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297 Cards in this Set

  • Front
  • Back
  • 3rd side (hint)
What type of cell is destroyed in MS?
oligodendrocytes
What type of cell is destroyed in Guillan-Barre?
schwann cells
What are the origins of CNS tissue?
neuroectoderm
What are the origins of PNS tissue?
neural crest
What do Meissner's corpuscles sense?
position sense
dynamic fine touch (maunipulation)
adapt quickly (precision)
What do Pacinian corpuscles sense?
vibration
pressure
What do Merkel's disks sense?
position sense
static touch (shapes, edges, textures)
adapt slowly (as compared to meissner's which adapt quickly)
Where are meissne'rs corpuscles found compared to markel's disks?
meissner's = hairless skin while merkel's = around hair follicle
Locus ceruleus function
stress and panic

synthesizes NE
Nucleus accumbens function
reward center
pleasure
addiction
fear

*synthesizes GABA
Which areas of the brain are not controlled by BBB?
area postrema (vomiting after chemo)

OVLT (osmotic sensing)

neurohypophysis
these are all inputs to the hypothalamus
What does the hypothalamus control?
TAN HATS:
Thirst/water balance
Adenohypophysis
Neurohypophysis
Hunger
Autonomic regulation
Temperature regulation
Sexual urges
Where within hypothalamus is ADH made?
supraoptic nucleus
Where within hypothalamus is oxytocin made?
paraventricular nucleus
What part of the hypothalamus promotes hunger?
lateral area
inhibited by leptin
What part of the hypothalamus promotes satiety?
ventromedial area
stimulated by leptin
What part of the hypothalamus promotes cooling?
anterior (A/C)
What part of the hypothalamus promotes heating?
posterior
Where is the circadian rhythym generated/controlled?
suprachiasmatic nucleus of the hypothalamus
What is the input to the VPL of the thalamus?
spinothalamic

dorsal columns/medial lemniscus
What is the input to the VPM of the thalamus?
trigeminal

gustatory pathway
What is the input to the LGN of the thalamus?
CNII
L for Light
What is the input to the MGN of the thalamus?
superior olive

inferior colliculus of pons
M for music
What parts of the brain are included in the limbic system?
cingulate gyrus
hippocampus
fornix
mammillary bodies
septal nucleus
What is the limbic system responsible for?
Feeding
Fleeing
Fighting
Feeling
sex
the 5F's
What are the input nerves of the cerebellum?
climbing and mossy fibers
What are the output nerves of the cerebellum?
Purkinje fibers
What is the order of the deep nuclei of the cerebellum?
L==>M (Don't Eat Greasy Food)

Dentate
Emboliform
Globose
Fastigial
What does the lateral cerebellum do?
controls/coordinates voluntary movement of extremities
Lateral = Limbs
What does the medial part (vermis) of the cerebullum control?
balance
truncal coordination
ataxia

*propensity to fall toward injured (ipsilateral) side when damaged
How is cortical input relayed through the cerebellum?
via middle cerebellar peduncle (contralateral)
How is proprioceptive input relayed through the cerebellum?
ipsilateral via inferior cerebellar peduncle
How is stimulatory feedback (output) to the cortex relayed in the cerebellum?
deep nuclei ==> superior cerebellar peduncle ==> contralateral cortex
What causes hemiballismus?
contralateral subthalamic nucleus lesion

loss of inhibition of thalamus through globus pallidus
Huntington's pathophys
neuronal death via NMDA and glutamate toxicity so caudate loses Ach and GABA to globus pallidus so stops inhibiting movement
Bilateral amygdala lesion
hyperorality
hypersexuality
disinhibited behavior
Frontal lobe lesion
disinhibition and deficits in concentration, orientation and judgment

may have reemergence of primitive reflexes
Right parietal lobe lesion
spatial neglect syndrome (agnosia of the CONTRAlateral world)
Where is the reticular activating system?
midbrain
Mammillary bodies lesion
Wernicke-Korsakoff syndrome
wernicke - confusion, ophthalmoglegia, ataxia

korsakoff - memory loss, confabulation, personality changes
basal ganglia lesion
chorea
tremor at rest
athetosis
Why are cerebellar hemisphere lesions ipsilateral?
cerebellum ==> SCP ==> contralateral cortex ==> corticospinal decussation in medulla = ipsilateral at destination
cerebellar hemisphere lesion
intention tremor

