This document discusses stroke, specifically focusing on ischemic and hemorrhagic stroke. It defines stroke as an abrupt onset of focal neurologic deficit lasting at least 24 hours presumed to be of vascular origin. Ischemic stroke, which accounts for 87% of cases, occurs from local thrombus formation or emboli blocking a cerebral artery. Hemorrhagic stroke can be subarachnoid, intracranial, or subdural depending on where the bleeding occurs in the brain. The document then examines the pathogenesis of ischemic stroke, outlining how arterial occlusion leads to decreased blood flow and nutrients, cell damage, and ultimately cell death within 2-3 hours. For hemorrhagic stroke, the presence
PRESENTED BY ,
SpurthiBS
Doctor of Pharmacy (PharmD)
Mallige college of pharmacy
STROKE : The silent killer
2.
INTRODUCTION
STROKE is definedas an abrupt onset of focal
neurologic deficit that lasts at least 24hrs and is presumed
to be vascular origin.
It affects the left side of the face, right arm and even small
area.
BASED ON ETIOLOGICAL CLASSIFICATION:
1. ISCHEMIC STROKE (87%)
2. HEMORRHOGIC STROKE (13%)
3.
ISCHEMIC STROKE
It occurseither by local thrombus formation or by
emboli phenomenon which results in occlusion of
cerebral artery.
CAUSES:
1) ATHEROSCLEROSIS (70%)
2) CRYPTOGENIC (30%)
4.
HEMORRHAGIC STROKE
SUB-ARACHNOID
HEMORRHAGE
Occurs whena blood
vessels on the surface of
the brain ruptures and
bleeds into the space
between the brain and
the skull.
INTRA-CRANIAL
HEMORRHAGE
Occurs when a blood
vessels bleeds into the
tissue deep within the
brain
SUB-DURAL
HEMATONA
Abnormal collection of
blood between
duramater and
arachnoid
5.
PATHOGENESIS OF ISCHEMICSTROKE
ARTERIAL OCCLUSION
Severe reduction in cerebral blood flow
Maintain membrane ISCHEMIC PENUMBRA
integrity (INFARCT CORE)
Decrease nutrients to ischemic cell
Decreased ATP,accumulation of extracelluar Na+,
intracellular Na+ , H20
ISCHEMIA
6.
Cell swelling andlysis of cell
Increased intracellur Ca2+ activates
Lipases, protease and endonucleases
Breakdown of membrane phospholipids liberate
Free fatty acids and Amino acids( GLUTAMATE AND ASPARATE)
Further continue neuronal cell damage and accumulation
of free fatty acids Arachidonic acid (activates COX and LOX
PROSTAGLANDINS, LEUKOTRIENE , FREE RADICALS
AND CYTOTOXIC SUBSTANCES.
7.
Attack cell membrane
Increasedintracellular acidosis
Imbalance b/w C02 and bicarbonates
All the events occurs within 2-3hrs of the onset of
ischemia leading to cell death.
CELL
DEATH
8.
PATHOGENESIS OF HEMORRHAGICSTROKE
Presence of blood in the brain parenchyma
Damage to surrounding tissue by mechanical effect and neuro
toxicity of blood components and degradation products.