jdlevenson's version from 2015-06-21 02:11


Question Answer
ACh release from presynaptic terminal vesicles happens as a result fromExtracellular calcium influx, occurring following depolarization, that opens voltage-gated calcium channels.
Neuronal AP depolarization occurs fromDEPENDS. Rapid sodium influx in skeletal muscle, smooth muscle, cardiac muscle and purkinje fibers but in SA node, initial upstroke is Ca influx.
Postsynaptic skeletal muscle end plateLigand gated sodium and potassium ion channels. This increased conductance generates motor end plate potential -> depolarization.
Overshoot isAmount over zero in membrane potential/ ‘overshoot of depolarization’
Depolarization in AP is generally fromMassive influx of Na+ through voltage gated Na+ channels whereas repolarization occurs due to closure of Na+ channels and opening of voltage gated K+ channels. K+ ion permeance is HIGHEST during repolarization.
Resting potential, which ions have high permeanceK+. Low to Na+. K+ efflux via non-gated K+ channels/ leak channels.
Repolarization isClosure of Na+ channels and simultaneous opening of K+ channels. Significant increase in K+ permeance.
Rifampin as prophylaxis for N. Menin is used post exposure to patient or post exposure to contacts Contacts, not to patient.
Chromatolysis / axonal reaction: Neuronal cell process following axonal injury in neuronal body* (vs. Wallerian degeneration in axon). Inreased protein synthesis to repair damaged protein will lead to appearance: round circular swelling/ edema, displacement of the nucleus to periphery, dispersion of nissl substance throughout cytoplasm as it becomes fine and granular. Axonal reaction becomes visible 24-48 hours after the injury and maximal changes occur 12 days after injury*.
Question Answer
Nissl substance isBasophilic, rough ER, responsible for protein synthesis
Nissl substance is lost in () and dispersed in ()Lost in acute neuronal injury/ red neuron vs dispersed in axonal reaction/ loss of axon. Also nucleus moves to peripheryin axonal reaction whereas it shrinks and becomes basophilic in acute neuronal injury.
In initial 3-6 hours after ischemic injury to neuron what happensNothing micro or macroscopically
Red neuron appearanceCytoplasm stains deeply eosinophilic, nucleus becomes pyknotic and nissl substance and nucleolus disappear and neuronal body becomes shrunken and separated from the surrounding tissue. 12-24 hours after injury (ischemia, hypoglycemia, hypoxia) and are followed by death of neuron.
Wallerian degenerationReaction in axon after injury -> degeneration of axon and myelin distal to a point of injury; swelling and irregularity in distal segment of axon and then axon is destroyed and its fragments are digested by Schwann cells and macrophages.
Lipid laden macrophages containing products of myelin within periventricular plaque like lesionsMS.
After macrophages eat up necrotic debris and a cyst forms, gliosis occurs from actions ofAstrocytes**
SCN regulates what hormone(s)Cortisol (stress hormone) and melatonin (induces sleep). Melatonin highest during night. Cortisol peaks in the morning and reaches lowest at night .
Which one is from neuroectoderm, astrocytes or oligodendrocytes?Both.
GFAPAstrocytes. Repair, structural support, blood brain barrier and metabolic functions.
Proliferating astrocytes/ gliosis contain a lot of?Glycogen granules. And fibrils. Form glial scar that compensates for volume loss that occurs after neuronal death.
Vertigo vs Imbalance, light-headedness, syncopeVertigo is sudden onset, interferes with walking and can cause N/V
Neurons are especially sensitive to hypoglycemia becauseDo not store glycogen. Interruption of cerebral blood flow for 5-10 seconds leads to loss of consciousness and permanent damage after 4-5 minutes.
Kinesin functionMicrotubule associated protein involved in anterograde transport of intracellular vesicles and organelles towards the plus/ rapidly growing ends of microtubules. Kinesin generally uses ATP hydrolysis to move along microtubule. Plus ends are generally farther from nucleus. In neuron, kinesin carries vesicles and organelles away from cell body and towards nerve terminal.
