Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
272 Cards in this Set
- Front
- Back
|
GFAP is a marker of what
|
Astrocytes product
-marker of Glioblastoma -astrocytes do reactive gliosis in response to injury |
|
|
CNS phagocytes
|
Microglia
|
|
|
Nissle substance
|
in neuronal cell body and dendrites, NOT axon
|
|
|
what forms multinucleated giant cells in CNS of HIV pt
|
HIV-infected microglia
|
|
|
cells providing myelination
|
in CNS, Oligodendrocytes; and these myelinate multiple CNS axons
-oligodendrocytes look like fried-eggs on H&E in periphery, Schwann Cells myelinate, and only myelinate 1 PNS axon...these cells are destroyed in Guillain-Barre syndrome |
|
|
what's cell in nervous system is destroyed in Guillain-Barre
|
Schwann cells
|
|
|
what's an acoustic neuroma?
|
type of schwannnoma; usually in Internal Acoustic Meatus (CN VIII), and a/w Neurofibromatosis Type 2
|
|
|
sensory receptor for Pain & temperature
|
Free nerve endings:
C = slow, unmyelinated fibers Adelta = fast, unmyelinated fibers |
|
|
difference btw C fibers & Adelta fibers
|
C fibers = slow, unmyelinated fibers for pain & temperature
Adelta = fast, myelinated fibers for pain & temperature |
|
|
in glabrous skin, receptor for position sense, dynamic fine touch
|
Meissner's corpuscles, adapt quickly
|
|
|
in hair follicles, receptors for postion sense, static touch, adapt slowly
|
Merkel's disks
-adapt SLOW (vs Meissner's corpuscles adapt fast) |
|
|
difference btw Merkel's disks and Meissner's corpuscles
|
Merkel's disks:
-SLOW adapting -position, static touch Meissner's corpuscles: -FAST adapting -position, static touch |
|
|
receptors for vibration and P
|
Pacinian corpuscles
|
|
|
Norepinephrine
-changes in anxiety, depression, mania -where made? |
Norepinephrine
-incr in anxiety, decr in depression, incr in mania -locus ceruleus, reticular formation, solitary tract |
|
|
Dopamine
-changes in Schizophrenia, PD, depression -where made? |
Dopamine
-incr in Schizophrenia, decr in PD, decr in depression -made in Ventral Tegmentum, SNc |
|
|
5HT
-changes in anxiety, depression -where made? |
5HT
-decr in anxiety, decr in depression -made in Raphe nucleus |
|
|
ACh
-changes in Alzheimer's Huntington's, REM, PD -where made? |
ACh
-decr in Alzheimer's, decr in Huntington's, decr in REM, incr in PD -made in Basal Nucleus of Meynert |
|
|
precursor to GABA, and what vitamin req'd for this?
|
Glycine → GABA
-vitamin B6 is req'd for this |
|
|
GABA
-changes in anxiety, Huntington's -where made, what from, what req'd? |
GABA
-decr in anxiety, decr in Huntington's -made in Nucleus Accumbens, from Glycine, and B6 is req'd for this |
|
|
why does infarction cause edema in the brain?
|
infarction destroys the endothelial cells, and the tight junctions that they form, leading to Vasogenic Edema
|
|
|
what makes up the blood brain barrier? (BBB)
|
BBB:
1) tight junctions btw nonfenestrated capillary endothelial cells 2) basement membrane 3) astrocyte process |
|
|
crossing of BBB?
|
glc & AAs can cross slowly by carrier-med'd transport
-nonpolar/lipid-soluble substances cross rapidly via diffusion (remember, incr lipid solubility of anesthetic, incr potency) |
|
|
supraoptic nucleus of hypothalamus makes_, while paraventricular nucleus makes_
|
Hypothalamus:
Supraoptic nucleus → ADH Paraventricular nucleus → Oxytocin (PO) |
|
|
destruction of Lateral area of hypothalamus
|
would lead to anorexia
-b/c Lateral area of Hypothal nrl'ly stim's hunger -Leptin inhibits the lateral area after meal -"destroy lateral nucleus of hypothal, shrink laterally; destroy ventromedial area, grow ventromedially" |
|
|
destruction of Ventromedial area of Hypothalamus
|
would lead to weight gain/hyperphagia
-b/c Ventromedial area of Hypothal nrl'ly stim's satiety -Leptin stim's ventromedial area after meal -"destroy ventromedial area of hypothal, grow ventral-medially" |
|
|
Anerior Hypothal vs Posterior Hypothal
|
Anterior hypothal → cooling, PNS
"A/C" Posterior hypothal → heating, SNS |
|
|
origin of Posterior Pituitary, and what does it secrete?
|
Posterior Pituitary from Neuroectoderm
-receives Oxytoxin from Paraventricular nuclei of hypothal -receives ADH from Supraoptic nuclei of hypothal |
|
|
Lateral Geniculate Nucleus of Thalamus for
|
Lateral Geniculate Nucleus of Thalamus for vision
-projects via optic radiations to occipital cortex "Lateral for Light" "Medial for Music (hearing), Lateral for Light (vision) |
|
|
Medial Geniculate Nucleus of Thalamus for
|
Medial Geniculate Nucleus of Thalamus for Auditory info
"Medial for Music" "Medial for Music (hearing), Lateral for Light (vision)" |
|
|
Ventral Posterior Nucleus, Lateral
|
Ventral Posterior Nucleus, Lateral:
body sensation (proprioception, P, pain, touch, vibration, via dorsal columns, spinothalamic tract) |
|
|
Ventral Posterior Nucleus, Medial part
|
Ventral Posterior Nucleus, Medial part:
-facial sensation, via CN V |
|
|
motor nucleus of the Thalamus
|
Ventral Anterior/Lateral
|
|
|
blood supply of Thalamus
|
Posterior communicating, PCA, ICA
|
|
|
infarction of Posterior communicating, PCA, ICA could damage what structure?
|
Thalamus
|
|
|
Limbic system 5 main functions?
|
Feeding, Fleeing, Fighting, Feeling, Fucking
|
|
|
60 y.o man presents w/ tremor at rest, rigidity in extremeties, instability w/ standing. what neurotransmitter changes seen (name TWO), and Bx of affected area would show what?
|
this is Parkinson's disease
-degeneration of Basal Ganglia, esp depigmentation of Substantia Nigra pars Compacta -thus, lose Dopamine neurons, so have LOW DA, and INCR in ACh -a/w Lewy Bodies composed of α-synuclein |
|
|
Bx of brain shows α-synuclein deposits in a old man w/ resting tremor
|
these are probably Lewy Bodies a/w depigmentation of the Substantia Nigra pars compacta, in Parkinson's Disease
-decr DA, incr ACh |
|
|
α-synuclein, decr DA, incr ACh, in degenerative brain condition
|
Parkinson's Disease
TRAP: Tremor at rest, Rigidity (cogwheel), Akinesia, Postural instability |
|
|
Bromocriptine, Pergolide
|
Bromocriptine, Pergolide
-ergot alkaloid Dopamine-agonists in Tx of Parkinson's Tx for PD incl BALSA: Bromocriptine Amantadine Levodopa w/ carbidopa Selegiline Antimuscarinics (since high ACh in PD) |
|
|
What is the #1 cause of digitoxin toxicity?
|
hypokalemia
|
|
|
Pramipexole, Ropinrole MoA and what for?
