PATHTALK Flashcards
DIABETIC NEUROPATHY
Peripheral nerves can be a common location of
complications from DM.
- The pathologic lesion is thought to arise from microvascular injury.
- Common nerve conditions include 3rd nerve palsy, mononeuropathy multiplex, diabetic amyotrophy, and autonomic neuropathy
Duret Hemorrhage
linear pontine hemorrhages seen almost exclusively in downward herniation through tentorium
cerebelli
-tearing paramedian branches of basilar leading to immediate death.
Resolving infarct
the frontal lobe has partial liquefactive necrosis with formation of a large cyst and smaller cysts.
Much of the remainder of the dead cerebral tissue would have cavitated in a similar fashion over the next several months if the patient had survived that long. With longer patient survival, the infarct could have continued its resolution by further loss of dead tissue and continued gliosis which, along with some blood vessels, would have been the final residue of the necrotic brain tissue
Infarcts from global cerebral ischemia/hypoxia:
– Most susceptible neurons: pyramidal cells of the hippocampus
and Purkinje cells of the cerebellum – Border zone (“watershed”) infarcts: wedge-shaped infarcts in
regions perfused by most distal portions of arteries. Usually seen
after hypotensive episodes.
• Infarcts from local cerebral ischemia:
– From cerebral arterial occlusion. Less damaging in areas of
collateral circulation. – Embolic etiology for infarct more common than thrombic. – Infarcts can be ischemic (bland, white, common; thrombolytic
therapy possible), hemorrhagic (less common; thrombolytic
therapy counterindicated), or “transformed” into hemorrhagic
(unclear incidence).
Infarcts from global cerebral ischemia/hypoxia:
– Most susceptible neurons: pyramidal cells of the hippocampus
and Purkinje cells of the cerebellum – Border zone (“watershed”) infarcts: wedge-shaped infarcts in
regions perfused by most distal portions of arteries. Usually seen
after hypotensive episodes.
• Infarcts from local cerebral ischemia:
– From cerebral arterial occlusion. Less damaging in areas of
collateral circulation. – Embolic etiology for infarct more common than thrombic. – Infarcts can be ischemic (bland, white, common; thrombolytic
therapy possible), hemorrhagic (less common; thrombolytic
therapy counterindicated), or “transformed” into hemorrhagic
(unclear incidence).
Hypertensive hemorrhage
Hypertension => hyaline arteriolar sclerosis of the deep penetrating arteries/arterioles supplying the basal ganglia, hemispheric white matter, and brain stem.
• Affected vessel walls are weakened and prone to rupture.
A mass effect with midline shift, often with secondary edema, may lead to herniation
Lacunar infarct
From the Latin lacuna for an empty space.
• Small (a few millimeters) cavity infarct in the deep
gray matter (basal ganglia and thalamus), internal capsule, deep white matter, and pons.
• Due to occlusion of a small deep penetrating artery as a consequence of aging, hypertension,
smoking, and diabetes mellitus
• May be clinically silent or => significant impairment.
- Marfan’s
- Ehlerdanlos
- autosomal polycystic kidney disease
predisposed to aneurysms.
Acute bacterial meningitis
After resolution of meningitis,
**adhesive arachnoiditis with obliteration of subarachnoid space leading to obstructive hydrocephalus
All age groups show systemic signs of infection and
meningeal irritation, headache, photophobia, irritability,
clouding of consciousness, neck stiffness.
• CSF: increased opening pressure, abundant neutrophils,
elevated protein, reduced glucose.
• Organisms:
– Neonates: E coli and group B streptococci.
– Adolescents and young adults: Neisseria meningitidis.
– Older patients: Streptococcus pneumoniae & Listeria
monocytogenes.
What is mutated in MS
superoxide dismutase -
converts oxygen free radial to hydrogen peroxide.
Glutathione peroxidase converts hydrogen peroxide to water.