Exam 2 Study Guide
1. Mechanisms of cerebral injury (hypoxia, ischemia, increased ICP)
● Hypoxia / ischemia
○ Primary problem: reduced oxygen (hypoxia) and/or blood flow (ischemia) →
ATP depletion.
○ Cellular cascad
...
Exam 2 Study Guide
1. Mechanisms of cerebral injury (hypoxia, ischemia, increased ICP)
● Hypoxia / ischemia
○ Primary problem: reduced oxygen (hypoxia) and/or blood flow (ischemia) →
ATP depletion.
○ Cellular cascade: failure of Na⁺/K⁺ ATPase → Na⁺/water influx → cytotoxic
edema; Ca²⁺ influx → activation of proteases, lipases, endonucleases →
membrane and mitochondrial damage; increased glutamate release →
NMDA-mediated excitotoxicity → further Ca²⁺ overload.
○ Reperfusion injury: ROS formation, inflammation, blood–brain barrier (BBB)
disruption.
○ Selective vulnerability: vulnerable regions: hippocampal CA1, neocortex layers
3/5, Purkinje cells in cerebellum.
● Increased intracranial pressure (ICP)
○ Causes: edema (cytotoxic or vasogenic), hemorrhage, mass lesion,
hydrocephalus.
○ Consequences: decreased cerebral perfusion pressure (CPP = MAP − ICP) →
worsened ischemia; herniation syndromes (uncal, central, tonsillar) → brainstem
compression, cranial nerve deficits, altered consciousness.
○ Clinical signs: headache, vomiting, altered mental status, papilledema, Cushing
triad (hypertension, bradycardia, irregular respiration) in advanced cases.
2. Stroke: risk factors, subtypes, deficits by region
● Risk factors
○ Non-modifiable: age, male sex, prior stroke/TIA, family history.
○ Modifiable: hypertension (biggest), atrial fibrillation (embolism), diabetes,
hyperlipidemia, smoking, carotid atherosclerosis, oral contraceptives (in some),
illicit drug use (cocaine), sedentary lifestyle.
● Subtypes
○ Ischemic (≈80–85%)
■ Thrombotic: in situ atherosclerotic plaque → occlusion (often at branch
points/cervical carotid, MCA).
■ Embolic: cardiac (AF, mural thrombus) or arterial-to-artery; sudden onset,
may be multiple territories.
■ Lacunar: small vessel lipohyalinosis → small subcortical infarcts (e.g.,
internal capsule) producing pure motor/sensory syndromes.
○ Hemorrhagic
■ Intracerebral hemorrhage (ICH): hypertension-related (basal ganglia,
thalamus), amyloid angiopathy (lobar in elderly).
■ Subarachnoid hemorrhage (SAH): ruptured aneurysm → thunderclap
headache, meningismus.
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