pathology Flashcards
treponema, RMSF, polio, HSV, cryptococcus, aspergillus, TB, rabies, SSPE (measles) / PML (JC virus) tropisms
blood -> neural tissues -> infx, dementia, sensory defects cerebral endothelial cells motor neurons in spinal cord and bulbar areas temporal lobes leptomeninges, lungs cerebral parenchyma -> abscesses meninges at base of brain around chiasm brainstem cerebral hemispheres
leptomeningitis
pachymeningitis
between pia and arachnoid
external to dura due to chronic infx
age and organism: neonates infant (3 mo to 3 yrs) adult close quarters
E. coli, GBS
H flu
Strep. pneumoniae
N. meningitidis
diagnosis of meningitidis
neutrophil presence! decreased glucose
lymphocytes for TB, viral, and cryptococcal meningitis; elevated protein but normal glucose
H flu meningitis
dense leukocytic exudate, rich in fibrin -> loculated barrier to antibiotics
TB meningitis gross and histologic appearance, stain
meningeal granulomas (spider-web appearance)
multinucleate giant cells with no PMN’s
AFB (acid fast bacilli) stain
TB meningitis complications
can cause meningeal fibrosis -> communicating hydrocephalus OR arteritis -> parenchymal infarcts
tuberculoma
hematogenous spread -> parenchymal involvement -> solitary spherical mass with central caseous necrosis
Pott’s disease
TB of spine
epidural granulomatous mass -> vertebrae destruction -> spinal cord compression
viral meningitis
lymphocytes, increased pro, normal glucose
enteroviri (including coxsackie B), echovirus, EBV, Herpes virus, mumps
most common viral CNS disease
C. neoformans
bird feces -> inhaled by immunocompromised -> pneumonia -> hematogenous spread -> lungs, leptomeninges -> disseminated and discrete white nodule lesions
number one AIDS meningitis
C. neoformans morphology
encapsulated sphere -> halo with india ink stain
latex agglutination from capsule antigens
cerebral abscess
blood -> richest capillary beds of cerebral cortex and subajacent white matter -> cerebritis (Acute inflammation) -> liquefactive necrosis -> expanding abscess
viral encephalitis
perivascular cuffs of lymphocytes involving small arteries / arterioles
intranuclear / intracytoplasmic inclusion bodies
inclusion body tropisms of: HSV / H zoster rabies CMV SSPE PML
eosinophilic intranuclear cytoplasmic negri bodies basophilic intranuclear basophilic intranuclear (measles virus) intranuclear ground glass appearance in oligodendrocytes (JC virus)
AVM prevalence, location, complications
most common congenital vascular malformation
second most common cause of a nontraumatic SAH
occurs at transition between artery and vein
results in seizure, SAH, intracerebral hemorrhage in 2nd or 3rd decade
cavernous angioma prevalence, structure, complication
much less common than AVM
large vascular spaces compartmentalized by prominent fibrous walls
usually asymptomatic, may cause intracranial bleed, epilepsy, or focal neuro disturbance
teleangiectasia
focal aggregate of small vessels with intervening parenchyma
may cause seizures but rarely ruptures
venous angioma
few enlarged veins randomly distributed in spinal cord or brain
asymptomatic
cerebral aneurysm prevalence, types
most common non-traumatic SAH
1. berry 2. atherosclerotic 3. mycotic 4. HTN
berry aneurysm
most common aneurysm
at bifurcation of arteries in circle of willis
muscle layer is lacking; only thin tunica adventita
berry location
ACA-AComm
ICA-PComm-ACA
MCA trifurcation
berry complications
rupture -> SAH or intracerebral / intraventricular H or CN 3, 4, 6 palsies or seizures due to medial temporal lobe compression
can rebleed if they survive
atherosclerotic aneurysm
vertebral, basilar or ICA
fusiform elargement due to progressive luminar narrowing due to atherosclerotic plaque
cause thrombosis but rarely rupture
mycotic aneurysm
infections of arterial walls due to septic emboli usually from infected cardiac valve (endocarditis)
often in MCA branches
proliferation -> inflammation -> destruction of arterial walls
SAH / intracerebral H or cerebral abscess / meningitis
Charcot-Bouchard aneurysm description
HTN -> lipohyalinosis in interparenchymal cerebral arterioles
associated with long-standing HTN -> small fusiform dilations on trunk of a vessel that are predisposed to rupture causing HTNsive intercerebral hemorrhage
Charcot-Bouchard aneurysm locations
Basal ganglia / thalamus
pons
cerebellum
Charcot-Bouchard aneurysm presentation / complications
hematoma -> HA and weakness -> transtentorial hernation or interventricular hemorrhage
interventricular hemorrhage
expanding 3rd and 4th ventricle -> compression of medulla by ventricle 4 -> death
cerebellar hemorrhage
abrupt ataxia, occipital HA, vomiting -> compression of medulla
cerebral ischemia histology
shrunken nuclei, eosinophilic cytoplasm, perineuronal halo
due to extracerebral or occlusive disease
infarct types
hemorrhagic - emboli
bland - thrombi
infarct histology
liquefactive necrosis -> neutrophils -> macrophages -> astrogliosis and capillary proliferation -> cystic healing and regressive neovascularity
striate and MCA thrombosis deficits
striate - from MCA, ischemia of internal capsule -> hemiparesis / hemiplasia
MCA trifurcation -> cerebral cortex ischemia -> motor and sensory defects, aphasia
frequent sites of atherosclerosis
most common - CCA, esp at bifurcation into ECA, ICA
lacunar infarcts
ischemic lesions due to stenosis of AComm and PComm (secondary atherosclerosis) -> multi-infarct dementia
hypertensive encephalopathy
fibrinoid necrosis of small arteries with petechiae due to HTN -> cerebral edema, papilledema -> HA, vomiting -> lethargy -> coma and death
fat embolism syndrome
traumatic leg fracture -> release of fat emboli -> occlude brain / lung capillaries -> distal capillary ischemia -> development of petechiae restricted to white matter
cause of cerebral contusions
anteroposteriro displacement
contra-coup contusion location
frontal and temporal lobes
occipital lobe protected by broad, smooth contour
herniations
subfalcine (cingulate gyrus)
tonsillar (coning)
transtentorial (uncal)
minimal force vs more force contusions
minimal - restricted to apex of gyri of cortex
greater force - destroy larger areas of cortex, deeper cavities that expand into white matter or lacerate -> cortical or subcortical hemorrhage and edema -> mass lesion
repair of contusions
permanent!
necrosis -> phagocytized -> astrogliosis -> pigmented crater lesion
subfalcine herniation
cingulate gyrus is pushed down and under the falx -> compression of ACA branches
tonsillar herniation
coning
tonsils of cerebellum are pushed down through foramen magnum -> compression of medulla
transtentorial herniation
medial temporal lobe (hippocampus) is compressed under tenterium -> compression of CN3 -> ipsilateral fixed pupil dilation, impaired EOM -> duret hemorrhage
duret hemorrhage
flame-shaped or linear necrotic and hemorrhagic lesions in the midline of the midbrain and pons