Kinesin deficiency/ insultDeficiency of synaptic vesicles at terminal
T-Tubule system locationLocated at junction of A and I bands of striated myocytes. Open to extracellular space and facilitate depolarization movement to inside of cell.
Length constant/ space constant is defined asMeasure of how far along an axon an electrical impulse can propagate (length at which original AP decreases to 37% of its magnitude). Would decrease from charge dissipation along the axon.
Demyelination would result in decreased length constant or temporal summation?Decreased length constant – since more impulse would dissipate along the axon. Whereas temporal summation refers to sequential impulses from same neuron over time and summation can only occur in dendrites, cell body and axon hillock, not axon.
Time constant vs length constant ?Time constant is time it takes for membrane potential to achieve 63% of new value; lower time constants allow quicker changes in membrane potential; myelination decreases membrane capcacitance and reduces time constant. Length constant is measure of how far along an axon an electrical impulse can propragate.


Question Answer
Only serotonin-relasing neurons in CNSRaphe nuclei. Neurons disseminate widely though in CNS.
Serotonin is implicated in what disordersAnorexia, depression and sleep disorders
Red nucleusAnterior midbrain; participate in the motor coordination of the upper extremities.
Striatum formed ofCaudate nucleus and putamen.
Huntington’s disease patients on imagingAtrophy of caudate and PET scans will show decreased metabolic activity in striatum.
Caudate separated by internal capsule fromGlobus pallidus and putamen.
Internal capsule separates () from ()anterior limb separates caudate from GP and P and posterior limb separates GP and P from thalamus.
Internal capsule posterior limb carriesCorticospinal motor and somatic sensory fibers as well as visual and auditory fibers***
Left homonymous hemianopia with macular sparing, lesion is wherePCA -> its ipsilateral occipital lobe. Macular sparing from collateral blood via MCA. Often presents instead with or is accompanied by contralateral paresthesias and numbness.
Central visual information is processed whereOccipital pole.
Homonymous hemianopia with macular involvement?MCA stroke (vs. PCA when without)
Hemiballism due toContralateral STN. Usually from lacunar stroke.
Lacunar stroke thinkHTN.
Wilson disease involves what portion of brainLentiform nucleus (GP and Putamen).
Burning or stabbing sensation of one half of body after strokeThalamic syndrome
Rapidly progressive dementia and myoclonic jerks?CJD/ prion disease.
PrP in alpha helical stateNormal
PrP in beta pleated sheetCJD/ pions disease. B pleted state is resistant to proteases. Affected gray matter undergo spongiform change ie multiple vacuoles in gray matter of brain.
CJD causesInfectious or sporadic or iatrogenic* - corneal transplants, HGH, or implantable electrodes.
Prion disease treatmentNone
Prion disease beyond CJDKuru and familial fatal insomnia.
All prion diseases share in commonno treatment; long incubation periods; PrP in beta; and spongiform enceph.
Cytoplasmic inclusions in oligodendrocytesProgressive Multifocal Leukoencephalopathy.
Microglial nodulars and multinucleated giant cellsViral infections of CNS. Found in HIV associated encephalopathy.
Pseudobulbar palsyHead ahd neck muscle weakness, dysphagia, dysarthria; pseudobulbar because nuclei of CNs remain intact particularly 9, 10 and 11.
Synaptophysin stainindicates neuronal origin. It is a protein in presynaptic vesicles of neurons, neuroendocrine and neuroectodermal cells.
Synaptophysin vs GFAPSynapto – neuronal origin vs. GFAP – glial (astrocytes, ependymal cells, oligodendrocytes).