limb ataxia
Cerebellar vermis lesion
truncal ataxia

dysarthria
Subthalamic nucleus lesion
contralateral hemibalismus
Hippocampus lesion
anterograde amnesia - inability to make new memories
Paramedian pontine reticular formation (PPRF) lesion
eye look AWAY from side of lesion
What causes central pontine myelinolysis?
very rapid correction of hyponatremia - osmotic shift damages pontine nerve fibers
What are the symptoms of central pontine myelinolysis?
acute paralysis
dysarthria
dysphagia
diplopia
loss of conciousness
Where is Broca's area?
inferior frontal gyrus
What is Broca's aphasia?
nonfluent aphasia with intact comprehension
broca's = broken boca
Where is Wernicke's area?
superior temporal gyrus
What is Wernicke's aphasia?
fluent aphasia with impaired comprehension
What does an arcuate fasciculus lesion cause?
conduction aphasia - poor repetition but fluent speech, intact comprehension
Anterior spinal artery infarct
contralateral hemiparesis (lower extremities)
medial lemniscus (dec. contralateral proprioception)
ipsilateral paralysis of CNXII
PICA infarct
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
AICA infarct
ipsilateral facial paralysis
ipsilateral cochlear nucleus
vestibular (nystagmus)
ipsilateral facial pain and temp
ipsilateral dystaxia
AICA infarct = lateral inferior pontine syndrome
Posterior cerebral artery infarct
contralateral hemianopia with macular sparing
supplies occipital cortex
Middle cerebral artery infarct
contralateral face and arm paralysis and sensory loss
aphasia
left-sided neglect
Anterior cerebral artery infarct
supplies medial surface of the brain so leg-foot area of motor and sensory cortices are lost
Anterior communicating artery infarct
most common site of circle of willis aneurysm

lesions may cause visual field defects
Posterior communication artery infarct
common area of aneurysm

causes CNIII palsy
Lateral striate artery infarct
divisions of middle cerebral artery that supply internal capsule, caudate, putamen, globus pallidus

infarct of the posterior limb causes pure motor hemiparesis
Where is the watershed zone in the brain and what symptoms does it cause when affected?
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
Basilar artery infarct
"locked-in" syndrome
In general stroke of anterior circle causes:
general sensory and motor dysfunction

aphasia
In general stroke of posterior circle causes:
cranial nerve deficits (vertigo, visual defects)
coma
cerebellar deficits (ataxia)
dominant hemisphere (ataxia)
nondominant (neglect)
What conditions are associated with Berry aneurysm?
adult polycystic kidney disease
ehlers-danlos syndrome
marfan's
What are Charcot-Bouchard microaneurysms?
associated with chronic HTN - affects small vessels (e.g. basal ganglia, thalamus)
What does an epidural hematoma look like on CT?
biconvex disk not crossing suture lines

CAN cross falx, tentorium
What does an subdural hematoma look like on CT?
crescent-shaped hemorrhage that crosses suture lines. gyri are preserved, since pressure is distributed equally

can NOT cross falx, tentorium
How do patients with subarachnoid hemorrhage present?
"worst headache of my life"
What causes subarachnoid hemorrhage?
ruptured berry aneurysm
Where does a parenchymal hemorrhage usually occur?
basal ganglia

internal capsule
What must you worry about 2-3 days post subarachnoid hemorrhage and how do you treat it?
vasospasm due to blood breakdown products irritating vessels

tx = calcium channel blockers
What is the time course for ischemic brain disease healing?
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
How do strokes appear on CT?
on nonconstrast:
ischemic = dark
hemorrhagic = bright
How does CSF return to circulation?
it gets absorbed by the arachnoid granulation then goes into the sup. sagittal sinus
What does the ventricular foramen of monro connect?
lateral ventricles to the third ventricle
What does the cerebral aqueduct connect?
third ventricle to fourth ventricle
What drains the 4th ventricle into the subarachnoid space?
Lateral = foramina of Luschka

