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297 Cards in this Set
- Front
- Back
- 3rd side (hint)
What type of cell is destroyed in MS?
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oligodendrocytes
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What type of cell is destroyed in Guillan-Barre?
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schwann cells
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What are the origins of CNS tissue?
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neuroectoderm
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What are the origins of PNS tissue?
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neural crest
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What do Meissner's corpuscles sense?
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position sense
dynamic fine touch (maunipulation) adapt quickly (precision) |
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What do Pacinian corpuscles sense?
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vibration
pressure |
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What do Merkel's disks sense?
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position sense
static touch (shapes, edges, textures) adapt slowly (as compared to meissner's which adapt quickly) |
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Where are meissne'rs corpuscles found compared to markel's disks?
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meissner's = hairless skin while merkel's = around hair follicle
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Locus ceruleus function
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stress and panic
synthesizes NE |
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Nucleus accumbens function
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reward center
pleasure addiction fear *synthesizes GABA |
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Which areas of the brain are not controlled by BBB?
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area postrema (vomiting after chemo)
OVLT (osmotic sensing) neurohypophysis |
these are all inputs to the hypothalamus
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What does the hypothalamus control?
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TAN HATS:
Thirst/water balance Adenohypophysis Neurohypophysis Hunger Autonomic regulation Temperature regulation Sexual urges |
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Where within hypothalamus is ADH made?
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supraoptic nucleus
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Where within hypothalamus is oxytocin made?
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paraventricular nucleus
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What part of the hypothalamus promotes hunger?
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lateral area
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inhibited by leptin
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What part of the hypothalamus promotes satiety?
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ventromedial area
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stimulated by leptin
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What part of the hypothalamus promotes cooling?
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anterior (A/C)
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What part of the hypothalamus promotes heating?
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posterior
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Where is the circadian rhythym generated/controlled?
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suprachiasmatic nucleus of the hypothalamus
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What is the input to the VPL of the thalamus?
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spinothalamic
dorsal columns/medial lemniscus |
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What is the input to the VPM of the thalamus?
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trigeminal
gustatory pathway |
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What is the input to the LGN of the thalamus?
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CNII
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L for Light
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What is the input to the MGN of the thalamus?
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superior olive
inferior colliculus of pons |
M for music
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What parts of the brain are included in the limbic system?
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cingulate gyrus
hippocampus fornix mammillary bodies septal nucleus |
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What is the limbic system responsible for?
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Feeding
Fleeing Fighting Feeling sex |
the 5F's
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What are the input nerves of the cerebellum?
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climbing and mossy fibers
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What are the output nerves of the cerebellum?
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Purkinje fibers
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What is the order of the deep nuclei of the cerebellum?
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L==>M (Don't Eat Greasy Food)
Dentate Emboliform Globose Fastigial |
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What does the lateral cerebellum do?
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controls/coordinates voluntary movement of extremities
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Lateral = Limbs
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What does the medial part (vermis) of the cerebullum control?
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balance
truncal coordination ataxia *propensity to fall toward injured (ipsilateral) side when damaged |
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How is cortical input relayed through the cerebellum?
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via middle cerebellar peduncle (contralateral)
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How is proprioceptive input relayed through the cerebellum?
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ipsilateral via inferior cerebellar peduncle
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How is stimulatory feedback (output) to the cortex relayed in the cerebellum?
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deep nuclei ==> superior cerebellar peduncle ==> contralateral cortex
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What causes hemiballismus?
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contralateral subthalamic nucleus lesion
loss of inhibition of thalamus through globus pallidus |
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Huntington's pathophys
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neuronal death via NMDA and glutamate toxicity so caudate loses Ach and GABA to globus pallidus so stops inhibiting movement
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Bilateral amygdala lesion
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hyperorality
hypersexuality disinhibited behavior |
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Frontal lobe lesion
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disinhibition and deficits in concentration, orientation and judgment
may have reemergence of primitive reflexes |
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Right parietal lobe lesion
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spatial neglect syndrome (agnosia of the CONTRAlateral world)
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Where is the reticular activating system?
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midbrain
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Mammillary bodies lesion
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Wernicke-Korsakoff syndrome
wernicke - confusion, ophthalmoglegia, ataxia korsakoff - memory loss, confabulation, personality changes |
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basal ganglia lesion
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chorea
tremor at rest athetosis |
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Why are cerebellar hemisphere lesions ipsilateral?
