4th Exam: Neurologic Disease Flashcards
Meningococcal Meningitis:
Carriers have nasopharyngeal bacteria, often in epidemics, outbreaks, young adults and kids, DIC = intravascular thrombosis (caps) (skin, adrenal lesions), can be fatal
Meningitis with WFS:
Adrenal gland hemorrhage = insufficiency, meningitis assoc w inflammation, inflammation → leaky vessels→ edema, seizures, confusion, coma, WFS: numerous skin hemorrhages
WFS sf:
Waterhouse-Friderichsen Syndrome
Brain Abscess sources:
local or distant infection
o Endocarditis, tooth extraction
• Endocarditis: emboli on valves travel to brain
Etiology of brain abscess:
usually bacterial, not a single species, but mixed flora
Signs of brain abscess:
signs of mass lesion w fever, headache, sizures, elevated WBC
Mortality, morbidity of brain abscesses:
10%, 50%
Abscess:
necrosis of tissue + inflammation, PMNs
What forms the capsule around an abscess?
collagen
Why does a capsule form around an abscess?
Attempt to wall-off infection and prevent spread
Myotonic Dystrophy:
Hatchet face with ptosis (droopy eyelids), dysphagia (be aware, may choke on saliva), muscle disease, dominant inheritance, progressive muscle weakness
Mito Disorders esp effect:
cells in organs that don’t turn over quickly (heart, skeletal muscle, brain)
Mito Myopathies:
Ptosis, dysphagia, too many mito, abnormal mitochondria
Abnormal mitochondria:
Differing sizes & shapes, whorled appearance (whirling cristae), crystal-like inclusions
Degenerative Diseases:
Selective vulnerability: distinct topography, often Idiopathic, hereditary/genetic/molecular basis, neurons primarily affected, atrophy + gliosis (astrocytes proliferate → scarring of the brain) + a unique change
Dementia:
Loss of cognitive function, decline from a previous level of function, slowly progressive, modalities affected: memory, judgment, reasoning, calculation, language, lesions in cerebrum
Causes of dementia:
Alzheimer’s & similar diseases, Huntington’s, Parkinson’s (movement disorders), vascular disease, infections, alcohol abuse, Vit deficiency
Alzheimer’s:
- 50-75% of all dementia cases
- Incidence increases w age
o 50% people > 85yo - 5-10yr survival after dx
- Disease of cerebral cortex- cerebral cortical atrophy, diffuse
- Senile plaques in Alzheimer’s
Alzheimers effects on cerebral cortex:
diffuse, sulci bw gyri are very wide, representing atrophy, ventricles dilated, loss of cortical neurons- almost 50%, neural connections to create memory, calculation and reasoning are lost, leads to dementia, senile plaques:
What are senile plaques in Alzheimer’s made of?
Core: amyloid, surrounded by degenerating neurites (damaged neurons)
Pathogenesis of Alzheimer’s – Amyloid
Several pws, all begin with Beta-amyloid deposits (plaques in brain), neurotoxic w loss of neurons (activates macs inducing inflammation, accelerates apoptosis of neurons)
Amyloid Formation and Breakdown:
APP (Amyloid Precursor Protein) formation, may be increased (Ex. Down’s Syndrome), cleavage/degradation may be reduced
APP:
normal membrane protein, 563-770 AAs
May lead to the reduction of amyloid breakdown:
Secretase enzymes break down APP, failure of breakdown → amyloid deposits
