basic neuropathology Flashcards
diagnose neuropaths
Diagnostic
•Neurosurgical
•CSF cytology
•Muscle & Nerve biopsies
•Ophthalmic pathology
•Autopsy
–Consent (Hospital) PMs
–Medicolegal (Coroner’s & Forensic) PMs
–High risk PMs (eg CJD)
Academic
•Research
•Teaching
cels can be found in LB
all brain tumours?
grading?
All CNS tumours graded (WHO I - IV)
Low Grade
–Well defined
–Slow growing
–Lack necrosis, mitoses, microvascular proliferation
•High Grade
–Diffusely infiltrative
–Rapidly growing (Ki67 proliferation index)
–Necrosis, many mitoses, vascular proliferation
geneic alterations in astrocytomas?
types of staiing for demntia?
silver stain, thioflavine S stain
CADASIL
CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) is the most common form of hereditary stroke disorder, and is thought to be caused by mutations of the Notch 3 gene on chromosome 19.[1] The disease belongs to a family of disorders called the Leukodystrophies. The most common clinical manifestations are migraine headaches and transient ischemic attacks or strokes, which usually occur between 40 and 50 years of age, although MRI is able to detect signs of the disease years prior to clinical manifestation of disease.[2][3]#
CADASIL may start with attacks of migraine with aura or subcortical transient ischemic attacks or strokes, or mood disorders between 35 to 55 years of age. The disease progresses to subcortical dementia associated with pseudobulbar palsy and urinary incontinence.
Ischemic strokes are the most frequent presentation of CADASIL, with approximately 85% of symptomatic individuals developing transient ischemic attacks or stroke(s). The mean age of onset of ischemic episodes is approximately 46 years (range 30–70). A classic lacunar syndrome occurs in at least two-thirds of affected patients while hemispheric strokes are much less common. Notably, ischemic strokes typically occur in the absence of traditional cardiovascular risk factors. Recurrent silent strokes, with or without clinical strokes, often lead to cognitive decline and overt subcortical dementia.
wernickes encephalopathy result of?
vitamin b1 defiieny
tumor cell lineage grading
GFAP antibody (grades astrocytic tumour)
molecular genetics of astrocytomas?
oligodendroglioma & 1p19q deletion
pilocytic astrocytoma?
Pilocytic astrocytoma (I)
• Slow growing
• Well defined
• Surgically curable
• No adjuvant treatment
• Normal life expectancy
glioblastoma?
Glioblastoma (IV)
• Rapidly growing
• Poorly defined
• Inoperable
• Palliative adjuvant
treatment
• >80% dead within 1 year