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cerebellum ==> SCP ==> contralateral cortex ==> corticospinal decussation in medulla = ipsilateral at destination
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cerebellar hemisphere lesion
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intention tremor
limb ataxia |
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Cerebellar vermis lesion
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truncal ataxia
dysarthria |
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Subthalamic nucleus lesion
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contralateral hemibalismus
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Hippocampus lesion
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anterograde amnesia - inability to make new memories
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Paramedian pontine reticular formation (PPRF) lesion
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eye look AWAY from side of lesion
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What causes central pontine myelinolysis?
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very rapid correction of hyponatremia - osmotic shift damages pontine nerve fibers
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What are the symptoms of central pontine myelinolysis?
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acute paralysis
dysarthria dysphagia diplopia loss of conciousness |
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Where is Broca's area?
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inferior frontal gyrus
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What is Broca's aphasia?
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nonfluent aphasia with intact comprehension
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broca's = broken boca
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Where is Wernicke's area?
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superior temporal gyrus
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What is Wernicke's aphasia?
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fluent aphasia with impaired comprehension
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What does an arcuate fasciculus lesion cause?
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conduction aphasia - poor repetition but fluent speech, intact comprehension
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Anterior spinal artery infarct
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contralateral hemiparesis (lower extremities)
medial lemniscus (dec. contralateral proprioception) ipsilateral paralysis of CNXII |
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PICA infarct
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contralateral loss of pain and temp ipsilateral facial pain and temp
ipsilateral dysphagia hoarseness dec. gag reflex vertigo diplopia nystagmus ipsilateral Horner's vomiting trigeminal nucleus ipsilateral ataxia |
PICA infarct = lateral medullary syndrome
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AICA infarct
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ipsilateral facial paralysis
ipsilateral cochlear nucleus vestibular (nystagmus) ipsilateral facial pain and temp ipsilateral dystaxia |
AICA infarct = lateral inferior pontine syndrome
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Posterior cerebral artery infarct
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contralateral hemianopia with macular sparing
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supplies occipital cortex
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Middle cerebral artery infarct
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contralateral face and arm paralysis and sensory loss
aphasia left-sided neglect |
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Anterior cerebral artery infarct
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supplies medial surface of the brain so leg-foot area of motor and sensory cortices are lost
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Anterior communicating artery infarct
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most common site of circle of willis aneurysm
lesions may cause visual field defects |
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Posterior communication artery infarct
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common area of aneurysm
causes CNIII palsy |
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Lateral striate artery infarct
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divisions of middle cerebral artery that supply internal capsule, caudate, putamen, globus pallidus
infarct of the posterior limb causes pure motor hemiparesis |
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Where is the watershed zone in the brain and what symptoms does it cause when affected?
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between anterior cerebral/middle cerebral artery and posterior cerebral/middle cerebral arteries
during severe hypotension ==> upper leg/upper arm weakness, defects in higher-order visual processing |
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Basilar artery infarct
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"locked-in" syndrome
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In general stroke of anterior circle causes:
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general sensory and motor dysfunction
aphasia |
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In general stroke of posterior circle causes:
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cranial nerve deficits (vertigo, visual defects)
coma cerebellar deficits (ataxia) dominant hemisphere (ataxia) nondominant (neglect) |
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What conditions are associated with Berry aneurysm?
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adult polycystic kidney disease
ehlers-danlos syndrome marfan's |
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What are Charcot-Bouchard microaneurysms?
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associated with chronic HTN - affects small vessels (e.g. basal ganglia, thalamus)
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What does an epidural hematoma look like on CT?
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biconvex disk not crossing suture lines
CAN cross falx, tentorium |
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What does an subdural hematoma look like on CT?
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crescent-shaped hemorrhage that crosses suture lines. gyri are preserved, since pressure is distributed equally
can NOT cross falx, tentorium |
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How do patients with subarachnoid hemorrhage present?
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"worst headache of my life"
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What causes subarachnoid hemorrhage?
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ruptured berry aneurysm
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Where does a parenchymal hemorrhage usually occur?
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basal ganglia
internal capsule |
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What must you worry about 2-3 days post subarachnoid hemorrhage and how do you treat it?
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vasospasm due to blood breakdown products irritating vessels
tx = calcium channel blockers |
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What is the time course for ischemic brain disease healing?
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12-48 hrs: red neurons
24-72 hours: necrosis and PMN's 3-5 days: macrophages 1-2 wks: reactive gliosis and vascular proliferation >2wks: glial scar |
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How do strokes appear on CT?
