Exam 2 (week 2) Flashcards
what is the name of the boundary between nasal cavity and nasopharynx
choanae
what are the boney portions of the nasal septum
perpendicular plate of ethmoid (superior)
vomer (inferior)
role of turbinates in nose
warm and circulate air
what bone are the conchae from
superior and middle from ethmoid
inferior is it’s own bone
how are spaces by nasal conchae named and what do they do
named for the conchae superior to them
used for drainage (tears and mucus)
most posterior sinus in face and what is it near
sphenoid sinus - right anterior to optic chiasm and inferior to pituitary
features of middle meatus and what drains into it
ostiomeatal complex:
- semilunar hiatus (frontal, maxillary, and anterior air cells)
- ethmoidal bulla
- uncinate process (ridge)
what drains into superior meatus
posterior ethmoid air cells
what drains into sphenoethmoidal recess
sphenoid sinus
sensory info to nose
V1 and V2
vasculature in nose (3)
- 3rd portion of maxillary
- ophthalmic artery
- facial artery
what is boundary between larynx and trachea
inferior border of cricoid cartilage
posterior articulation of cricoid cartilage
superiorly articulates with the arytenoid cartilage, inferiorly with tracheal cartilage
anterior articulation of cricoid cartilage
superiorly articulates with cricothyroid ligament
inferiorly with tracheal cartilage
posterior articulation of arytenoid cartilage
superiorly articulates with corniculate cartilage
inferiorly articulates with cricoid cartilage
anterior articulation of arytenoid cartilage
anteriorly articulates with vocal ligament
ligamentous articulations of epiglottis
superiorly articulates with hyoid bone via hyoepiglottic ligament
inferiorly articulates with thorid bone via stalk of the epiglottis
cavities of larynx from superior to inferior (4)
- laryngeal vestibule
- middle part of laryngeal cavity
- laryngeal vestibule
- infraglottic cavity
purpose of vestibular folds
protection - not vocal folds. mucus membrane that extends between thyorid cartilage and cuneiform ligament
blood supply and drainage from larynx comes off what what vessels
inferior and superior thyroid vessels
what nerve is responsible for the sensation that you need to cough and what is it a branch of
internal laryngeal nerve, branch of superior laryngeal nerve, branch of vagus
what nerves are responsible for motor innervation to larynx and what are they branches of (2)
external laryngeal, branch of superior laryngeal, branch of vagus
inferior laryngeal nerve, branch of recurrent laryngeal nerve, branch of vagus
what does cricothyroid muscle do and what is it innervated by
stretches and tenses vocal ligament
only muscle innervated by external laryngeal nerve
what does posterior cricoarytenoid muscle do
abducts vocal fold
innervated by internal laryngeal/recurrent laryngeal
what muscles are responsible for phonation (2)
transverse and oblique arytenoid muscles
what muscle is repsonsible for forced inspiration
posterior cricoarytenoid muscle
what additional action happens in forced closure of folds (valsalva)
vestibular folds close too
what muscle will lower tone voice
posterior cricoarytenoid
what muscles will make higher tone of voice
transverse and oblique arytenoid
what muscle will let you whisper
lateral cricoarytenoid
which muscles will lower pitch of voice
thyroartenoid and vocalis muscles retract thyroid cartilage, loosening vocal cords, lowering pitch of voice
which muscle will raise pitcho f voice
criothyroid muscle, whcih tilts and stretches vocal cords
loss of function of what muscle will lead to monotonous voice
cricothyroid - innervated by superior laryngeal nerve. changes pitch of voice. can’t stretch vocal ligament
exertional sexual headache thunderclap, goes home, few days later dies when running
sentinal bleed subarachnoid hemorrhage
type 2 chiari malformation presentation/associations
bone formation problem:
vermis gets herniated out along with brainstem - associated with hydrocephalus and lumbosacral myelomeningiocele
dandy walker malformation presrentation/associations
failure of development of cerebellar tissue: vermis is gone, associated with dilated, cystic 4th ventricle
what happens in a subfalcine herniation
cingulate gyrus cause midline shift and compression of the ACA
what happens in a transtentorial herniation