|
Pramipexole & Ropinrole
-non-ergot alkaloid Dopamine-Agonists -Tx for PD incl BALSA: Bromocriptine (DA-agonist, also Pergolide, Ropinrole, Pramipexole) Amantadine (incr DA release) L-dopa w/ Carbidopa Selegiline (MAO-B inhibitor) Antimuscarinics (Benztropine, since incr ACh in PD) |
|
|
Amantadine, MoA, and why for PD?
|
Amantadine
-may incr DA release for PD |
|
|
L-dopa/Carbidopa
|
converted to DA in CNS
-for PD |
|
|
Selegiline, MoA, what for?
|
Selegiline
-for PD -MAO type B inhibitor -MAO-B degrades DA selectively, while MAO-A degrades 5HT & NE (for depression) |
|
|
Entacapone, Tolcapone
|
Etacapone, Tolcapone
-inhibit COMT to prevent L-dopa degradation, incr'ing DA activity |
|
|
MAO-B inhib vs COMT inhibitor for Parkinson's
|
MAO-B inhibitor = Selegiline
-incr's DA availability by inhibiting its breakdown COMT inhibitors = Entacapone, Tolcapone -stop L-dopa degredation |
|
|
Benztropine's nuerodegenerative use?
|
Benztropine
-anti-muscarinic |
|
|
PD Rx w/ risk of arrhythmia from peripheral conversion; long term can → Dyskinesia
|
L-Dopa
-can get arrhythmias from peripheral conversion to DA -Carbidopa helps inhibit L-dopa breakdown since its a decarboxylase inhibitor |
|
|
Selegiline's SE
|
Selegiline mainly incr's SE of L-dopa:
-can get arrhythmias from peripheral conversion to DA |
|
|
sudden, wild flailing of an extremety, what is this, and where's the brain lesion
|
this is Hemiballismus
-the lesion is m/c in the Subthalamic Nucleus -w/o Subthalamic Nucleus, you release inhibition on the Thalamus |
|
|
injury to Subthalamic Nucleus
|
Hemiballismus
lose activation of Globus Pallidus internus, so lose inhibition of Thalamus, Thalamus is free to stimulate movment |
|
|
50 y.o pt has increasing defects in memory, jerky uncontrolled mvmnts of R arm, starting to feel somewhat 'down', what is this?
|
Huntington's Disease
-autosomal dominant -CAG repeat expansion (shows anticipation) -Caudate loses ACh & GABA -C's of Huntington's: Crazy, Chorea, CAG repeat, Caudate degeneration, Chrom Cuatro, onset ~'Cuarenta' Tx: DA-antagonists, Haloperidol, Benzo's, Phenothiazines |
|
|
39 y.o F presents w/ changes in mentation, spasticity of her R leg. similar problem in grandma starting around 64, and in dad starting around 50.
|
Huntington's Disease
-the age decrease in onset is due to the Anticipation seen w/ trinucleotide repeat diseases -CAG repeat expansion → changes of Huntington's: Chorea, Caudate loss of ACh & GABA, Depression, progressive Dementia |
|
|
Reserpine & Tetrabenazine can be used for
|
Reserpine & Tetrabenazine
-Rx for Huntington's -these are Amine depleting -Huntington's = incr DA, decr GABA & ACh |
|
|
Haloperidol, why for Huntington's?
|
Haloperidol in Huntington's b/c its a DA-R antagonist
|
|
|
slow, writhing mvmnts, esp of fingers is what
|
Athetosis
|
|
|
sudden, brief muscle contraction
|
Myoclonus
jerks, hiccups (singulitis) |
|
|
finger-to-nose testing, pt shows slow zigzag motion of finger, what is this indicative of?
|
Intention Tremor a/w Cerebellar dysfunction
|
|
|
difference btw Broca's area and Wernicke's areas (hemisphere, function)
|
BOTH in dominant hemisphere
Broca's area = Motor speech; is anterior to temporal lobe Wernicke's area = Auditory Association; posterior to temporal lobe |
|
|
planning, inhibition, concentration, language, judgement are some functions of which part of the brain
|
Frontal Lobe
|
|
|
frontal lobe lesion, usual first S/Sx
|
lack of Social Judgement
|
|
|
spacial neglect syndrome a/w what brain lesion
|
R parietal lobe
|
|
|
hyperorality, hypersexuality, disinhibited behavior is what, and a/w what lesion?
|
hyperorality, hypersexuality, disinhibited behavior is Kluver-Bucy syndrome
-a/w a bilateral Amygdala lesion |
|
|
reduced levels of arousal & wakefulness is a/w what lesion in the brain?
|
Reticular Activating System (in Midbrain)
|
|
|
falling towards side of a brain lesion is characteristic of _
|
Ipsilateral Cerebellar lesion
(cerebellum → SCP → contralateral cortex → corticospinal decussation = ipsilateral) |
|
|
acute paralysis, dysarthria, dysphagia, diplopia, loss of consciousness
|
Central Pontine Myelinolysis
-often caused by Rapid Correction of Hyonatremia |
|
|
what can too rapid correction of hyponatremia cause?
|
Central Pontine Myelinolysis:
Acute paralysis, dysarthria, dysphagia, diplopia, loss of consciousness *irreversible!* |
|
|
in Tx of hyponatremia, pt develops paralysis, trouble w/ speech, trouble swallowing, double vision, comatose
|
Central Pontine Myelinolysis
-too rapid correction of hyponatremia causing acute paralysis, dysarthria, dysphagia, diplopia, loss of consciousness |
|
|
loss of all laryngeal muscles except the cricothyroid would be due to
|
Recurrent Laryngeal n injury
-also would have hoarsness -common result after thyroidectomy |
|
|
sensation below vocal folds of laryngeal mucosa
|
recurrent laryngeal n
vs Internal branch of Superior Laryngeal n is for sensation above vocal folds |
|
|
sensation in laryngeal mucosa above vocal folds
|
Internal branch of Superior Laryngeal n
vs Recurrent Laryngeal n is for sensation in Laryngeal Mucosa below vocal folds |
|
|
inability to speak, intact comprehension
|
Broca's aphasia
-lesion to inferior frontal gyrus |
|
|
lesion to the inferior frontal gyrus would manifest as how?
|
Broca's aphasia
-inability to speak, but nrl comprehension |
|
|
asking a pt 'how arrive at the hospital', and responds with great difficulty, but understands question and tries to answer it
|
Broca's aphasia
-lesion to inferior frontal gyrus |
|
|
fluent aphasia, but inability to comprehend
|
Wernicke's aphasia
-lesion to superior temporal gyrus |
|
|
pt cannot understand others, can speak fluently, but speech does not make sense
|
Wernicke's aphasia
-lesion to superior temporal gyrus |
|
|
pt cannot understand others, and cannot speak fluently
|
Global aphasia
-both Wernicke's (superior temporal gyrus) and Broca's (inferior frontal gyrus) are lesioned |
|
|
lesion to superior temporal gyrus, and inferior frontal gyrus would lead to what?
