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STROKE :silhouette: - Coggle Diagram

- - - - 1. 87% of all strokes are ischemic, and occur due to an obstruction in cerebral blood flow, most commonly from thromboembolic events or large artery atherosclerosis. The reduction in cerebral perfusion below the critical threshold triggers a cascade of biochemical events leading to neuronal injury.
        
        Energy failure + ionic imbalance: Depletion of adenosine triphosphate (ATP) leads to the failure of ATP-dependent ion pumps, mostly the Na+/K+ ATPase and Ca2+ ATPase pumps.
        
        Membrane depolarization: Increased sodium influx and cytotoxic edema.
        
        Intracellular calcium overload: Activation of calcium-dependent enzymes such as proteases, phospholipases, and endonucleases, leading to cellular damage.
        
        2. Neurotransmitter dysfunction: The brain experiences excessive release of glutamate, which binds to N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors.
        
        Results in: Mitochondrial dysfunction: Release of reactive oxygen species (ROS).
        
        Results in: Activation of apoptotic pathways: cellular apoptosis and necrosis
        
        3. Oxidative stress and free radical damage: The accumulation of ROS, including superoxide anions, hydrogen peroxide, and hydroxyl radicals, results in lipid peroxidation and protein oxidation+DNA damage.
        
        Protein oxidation and DNA damage: Activation of pro-apoptotic cascades and neurodegeneration.
        
        Lipid peroxidation: Disruption of the blood-brain barrier.
        
        4. Inflammatory response: Post-ischemic neuroinflammation is mediated by the activation of resident microglia and infiltration of peripheral immune cells, releasing pro-inflammatory cytokines such as interleukin-1β, tumor necrosis factor-alpha, and interleukin-6.
        
        Results in: Increased risk of post-stroke infections due to immune suppression.
        
        Results in: Exacerbation of secondary neuronal damage
        
        5. Reperfusion injury: Restoring blood flow after an ischemic event can worsen damage due to the burst of oxidative stress and ROS generation, increased inflammatory infiltration and BBB breakdown, and risk of hemorrhagic transformation.
    - - Hemorrhagic stroke (intracerebral and subarachnoid hemorrhage) results from the rupture of cerebral blood vessels due to hypertension, aneurysm rupture, or cerebral amyloid angiopathy.
        
        2. Toxic Effects of Blood Components: Hemolysis releases hemoglobin, which gets converted into heme and iron.
        
        Oxidative stress Free radical-mediated neuronal damage.
        
        BBB breakdown: Edema formation and worsening neurological deficits.
        
        Neuroinflammation: Activation of microglia and astrocytes.
        
        1. Hematoma Expansion and Mass Effect: Increased intracranial pressure (ICP), resulting in herniation and decreased cerebral perfusion
        
        3. Cerebral Vasospasm and Delayed Ischemia: In subarachnoid hemorrhage, vasoactive substances contribute to prolonged vasoconstriction, increasing the risk of delayed ischemia and infarction
  - - - Post-stroke epilepsy from excitotoxic injury and gliosis.
      - Hemorrhagic transformation of ischemic stroke due to BBB disruption.
      - Dementia and cognitive decline linked to chronic neuroinflammation.
    - - Deep vein thrombosis and pulmonary embolism due to immobility.
      - Infections (pneumonia, urinary tract infections) from post-stroke immunosuppression.
      - Cardiac complications, including arrhythmias and heart failure.
        
        Cardiac complications following a stroke arise due to autonomic dysfunction, inflammation, and excessive catecholamine release
  - - - Brief disruption of blood flow of cerebral hemisphere
- - - - Annual Incidence: Each year, over 12.2 million people worldwide suffer a new stroke, underscoring the vast reach of this cerebrovascular event.
  - - - Incidence: Approximately 1.98 million strokes occur annually in individuals aged 15 to 49
      - Trends: Recent data indicates a concerning rise in stroke rates among younger adults
      - Contributing Factors: linked to rising rates of cardiovascular risk factors such as obesity, hypertension, and diabetes.
    - - Prevalence: In the United States, stroke prevalence among adults aged 45–64 years increased by 15.7% from 2011–2013 to 2020–2022.
      - Risk Factors
    - - Trends: the absolute number of strokes remains substantial due to the aging population.
      - Mortality: Advanced age
      - Prevalence: Stroke prevalence is highest among older adults. In the United States, 38% of people hospitalized for stroke in 2014 were less than 65 years old, indicating a significant proportion of strokes occur in those 65 and older.
- - - - Family History: A positive family history of stroke increases an individual's risk
      - Monogenic Disorders: Certain genetic conditions, such as Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy
    - - ABO Blood Group: a 16% higher likelihood of experiencing an early-onset ischemic stroke before age 60
        
        Those with blood type O have a 12% reduced risk compared to other blood types.
    - - CHIP: This condition involves age-related mutations in hematopoietic stem cells,
- - - - PT/INRR/PTT: risks for clotting
- - - - Ateplase: IV thrombolytic
        
        Binds to fibrin in a thrombusand converts plasminogen to plasmin, which breaks down fibrin and dissolves the clot.
      - Tenecteplase: Newer thrombolytic, fewer complications
        
        Similar to alteplase but has greater fibrin specificity and a longer half-life. Converts plasminogen to plasmin, enhancing clot dissolution.
      - Antiplatelets: aspirin, clopidogrel -> prevent clot formation
        
        Aspirin: Irreversibly inhibits cyclooxygenase-1 (COX-1) -> decreases thromboxane A2 -> prevents platelet aggregation.
        
        Clopidogrel: Inhibits the P2Y12 ADP receptor on platelets -> reduces platelet activation and aggregation.
      - Anticoagulants: warfarin, etc. -> used in embolic stroke
        
        Inhibits vitamin K epoxide reductase, preventing the activation of vitamin K-dependent clotting factors -> reduces blood coagulability.
    - - BP management: Labetalol, nicardipine
        
        Labetalol: Mixed alpha-1 and beta-blocker -> reduces systemic vascular resistance and BP without increasing ICP.
        
        Nicardipine: Calcium channel blocker -> relaxes vascular smooth muscle, lowering BP.
      - Reversal agents: vitamin K (warfarin)
        
        Restores synthesis of vitamin K-dependent clotting factors -> reverses effects of warfarin.
  - - - Diet/exercise
  - - - Stroke awareness: FAST
      - Targeting at-risk populations: elderly, ethnic groups, genetics
- - - - Common sudden signs: visual disturbances, unexplained headache, unilateral weakness/numbness
      - Often misdiagnosed as migraine, drug usage, anxiety
    - - Classic FAST symptoms
      - May present: pronounced hemiplegia, aphasia, visual field defects
    - - Sudden lethargy, delirium, falls, increase in dementia symptoms, silent strokes
- - - - Often is uninsured and expensive
- - - - The incident was captured on her nanny cam, unable to move the left side of her body she still managed to call 911
        
        EMTS transported her to New York-Presbyterian's Weill Cornell Medical Center, where she received thrombolytic treatment, restoring her movement within 15 minutes.
        
        Doctors later identified a previously undetected congenital heart condition & patent foramen ovale as the cause, which she had surgically corrected.
        
        Krista is now an advocate for stroke awareness, emphasizing the importance of recognizing symptoms and seeking immediate medical attention