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on nonconstrast:
ischemic = dark hemorrhagic = bright |
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How does CSF return to circulation?
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it gets absorbed by the arachnoid granulation then goes into the sup. sagittal sinus
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What does the ventricular foramen of monro connect?
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lateral ventricles to the third ventricle
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What does the cerebral aqueduct connect?
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third ventricle to fourth ventricle
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What drains the 4th ventricle into the subarachnoid space?
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Lateral = foramina of Luschka
Medial = foramen of Magendie |
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What level is most common for vertebral disk herniation?
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L5-S1
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Where does the spinal cord stop?
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L1-L2
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What does the dorsal column/medial lemniscal pathway do?
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ascending pressure, vibration, touch and proprioception
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What does the spinothalamic tract do?
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ascending pain and temperature
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What does the lateral corticospinal tract do?
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descending voluntary movement of contralateral limbs
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What is the course of the dorsal column tract?
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dorsal (posterior) root ganglion ==> ascends ipsilateral in dorsal column ==> synapses in the nucleus cuneatus/gracilis of the medulla ==> decussates ==> ascends contralaterally in medial lemniscus ==> synapses in VPL of thalamus ==> sensory cortex
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What is the course of the spinothalamic tract?
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dorsal (posterior) root ganglion ==> synapses on ipsilateral side in the gray matter ==> decussates at anterior white commissure ==> ascends contralaterally ==> VPL of thalamus ==> sensory cortex
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What is in the anterior horn of the spinal cord?
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alpha-motor neuron cell bodies
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What is the path of the lateral corticospinal tract?
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primary motor cortex ==> descends ipsilaterally (through internal capsule) ==> decussates at caudal medulla (pyramidal decussation) ==> descends contralaterally ==> synapses in the cell body of the anterior horn of SC ==> leaves spinal cord on same side ==> synapses at NMJ
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What is the lesion in polymyelitis?
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anterior horn destruction leading to lower moter neuron deficit - atrophy, weakness, fasciculations, hyporeflexia
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What is Werdnig-Hoffman disease and what causes it?
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aka infantile spinal muscular atrophy
"floppy baby" at birth tongue fasciculations caused by AD inheritance of degenerative anterior horn cell bodies so LMN involvement only |
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What is the lesion in AML?
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upper and lower motor neuron degeneration
fasciculations ==> atrophy |
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AML tx?
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riluzole tx modestly lengthens survival by decreasing presynaptic glutamate release
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What is the lesion in tabes dorsalis?
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degeneration of dorsal columns ==> impaired proprioception and locomotor ataxia
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What are the signs of tabes dorsalis?
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absence of DTRs
positive Romberg sensory ataxia at night |
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What is the lesion in Friedreich's ataxia?
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dorsal columns
lateral spinothalamic spinocerebellar |
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What are the sign/findings in Friedreich's ataxia?
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staggering gait
frequent falling nystagmus dyarthria pes cavus hammer toes hypertrophic cardiomyopathy kyphoscoliosis |
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What is the lesion in Brown-Sequard syndrome?
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hemisection of spinal cord:
ipsilateral UMN signs (corticospinal tract) below the lesion ipsilateral loss of tactile, vibration proprioception sense (dorsal column) below the lesion contralateral pain and tem loss (spinothalamic tract) below the lesion ipsilateral loss of all sensation at the level of lesion LMN sign at level of lesion |
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What is Horner's syndrome associated with?
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lesions of the spinal cord above T1
(Pancoast's tumor, Brown-Sequard, late state syringomyelia) |
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What is the biceps reflex testing?
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C5, C6
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What is the triceps reflex testing?
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C7, C8
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What is the patella reflex testing?
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L3, L4
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What is the Achilles reflex testing?
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S1, S2
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Superior colliculi
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just below pineal body in the brain stem
conjugate vertical gaze center |
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Inferior colliculi
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in midbrain below pineal body
auditory relay/processes center |
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Parinaud syndrome
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paralysis of conjugate vertical gaze due to lesion in superior colliculi
(e.g. from pinealoma) |
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What are the functions of oculomotor nerve? CNIII
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eye movt. (SR, IR, MR, IO)
pupillary constriction (PS: E-W nucleus, muscarinic receptors) accommodation eyelid opening (levator palpebrae) |
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What is the function of the Trochlear (CNIV) nerve?
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eye movement (SO)
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What is the function o f the trigeminal nerve (CNV)?