Medial = foramen of Magendie
What level is most common for vertebral disk herniation?
L5-S1
Where does the spinal cord stop?
L1-L2
What does the dorsal column/medial lemniscal pathway do?
ascending pressure, vibration, touch and proprioception
What does the spinothalamic tract do?
ascending pain and temperature
What does the lateral corticospinal tract do?
descending voluntary movement of contralateral limbs
What is the course of the dorsal column tract?
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
What is the course of the spinothalamic tract?
dorsal (posterior) root ganglion ==> synapses on ipsilateral side in the gray matter ==> decussates at anterior white commissure ==> ascends contralaterally ==> VPL of thalamus ==> sensory cortex
What is in the anterior horn of the spinal cord?
alpha-motor neuron cell bodies
What is the path of the lateral corticospinal tract?
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
What is the lesion in polymyelitis?
anterior horn destruction leading to lower moter neuron deficit - atrophy, weakness, fasciculations, hyporeflexia
What is Werdnig-Hoffman disease and what causes it?
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
What is the lesion in AML?
upper and lower motor neuron degeneration

fasciculations ==> atrophy
AML tx?
riluzole tx modestly lengthens survival by decreasing presynaptic glutamate release
What is the lesion in tabes dorsalis?
degeneration of dorsal columns ==> impaired proprioception and locomotor ataxia
What are the signs of tabes dorsalis?
absence of DTRs
positive Romberg
sensory ataxia at night
What is the lesion in Friedreich's ataxia?
dorsal columns
lateral spinothalamic
spinocerebellar
What are the sign/findings in Friedreich's ataxia?
staggering gait
frequent falling
nystagmus
dyarthria
pes cavus
hammer toes
hypertrophic cardiomyopathy
kyphoscoliosis
What is the lesion in Brown-Sequard syndrome?
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
What is Horner's syndrome associated with?
lesions of the spinal cord above T1

(Pancoast's tumor, Brown-Sequard, late state syringomyelia)
What is the biceps reflex testing?
C5, C6
What is the triceps reflex testing?
C7, C8
What is the patella reflex testing?
L3, L4
What is the Achilles reflex testing?
S1, S2
Superior colliculi
just below pineal body in the brain stem
conjugate vertical gaze center
Inferior colliculi
in midbrain below pineal body

auditory relay/processes center
Parinaud syndrome
paralysis of conjugate vertical gaze due to lesion in superior colliculi
(e.g. from pinealoma)
What are the functions of oculomotor nerve? CNIII
eye movt. (SR, IR, MR, IO)
pupillary constriction (PS: E-W nucleus, muscarinic receptors)
accommodation
eyelid opening (levator palpebrae)
What is the function of the Trochlear (CNIV) nerve?
eye movement (SO)
What is the function o f the trigeminal nerve (CNV)?
facial movement
taste from anterior 2/3 of tongue (via chordi tympani)
lacrimation
salivation (non parotid)
eyelid closing (orbicularis oculi)
stapedius muscle in ear
What is the function of the glossopharyndeal nerve (CNIX)?
taste from posterior 1/3 of tongue
swallowing
salivation (parotid)
monitoring carotid body and sinus chemo/baro receptos
stylopharyngeus muscle (elevates pharynx, larynx)
What is the function of the vagus nerve (CNX)?
taste from epiglottic region
swallowing
palate elevation
midline uvula
talking
coughing
thoracoabdominal viscera
monitoring aortic arch chemo- and baraoreceptors
What is the function of the accessory nerve (CNXI)?
head turning
shoulder strugging

(SCM and trapezius muscles)
Which cranial nerve nuclei are located in the midbrain?
CN III and IV
Which cranial nerve nuclei are located in the pons?
CN V, VI, VII, VIII
Which cranial nerve nuclei are located in the medulla?
CN IX, X, XI, XII
What conducts the corneal reflex?
afferent: V1 (ophthalmic)

efferent: VII (temporal branch)
What conducts the lacrimation reflex?
afferent V1