supratentorial component herniates down, causing CN3 ccompression, ipsilateral hemiparesis and PCA compression
what do you see on histology for pilocytic astrocytoma
biphasic appearance - some loose some packed
what do you see on CT for pilocytic astrocyoma
well circumscribed borders, but no contrast enhancement
what does astrocytoma look like on CT
no contrast enhancement
what do you see for astrocytoma on gross
enlargement but no clear borders
what do you see on histology for diffuse astrocytoma
increased cellularity and always compacted. increased pleomophism, NO mitoses NO necrosis
what do you see on CT for anaplastic astrocytoma
contrast enhancement
what do you see on histology for anaplastic astrocytoma
increased cellularity, increased pleomorphism, MITOSES
what do you see on CT for glioblastoma
ring enhancing lesions (looks like toxoplasmosis), mass effect - midline shift
what do you see on gross for glioblastoma
necrosis, hemorrhage, can cross contralateral hemisphere - “butterfly glioma”
features for glioblastoma on histology
hypercellularity, pleomorphism, mitoses, AND vascular proliferation and palisading necrosis
are ependymomas diffuse or circumscribed
circumscribed
what do ependymomas look like in histology
perivascular psuedorosettes - no lumen. more pseudorosettes than true rosettes
oligodendroglioma imaging findings
see calcification
oligodendroglioma on microscopy
“fried egg” - nucleus is right in center of cell, and “chicken wire” capillary network
what grade is medulloblastoma characterized as
grade 4
what do you see for medulloblastoma on CT
contrast enhancing lesion
what do you see on histology for medulloblastoma
“small round blue cell tumor”
Homer Wright rosettes (no lumen)
high mitotic activity, shows neuronal or glial differentiation
what does medulloblastoma look like in gross
similar to ependymoma
progression of medulloblastoma
can disseminate down spinal cord
what cells are meningiomas derived from
arachnoid cap cell of leptomeninges
who gets meningiomas
mostly adult females (progesterone)
what do you see for meningiomas for CT
Extra axial isodense mass with contrast enhancement - “dural tail”
what do you see for meningiomas in histology
spindles and whorls, mitoses, psammoma bodies (round concentric calcifications)
genetics of meningioma
chromosome 22. can see neurofibromatosis type 2 - bilateral schwannoma, multiple meningiomas
what do you see on histology for schwannoma
biphasic - antoni A (dense) antoni B (loose)
palisading - zebra stripe verocay bodies.
NF type 2 you see what
bilateral schwannoma and multiple meningiomas
NF type 1 what do you see
neurofibroma
what do you see with neurofibroma on microscopic
loose myxoid background with comma or wavy shaped schwann cell nuclei
where do you see most mets in the brain (3)
- gray-white matter junction of cerebral hemispheres
- subarachnoid space (carcinomatous meningitis)
- dural infiltration (breast and prostate)
if you see multiple lesions what do you think it could be (in brain)
more likely metastasis
what’s the medial survival for multiple mets to the brain
3-6 months
definition of epilepsy
recurrent unprovoked seizures more than 24 hr apart
majority of seizures in children caused by what
unknown (no inborn error or no CT abnormalities)
second most common etiology of seizures in children
congenital
what cause of seizures becomes more common in adulthood
vasculature - stroke
what percentage of epilepsy cases are treated successfully with medications
60-70%
what do you do for intractable seizures
surgical resection (if appropriate)
how many meds do you have to fail to be classified as intractable epilepsy
2
focal vs generalized onset seizures
focal starts on one side of brain in one spot, generalized starts on both sides of brain but not entire cortex (genetic epilepsy)
difference between simple partial and complex partial
simple = aware complex = confusion/altered awareness
which generalized seizure does not have motor component
absence - looks like they’re spacing out
myoclonic seizure symptom
jerk, like when you’re falling asleep
atypical absence seizure
blank staring with twitching
myoclonic-atonic seizure
twitching fallowed by loss of tone and falling
what do you see on EEG for absence seizures
3 spikes per second/ 3Hz spike-wave
what is the onset of tonic-clonic seizure
can be either focal or generalized. focal will have aura or unilateral onset.
