Hemorrhagic Stroke: Pathogenesis

Hemorrhagic Stroke: Pathogenesis
1° ICH (-75%) 2° ICH (-25%) * MD Amyloid Angiopathy Hypertension Unknown Vascular Malformations Aneurysm Drugs Amyloid deposits in Lipohyalinosis replacing Dilation of a weakened e.g. cocaine, crystal blood vessels and can cause walls to weaken arterial musculature and weakens blood vessels blood vessel meth, decongestants, anticoagulants
Authors: Andrea Kuczynski Reviewers: Sina Marzoughi Usama Malik Michael D Hill* at time of publication
Abbreviations: Blood vessel ruptures and ATP: adenosine triphosphate Glu: glutamate bleeds, 1% intracranial pressure Note: the pathophysiology and exact Hb: hemoglobin mechanism is not well known ICH: intracerebral hemorrhage Blood cytotoxicity and sudden focal internal ICP: intracranial pressure brain trauma from hematoma mass effect LOC: level of consciousness RBC: red blood cell • RBC lysis 4, ATP 1′ lactate Cytotoxic Hb (heme, iron) release Astrocytes release Glu Dysfunction of Nalr ATPase pump on neurons Astrocyte death Tiv Fenton-type free Excitotoxicity t Nat, Ca2+ H2O influx with Nat Microglia clear debris radical generation influx, Kt outflux Release inflammatory Oxidative damage to proteins, nucleic acids, carbohydrates, lipids Depolarization • markers (TNFa, IFy, IL-11i) Activate mGluR Neurons release Glu Edema • Inflammation Necrosis 1′ Ca2+ influx

Neurological signs: focal motor weakness, aphasia, vision loss, sensory loss, imbalance/incoordination, change in LOC
Legend:
Pathophysiology Mechanism
Sign/Symptom/Lab Finding
General findings: nausea, vomiting, headache, seizures, lethargy
Complications
Increased ICP: papilledema, sudden headache, non-reactive pupils, decreased LOC, nausea/vomiting