efferent VII
What conducts the pupillary reflex?
afferent: CNII

efferent: CNIII
What conducts the gag reflex?
Afferent: IX

Efferent: IX, X
What type of info is relayed via the Nucleus Solitarius?
visceral sensory (e.g taste, baroreceptors, gut distention)
VII, IX, X
What type of info is relayed via the Nucleus ambiguus?
motor innervation of pharynx, larynx and upper esophagus (e.g. swallowing, palate elevation)
IX, X, XI
What type of info is relayed via the Dorsal (motor) nucleus?
sends autonomic (parasympathetic fibers) to heart, lungs and upper GI
what travels through the optic canal?
CNII
ophthalmic artery
central retinal vein
what travels through the superior orbital fissure?
CNIII, IV, V1,
ophthalmic vein
sympathetic fibers
what travels through the foramen rotundum?
CNV2
what travels through the foramen ovale?
CNV3
what travels through the spinosum?
middle meningeal artery
what travels through the internal auditory meatus?
CNVII, VIII
What exits through the jugular foramen?
CNIX, X, XI
jugular vein
What exits through the hypoglossal canal?
CN XII
What exits through the foramen magnum?
spinal roots of CN XI
brain stem
vertebral arteries
What passes through the cavernous sinus?
CN III, IV, V1/V2, VI
post-ganglionic parasympathetic fibers
CNXII lesion (LMN)
tongue deviates toward the side of the lesion (lick your wound)

that's because it decussates before medulla and synapse on contralateral hypoglossal nucleus
CN V motor lesion
jaw deviates toward side of lesion

bilateral cortical input to lateral pterygoid muscle (UMN)
CNX lesion
uvula deviates away from side of lesion

weak side collpses and uvula points away
CN XI lesion
weakness turning head to contralateral side of lesion (SCM)

shoulder droop on side of lesion (trapezius)
UMN lesion of CN VII
contralateral paralysis of lower face only, since upper face receives bilateral UMN innervation
LMN lesion of CN VII
Ipsilateral paralysis of upper and lower face
Bell's palsy deficits
peripheral ipsilateral facial paralysis with inability to close eye on involved side
KUH sound tests what?
palate elevation (CNX)
LA sound tests what?
tongue - CNXII
MI sound test what?
lips - CNVII
What are the muscles of mastication?
muscles that close:
Masseter
Temporalis
Medial pterygoid

muscle that opens:
lateral pterygoid
Lateral Lowers

M's Munch
How is near vision produced?
ciliary muscle contracts==> zonular fibers relax/lengthen ==> lens relaxes and becomes more convex
How is far vision produced?
ciliary muscle relaxes==> zonular fibers shorten/tense ==> lens flattens
CN III palsy
eye looks down and out

pupillary dilation

loss of accomodation
CN IV palsy
eye drifts up ==> vertical diplopia

(problems reading newspapers or going down stairs)
CN VI palsy
medially directed eye (horizontal diplopia)
How is pupillary constriction (miosis) controlled?
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
What is Marcus Gunn pupil and what is it a sign of?
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
What is the tract/pathway for pupillary dilation?
T1 preganglionic sympathetic ==> superior cervical ganglion ==> postganglionic sympathetic ==> long ciliary nerve
the fact that it has to pass through cervical ganglion explains why Horner's happens in ppl with masses in that area
Which part of the visual field crosses over at the optic chiasm?
lateral fields (medial retina)
Lesion of left optic nerve before the chiasm would result:
left anopia
Lesion of the optic nerve at the chiasm would cause:
bitemporal hemianopia
Lesion of the right optic track on the would cause:
left homonnymous hemianopsia
Lesion of Meyer's loop (temporal lobe) on the right would cause:
left upper quadrant anopia
Lesion of dorsal optic radiation (parietal lobe) on the right would cause:
left lower quadrant anopia
Internuclear ophthalmoplegia is caused by?
lesion in the medial longitudinal fasciculus

common in MS
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
What genes are associated with Alzheimer's?
early onset: APP (21), presenilin-1, presenilin-2

later onset: ApoE4
Which lobe is spared in Alzheimer's?
occipital
What are the histologic findings in Alz?
senile plaques: extracellular Beta-amyloid core

neurofibrillary tangles (intracellular, abnormally phosphorylated tau protein = insoluble cytoskeletal elements)
What part of the brain is most atrophied in Pick's disease?
frontotemporal
What is the histologic finding in Pick's disease?
Pick bodies = intracellular, aggregated tau proteins
What are the symptoms of Pick's disease?
dementia
aphasia
parkinsonian aspects
change in personality/behavior
What are the symptoms of Lewy body dementia?
Parkinsonism with dementia and hallucinations
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
MS treatment
chronic - beta-interferon or immuno-suppressive therapy