|
Global aphasia
-inability to speak or comprehend others speech |
|
|
most common locations of Berry Aneurysm
|
bifurcations in Circle of Willis
-m/c in Anterior Comm a, and Posterior Comm a -a/w ADPKD, Ehlers-Danlos, Marfan's |
|
|
chronic HTN is m/l to cause what type of aneurysms in brain
|
m/c will cause Charcot-Bouchard microaneurysms
|
|
|
pt suffers head trauma, gets lucid interval, now has L eye 'down & out'
|
Epidural Hematoma
-m/l rupture of MCA -biconcave disk on CT that does NOT cross suture lines (subdural can), can cross Falx & Tentorium -'down & out' eye due to CN III palsy |
|
|
CT shows 'biconcave disk'- appears as balloon being blown up just outside brain, into calvarium
|
Epidural Hematoma
-usually has lucid interval after injury -canNOT cross suture lines (subdural can), can cross falx, can cross tentorium |
|
|
head injury common to old or alcoholic, blood slowly gathering in calvarium
|
Subdural Hematoma
-rupture of bridging veins -Cresent-shaped on CT -CAN cross suture lines (Epidural cannot), canNOT cross falx or tentorium (epidural can) |
|
|
CT shows cresent-shaped hemorrhage (like quarter moon forming in calvarium)
|
Subdural hematoma
-CAN cross suture lines (Epidural cannot) -canNOT cross falx or tentorium (Epidural can) |
|
|
difference btw Epidural & Subdural hematoma's
|
Epidural
-arterial (usually MCA) -biconcave disk on CT Subdural -venous (usually bridging veins) -cresent-shaped on CT |
|
|
rupture of an aneurysm or AVM can lead to
|
Subarachnoid hemorrhage
-"worst HA of my life" -Marfan's, Ehler's-Danlos, ADPKD -spinal tap bloody if acute, or xanthochroma (yellow) if a few days old -2-3d later, risk of vasospasm due to blood breakdown products that irritate blood vessels (Tx w/ Ca chnnl blockers) |
|
|
worst HA of my life
|
Subarachnoid hematoma
-m/c rupture of aneurysm or AVM -bloody spinal tap in acute -xanthochromia if few days later (yellow) |
|
|
hematoma of Lenticulate Striae arteries m/c a/w _
|
Parenchymal hematoma
|
|
|
most vulnerable areas of brain to ischemia
|
watershed areas
-irreversible damage occurs after 5 min |
|
|
red neurons in brain
|
12-48 hr after ischemic brain attack
|
|
|
necrosis & neutrophils in brain
|
24-72 hr after ischemic brain attack
|
|
|
macrophages in ischemic brain
|
3-5 days after ischemic brain attack
|
|
|
reactive gliosis & vascular proliferation in ischemic brain
|
1-2 wks after ischemic attack
|
|
|
glial scar in brain
|
>2wks after ischemic attack
|
|
|
difference btw hemorrhagic & ischemic strokes
|
Hemorrhagic
-intracerebral bleeding -usually due to aneurysm rupture Ischemic -embolus blocking cerebral blood flow -lacunar strokes block small vessels, are 2ndary to HTN -Tx = tPA w/in 3 hrs |
|
|
ischemia on imaging after few hours (btw CT & MRI)
|
-CT will NOT show ischemia w/in 24 hrs (WILL show hemorrhage)
-MRI will show ischemia w/in 30 min |
|
|
how does CSF get from subarachnoid to Superior Sagittal sinus
|
thru the arachnoid granulations
|
|
|
outline the flow of CSF in the ventricular system
|
Lateral ventricle → foramen of Monro → 3rd ventricle → Cerebral Aqueduct of Sylvius → 4th ventricle → subarachnoid space via Foramen of Luschka (Lateral) & Foramen of Magendie (Medial)
|
|
|
where is CSF made, and where reabsorbed?
|
CSF made by Choroid Plexus, reabsorbed by Venus Sinus Arachnoid Granulations (to get to the superior sagital sinus)
|
|
|
pt w/ dementia, ataxia, urinary incontinence, what occuring in brain?
|
Nrl P Hydrocephalus
"wet, wobbly, & wacky" -expansion of ventricles distorts fibers of coronia radiata & → clinical triad of dementia, ataxia, urinary incontinence *reversible cause of dementia in eldery* |
|
|
decrease in CSF absorption by arachnoid villi can lead to
|
"Communicating Hydrocephalus"
decr CSF reabsorption by arachnoid villi → incr ICP, papilledema, herniation -'communicating' b/c CSF is still flowing from lateral to 4th ventricle |
|
|
structural blockage of CSF circulation in ventricular system can lead to
|
Obstructive (noncommunicating) hydrocephalus
|
|
|
appearance of incr CSF in atrophy of the cerebri
|
Hydrocephalus ex vacuo
-ICP is nrl, triad not seen |
|
|
where do spinal nerves exit as leave IV foramen?
|
C1-C7 exit via IV foramen ABOVE vertebra
-all other exit below |
|
|
how far does the spinal CORD extend? subarachnoid space?
|
to L1/L2
-subarachnoid space extends to lower S2 |
|
|
for Lumbar Puncture, where usually insert needle?
|
L4, find ASIS- that corresponds to L4 & L5
|
|
|
layers of lumbar puncture
|
Skin → superficial fascia → deep fascia → supraspinous ligament → interspinous ligament → interlaminar space → ligamentum flavum → epidural space → dura mater → subdural space → arachnoid → subarachoid space to collect CSF
|
|
|
spastic paralysis, hyperreflexia, incr tone are signs of what type of cord lesion
|
Upper Motor Neuron lesion
-also: clonus, weakness, hyperreflexia, incr tone, (+)Babinski, spastic paralysis, clasp knife spasticity |
|
|
weakness, atrophy, fasciculations are signs of what type of spinal cord lesion?
|
Lower Motor Neuron lesion
also: weakness, atrophy, fasciculations, hyporeflexia, decr tone, flacid paralysis |
|
|
test of motor function at lowest level of the spine
|
Anal Reflex
-contraction of the anal sphincter on stimulation of perianal skin -(+) in nrl adult |
|
|
Poliomyelitis and Werdnig-Hoffmann disease will affect what part of spinal cord
|
Lower Motor Neuron
-due to destruction of anterior horns → flaccid paralysis |
|
|
Multiple Sclerosis mostly affects what part of the spine
|
MS targets the white matter, esp in Cervical region
-random & asymmetric -lesions are due to demyelination -Sx: scanning speech, intention tremor, nystagmus (Charcot's Triad) |
|
|
what does poliomyelitis do before it infects the CNS, and once in the CNS, what does it do?