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facial movement
taste from anterior 2/3 of tongue (via chordi tympani) lacrimation salivation (non parotid) eyelid closing (orbicularis oculi) stapedius muscle in ear |
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What is the function of the glossopharyndeal nerve (CNIX)?
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taste from posterior 1/3 of tongue
swallowing salivation (parotid) monitoring carotid body and sinus chemo/baro receptos stylopharyngeus muscle (elevates pharynx, larynx) |
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What is the function of the vagus nerve (CNX)?
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taste from epiglottic region
swallowing palate elevation midline uvula talking coughing thoracoabdominal viscera monitoring aortic arch chemo- and baraoreceptors |
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What is the function of the accessory nerve (CNXI)?
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head turning
shoulder strugging (SCM and trapezius muscles) |
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Which cranial nerve nuclei are located in the midbrain?
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CN III and IV
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Which cranial nerve nuclei are located in the pons?
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CN V, VI, VII, VIII
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Which cranial nerve nuclei are located in the medulla?
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CN IX, X, XI, XII
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What conducts the corneal reflex?
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afferent: V1 (ophthalmic)
efferent: VII (temporal branch) |
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What conducts the lacrimation reflex?
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afferent V1
efferent VII |
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What conducts the pupillary reflex?
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afferent: CNII
efferent: CNIII |
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What conducts the gag reflex?
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Afferent: IX
Efferent: IX, X |
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What type of info is relayed via the Nucleus Solitarius?
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visceral sensory (e.g taste, baroreceptors, gut distention)
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VII, IX, X
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What type of info is relayed via the Nucleus ambiguus?
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motor innervation of pharynx, larynx and upper esophagus (e.g. swallowing, palate elevation)
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IX, X, XI
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What type of info is relayed via the Dorsal (motor) nucleus?
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sends autonomic (parasympathetic fibers) to heart, lungs and upper GI
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what travels through the optic canal?
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CNII
ophthalmic artery central retinal vein |
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what travels through the superior orbital fissure?
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CNIII, IV, V1,
ophthalmic vein sympathetic fibers |
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what travels through the foramen rotundum?
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CNV2
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what travels through the foramen ovale?
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CNV3
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what travels through the spinosum?
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middle meningeal artery
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what travels through the internal auditory meatus?
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CNVII, VIII
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What exits through the jugular foramen?
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CNIX, X, XI
jugular vein |
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What exits through the hypoglossal canal?
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CN XII
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What exits through the foramen magnum?
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spinal roots of CN XI
brain stem vertebral arteries |
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What passes through the cavernous sinus?
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CN III, IV, V1/V2, VI
post-ganglionic parasympathetic fibers |
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CNXII lesion (LMN)
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tongue deviates toward the side of the lesion (lick your wound)
that's because it decussates before medulla and synapse on contralateral hypoglossal nucleus |
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CN V motor lesion
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jaw deviates toward side of lesion
bilateral cortical input to lateral pterygoid muscle (UMN) |
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CNX lesion
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uvula deviates away from side of lesion
weak side collpses and uvula points away |
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CN XI lesion
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weakness turning head to contralateral side of lesion (SCM)
shoulder droop on side of lesion (trapezius) |
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UMN lesion of CN VII
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contralateral paralysis of lower face only, since upper face receives bilateral UMN innervation
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LMN lesion of CN VII
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Ipsilateral paralysis of upper and lower face
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Bell's palsy deficits
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peripheral ipsilateral facial paralysis with inability to close eye on involved side
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KUH sound tests what?
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palate elevation (CNX)
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LA sound tests what?
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tongue - CNXII
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MI sound test what?
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lips - CNVII
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What are the muscles of mastication?
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muscles that close:
Masseter Temporalis Medial pterygoid muscle that opens: lateral pterygoid |
Lateral Lowers
M's Munch |
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How is near vision produced?
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ciliary muscle contracts==> zonular fibers relax/lengthen ==> lens relaxes and becomes more convex
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How is far vision produced?
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ciliary muscle relaxes==> zonular fibers shorten/tense ==> lens flattens
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CN III palsy
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eye looks down and out
pupillary dilation loss of accomodation |
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CN IV palsy
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eye drifts up ==> vertical diplopia
(problems reading newspapers or going down stairs) |
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CN VI palsy
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medially directed eye (horizontal diplopia)
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How is pupillary constriction (miosis) controlled?
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light goes in through CNII and activates pretectal nucleus which sends signals out to Edinger-Westphal nuclei on both sides. This then sends efferent info to the pupillary constrictor muscle via CN III causing it to contract
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What is Marcus Gunn pupil and what is it a sign of?