acute - corticosteroids
What is Gullain-Barre syndrome?
inflammation and demyelination of peripheral nerves and motor fibers of ventral roots causing symmetric ascending muscle weakness
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
Acute disseminated (postinfectious) encephalomyelitis
multifocal perivenular inflammation and demyelination after infection or certain vaccines
Metachromatic leukodystrophy
autosomal-recessive lysosomal storage disease, most commonly due to arylsulfatase A deficiency. Buildup of sulfatides leads to impaird production of myelin sheath
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
Where do partial seizures usually originate?
mesial temporal lobe
How can you differentiate peripheral and central vertigo with positional testing?
peripheral - delayed nystagmus horizontal only

central - immediate nystagmus in any direction
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
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
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)
Glioblastoma multiforme histology
psudopalisading pleomorphic tumor cells - border central areas of necrosis and hemorrhage
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
Meningioma histology
spindle cells concentrically arranged in a whorled patter

psammoma bodies (laminated calcifications)
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
Who gets bilateral schwannomas?
NF-2
Oligodendroglioma general characteristics
relatively rare
slow growing
most often in frontal lobes
Oligodendroglioma histology
chicken-wire capillary patter around oligodendrocytes which look like "fried eggs" - round nuclei with clear cytoplasm

often calcified
Pilocytic (low-grade) astrocytoma general characteristics
usually well circumscribe, benign, good prognosis in kids

found in posterior fossa

GFAP+
Pilocytic (low-grade) astrocytoma histology
Rosenthal fibers - eosinophilic, corkscrew fibers. Cystic + solid (gross)
Medulloblastoma general characteristics
Highly malignant cerebellar tumor
a form of primitive neuroectodermal tumor (PNET)
can compress 4th ventricle causing hydrocephalus
Medulloblastoma histology
rosettes or perivascular psuedorosette pattern of cells

solid tumor
small blue cells
Ependymoma general characteristics
kids
ependymal cell tumors most commonly found in 4th ventricle so can cause hydrocephalus
poor prognosis
Ependymoma histology
characteristic perivascular pseudorosettes
rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus
Hemangioblastoma general
kids
most often cerebellar
associated with VHL when found with retinal angiomas
can produce EPO --> secondary polycythemia
Hemangioblastoma histology
foamy cells and high vascularity are characteristic (stokes, clots)
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
Craniopharyngioma histology
derived from remnants of Rathke's pouch
calcification is common (tooth and enamel-like)
cysts
hyposecretion of mixed hormones
Clinical signs of uncal herniation
1) ipsilateral dilated pupil/ptosis
2) contralateral homonymous hemianopia
3) ipsilateral paresis
4) duret hemorrhages - paramedian artery rupture
Which brain lesions are ring-enhancing?
mets
abscesses
toxo
AIDS lymphoma
Which brain lesions are uniformly enhancing?
lymphoma
meningioma
mets (usually ring-enhancing)
Which brain lesions are heterogeneously enhancing?
Glioblastoma multiforme
What might a cingulate herniation under falx cerebri cause?
compression of anterior cerebral artery
what can a downward transtentorial (central) herniation cause?
if it compresses the brain stem ==> coma and death
Timilol MOA/use
beta-blocker that dec. aqueous humor production so good for glaucoma
Brimonidine MOA/use
alpha-agonist that decreases aqueous humor secretion so good for glaucoma
Pilocarpine, carbachol MOA/use
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
Physostigmin, echothiophate MOA
Indirect cholimimetics (AchE inhibitors)
inc. the outflow of aqueous humor by contracting ciliary muscle and opening trabecular meshwork
causes miosis and cyclospasm
Latanoprost MOA
a PGF2alph agonist that inc. outflow of aqueous humor
darkens color of iris (browning)
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
What are the clinical uses of opiods?
cough suppressant - dextromethorphan)
diarrhea - loperamide and diphenoxylate
acute pulmonary edema
rehab (methadone)
Butorphanol MOA
partial agonist at opioid mu receptors, agonist at kappa receptors
Butorphanol clinical use
pain (causes less respiratory depression than full agonists)
Butorphanol toxicity
causes withdraw symptoms if on a full opioid agonist
Tramadol MOA
very weak opioid agonist

inhibits serotonin and NE reuptake
Tramadol clinical use
chronic pain
Tramadol toxicity
less abuse potential

similar to opioids

decreases seizure threshold
What is first line tx for tonic-clonic seizures?
phenytoin (also can be used for prophylaxis)