if you’re having a focal dyscognitive seizure, and you have automatism of the right hand, what side of the brain is the seizure originating from
right side - ipsilateral automatism.
contralateral posturing
which kind of generalized tonic clonic seizures have better prognosis, primary generalized or secondarily generalized?
primary generalized - more responsive to meds
seizure that lasts 30 or more minutes is called what
status epilepticus
which types of seizures are potential subjects for sx
focal if they fail multiple meds
where does lateral olfactory and medial olfactory stria go in the olfactory system
medial crosses over in anterior commissure to contralateral piriform cortex and amygdala
lateral stays ipsilatera
where is olfactory association cortex, what are its inputs, and what information does it process
lateral part of orbital surface of frontal lobe (lateral to olfactory tract)
recieves afferents from DMN of thalamus and from primary olfactory area
involved in behavioral reactions to recognized odors
uncus (associated with olfaction) is part of what gyrus
parahippocampal
septal area includes what, and is part of what lobe
part of limbic lobe, includes nucleus accumbens and is pleasure/reward center via dopa
where is septal areal located
medially, right below lateral ventricles
what are the parts of the limbic system (5)
- limbic lobe
- hippocampal formation
- amygdala
- hypothalamus (mammillary bodies)
- anterior thalamic nuclei
what are the parts of the limbic lobe (3)
- cingulate gyrus (including anterior cingulate cortex)
- parahippocampal gyrus (uncus and entorrhinal area)
- septal area
where is amygdala in relation to hippocampus and uncus
slightly anterior to hippocampus (closer to optic chiasm)
deep to uncus
amygdala connects to what other brain structures/areas (3) and what reactions do they control
- olfactory system (pheromonal information)
- cerebral cortex (conscious emotions)
- hypothalamus and brainstem visceral nuclei (autonomic/drive responses to emotions - sweating, dry mouth, crying)
output from amygdala for autonomic responses down brainstem - how does it travel
MFB
Kluver Bucy syndrome
bilateral destruction of amygdala - becomes placid, can’t recognize things, examine everything orally, hypersexual and indiscriminate
connection between mamillary bodies to hippocampus
fornix
inputs and outputs to hippocampus enter/exit through what structure
fimbria, which continues on to become fornix
what is declarative memory
knowledge and recall of facts
hippocampal efferents (2) and what are they responsible for
- fornix (to mammillary and then to anterior thalamic nuclei to be able to recall the scene for a particular memory)
- perforant pathway (to entorhinal cortex for formation of long-term memory)
Korsakoff’s syndrome - associated with that, and causes what
associated with chronic alcoholism
damage to ammillary bodies and projections into thalamus - amnestic confabulatory syndrome (don’t remember, but will lie about what’s happened)
what are prions in humans
proteins - abnormal protein caused by infection, causes neurodegenerative disorder.
normal protein is PrPc
abnormal is PrPSc which causes beta-pleated sheets aggregates which are resistant to proteinases, heat or ionization
are prions transmissible?
yes. usually not between species though besides mad cow
genetic predisposition for susceptibility to prion disease
if you are homozygous Met/Met at residue 129 on PRNP gene of chromosome 20
what does prion disease look like on histo
“spongiform” vacules
what is the incubation period for prion diseases
most commonly takes years, sporadic creutzfeld jacob kills you in 4-5 months however
most common inherited prion disease
Famililal Creutzfeld-Jakob Disease (younger age on onset than sporatic form)
inheritance pattern of inherited prion disease
Autosomal dominant inherit the germline mutation
clinical course of sporadic cerutzfeld-Jakob disease
3 stages of clinical course:
initial symptoms of fatigue, disordered sleep, behavioral changes, visual or motor deficits
rapidly progresses to cognitive decline/dementia
late: myoclonus right before death. die within 4-5 months of onset
pathogenesis of sporadic CJD (2)
NO germline mutation
either:
1. random mis-folding of PrPc protein, which then causes flipping of others
- somatic mutation in PRNP gene
who gets sporadic CJD
older (~60y/o) individuals of any race or gender
1 in a million
kuru clinical presentation
younger age of onset, tremors, ataxia, cerebellar involvement
kuru histo/gross presentation
75% had amyloid plaques on brain pathology (cerebellar)
kuru genetics
see Met/Met homozygosity at PRNP codon 129
what kind of CJD can you detect outside of the CNS and why
variant CJD - from eating cattle. can see in lymphoid tissue. probably because it’s acquired through GI tract
can see it in the muscles of cows
genetics of vCJD
until 2016, everyone with vCJD had Met/Met homozygous
maybe it just means that heterozygous takes a longer time to present, but we haven’t seen that happen
clinical presentation of vCJD
psychiatric/behavioral changes, painful dysesthesias
imaging of CJD
for variant form only, pulvinar sign (high MRI signal bilaterally in posterior thalamus)
EEG for CJD
see classic findings for sCJD (periodic sharp waves)
can you use CSF for diagnosing CJD?