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When you shine light in the affected eye both eyes show decreased pupillary constriction
This is a sign of retinal detachment or optic nerve damage |
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What is the tract/pathway for pupillary dilation?
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T1 preganglionic sympathetic ==> superior cervical ganglion ==> postganglionic sympathetic ==> long ciliary nerve
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the fact that it has to pass through cervical ganglion explains why Horner's happens in ppl with masses in that area
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Which part of the visual field crosses over at the optic chiasm?
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lateral fields (medial retina)
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Lesion of left optic nerve before the chiasm would result:
|
left anopia
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Lesion of the optic nerve at the chiasm would cause:
|
bitemporal hemianopia
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Lesion of the right optic track on the would cause:
|
left homonnymous hemianopsia
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Lesion of Meyer's loop (temporal lobe) on the right would cause:
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left upper quadrant anopia
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Lesion of dorsal optic radiation (parietal lobe) on the right would cause:
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left lower quadrant anopia
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Internuclear ophthalmoplegia is caused by?
|
lesion in the medial longitudinal fasciculus
common in MS |
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What is the deficit in Internuclear ophthalmoplegia?
|
When you try to look left your left eye can do it but your right eye gets stuck. This causes horizontal nystagmus of the left eye
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What genes are associated with Alzheimer's?
|
early onset: APP (21), presenilin-1, presenilin-2
later onset: ApoE4 |
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Which lobe is spared in Alzheimer's?
|
occipital
|
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What are the histologic findings in Alz?
|
senile plaques: extracellular Beta-amyloid core
neurofibrillary tangles (intracellular, abnormally phosphorylated tau protein = insoluble cytoskeletal elements) |
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What part of the brain is most atrophied in Pick's disease?
|
frontotemporal
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What is the histologic finding in Pick's disease?
|
Pick bodies = intracellular, aggregated tau proteins
|
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What are the symptoms of Pick's disease?
|
dementia
aphasia parkinsonian aspects change in personality/behavior |
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What are the symptoms of Lewy body dementia?
|
Parkinsonism with dementia and hallucinations
|
|
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Histologic finding in Lewy body dementia:
|
defective alpha-synuclein (like in Parkinson's)
no tangles or plaques as with the other dementias |
|
|
How can MS present?
|
optic neuritis
MLF syndrome hemiparesis/loss of sensation incontinence Scanning speech intention tremor |
|
|
MS diagnosis
|
inc. protein in CSF
oligoclonal bands MRI - high signal lesions periventricular plaques (area of oligodendrocyte loss and gliosis) with intact axons |
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MS treatment
|
chronic - beta-interferon or immuno-suppressive therapy
acute - corticosteroids |
|
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What is Gullain-Barre syndrome?
|
inflammation and demyelination of peripheral nerves and motor fibers of ventral roots causing symmetric ascending muscle weakness
|
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Progressive multifocal leukoencephalopathy (PML)
|
demyelination of CNS due to destruction of oligodendrocytes. Associated with JC virus and seen in AIDS patient. Rapidly progressive usually fatal
|
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Acute disseminated (postinfectious) encephalomyelitis
|
multifocal perivenular inflammation and demyelination after infection or certain vaccines
|
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Metachromatic leukodystrophy
|
autosomal-recessive lysosomal storage disease, most commonly due to arylsulfatase A deficiency. Buildup of sulfatides leads to impaird production of myelin sheath
|
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Charcot-Marie-Tooth disease
|
also known as hereditary motor and sensory neuropathy. group of progressive hereditary nerve disorders related to the defective production of proteins involved in the structure and function of peripheral nerves or the myelin sheath
|
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Where do partial seizures usually originate?
|
mesial temporal lobe
|
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How can you differentiate peripheral and central vertigo with positional testing?
|
peripheral - delayed nystagmus horizontal only
central - immediate nystagmus in any direction |
|
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What are the neurocutaneous disorders?