|
poliovirus replicates in oropharynx & small intestine before spreading to CNS via blood
-in CNS, destroys cells in anterior horn of spine → LMN lesions -Sx: malaise, HA, fever, N, abd pain, pharyngitis, weakness & atrophy, fasciculations, fibrillation, hyporeflexia -CSF: lymphocytic pleocytosis, ~incr in protein (no change in CSF glucose) -virus in stool or throat |
|
|
pt presents w/ malaise, HA, fever, N, muscle weakness & atrophy, fasciculations, fibrillations
|
Poliomyelitis
-virus replicates in oropharynx & small intestine before spreading via blood to CNS where destroys anterior horn cells to → LMN destruction -CSF: lymphocytic pleocytosis, slight elevation in protein, no change in glucose |
|
|
infant w/ spinal muscular atrophy, poor suckling and swallowing, tongue fasciculations
|
Werdnig-Hoffman disease
-like Poliomyelitis, destroys the anterior horn of the spine → flaccid paralysis -due to continued cell death by apoptosis |
|
|
young infant w/ poor suckling and swallowing, tongue fasciculations
|
Werdnig-Hoffman disease
-similar to Poliomyelitis, it causes destruction of LMNs only via the anterior horn cells |
|
|
pt presents w/ fasciculations, hyperreflexia of patellar joint, but hyporeflexia of tricpes joint, sensory, cognitive, oculomotor functions are in tact
|
Amyotrophic Lateral Sclerosis
-commonly caused by defect in Superoxide Dismutase 1 (SOD1) -if notice, Sx incl BOTH UMN & LMN signs |
|
|
which part of the spine would Tabes Dorsalis affect (and what Tabes Dorsalis)
|
Tabes Dorsalis = tertiary syphilis
-degeneration of dorsal roots & dorsal columns, impaired proprioception, locomotor ataxia |
|
|
34 y.o M w/ loss of Deep Tendon Reflexes, (+) Romberg, pupils unresponsive to light, but do accomodate
|
Tabes Dorsalis of Tertiary Syphilis
-damage to dorsal roots & dorsal columns of spine -impaired proprioception and locomotor ataxia -the pupils described are "Argyll Robertson pupils" aka Prostitutes Pupils, b/c they accommodate but do not react |
|
|
pt w/ staggering gait, frequent falling, nystagmus, dysarthria, grandfather had similar problem
|
Friedreich's Ataxia
-Auto-recessive trinucleotide repeate d/o of Frataxin gene; GAA repeat -affects UMN & LMN -loss of tactile discrimination & position/vibration sense (dorsal columns), spastic paralysis (CS tracts), limb dystaxia (spinocerebellar tracts) -presents in childhood w/ kyphoscoliosis -common cause of death is Hypertrophic Cardiomyopathy |
|
|
young female is frequently falling, has a staggering gait and bumbs into things, has nystagmus, starting to develop kyphoscoliosis and a heart murmur
|
Friedriech's ataxia
-GAA repeat expansion, auto-recessive -impaired mitochondrial functioning -affects UMN & LMN -lose tactile discrimination & position/vibration sense (dorsal columns), spastic paralysis (CS tracts), limb dystaxia (spinocerebellar tracts) |
|
|
hemisection of spinal cord will affect:
UMN signs? Tactile Vibration Proprioception Pain Temperature Sensation Motor control |
Spinal Cord hemisection
UMN signs: Ipsilateral loss below lesion (corticospinal tract) Tactile: Ipsilateral loss below lesion (dorsal column) Vibration: Ipsilateral loss below lesion (dorsal column) Proprioception: Ipsilateral loss below lesion (dorsal column) Pain: Contralateral loss below lesion (spinothalamic tract) Temperature: Contralateral loss below lesion (spinothalamic tract) Sensation: Ipsilateral loss AT level of lesion Motor control: LMN signs (flaccid paralysis) AT level of lesion |
|
|
a hemisection of spinal cord above T1 can present w/ _
|
Horner's syndrome in addition to:
UMN signs: Ipsilateral loss below lesion (corticospinal tract) Tactile: Ipsilateral loss below lesion (dorsal column) Vibration: Ipsilateral loss below lesion (dorsal column) Proprioception: Ipsilateral loss below lesion (dorsal column) Pain: Contralateral loss below lesion (spinothalamic tract) Temperature: Contralateral loss below lesion (spinothalamic tract) Sensation: Ipsilateral loss AT level of lesion Motor control: LMN signs (flaccid paralysis) AT level of lesion |
|
|
pt presents w/ drooping of eyelid, dry skin on same side, and miosis on eye of same side
|
Horner's Syndrome
-Ptosis (eyelid droop), Anhidrosis (no sweating), Miosis on same side -due to lesion to spinal cord above T1 (Pancoast's tumor, Brown-Sequard syndrome, late-stage Syringomyelia) *Cluster HA's can → Ptosis & Miosis |
|
|
how remember where is T4 and T10 dermatomes?
|
T4 at the 'teat pore' - nipple level
T10 at the belly butTEN - at umbilicus (important to early appendicitis pain referral) |
|
|
how would stretching a muscle affect it (think reflex arc)
|
Muscle Spindle used here
-intrafusal muscle spindle senses stretch → stimulates Ia afferent → thru dorsal horn of spine → stim's alpha motor neuron → reflex muscle contraction via extrafusal fibers |
|
|
Function of Golgi Tendon Organs?
|
these lie perpendicular to intrafusal muscle, when over-stretched, stim Ib afferent to inhibit alpha-motor neuron
-function is to prevent tear by overstretching |
|
|
how do Muscle Spindle, Ia afferent, and Golgi Tendon Organ work together?
|
muscle spindle lies parallel w/ extrafusal muscle fibers, if sense sudden stretch by Ia afferent to stim alpha-motor neuron to give extrafusal contraction
-the Golgi Tendon Organs lie perpendicular to intrafusal muscle, sense too much stretch and inhibit alpha-motor neurons to avoid over-stretching |
|
|
what is the gamma-motor neuron for?
|
it changes sensitivity of the intrafusal fiber reflex arc
-contracting gamma-motor n more will make it more sensitive to stretch -relaxing gamma-motor n will make it less sensitive to stretch |
|
|
Reflexes are testing which nerve root:
Biceps: Triceps: Patella: Achilles: Babinski: |
Biceps: C5
Triceps: C7 Patella: L4 Achilles: S1 Babinski: dorsiflexion of big toe & fanning of other toes; sign of UMN lesion, but nrl in 1st yr of life |
|
|
melatonin secretion & circadian rhythm done by?
|
melatonin secretion & circadian rhythm done by the Pineal Gland
|
|
|
Conjugate Vertical Gaze Center is _
|
Conjugate Vertical Gaze Center is in Superior Colliculi of brain stem
vs Inferior Collicular are for auditory (youre eyes are above your ears, and the superior colliculus (visual) is above your inferior colliculus (auditory)" |
|
|
Auditory center in brain stem is in
|
Auditory center in brain stem is in Inferior Colliculi
vs Conjugate Vertical Gaze Center is in Superior Colliculi "your eyes are above your ears, and the superior colliculus (visual) is above the inferior colliculus (auditory)" |
|
|
paralysis of conjugate vertical gaze can be caused by
|
paralysis of Conjugate Vertical gaze due to lesion of Superior Colliculi, m/c by a Pinealoma
-this is Parinaud's syndrome -can also cause pupillary disturbances, noncomm hydrocephalus |
|
|
cranial nerves III thru XII lie where?
|
Midbrain: III & IV
Pons: V, VI, VII, VIII Medulla: IX, X, XI, XII |
|
|
Corneal reflex involves what nerves?
|
Corneal reflex:
V1 afferent, VII efferent |
|
|
Lacrimation reflex involves what nerves?
|
Lacrimation reflex:
V1 afferent, VII efferent |
|
|
Jaw jerk reflex involves what nerves?
|
V3 afferent, V3 motor
|
|
|
Pupillary reflex involves what nerves?
|
Pupillary reflex:
II afferent, III efferent |
|
|
Gag reflex involves what nerves?
|
IX ipsilaterally afferent, IX & X bilaterally efferent
|
|
|
tongue deviates to L, what could be wrong here
|
tongue deviation to L:
LEFT CN XII -hyoglossus pushes tongue out, so if deviating L, R hyoglossus is working -tongue deviates TOWARD side of lesion |
|
|
jaw deviating to R, what could be wrong here?
