pathology

Question 1

treponema, RMSF, polio, HSV, cryptococcus, aspergillus, TB, rabies, SSPE (measles) / PML (JC virus) tropisms

Answer 1

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

Question 2

leptomeningitis

pachymeningitis

Answer 2

between pia and arachnoid

external to dura due to chronic infx

Question 3

age and organism:
neonates
infant (3 mo to 3 yrs)
adult
close quarters

Answer 3

E. coli, GBS
H flu
Strep. pneumoniae
N. meningitidis

Question 4

diagnosis of meningitidis

Answer 4

neutrophil presence! decreased glucose

lymphocytes for TB, viral, and cryptococcal meningitis; elevated protein but normal glucose

Question 5

H flu meningitis

Answer 5

dense leukocytic exudate, rich in fibrin -> loculated barrier to antibiotics

Question 6

TB meningitis gross and histologic appearance, stain

Answer 6

meningeal granulomas (spider-web appearance)
multinucleate giant cells with no PMN’s
AFB (acid fast bacilli) stain

Question 7

TB meningitis complications

Answer 7

can cause meningeal fibrosis -> communicating hydrocephalus OR arteritis -> parenchymal infarcts

Question 8

tuberculoma

Answer 8

hematogenous spread -> parenchymal involvement -> solitary spherical mass with central caseous necrosis

Question 9

Pott’s disease

Answer 9

TB of spine

epidural granulomatous mass -> vertebrae destruction -> spinal cord compression

Question 10

viral meningitis

Answer 10

lymphocytes, increased pro, normal glucose
enteroviri (including coxsackie B), echovirus, EBV, Herpes virus, mumps
most common viral CNS disease

Question 11

C. neoformans

Answer 11

bird feces -> inhaled by immunocompromised -> pneumonia -> hematogenous spread -> lungs, leptomeninges -> disseminated and discrete white nodule lesions
number one AIDS meningitis

Question 12

C. neoformans morphology

Answer 12

encapsulated sphere -> halo with india ink stain

latex agglutination from capsule antigens

Question 13

cerebral abscess

Answer 13

blood -> richest capillary beds of cerebral cortex and subajacent white matter -> cerebritis (Acute inflammation) -> liquefactive necrosis -> expanding abscess

Question 14

viral encephalitis

Answer 14

perivascular cuffs of lymphocytes involving small arteries / arterioles
intranuclear / intracytoplasmic inclusion bodies

Question 15

inclusion body tropisms of: 
HSV / H zoster
rabies
CMV
SSPE
PML

Answer 15

eosinophilic intranuclear
cytoplasmic negri bodies
basophilic intranuclear
basophilic intranuclear (measles virus)
intranuclear ground glass appearance in oligodendrocytes (JC virus)

Question 16

AVM prevalence, location, complications

Answer 16

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

Question 17

cavernous angioma prevalence, structure, complication

Answer 17

much less common than AVM
large vascular spaces compartmentalized by prominent fibrous walls
usually asymptomatic, may cause intracranial bleed, epilepsy, or focal neuro disturbance

Question 18

teleangiectasia

Answer 18

focal aggregate of small vessels with intervening parenchyma

may cause seizures but rarely ruptures

Question 19

venous angioma

Answer 19

few enlarged veins randomly distributed in spinal cord or brain
asymptomatic

Question 20

cerebral aneurysm prevalence, types

Answer 20

most common non-traumatic SAH

1. berry 2. atherosclerotic 3. mycotic 4. HTN

Question 21

berry aneurysm

Answer 21

most common aneurysm
at bifurcation of arteries in circle of willis
muscle layer is lacking; only thin tunica adventita

Question 22

berry location

Answer 22

ACA-AComm
ICA-PComm-ACA
MCA trifurcation

Question 23

berry complications

Answer 23

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

Question 24

atherosclerotic aneurysm

Answer 24

vertebral, basilar or ICA
fusiform elargement due to progressive luminar narrowing due to atherosclerotic plaque
cause thrombosis but rarely rupture

Question 25

mycotic aneurysm

Answer 25

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

Question 26

Charcot-Bouchard aneurysm description

Answer 26

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

Question 27

Charcot-Bouchard aneurysm locations

Answer 27

Basal ganglia / thalamus pons cerebellum

Question 28

Charcot-Bouchard aneurysm presentation / complications

Answer 28

hematoma -> HA and weakness -> transtentorial hernation or interventricular hemorrhage

Question 29

interventricular hemorrhage

Answer 29

expanding 3rd and 4th ventricle -> compression of medulla by ventricle 4 -> death

Question 30

cerebellar hemorrhage

Answer 30

abrupt ataxia, occipital HA, vomiting -> compression of medulla

Question 31

cerebral ischemia histology

Answer 31

shrunken nuclei, eosinophilic cytoplasm, perineuronal halo | due to extracerebral or occlusive disease

Question 32

infarct types

Answer 32

hemorrhagic - emboli | bland - thrombi

Question 33

infarct histology

Answer 33

liquefactive necrosis -> neutrophils -> macrophages -> astrogliosis and capillary proliferation -> cystic healing and regressive neovascularity

Question 34

striate and MCA thrombosis deficits

Answer 34

striate - from MCA, ischemia of internal capsule -> hemiparesis / hemiplasia MCA trifurcation -> cerebral cortex ischemia -> motor and sensory defects, aphasia

Question 35

frequent sites of atherosclerosis

Answer 35

most common - CCA, esp at bifurcation into ECA, ICA

Question 36

lacunar infarcts

Answer 36

ischemic lesions due to stenosis of AComm and PComm (secondary atherosclerosis) -> multi-infarct dementia

Question 37

hypertensive encephalopathy

Answer 37

fibrinoid necrosis of small arteries with petechiae due to HTN -> cerebral edema, papilledema -> HA, vomiting -> lethargy -> coma and death

Question 38

fat embolism syndrome

Answer 38

traumatic leg fracture -> release of fat emboli -> occlude brain / lung capillaries -> distal capillary ischemia -> development of petechiae restricted to white matter

Question 39

cause of cerebral contusions

Answer 39

anteroposteriro displacement

Question 40

contra-coup contusion location

Answer 40

frontal and temporal lobes | occipital lobe protected by broad, smooth contour

Question 41

herniations

Answer 41

subfalcine (cingulate gyrus) tonsillar (coning) transtentorial (uncal)

Question 42

minimal force vs more force contusions

Answer 42

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

Question 43

repair of contusions

Answer 43

permanent! | necrosis -> phagocytized -> astrogliosis -> pigmented crater lesion

Question 44

subfalcine herniation

Answer 44

cingulate gyrus is pushed down and under the falx -> compression of ACA branches

Question 45

tonsillar herniation

Answer 45

coning | tonsils of cerebellum are pushed down through foramen magnum -> compression of medulla

Question 46

transtentorial herniation

Answer 46

medial temporal lobe (hippocampus) is compressed under tenterium -> compression of CN3 -> ipsilateral fixed pupil dilation, impaired EOM -> duret hemorrhage

Question 47

duret hemorrhage

Answer 47

flame-shaped or linear necrotic and hemorrhagic lesions in the midline of the midbrain and pons