|
Sturge-Weber syndrome
Tuberous sclerosis NF-1 VHL |
|
|
Sturge-Weber syndrome presentation
|
port wine stains (nevus flemmeus) in a V1 distribution usually
ipsilateral leptomeningeal angiomas pheochromocytomas can cause: glaucoma, seizures, hemiparesis, mental retardation |
pheos
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Tuberous sclerosis presentation
|
Hamartomas in CNS, skin, organs
Cardiac rhabdomyoma Renal angiomylolipoma subependymal giant cell astrocytoma mental retardation seizures hypopigmented "ash leaf spots" sebaceous adenoma shagreen patch |
AD
|
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NF-1 presentation
|
Cafe-au-lait spots
Lisch nodules (pigmented iris hamartomas) neurofibromas of skin optic gliomas phechromocytomas |
AD
pheos |
|
VHL presentation
|
cavernous hemangiomas in skin, mucosea, organs
bilateral renal cell carcinoma hemangioblastoma in retina, brain stem, cerebellum pheochromocytomas |
AD
pheos |
|
Glioblastoma multiforme (grade IV astrocytoma) general characteristics
|
most common primary brain tumor in adults
can cross corpus collosum (butterfly glioma) poor prognosis (<1yr) stains for astrocytes (GFAP) |
|
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Glioblastoma multiforme histology
|
psudopalisading pleomorphic tumor cells - border central areas of necrosis and hemorrhage
|
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Meningioma characteristics
|
2nd most common primary brain tumor in adults
most commonly occurs in convexities of hemispheres and parasagittal region arises from arachnoid cells external to brain resectable |
|
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Meningioma histology
|
spindle cells concentrically arranged in a whorled patter
psammoma bodies (laminated calcifications) |
|
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Schwannoma general characteristics
|
3rd most common primary brain tumor in adults
often localized to CN VIII ==> acoustic schwannoma found at cerebellopontine angle S-100+ resectable |
|
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Who gets bilateral schwannomas?
|
NF-2
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Oligodendroglioma general characteristics
|
relatively rare
slow growing most often in frontal lobes |
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Oligodendroglioma histology
|
chicken-wire capillary patter around oligodendrocytes which look like "fried eggs" - round nuclei with clear cytoplasm
often calcified |
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Pilocytic (low-grade) astrocytoma general characteristics
|
usually well circumscribe, benign, good prognosis in kids
found in posterior fossa GFAP+ |
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Pilocytic (low-grade) astrocytoma histology
|
Rosenthal fibers - eosinophilic, corkscrew fibers. Cystic + solid (gross)
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Medulloblastoma general characteristics
|
Highly malignant cerebellar tumor
a form of primitive neuroectodermal tumor (PNET) can compress 4th ventricle causing hydrocephalus |
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Medulloblastoma histology
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rosettes or perivascular psuedorosette pattern of cells
solid tumor small blue cells |
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Ependymoma general characteristics
|
kids
ependymal cell tumors most commonly found in 4th ventricle so can cause hydrocephalus poor prognosis |
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Ependymoma histology
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characteristic perivascular pseudorosettes
rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus |
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Hemangioblastoma general
|
kids
most often cerebellar associated with VHL when found with retinal angiomas can produce EPO --> secondary polycythemia |
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Hemangioblastoma histology
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foamy cells and high vascularity are characteristic (stokes, clots)
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Craniopharyngioma general
|
benign childhood tumor, confused with pituitary adenoma because it too causes bitemporal hemianopia
it is a like a teratoma of the brain unlike most childhood brain tumors it is often found supratentorial |
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Craniopharyngioma histology
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derived from remnants of Rathke's pouch
calcification is common (tooth and enamel-like) cysts hyposecretion of mixed hormones |
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Clinical signs of uncal herniation
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1) ipsilateral dilated pupil/ptosis
2) contralateral homonymous hemianopia 3) ipsilateral paresis 4) duret hemorrhages - paramedian artery rupture |
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Which brain lesions are ring-enhancing?
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mets
abscesses toxo AIDS lymphoma |
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Which brain lesions are uniformly enhancing?
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lymphoma
meningioma mets (usually ring-enhancing) |
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Which brain lesions are heterogeneously enhancing?
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Glioblastoma multiforme
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What might a cingulate herniation under falx cerebri cause?
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compression of anterior cerebral artery
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what can a downward transtentorial (central) herniation cause?