|
Jaw Deviation to R
-L Lateral Pterygoid is pulling jaw forward and to R -thus, the R CN V is lesioned distally -jaw deviates TOWARD side of CN V lesion -must be distal b/c Lateral Pterygoids get bilateral input |
|
|
on saying 'ah', pt's Uvula deviates to the R
|
Uvula deviating to R:
-L CN X lesion -'uvula deviates AWAY from side of lesion'- weak side collapses and uvula points away |
|
|
weakness turning head to L, what could be wrong?
|
weakness turning head to L:
R CN XI probably lesioned -sternocleidomastoid is innervated by CN IX, and pulls head to opposite side (L sternocleidomastoid pulls from clavicle/manubrium on the occipital bone to pull head to opposite side) |
|
|
difference btw an UMN & LMN lesion for CN V?
|
UMN CN V lesion:
-contralateral lower face paralysis...only lower b/c upper face gets bilateral UMN innervation LMN CN V lesion: -ipsilateral paralysis of upper & lower face |
|
|
when smiling, pt has inability to make a smile on right side; what nerve can be lesioned here
|
LEFT UMN CN V
-CN V UMN lesion causes contralateral paralysis of lower face only, since upper face gets bilateral innervation |
|
|
what is Bell's Palsy
|
destruction of facial nucleus or branchial efferent fibers
-Peripheral ipsilateral facial paralysis w/ inability to close eye on involved side -complication of: Aids, Lyme, Herpes zoster, Sarcoidosis, Tumors, Diabetes (ALexander graHam BELL w/ STD) |
|
|
pt cannot make 'la-la-la' sound, what is wrong
|
CN XII lesion (hypoglossal to tongue)
-kuh = CN X (palate elevation, CN X) -la = CN XII (tongue, CN XII) -mi = CN VII (lips, CN VII) -"it'd be a KaLaMity to lose CN X, XII, or VII" |
|
|
pt cannot make 'mi-mi'mi' sound, whats wrong?
|
CN VII lesion
-kuh = CN X (palate elevation, CN X) -la = CN XII (tongue, CN XII) -mi = CN VII (lips, CN VII) -"it'd be a KaLaMity to lose CN X, XII, or VII" |
|
|
pt cannot make 'kuh-kuh-kuh sound', what's wrong?
|
CN X lesion
-kuh = CN X (palate elevation, CN X) -la = CN XII (tongue, CN XII) -mi = CN VII (lips, CN VII) -"it'd be a KaLaMity to lose CN X, XII, or VII" |
|
|
which muscles close the jaw?
|
Masseter, teMporalis, Medial pterygoid all Munch
-Lateral pterygoid opens -ALL are innervated by V3 |
|
|
which muscle(s) open the jaw?
|
Lateral Pterygoid opens the jaw
-Masseter, teMporalis, Medial pterygoid all Munch ALL innervated by V3 |
|
|
muscles w/ '-glossus' are innervated by _
|
all muscles w/ "-glossus" are innervated by CN XII
*except the Palatoglossus, this is CN X |
|
|
all muscles w/ "palat" in name are innervated by _
|
all muscles w/ "palat" in name are innervated by CN X
*except the Tensor Veli Palatini, thats CN V |
|
|
nrl'ly, which conducts air better, air or bone?
|
nrl, air (AC) > bone conduction (BC)
-Rinne test |
|
|
pt w/ trouble hearing on R; if Weber test lateralizes to Right ear, what could be wrong?
|
conduction deafness in R ear
vs if trouble hearing on R, and Weber lateralized to L, sensorineural deficit in R |
|
|
pt w/ trouble hearing on R; if Weber test lateralizes to Left ear, what could be wrong?
|
Sensorineural loss in R ear
vs if trouble hearing on R, and Weber lateralized to R, conduction deficit in R |
|
|
nerves in Cavernous sinus
|
III, IV, V1, V2, VI
-1st to get hit by Pituitary adenoma would be VI |
|
|
pt loses ability to Abduct R eye, and on R side of face has ophthalmic & maxillary sensory loss...what's going on?
|
Cavernous Sinus Syndrome
-due to mass defect |
|
|
DDx for "cherry-red spot on macula"
|
DDx for "cherry-red spot on macula"
-Tay-Sachs disease (no hepatosplenomegaly), Niemann-Pick (hepatosplenomegaly), occlusion of central retinal vessel |
|
|
1st hearing to go in elderly
|
as age, lose High Frequency hearing 1st
*this is why old man can't hear his wife screaming |
|
|
how is the eye Ciliary Process affected by β stimulation
|
stim β-R on Ciliary process → Aqueous Humor PRODUCTION
-this is why β-blockers are used for glaucoma -α-agonists would be used b/c α-R stim → mydriasis |
|
|
how is eye dilator/radial muscle affected by α stimulation?
|
α-stimulation → Mydriasis
-this is why α-agonists are used in Glaucoma: they decr aqueous production & incr trabecular outflow |
|
|
cupping of optic disc
|
incr Intraocular P
|
|
|
whats the difference btw Open/Wide Angle Glaucoma, and Closed/Narrow Angle Glaucoma
|
Wide/Open Angle Glaucoma:
-obstruction of Aqueous Humor outflow, aka, the Canal of Schlemm is blocked -a/w myopia, incr age, Black -more common, and is 'silent' & painless Closed/Narrow Angle Glaucoma -Aqueous Humor flow is obstructed btw iris & cornea → P buildup in Posterior Chamber, which is **an Ophthalmmologic Emergency**, do NOT give Epi or Atropine |
|
|
why is atropin bad for closed/narrow angle glaucoma?
|
Atropine will block Muscarinic-R, which will allow SNS stimulation to dominate → Mydriasis → narrow angle in anterior chamber of eye → back up fluid, worsen incr Intraocular P
|
|
|
what drugs do you use for glaucoma?
|
alpha-agonists, beta-blockers, Diuretics, Cholinomimetics, Prostaglandin
|
|
|
why use Epi for Glaucoma, and any CI's?
|
Epi will cause vasoconstriction, so will decr aqueous humor production
**DO NOT give for Closed/Narrow angle glaucoma b/c this will cause mydriasis, and mydriasis further narrows angle obstructing outflow |
|
|
Brimonidine used for what in eye?
|
Brimonidine is an alpha-agonist, used for Glaucoma
|
|
|
Timolol, Betaxolol, Carteolol used for what?
|
these are beta-blockers used for glaucoma, b/c they stop aqueous humor production (remember beta-stimulation of ciliary process stimulates humor production)
|
|
|
what diuretics would you use in Glaucoma
|
Diuretics for Glaucoma:
Acetazolamide- Carbonic Anhydrase inhibitor, which decreases HCO3 for aqueous humor production Mannitol used for Acute, Closed angle glaucoma |
|
|
Pilocarpine, Carbachol can be used for _
|
Pilocarpine, Carbachol = direct cholinomimetics for Glaucoma
-incr aqueous humor outflow -remember, muscarinic blockade allows mydriasis that further narrows humor outflow angle; but muscarinic agonism will → miosis to open it up *Pilocarpine esp good for emergencies b/c fast opening of canal of Schlemm |
|
|
Physostigmine, Echothiophate used for _
|
Physostigmine, Echothiophate
-indirect cholinomimetics for Glaucoma Tx -incr outflow of humor, contract ciliary muscle & open trabecular meshwork |
|
|
what product of the arachidonic acid pathway would you use for Glaucoma?