only for sporadic form - can use real time quiaking induced conversion (RT-QuIC) to amplify protein for diagnosis
how to do histo for prion disease
you pretreat the sample to denature normal protein, and then stain with anti-PrP antibody - which will reveal PrPSc plaques
2 common causes of acute pyogenic meningitis in neonates
- group B strep
2. E. Coli
2 common causes of acute pyogenic meningitis in children
- strep pneumo
2. H. flu (w/o vaccinations)
2 common causes of acute pyogenic meningitis in otherwise healthy adults
- strep pneumo
2. neisseria (college or military)
3 causes of acute pyogenic meningitis in adults with underlying medical conditions
- gram neg rods (kleb or pseudomonas)
- listeria
- staph aureas
why can acute pyogenic meningitis be fatal?
can get into bloodstream - septisemia - and can settle in adrenal glands - necrosis - no corticosteroids causes systemic collapse and death
most common viral agent in meningitis
enterovirus (polio, echo-, coxackie)
clinical presentation of viral meningitis
spontanoues remission, less fulinant meningitis
how do diagnose viral agent in meningitis
culture throat or stool, or serum titer in acute and convalescent stages
brain abscess agents in healthy adults (2)
staph and strep (normal flora in mouth)
brain abscess agents in immunocompromised adults (5)
toxo, nocardia, listeria, mycobacteria, fungi
do you do a spinal tap in brain abscess?
no because you help pull the brain further down - bad
brain abscess on histology
3 zones:
- outer necrosis
- rim of granulation tissue (BVs, fibrous, inflammation)
- swollen brain with reactive astrocytes
mycobacterium TB meningitis on histo
caseating granulomatous inflammation
clinical course for mycobaterium TB
long clinical course before dx (years)
can get miliary TB - infection in vertebral body and then collapse, escape into epidural space and epidural abcess (POTTS disease)
causative agent of meningitis in neurosyphilis
treponema pallidum
CNS clinical manifestations in neurospyhilis (3)
- can be limited to mesodermally derived structures (meningovascular syphilis)
- parenchyma of brain - “general paresis of the insane” gradual loss of cognition
- parenchyma of spinal cord - “tabes torsalis” loss of position sense and pain sensation “charcot joints”
if you see infectious lesion in CNS with a bunch of plasma cells, what do you think
syphilis
histo of neurosyphilis
gumma granuloma (not caseating)
lyme disease and meningitis
rod cell activation in aseptic meningitis
if you see microglial nodule in CNS tissue, what do you think
viral meningoenchephalitis
leptin resistance and astrocytes and microglia (2)
fat crosses BB barrier, bind to toll like receptors in microglia, activates and releases inflammatory cytokines, which bind to neurons and lead to impairment of leptin receptor-mediated signalling
astrocytes express leptin receptors. reactive astrocytes reduce leptin receptor expression and reduce leptin transport across BBB
what does leptin do?