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if it compresses the brain stem ==> coma and death
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Timilol MOA/use
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beta-blocker that dec. aqueous humor production so good for glaucoma
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Brimonidine MOA/use
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alpha-agonist that decreases aqueous humor secretion so good for glaucoma
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Pilocarpine, carbachol MOA/use
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direct cholimimetics that inc. the outflow of aqueous humor by contracting ciliary muscle and opening trabecular meshwork
*use pilocarpine in emergencies |
causes miosis and cyclospasm
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Physostigmin, echothiophate MOA
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Indirect cholimimetics (AchE inhibitors)
inc. the outflow of aqueous humor by contracting ciliary muscle and opening trabecular meshwork |
causes miosis and cyclospasm
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Latanoprost MOA
|
a PGF2alph agonist that inc. outflow of aqueous humor
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darkens color of iris (browning)
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How do opiod analgesics work?
|
bind to mu receptor causing K+ channel opening and Ca2+ channel closing ==> dec. synaptic transmission
inhibit release of Ach, NE, 5-HT, glutamate, substance P |
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What are the clinical uses of opiods?
|
cough suppressant - dextromethorphan)
diarrhea - loperamide and diphenoxylate acute pulmonary edema rehab (methadone) |
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Butorphanol MOA
|
partial agonist at opioid mu receptors, agonist at kappa receptors
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Butorphanol clinical use
|
pain (causes less respiratory depression than full agonists)
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Butorphanol toxicity
|
causes withdraw symptoms if on a full opioid agonist
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Tramadol MOA
|
very weak opioid agonist
inhibits serotonin and NE reuptake |
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Tramadol clinical use
|
chronic pain
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Tramadol toxicity
|
less abuse potential
similar to opioids decreases seizure threshold |
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What is first line tx for tonic-clonic seizures?
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phenytoin (also can be used for prophylaxis)
carbamazepine |
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Phenytoin MOA
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inc. Na+ channel inactivation
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Carbamazepine MOA
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inc. Na+ channel inactivation
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What is the first line treatment for trigeminal neuralgia?
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Carbamazepine
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Lamotrigine MOA
|
blocks voltage-gated Na+ channels
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Lamotrigine clinical use
|
partial seizures
tonic-clonic |
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Gabapentin MOA
|
GABA analog but primarily inhibits HVA Ca2+ channels
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Tramadol MOA
|
very weak opioid agonist
inhibits serotonin and NE reuptake |
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Tramadol clinical use
|
chronic pain
|
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Tramadol toxicity
|
less abuse potential
similar to opioids decreases seizure threshold |
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|
What is first line tx for tonic-clonic seizures?
|
phenytoin (also can be used for prophylaxis of status epilepticus)
carbamazepine valproic acid |
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Phenytoin MOA
|
inc. Na+ channel inactivation
|
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Carbamazepine MOA
|
inc. Na+ channel inactivation
|
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What is the first line treatment for trigeminal neuralgia?
|
Carbamazepine
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Lamotrigine MOA
|
blocks voltage-gated Na+ channels
|
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Lamotrigine clinical use
|
partial seizures
tonic-clonic |
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Gabapentin MOA
|
GABA analog but primarily inhibits HVA Ca2+ channels
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Gabapentin clinical use
|
partial
tonic-clonic |
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Topiramate MOA
|
blocks Na+ channels
inc. GABA action |
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Topiramate clinical use
|
partial
tonic-clonic |
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What is the first line anti-seizure med in pregnancy and children?
|
phenobarbital
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Phenobarbital MOA
|
inc. GABA-A action
|
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Phenobarbital clinical use
|
partial
tonic-clonic |
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Valproic acid MOA
|
inc. Na+ channel inactivation
inc. GABA concentration |
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Valproic acid clinical use
|
partial
tonic-clonic absence myoclonic |
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Ethosuximide MOA
|
blocks thalamic T-type Ca2+ channels
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Ethosuximide clinical use
|
absence seizures
|
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How can benzos be used for seizures?
|
1st line for acute status epilepticus and eclampsia (along with Mg2+)
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Tiagabine MOA
|
inhibits GABA reuptake
|
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Tiagabine clinical use
|
partial seizures only
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Vigabatrin MOA
|
irreversibly inhibits GABA transaminase ==> inc. GABA
|
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Vigabatrin clinical use
|
partial seizures only
|
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Levetiracetam MOA
|
unknown; may modulate GABA and glutamate release
low side efx - good drug |
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Levetiracetam clinical use
|
partial
tonic-clonic |
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Carbamazepine toxicity
|
diplopia
ataxia agranulocytosis and aplastic anemia liver toxicity teratogenesis induction of P-450 SIADH |
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Ethosuximide toxicity
|
GI distress
fatigue headache urticaria Stevers-Johnson syndrome |
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Phenobarbital toxicity
|
sedation
tolerance dependence induction of P-450 |
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Phenytoin toxicity
|
nystagmus
diplopia ataxia sedation gingival hyperplasia hirsutism megaloblastic anemia teratogenesis SLE-like syndrome P-450 inducer |
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Valproic acid toxicity
|
GI distress
rare but fatal hepatoxicity neural tube defects in fetus tremor weight gain |
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Lamotrigine toxicity
|
Stevens-Johnson syndrome
|
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Gabapentin toxicity
|
sedation
ataxia |
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Topiramate toxicity
|
sedation
mental dulling kidney stones weight loss |
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What are the barbiturates?