|
Prostaglanding PGF2alpha (Latanoprost)
-for long term open angle glaucoma -incr's outflow of aqueous humor -brown's iris & lengthen's eye lashes |
|
|
painless opacification of lens of eye
|
Cataract
-incr risk w/ age, smoking, EtOH, sunlight, classic galactosemia, galactokinase deficiency, DM, trauma, infection, rubella |
|
|
incr in ICP → elevated optic disk w/ blurred margins, bigger blind spot
|
Papilledema
|
|
|
which extraocular muscles innervated by which CN?
|
Lat Rectus (abduction) by CN VI
Superior Oblique (depression from adduction) by CN IV all others = CN III LR6SO4Rest3 |
|
|
eye stuck looking medially
|
CN VI damage
|
|
|
eye looking down & out
|
CN III damage
|
|
|
eye w/ diplopia and defective downward gaze
|
CN IV defect
|
|
|
what is strabismus
|
misalignment of the eyes
|
|
|
what is amblyopia, and what is common cause?
|
reduction of vision b/c disuse in critical period
-can be 2ndary to strabismus, deprivation, bad refractice errors |
|
|
which muscle causes eye Miosis? and innvervation?
|
Pupillary Sphincter muscle, gets CN III from Edinger-Westphal nucleus via Ciliary Ganglion
|
|
|
which muscle causes eye Mydriasis? and innervation?
|
Radial muscle, gets Long Ciliary n from T1 preganglionic to Superior Cervical ganglion
|
|
|
pathway causing pupillary light reflex?
|
light into either retina → CN II carries info to Pretectal nuclei in Midbrain, activates Edinger-Westphal nuclei → via CN III to cause Bilateral pupil contraction
|
|
|
testing pupillary light reflex, shining light into R eye causes dilation of pupils, what's wrong?
|
Marcus Gunn pupil
-Afferent pupillary defect (common = optic n damage or retinal detachment) → pupillary dilation as eyes try to get as much light possible |
|
|
arrangement of different types of fibers in CN III
|
CN III:
-parasympathetic output is in periphery -somatosensory motor info is in center of CN III -'blown pupil' can result if start to compress parasympathetic portion of CN III |
|
|
painless loss of central vision in 78 y.o man
|
Age-Related Macula Degeneration
-"dry"/atrophic ARMD is slow, due to fat deposits & get gradual vison loss and pigment changes w/o scarring or hemorrhage -"wet" ARMD is rapid, due to neovascularization (can bleed & leak fluid & scar) |
|
|
Nystagmus and cold/hot H2O testing
|
COWS:
Cold water: nystagmus toward lesion and quick-phase to Opposite side Warm water: nystagmus to opposite side and quick-phase to Same side |
|
|
which side is lesion on if cold water gives nystagmus to left, and quick phase to right; warm water gives nystagmus right, quick phase to left
|
Lesion on Left side
COWS: Cold water: nystagmus towards lesion, quick phase Opposite Warm water: nystagmus away from lesion, quick phase to Same side of lesion |
|
|
how get conjugate gaze to when right or left?
|
when looking R, R Lat Rectus (CN VI) fires, and sends signal to L MLF (Medial Longitud Fasciculus) to cause L Med Rectus to fire and adduct (to look R), same if looking L
|
|
|
trying to look Right, Right eye has nystagmus to R, Left eye doesn't move; but convergence is nrl
|
Internuclear Ophthalmoplegia (MLF Syndrome (Medial Longitudinal Fasciculus))
***this is common Sx of Multiple Sclerosis*** |
|
|
common occular manifestation of Multiple Sclerosis
|
Internuclear Ophthalmoplegia MFL (Med Longitud Fasciculus) Syndrome
-ex: if looking Left: L eye has nystagmus, R eye doesn't move |
|
|
loss of vision in Right eye
|
Optic nerve
|
|
|
loss of bilateral outer visual fields
|
Bitemporal Hemianopia
-m/c optic chiasm lesion |
|
|
loss of outer visual field in L eye, inner visual field in R eye
|
R Optic Tract lesion
|
|
|
55 y.o man has increasing difficulty remembering things, CT shows widespread cortical atrophy, what chemical & histological changes expect?
|
this is Alzheimer's
-would expect Senile Plaques!!! of extracellular β-amyloid angiopathy -Neurofibrillary Tangles!!!- intracellular abnrl'ly PO4'd tau protein (these DO correlate w/ degree of dementia) -would expect a decrease in ACh -late onset, often ApoE4 is culprit; nrl function = chaperone to prevent beta-pleated sheet formation |
|
|
what changes in brain expect in Alzheimer's?
|
-widespread cortical atrophy
-decr ACh -Senile Plaques (extracell beta-amyloid core) -Neurofibrillary Tanlges (hypER-PO4'd tau; DO correlate w/ dementia severity) -ApoE4 in late onset, APP in early onset (on chr 21, which is why Alzheimer's is common in Down's pts) |
|
|
why is Alzheimer's common in Down's patients?
|
b/c 3 copies of Chr 21 means APP is present in much greater amount
-predisposed to early onset AD AD -widespread cortical atrophy -decr ACh -Senile Plaques of extracellular beta-amyloid -Neurofibrillary Tangles of abnrl'ly PO4'd tau proteins |
|
|
is any part of cerebrum spared in Alzheimer's?
|
Occipital Lobe
|
|
|
elderly man w/ changes in cognition, behavioral changes, resting tremor, what would CT and Histology show?
