406 E2 neuro pathogenesis Flashcards
change in neurotransmitter levels in CNS (increase of neuronal depolarization resulting in hyper activity)
-blood vessel tone (vasodilation)
migraines
destruction of substantia nigra in basal ganglia -> dopamine levels decrease -> imbalance between dopamine & ACh -> relative excess of ACh -> loss of controlled movement and balance
parkinson’s disease
antibodies attack ACh receptors -> decrease in ACh receptor sites at the neuromuscular junction -> this prevents ACh molecules from attaching and stimulating muscle contraction
(body is producing enough AHc but not enough receptor sites)
myasthenia gravis
T lymphocytes migrate to the CNS and cross the blood brain barrier -> antigen antibody reaction in CNS initiates an inflammatory response -> axons are de myelinated & plaques / sclerosis forms -> axons are destroyed
multiple sclerosis
motor neurons in the brainstem, cerebral cortex & spinal cord gradually degenerate -> death of neurons results in axonal degeneration, demyelination & sclerosis (scarring) -> damage causes motor neuros to no longer send messages to the muscles so the muscles cannot function
ALS
autoimmune disorder where the myeline sheath is damaged by autoantibodies usually triggered by a viral infection (GI or resp) + few cases caused by bacterial infection (campylobacter jejuni, food borne illness), post surgery and very rarely w/ flu vaccines
GBS
meningocooci or pneumococci is inhaled & attaches to the epithelial cells which cross the BBB to enter the blood stream -> infection of arachnoid mater and CSF -> inflammatory response (inc neutrophils) and pus secretion -> increase in CSF production -> increase in ICP
meningitis
acute inflammation of the brain d/t viral infection (mosquitoes cause west nile, measles, chicken px, mumps, HSV1)
encephalitis
accumulation of pus within the brain tissues caused by local or systemic infection (most common: ear, tooth, mastoid or sinus infection)
brain abscess
acute, focal cerebral insufficiency lasting <24 hrs (usually <60min) w/ no residual effects
TIA
occlusion -> oxygen deprivation -> neuro deficits within 1 min -> continued loss of supply leads to irreversible damage
ischemic stroke
bleeding within the brain parenchyma associated w/ standing, severe htn
hemorrhagic stroke