|
-barbital and thiopental (surgery)
|
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Barbiturates MOA
|
facilitate GABA-a action by inc. duration of Cl- channel opening, thus dec. neuron firing (due to hyperpolarization)
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Benzos MOA
|
facilitate GABAa action by inc. the frequency of Cl- channel opening
|
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Halothane toxicity
|
hepatotoxic
|
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Methoxyflurane toxicity
|
nephrotoxic
|
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Enflurane side effect
|
proconvulsant
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Thiopental clinical use
|
high potency, high lipid solubility rapid entry into the bran. used for induction of anesthesia and short surgical procedures
rapidly redistrubtuion into tissue and fat |
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Midazolam clinical use
|
endoscopy
|
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Ketamine clinical use/MOA
|
PCP analog that act as a dissociative anesthetics. Blocks NMDA receptors. causes disorientation, hallucination and bad dreams.
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Propofol MOA/clinical use
|
used for rapid anesthesia induction and short procedure
less postoperative nausea than thiopental potentiates GABA |
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MOA of local anesthetics (-caines)
|
Block Na+ channels by binding to specific receptors on inner portion of channel.
Preferentially bind to activated Na+ channels so most effective in rapidly firing neurons. have to be in an uncharged state to cross membrane |
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Succinylcholine MOA
|
depolarizing neuromuscular blocker selective for motor nicotinic receptor
|
|
|
How do you reverse neuromuscular blockade induced by succinylcholine?
|
during phase I you can't do anything
during phase II you can give neostigmine (AchE inhibitor) |
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Tubocurarine MOA
|
Competitive antagonist of Ach receptors
(non-depolarizing neuromuscular blockade) |
|
|
What are the complications of succinylcholine?
|
hypercalcemia
hyperkalemia |
|
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Dantrolene MOA
|
prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle
|
|
|
Dantrolene clinical use
|
treatment of malgnant hyperthermia and neuroleptic malignant syndrome
|
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|
Tx for parkinson's
|
BALSA:
Bromocriptine Amantadine Levodopa (w/carbidopa) Selegiline (and COMT inhibitors) Antimuscarinics |
|
|
Which antimuscarinic is typically used in parkinson's?
|
Benztropine - improves tremor and rigidity but has little effect on bradykinesia)
|
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|
Why do you give carbidopa with L-dopa in parkinson's
|
carbidopa is a peripheral decarboxylase inhibitor so it inc. the amount of L-dopa that makes it to the brain and it prevent peripheral side effects
|
|
|
Levodopa toxicity
|
cardiac arrhythmias
dyskinesia akinesia |
|
|
Selegiline MOA
|
selectively inhibits MAO-B, which preferentially metabolizes dopamine over NE and 5-HT, thereby increasing the availability of dopamine
|
|
|
Memantine MOA
|
NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+)
|
|
|
Memantine clinical use
|
Alzheimer's
|
|
|
Memantine toxicity
|
dizziness, confusion, hallucinations
|
|
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Donepezil MOA
|
AchE inhibitor
|
|
|
Donepezil clinical use
|
Alzheimers
|
|
|
Donepezil toxicity
|
nausea, dizziness, insomnia
|
|
|
Galantamine, rivastigmine MOA
|
AchE inhibitor
|
|
|
Galantamine, rivastigmine clinical use
|
Alzheimers
|
|
|
Galantamine, rivastigmine toxicity
|
nausea, dizziness, insomnia
|
|
|
How do you treat Huntington's?
|
you need to reverse the increased dopamine and decreased GABA/Ach
Reserpine + tetrabenazine - amine depleting Haloperidol - dopamine receptor antagonist |
|
|
Sumatriptan MOA
|
5-HT1b/1d agonist.
causes vasoconstriction, inhibition of trigeminal activation and vasoactive peptide release |
|
|
Sumatriptan clinical use
|
migraines
cluster headache attacks |
|
|
Sumatriptan toxicity
|
coronary vasospasm (don't use if CAD or Prinzmetal's angina)
mild tingling |
|