|
this is Pick's Disease (Frontotemporal Dementia)
-CT = Frontotemporal atrophy -Histo = Pick Bodies (intracellular (in neurons), aggregated tau protein) that can stain w/ silver -Parietal lobe & posterior 2/3 of Superior Temporal gyrus spared |
|
|
Pick Bodies present in _
|
Pick bodies = neuronal aggregates of tau protein seen in Pick's Disease (Frontotemporal Dementia)
-dementia, aphasia, personality/behavior changes |
|
|
Resting tremor and cogwheel rigidity in a pt w/ dementia and visual hallucinations, cognition fluctuates
|
Lewy Body Dementia
-expect to see Lewy Bodies (abnrl α-synuclein protein deposits) -incr falls & syncope |
|
|
histology shows deposits of α-synuclein in brain of pt
|
Parkinson's OR Lewy Body Dementia
|
|
|
neuronal deposits of α-synuclein in a pt w/ dementia & visual hallucinations
|
Lewy Body Dementia
|
|
|
rapidly progressive dementia w/ dementia, sudden involuntary muscle twitches, memory deficits
|
Creutzfeldt-Jakob Disease (CJD) due to Prion proteins
-Myoclonus = sudden invol muscle twitches, rapid dementia, memory deficits |
|
|
intention tremor, incontinence, internuclear ophthalmoplegia, muscle pain that comes severely then remits
|
Multiple Sclerosis
-autoimmune inflamm & demyelination of CNS -Bx would show lymphocytic infiltrate w/ active digestion of myelin products |
|
|
25 y.o F w/ Hx of periodic pain, bladder/bowel incontinence, internuclear ophthalmolpegia has CSF drawn- incr IgG
|
Multiple Sclerosis
-autoimmune inflamm & demyelination of CNS -CT shows Dawson's Finger's -main neural changes: demyelination, gliosis, inflamm, axonal damage -a/w HLA-DR2, HLA-DR3, HLA-B7 -as inflamm & demyelin subside, astrocyte hypertrophy & hyperplasia → Gliosis (glial cell proliferation & astrocytosis) |
|
|
Dawson's Fingers on CT
|
common finding of Multiple Sclerosis
|
|
|
autoimmune inflamm & segmental demyelination of peripheral nerves & motor fibers of ventral roots → symmetric ascending muscle weakness, often starting in distal LE
|
Guillain-Barre Syndrome
-**NO Sensory changes!!** -often follows GI infection (Campylobacter jejuni or herpesvirus common) -almost all survive & recover after weeks to months -incr CSF protein w/ nrl cell count, can → papilledema |
|
|
symmetric ascending muscle weakness that started w/ difficulty to dorsiflex the feet, sensation spared
|
Guillain-Barre Syndrome
-often follows GI infection of Campylobacter or Herpesvirus |
|
|
aphasia, hemiparesis, cortical blindness, ataxia in pt w/ demyelination of CNS
|
Progressive Multifocal Leukoencephalopathy (PML)
-a/w JC virus infection |
|
|
fever, HA, drowsiness, seizures, ~coma in pt who had recent viral infection that caused fever, maculopapular, erythematous rach over body
|
this pt probably had Measles and now has Acute Disseminated (Postinfectious) Encephalomyelitis (post-measles is Subacute Sclerosing Panencephalitis
|
|
|
dementia, ataxia, Bx shows accumulation of Cerebroside Sulfate
|
Metachromatic Leukodystrophy
-lysosomal storage disease w/ deficiency of Arylsulfatase A -Central & Peripheral demyelination |
|
|
child who appears 'clumsy', falls a lot w/ knee & ankle injuries could possibly have _
|
Charcot-Marie-Tooth disease
-hereditary nerve d/o w/ bad production of proteins involved in structure & function of periph nerves or myelin sheath |
|
|
difference btw a Simple Partial seizure and Complex Partial seizure
|
Simple Partial Seizure
-consciousness intact Complex Partial Seizure -impaired consciousness -"partial seizure" = 1 area of brain affected, m/c origin is Mesial Temporal Lobe |
|
|
young child who periodically stops and stares blankely into space for ~30 sec then returns to nrl as if nothing happened; and what's common Tx?
|
Absence seizure
-Tx = Ethosuximide |
|
|
what is:
Myoclonic seizure: Tonic-clonic seizure: Tonic seizure: Atonic seizure: |
Myoclonic seizure: quick, repetitive jerks of part or whole body
Tonic-clonic seizure: "grand-mal" seizure w/ alternating stiffening & mvmnt Tonic seizure: stiffening of muscles Atonic seizure: 'drop' seizures, commonly mistaken for fainting- sudden loss of muscle tone, no loss of bowel/bladder function |
|
|
what is NOT being irritated in HA's?
|
Brain parenchyma is not
is: dura, cranial nerves, extracranial structures, etc |
|
|
what Rx is CI'd in a F w/ Migraines w/ aura?
|
OCP's
-can incr risk Thrombotic Stroke |
|
|
phases of Migraine?
|
Phase I of Migraine = Vasoconstriction
Phase II of Migraine = Vasodilation |
|
|
bilateral HA of >30 min, not aggravated by light or noise, no aura
|
Tension HA
-(+) FHx -more common in F |
|
|
unilateral repeated brief HA, periorbital pain, more often in M
|
Cluster HA
-a/w ipsilateral lacrimation, rhinorrhea, Horner's syndrome Tx = O2!!, then Sumitriptan |
|
|
difference btw Migraine, Tension, Cluster HA's
|
Migraine = Unilateral, of 4-72 hr duration, many assoc Sx (photophobia, phonophobia, aura)
Tension HA = Bilateral, >30min, not affected by light or noise, no aurea Cluster HA = Unilateral, repeated brief HA |
|
|
red rash in V1 dermatome distribution present since birth
|
Sturge-Weber syndrome
|
|
|
spots of depigmentation, spots of leathery skin w/ orange-peel like dimpling, benign CNS enlargments, MV regurg
|
Tuberous Sclerosis
-'spots of depigmentation' = ash-leaf spots -'spots of leathery skin w/ orange-peel like dimpling' = Shagren's patches -'benign CNS enlargements' = hamartomas -also: cardiac rhabdomyoma, renal angiomyoplipoma, subependymal giant cell astrocytoma **Auto-Dominant |
|
|
spots of heavier pigmentation on skin, pigmented iris hamartomas, pheochromocytoma, skin neurofibroma
|
Neurofibromatotis Type I "von Recklinghausen's Diseaes"
-'spots' of heavier pigmentation on skin' = cafe-au-lait spots -'pigmented iris hamartomas' = Lisch Nodules -also: optic gliomas -Auto-Dominant, mutated NF-1 gene on chr 17 |
|
|
hemangiomas in skin, bilateral renal cell carcinoma, retinal hemangioblastoma, pheochromocytoma
|
von Hippel-Lindau Disease
-Auto-Dominant -mutated tumor suppressor VHL |
|
|
m/c adult brain tumor
|
Glioblastoma Multiforme
-m/c and most aggressive -pseudopalisading pleomorphic tumor cells bordering central areas of Necrosis & Hemorrhage -MGM Studios: Mets, Glioblastoma, Meningioma, Schwannoma |
|
|
serpentine pseudopalisading pleomorphic tumor cells w/ necrosis & hemorrhage in adult brain tumor
|
Glioblastoma Multiforme
-m/c and most aggressive -MGM Studios: Mets, Glioblastoma, Meningioma, Schwannoma |
|
|
adult brain tumor w/ whorled pattern of cells w/ laminated calcifications
|
'laminated calcifications' = the "rings on a tree" pattern of Psammoma Bodies, common in Meningioma
-Psammoma Bodies in PSaMMoma: Papillary adenocarcinoma of thyroid, Serous cystadenocarcinoma of ovary, Meningioma (here), Mesothelioma |
|
|
brain tumor S-100 (+), commonly found in Neurofibromatosis Type 2
|
Schwannoma
-often localizes to CN VIII → acoustic schwannoma |
|
|
oligodendrocytes w/ round nuclei & clear cytoplasm, chicken-wire capillary network in white matter