tells you to stop eating
bilateral lesion to lateral hypothalamic area causes what in mice
decreased feeding (decreased food-seeking locomotion/behaviors)
bilateral lesion to ventromedial hypothalamic lesion causes what in mice
increased feeding - satiety center is destroyed
which areas of CNS regulate eating based on maintaining energy homeostasis
- nucleus of solitary tract
2. hypothalamus (lateral hypothalamus)
opium signalling and eating
pleasure-driven eating
domamine signalling and eating
craving/addiction - driven eating
how do GI hormones regulate neural feeding patterns (2)
- GI peptides circulate to arcuate nucleus of hypothalamus (outside the BBB)
- GI hormones bind to vagal sensory nerve which stimulates AP which is relayed to the solitary tract nucleus
ghrelin does what
binds to receptors in arcuate nucleus or nucleus solitary tract which increase apetite and food intake
CCK does what
decreases appetite through hypothalamus and nucleus solitaris to
what neurotransmitter is used in lateral hypothalmic necleus
orexin - increases eating
what does PoMC (pro-opiomelanocortin) do
PoMC is in anorexigenic neurons, produce melanocyte stimulating hormone and decreases eating
is thyroid hormone production increased in relation to anorexogenic or orxigenic pathways
anorexogenic - leptin increases thyroid hormone to increase metabolism
mutations in alpha melanocyte stimulating hormone (alpha MSH) cuases what
obesity
where does CMV like to go in meningoehcephalitis
subventricular region/zone
where does polio like to go in meningoenchephalitis
lower motor neurons of spinal cord and brainstem
where does JC virus like to go in meningoenchephalitis
oligodendrocytes
where does HSV and VZV like to go in meningoenchephalitis
ganglion cells of dorsal root and cranail nerve ganglia
where does “herpes brain” affect (HSV1)
necrotizing bloody medial temporal lobe, limbic regions - people think it’s a stroke
on histo what do you see for VZV
intranucleuar inclusions in neurons and glia
fetal infection with CMV
microcelphaly, periventricular calcifications
if you get retinitis in immunocompromised patient, what infection do you think
CMV
why is rabid dog bite more concerning in children than adults
because there’s less distance to get to brain in a child - because they’re smaller
SSPE complication from what virus
measels before 2 years of age. latent, eventually attacks neurons and glia -fatal.
PML complication from what virus
JC virus. latent since childhood in everyone. if immunocompromised, will reactivate and attack oligodendrocytes
what does acute HIV encephalitis look like on histo
multinucleated giant cells within microglial nodule
rickettsial infections of CNS (2)
Rocky mountain spotted fever
Typhus
fungal CNS histo
granulomatous inflammatory response, or minimal response due to immunocompromised status
worldwide most common cause of pediatric epilepsy
cystercircosis - tenia solium
toxo in fetus
pan encephalitis, destruction of white and gray matter of fetus
in immunosuppressed host, where does toxo go in brain
basal ganglia
if someone comes in and you suspect bacterial meningitis what do you start
ceftriaxone and vancomycine
and dexamethasone steroids to reduce inflammation
if someone is taking eculizumab/soliris for atypical hemolytic uremic syndrome, what is he at risk for developing
meningococcal menintitis
if you see someone with acute meningoencephalitis, cerebral bleeds/infarcts, and uveitis, that (if you survive) could cause cognitive deficits what do you think it could be
ebola
if you see lesion in brainstem in someone who ate a bunch of cheeses, what could it be
listeria encephalitis
tx for toxo (3)
- pyrimethamine
- sulfadiazine
- folinic acid
for a few weeks
see a multiloculated brain abcess
nocardia
tx for cystercercosis
admit to hospital, give albendazole with praziquantel
AND corticosteroids
treat for a long time
(or don’t treat them because you don’t want the cysts to burst)
young kid with over past 2 weeks worsening headaches, vomitting, clumsiness, falling, L eye turned in. what is it?
medulloblastoma
kid with multiple cranial nerve palsies, headaches, cerebellar disfunction, cross hemiparesis
brain stem gliomas
Subtypes of declarative memory
Episodic (personal memory)
Semantic (facts, math etc)
Who is HM?