High frequency sounds heard best atBase of cochlea (thin rigid membrane)
Low frequency sounds heard best atTip of cochlea near helicotrema (wide and flexible)
Conductive vs Sensorineural hearing loss, Rhinne test?Conductive will be abnormal; bone will hear more than air** (normal – air more than bone)
Conductive vs Sensorineuarl hearing loss, Weber test?Sensorineural- sound will localize to unaffected ear whereas conductive- sound will localized to affected hear
How do sudden loud noises lead to hearing lossTympanic membrane rupture
What type of sound is lost firstHigh frequency


Question Answer
Most common brain tumor in immunosuppressedCNS lymphoma; arise from B cells. Universally associated with EBV***
Most common cause of intracranial tumor in adultsMetastases
Tumor along grey-white junctionMetastatic brain lesions. Usually well circumscribed. And may have central necrosis with surounding areas of reactive gliosis and edema.
Optic glioma, thinkNF1.
Rosenthal fibers may bePCA or optic glioma (accompanying immature astrocytes with microcystic degeneration)
PCA in children on biopsyRosenthal fibers and granular eosinophilic bodies. And spindle cells with hair like glial processes known as microcysts.
PCA locationCerebellum. (And brainstem, HT, optic pathways).
PCA and Medulloblastoma both arise in cerebellum, how to differentiatePCA -> Rosenthal fibers vs. Medulloblastoma is a PNET (primitive neuroectodermal tumor) and hence has sheets of small cells with deeply basophilic nuclei and scant cytoplasm (small, round blue cells) and abundant mitoses.
Neuroblastoma pathognomonicNeuropil/ neuritic process. Also Homer-Wright rosettes (also seen in medulloblastoma).
Medulloblastoma symptomsGait instability and limb ataxia (since in cerebellum); increased ICP (morning headache, vomiting, lethargy) and cerebellar dysfunction.
PCA vs Medulloblastoma, which has beter prognosisPCA.
Glioblastoma are not ring enhancing, true or falseFALSE. Ring-enhancing and butterfly shaped.


Question Answer
Most common extracranial solid tumor in childrenNeuroblastoma.
Neuroblastoma originates fromNeural crest cells; specifically neuroblasts in the adrenal medulla.
NeuroblastomaAge- 2; micro- solid sheets of small cells with dark nuclei and scant cytoplasm; clinical- retroperitoneal mass that displaces kidney (firm, irregular, can cross midline vs Wilms which is smooth unilateral***), HTN, anorexia and opsoclonus-myoclonus; mets – invasion of epidural space as ‘dumbell tumor’ compressing spinal cord, pancytopenia, hepatomegaly, palpabale nodules, periorbital proptosis and eccymoses and OPSOCLONUS-MYOCLONUS with truncal ataxia; biochem - increased excretion of catecholamines (HVA, from Dopamine, and VMA, from NE) in urine; genetic- N-MYC amplification; progrnosis – better if <1 year and worse with more N-MYC
Neuroblastoma vs Wilmsretroperitoneal mass that displaces kidney (firm, irregular, can cross midline vs Wilms which is smooth unilateral***
Non-rhythmic conjugate eye movements in various directions + myoclonusParaneoplastic syndrome of neuroblastoma
Neuroblastoma labsN-MYC gene amplification and HVA and VMA
Breakdown product of DopamineHVA
Ependymomas are characterized byPseudorosettes with GFAP positive processes tapering toward blood vessels. Poor prognosis. 3rd most common brain neoplasm in children. Arise in walls of ventriculi and can hamper CSF flow and cause hydrocephalus.
Neuroblastomas biologic markerN-MYC. As well as elevated HVA, VMA. Positive for Chromagranin, S100.
Meningiomas from what cellCells of arachnoid villi.
Whorled cells with or without psamomma bodies (core of dense calcification with surrounding collagen-fiber bundles)Meningioma.
New onset seizures in adult?Meningioma. Classic presentation.
Meningiomas are commonly located on cerebral surface; when parasagittal it leads toContralateral spastic paresis of leg due to compression of leg-foot motor area. May also lead to seizures.
2nd most common brain tumorMeningioma