequence including decrease blood supply lead to low oxygen and nutrient supply so infarction in the area that supplied by. affected vasculature Hemorrhage associated with rupture vessel which lead to direct tissue. damage ,hypoxia ,ischemia and infarction -: Global cerebral ischemia -: Ischemia – hypoxic injury can occur in. Severe systemic hypotension -1. Cardiac arrest -2. Shock -3 Clinical outcome is vary Mild and transient post ischemic insult with. eventual recovery ( cofusional state ) Severe insult lead to wide spread neuronal. death ( global ischemia ) Some area is more vulnerable to ischemia and ? neuronal death even with mild insult ? Home work  -: Morphology.Ischemic change ( infarction ) -: Early change Acute neuronal cell change (red neuron) occur. 12-24 hr after insult  -: Characterized by Micro vacuolization followed by cytoplasmic *. eosinophilia. Nuclear pyknosis and karyohexsis *. Neutrophils infiltration *  -: Sub acute change. occurring at 24 hr to 2weeks , include tissue necrosis , influx of macrophage. vascular proliferation and reactive gliosis Gliosis = fibrous proliferation of glial cell in. injured areas of CNS  -: Repair After 2 weeks ,characterized by removal of all necrotic tissue ,loss of organized CNS. structure and gliosis  -: Focal cerebral ischemia Cerebral arterial occlusion lead to focal. ischemia then infarction Initially may be modified by collateral blood. flow which limit the damage Embolic infarction are more common than.infarction due to thrombosis  -: Predisposing factor. Cardiac mural thrombi *. Myocardial dysfunction *. Valvular disease *. Atrial fibrillation *. DVT *. Atherosclerosis *  -: Common site for occlusion carotid bifurcation origin of middle cerebral. artery Supply lateral side of the frontal ,temporal. and parietal lobe  -: Morphology -: Non hemorrhagic During first 6 hr the tissue unchanged 48 hr. tissue become pale. day brain turns gelatinous and friable 2-10. After 10 days become liquifactive necrosis  Hemorrhagic infarction Same picture which addition of blood. extravasation and resorption  Intracranial hemorrhage. Bleeding with in the brain -: Risk factor HTN 2- Arteiovenous and cavernous -1. malformation. 3- Tumors Primary brain parenchymal hemorrhage Non traumatic* Most common in mid to late adult life.( 60 years of age ) -; Risk factor HTN basal ganglia ,thalamus ,Pons ,. cerebellum ( common site of bleeding ). Small blood vessel rupture - Clinical manifestation varying according to site. and size of bleeding  Cerebral amyloid angiopathy condition caused by amyloid peptide deposition in medium and small caliber meningeal and cortical vessel which weaken vessels wall and increase risk of. hemorrhage main site lobe of cerebral cortex (lobar.hemorrhage )  Subarachnoid hemorrhage Hemorrhage in the subarachanoid space -; Causes Rupture of berry aneurysm most common of -1. non traumatic cause. Vascular malformation -2 Trauma -3. Tumors -4 Bleeding can occur at any time but commonly associated with acute increase in intracranial. pressure -; C/F. Headache- -. Rapidly lose consciousness. t0 50 % die from first bleeding % 25 - Hydrocephalus common complication - consequence of healing and fibrosis and scar. formation -: Berry aneurysm occur in the anterior circulation near % 90. major arterial branch point. Maybe single or multiple. Congenital condition develop over time* increased risk in patients with autosomal dominant polycystic kidney disease as well as in those with genetic disorder of extra cellular. matrix protein. Probability of rupture related to size *  Vascular malformation -: Type. Arteriovenous malformation (AVM ) -1. Cavernous malformation -2. Capillary telangiectasia -3. Venous angioma -4  AVM. Most common and most danger Male to Female ratio 2:1. Age 10 – 30year C\F Seizure , intracerebral hemorrhage or *. subarachnoid. Lead to HF in newborn * Multiple type associated with heridadatory. telengectasia.  Other vascular disease Hypertensive CVA -1 Vasculitis -2  Hypertensive CVA Hypertension casue hyaline arteriolar and -: arterial sclerosis in the following area Basal ganglia -1 White matter -2 Brain stem -3 The affected vasculature become weak and. more vulnerable to rupture. pathology may be infarction or hemorrhage Acute hypertensive encephalopathy The most lethal clinical consequence of. hypertension Def :- sustained rises in diastolic blood. pressure to greater than 130 mmHg Cause increased intracranial pressure. and global cerebral dysfunction -: C/F Headache , confusion ,vomiting ,convulsion ,. and some time coma ? Other consequence ? Mention  Vasculitis -: Def Inflammatory process involving blood vessel may compromise blood flow and cause. ischemia -: Type. Infectious affect small and large vessel -1 Causes :- TB ,Syphilis , opportunistic.infections Systemic involve cerebral vessel cause -2 multiple and single infarct ( poly arteritis. nodosa ). Primary angiitis -3  -: Primary angiitis Form of vasculitis involve multiple small to medium size caliber parenchymal and.subarachnoid vessels THANKS