Patient who had bilateral removal of medial temporal lobe - could not make new memories, but could learn non declarative skills
Memory loss with ECT
6mo before shock, 2 mo after shock
Hippocampus being destroyed caused what kind of amnesia
Anterograde amnesia
what’s the issue with radiation in pediatric brain tumors
decreases IQ permanently
what info is processed by the prerhinal cortex
object features from various cortices
what info is processed by the parahippocampal cortex
spatial context of object by parietal cortex
what is multiple trace theory
the more you think of something, more memory traces are built in the hippocampus = become more resistant to partial damages (become consolidated in the hippocampus)
what does prefrontal cortex do for memory
links memory to context - selects relevant info to be remembered and retrieved ONLY
pertinent to the task goal or context (suppresses others and intentional forgetting)
if someone has defect in PFC how can their memory be affected
have difficulty remembering SOURCE of memory - difficulty remembering if they were abducted by aliens, or if they watched a movie about alien abduction - results in confabulation
role of anterior thalamic nucleus in memory
direct connection to mediodorsal thalamic nucleus (MTL)
role of mediodorsal thalamic nucleus in memory
interconnected with prefrontal cortex (damage causes confabulation)
does cerebellum control ipsilateral or contralateral body
ipsilateral
what is asynergia, what is it caused by
lack of cooperation of muscles that usually work together
caused by damage to cortico-ponto-cerebellar pathways, or spinocerebellar inputs
what is dysmetria
overshooting or undershooting a target as you approach
what is dysdiadochokinesia
rapid alternating movements that are clumsy or irregular in rhythm
what does posterolateral fissure in cerebellum separate
separates cerebellar hemispheres from flocculonodular lobe
what does primary fissure in cerebellum separate out
anterior and posterior cerebellar lobes
what is first part of cerebellum to develop
flocculonodular lobe
what kinds of inputs does flocculonodular lobe process
processes vestibular inputs
“vestibulocerebellum”
what inputs does anterior cerebellar lobe process
spinal cord inputs
“spinocerebellum”
what inputs does posterior cerebellar lobe process
input from ons and cerebral cortex
“cerebrocerebellum”
what’s the last cerebellar lobe to form in development
posterior lobe
where do fibers cross in cerebellum
superior cerebellar peduncles
what is the most medial nucleus in cerebellum
fastigial nucleus
what nuclei are right lateral to fastigial nuclei
globose nucleus
what nucleus is right lateral to globose nuclei
emboliform nucleus
what are the most lateral cerebellar nuclei
dentate nuclei
what is the largest cerebellar nucleus
dentate
dorsal spinocerebellar tract carries what info to cerebellum
muscle spindle/tone from lower extremities (ipsilateral)
ventral spinocerebellar tract carries what info to cerebellum
crosses twice, so caries ipsilataeral info about whole muscle movement
cuneocerebellar tract carries what info to cerebeelum
info regarding muscle spindle/tone to upper extermity (ipsilateral)
which are mossy fibers in cerebellum (4)
- spinal cord fibers
- vestibular fibers
- reticular fibers
- pontocerebellar fibers
which are climbing fibers in cerebellum
- inferior olivary nucleus fibbers
how many neuron layers in cerebeelum cortical gray and what are they
- molecular layer (external)
- purkinje cell layer (monolayer)
- granule cell layer (inner, overlying white matter)
what are paraellel fibers
axons of granule cell layer in cerebellum
in what plane can you see the arborization of purkinje fibers?
only in sagittal section (do so to intersect with multiple processes of granule cell dendrites run into them)
what direction do granule cell dentrite processes travel
parallel to folia
where to climbing fibers synapse
directly on dendrites of purkinje cells (direct connection from inferior olive to purkinje cells)
where do mossy fibers synapse
on granule cells in granular cell layer
is purkinje cell output inhibitory or excitatory to deep cerebellar nuclei - why is it important
inhibitory - modulates excitatory inputs from climbing and mossy fibers on deep cerebellar nuclei
purkinje cells in vermis project to what cerebellar nucleus
fastigial
purkinje cells in intermediate zone project to what cerebellar nucleus
interposed nucleis (globos + emboliform)
lateral cell purkinje fibers project to what cerebellar nuclei
dentate nucleus
output of fastigial nuclei - and through what peduncle
vestibular and reticular formation (via inferior cerebellar peduncle) extensor motor, adjusts posture
output of interposed nuclei- and through what peduncle
to red nucleus (via superior cerebellar peduncle) - flexor motor, adjusts limbs
output of dentate nuclei- and through what peduncle
to VA/VL nuclei (fine motor) in thalamus (via middle cerebellar peduncle)