|
Oligodendroglioma
-m/c in frontal lobe, and a/w seizures |
|
|
origin of m/c tumor to cause bitemporal hemianopia
|
bitemporal hemianopia m/c a/w Rathke's Pouch of Pituitary Adenoma
|
|
|
m/c tumor in kids
|
Pilocytic (low-grade) Astrocytoma
-well-circumscribed, supratentorial w/ GFAP (+) staining Rosenthal fibers; S-100 (+) -benign w/ good prognosis |
|
|
child w/ brain tumor, GFAP (+)
|
Pilocytic (low-grade) Astrocytoma, the m/c childhood brain tumor
|
|
|
child brain tumor w/ Homer-Wright Rosettes/Pseudorosettes around central tangle of fibrils
|
Medulloblastoma
-2nd m/c child brain tumor, GFAP (+) |
|
|
child brain tumor- ependymal cell origin m/c in 4th ventricle that can cause hydrocephalus
|
-Ependymoma
|
|
|
child w/ polycythemia, brain tumor that shows foamy cells & high vascularity
|
Hemangioblastoma
-can produce EPO → 2ndary Polycythemia -a/w von-Hippel-Lindau syndrome |
|
|
benign childhood tumor, bitemporal hemianopia; what is it/origin
|
Craniopharyngioma, from remnants of Rathke's Pouch
-common to have calcification |
|
|
common cause of blown pupil
|
transtentorial herniation
|
|
|
Cushing's Triad
|
bradycardia, HTN, irreg respiration
|
|
|
DDx for "Ring-Enhancing Lesions" in brain on imaging
|
Mets, Abscesses, Toxoplasmosis, AIDS lymphoma
|
|
|
DDx for "uniformly enhancing lesion"
|
lymphoma, meningioma, mets (tho usually ring-enhancing)
|
|
|
DDx for "Heterogenously Enhancing Lesion"
|
Glioblastoma Multiforme
|
|
|
Fentanyl, Meperidine, Dextromethorphan
|
Opioid Analgesics
others: morphine, codeine, heroin, methadone MoA: agonists @ opioid-R (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission- open K chnnl, close Ca chnnl → decr synaptic transmission -inhibit release of ACh, NE, 5HT, Glutamate, Substance P SE: addiction, respiratory depression, constipation, Miosis; NO tolerance to constipation or miosis; Tx toxicity w/ Naloxone or Naltrexone |
|
|
Butorphanol
|
partial agonist at opioid mu receptors and kappa receptors
-less respiratory depression than full agonists SE: w/drawal if on full opioid agonist |
|
|
parital agonist mu opioid-R, and kappa opioid-R
|
Butorphanol
|
|
|
Tramadol
|
Tramadol
very weak opioid agonist, also inhibits 5HT & NE reuptake -for chronic pain, w/ less addiction risk SE: as opioids, decreases seizure threshold (Buproprion did that too) |
|
|
weak opioid agonist that inhibits 5HT and NE reuptake
|
Tramadol
SE: decreases seizure threshold (like Buproprion), SE of full opioids |
|
|
two Rx's that decr seizure threshold
|
Tramadol & Bupropion
|
|
|
3 first line Rx's for Tonic-Clonic seizures
|
Phenytoin, Carbamazepine, Valproate
main SE's of: Phenytoin: nystagmus, Gingival Hyperplasia, hirsutism, megaloblastic anemia, teratogen, drug-induced SLE, P450 induction Carbemazepine: diplopia, ataxia, hepatotoxic, P450 induction, Stevens-Johnson Valproate: GI distress, hepatotoxicity, neural tube defects in fetus, tremor, wt gain, dose-related thrombocytopenia |
|
|
1st & 2nd choices for Abscence seizures
|
1st: Ethosuximide
2nd: Valproate |
|
|
commonly used for seizures in eclampsia
|
Benzodiazepines (tho 1st line is MgSO4!!!)
|
|
|
Phenobarbital, Pentobarbital, Thiopental, Secobarbital:
MoA, Toxicity |
Phenobarbital, Pentobarbital, Thiopental, Secobarbital
MoA: facilitate GABAa action by incr DURATion of Cl chnnl opening **CI'd in Porphyria** -SE: dependence, additive CNS effects w/ EtOH, resp or cardio depression, Induction of P450 (liver microsomal enzymes) |
|
|
Diazepam, Lorazepam, Triazolam, Temazepam:
MoA, Toxicity |
Diazepam, Lorazepam, Triazolam, Temazepam, Oxazepam, Midazolam, Chlordiazepoxide, Alprazolam = Benzodiazepines ("-epam" & "-olam")
MoA: facilitate GABAa by incr FREquency of Cl chnnl opening |
|
|
Tx of Benzodiazepine toxicity?
|
Flumazenil
Benzo's do NOT induce liver microsomal enzymes (like Barb's do) |
|
|
if want an inhaled anesthetic to have high potency, want _
|
high potency, want LOW MAC
-potency α 1/MAC -potency is MOST a/w Lipid Solubility |
|
|
how does Blood-Gas Partition Coefficient affect inhaled anesthetic
|
-less Blood Solubility means anesthetic will reach equilibrium more quickly, thus have faster onset of action w/ less blood solubility
|
|
|
toxicity of:
Halothane: Methoxyflurane: Enflurane: |
these, along w/ Isoflurane, Sevoflurane, NO are inhaled anesthetics
SE of: Halothane: Hepatotoxic (H &H) Methoxyflurane: Nephrotoxic (Meth is Neph) Enflurane: Epileptic (seizures...E & E) -other general inhaled anesthetic SE: malignant hyperthermia, expansion of trapped gas (NO) |
|
|
IV anesthetic w/ high potency & high lipid solubility used for induction of anesthesia
|
Thiopental, a Barbiturate
-high potency & lipid solubility -for anesthesia induction & short procedures *this decreases cerebral blood flow, while Ketamine incr's CBF |
|
|
Ketamine used for
|
Ketamine
IV anesthetic -PCP analog -block NMDA-R, cardio stimulant -disorientation, hallucination, bad dreams (worse in adults than kids), incr Cerebral Blood Flow (vs Barb's decr CMF) |
|
|
used for rapid IV induction of anesthesia, high TG content
|
Propofol
-potentiates GABAa |
|
|
how tell which local anesthetic is ester, which is amide?
|
amIdes have 2 I's in name: Lidocaine, Mepivicaine, Bupivicaine
esters: Procaine, Cocaine, Tetracaine -all block Na chnnls -give all except cocaine w/ vasoconstrictors to enhance local action -Order of nerve blockade: small before large, myelinated before unmyelinated, size before myelination -order of loss: pain 1st > temp > touch > P (so will still feel P often) |
|
|
what's Succinylcholine?
|
Depolarizing Neuromuscular blocking drug
-Phase I = prolonged depol; no antidote, block potentiated by AChE-I -Phase II = repolarized but blocked; antidote is AChE-I (Neostigmine) |
|
|
Tubocurarine, Atracurarium, Mivacurium, Rocuronium
|
Nondepolarizing Neuromuscular blocking drugs
-competative- compete w/ ACh for receptors Tx = Neostigmine, Edrophonium, other AChE-I |
|
|
how reverse neural blockade of Tubocurarine, Atracurium, Mivacurium, Rocuronium, etc
|
these are the Nondepolarizing Neuromuscular blockers
-compete w/ ACh for receptors -reverse w/ Neostigmine, Edrophonium, other AChE-I |
|
|
how Tx condition resulting from combining Inhaled anesthetics and Succinylcholine
|
condition that can result is Malignant Hyperthermia
Tx = Dantrolene, that prevents Ca release from SR of skeletal muscle -Dantrolene can also be used for Tx of Neuroleptic Malignant Syndrome, toxicity of antipsychotic's |
|
|
Dantrolene
|
used for Malignant Hyperthermia Tx, or Neuroleptic Malignant Syndrome Tx
|
|
|
Memantine
|
NMDA-R antagonist
-for Tx of Alzheimer's SE: dizziness, confusion, hallucinations |
|
|
Donepezil, Galantamine, Rivastigmine
|
AChE-I for Tx of Alzheimer's
SE: N, dizziness, insomnia |
|
|
Sumatriptan
|
Sumatriptan, Risatriptan, and other "-triptans" are 5HT agonists that → vasoconstriction for Tx of acute migraine, cluster HA
SE: coronary vasospasm (CI'd in pts w/ CAD, Prinzmetal's angina, Pregnancy) |