carbamazepine
Phenytoin MOA
inc. Na+ channel inactivation
Carbamazepine MOA
inc. Na+ channel inactivation
What is the first line treatment for trigeminal neuralgia?
Carbamazepine
Lamotrigine MOA
blocks voltage-gated Na+ channels
Lamotrigine clinical use
partial seizures

tonic-clonic
Gabapentin MOA
GABA analog but primarily inhibits HVA Ca2+ channels
Tramadol MOA
very weak opioid agonist

inhibits serotonin and NE reuptake
Tramadol clinical use
chronic pain
Tramadol toxicity
less abuse potential

similar to opioids

decreases seizure threshold
What is first line tx for tonic-clonic seizures?
phenytoin (also can be used for prophylaxis of status epilepticus)

carbamazepine

valproic acid
Phenytoin MOA
inc. Na+ channel inactivation
Carbamazepine MOA
inc. Na+ channel inactivation
What is the first line treatment for trigeminal neuralgia?
Carbamazepine
Lamotrigine MOA
blocks voltage-gated Na+ channels
Lamotrigine clinical use
partial seizures

tonic-clonic
Gabapentin MOA
GABA analog but primarily inhibits HVA Ca2+ channels
Gabapentin clinical use
partial

tonic-clonic
Topiramate MOA
blocks Na+ channels

inc. GABA action
Topiramate clinical use
partial

tonic-clonic
What is the first line anti-seizure med in pregnancy and children?
phenobarbital
Phenobarbital MOA
inc. GABA-A action
Phenobarbital clinical use
partial

tonic-clonic
Valproic acid MOA
inc. Na+ channel inactivation

inc. GABA concentration
Valproic acid clinical use
partial
tonic-clonic
absence
myoclonic
Ethosuximide MOA
blocks thalamic T-type Ca2+ channels
Ethosuximide clinical use
absence seizures
How can benzos be used for seizures?
1st line for acute status epilepticus and eclampsia (along with Mg2+)
Tiagabine MOA
inhibits GABA reuptake
Tiagabine clinical use
partial seizures only
Vigabatrin MOA
irreversibly inhibits GABA transaminase ==> inc. GABA
Vigabatrin clinical use
partial seizures only
Levetiracetam MOA
unknown; may modulate GABA and glutamate release

low side efx - good drug
Levetiracetam clinical use
partial

tonic-clonic
Carbamazepine toxicity
diplopia
ataxia
agranulocytosis and aplastic anemia
liver toxicity
teratogenesis
induction of P-450
SIADH
Ethosuximide toxicity
GI distress
fatigue
headache
urticaria
Stevers-Johnson syndrome
Phenobarbital toxicity
sedation
tolerance
dependence
induction of P-450
Phenytoin toxicity
nystagmus
diplopia
ataxia
sedation
gingival hyperplasia
hirsutism
megaloblastic anemia
teratogenesis
SLE-like syndrome
P-450 inducer
Valproic acid toxicity
GI distress
rare but fatal hepatoxicity
neural tube defects in fetus
tremor
weight gain
Lamotrigine toxicity
Stevens-Johnson syndrome
Gabapentin toxicity
sedation
ataxia
Topiramate toxicity
sedation
mental dulling
kidney stones
weight loss
What are the barbiturates?
-barbital and thiopental (surgery)
Barbiturates MOA
facilitate GABA-a action by inc. duration of Cl- channel opening, thus dec. neuron firing (due to hyperpolarization)
Benzos MOA
facilitate GABAa action by inc. the frequency of Cl- channel opening
Halothane toxicity
hepatotoxic
Methoxyflurane toxicity
nephrotoxic
Enflurane side effect
proconvulsant
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
Midazolam clinical use
endoscopy
Ketamine clinical use/MOA
PCP analog that act as a dissociative anesthetics. Blocks NMDA receptors. causes disorientation, hallucination and bad dreams.
Propofol MOA/clinical use
used for rapid anesthesia induction and short procedure

less postoperative nausea than thiopental

potentiates GABA
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
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)
Tubocurarine MOA
Competitive antagonist of Ach receptors

(non-depolarizing neuromuscular blockade)
What are the complications of succinylcholine?
hypercalcemia

hyperkalemia
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
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)
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
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