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Neuro Flashcards

1
Q

Arnold-Chiari Type I

A

Adults: low-lying cerebellar tonsils below formen magnum–> vertebral canal
- Symptoms: headaches, cerebellar symptoms (ataxia), syringomyelia

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2
Q

Arnold-Chiari Type II

A

Babies: Cerebellar tonsil and vermian heniation through foramen magnum

  • Aqueductal stenosis and hydrocephalus
  • Thoraco-lumbar myelomeningocele
  • paralysis below defect

Symptoms: difficulty swallowing, dysphonia, stridor, apnea

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3
Q

Dandy-Walker syndrome

A

Agenesis of cerebellar vermis with cystic enlargement of 4th ventricle (fills posterior fossa)

  • hydrocephalus
  • Spina bifida

Symptoms: postural instability, gait problems

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4
Q

Meissner’s corpuscles

A

Large, myelinated fibers (adapt quickly)
Seen in glabrous (hairless) skin

Dynamic, fine/light touch; position sense

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5
Q

Pacinian corpuscles

A

Large, myelinated A-beta fibers
- Deep skin layers, ligaments, joints

Rapid vibration, pressure sense

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6
Q

Merkel’s discs

A

Large, myelinated fibers; adapt slowly
- Hair follicles

Pressure, deep static touch (shapes, edges), position sense

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7
Q

Endoneurium

A

Invests single nerve fibers

- Guillain-Barre= inflammation of endoneurium

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8
Q

Perineurium

A

Surrounds fasicle of nerve fibers

  • Permeability layer
  • Rejoined in microsurgery for limb reattachment
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9
Q

Epineurium

A

Surrounds entire nerve (dense connective tissue)

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10
Q

Golgi Tendon Organ

A

Sensory receptor at muscle-tendon junction
- in SERIES with extrafusal muscle fibers
- Ib innervation–> inhibitory
GTO activated with excess contraction—> relaxation

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11
Q

Intrafusal muscle spindles

A

Ia and II innervation

- Sensitive to stretch (stops excess stretch force)

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12
Q

Locus Ceruleus

A

Site of NE formation
- SAM required to transform NE to epi

NE= tyrosine derived (like DA, epi)

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13
Q

Dopamine

A

Tyrosine-derived neurotransmitters

- Found in Ventral tegmentum, SNc (substantia nigra pars compacta)

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14
Q

5-HT (serotonin)

A

Tryptophan–> BH4 (pyridoxine= B6)–> 5-hydroxytryptamine–> serotonin
- found in Raphe nucleus (pons)

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15
Q

Basal nucleus of Meynert

A

ACh synthesis

  • Decreased in Alzheimer’s, Huntington’s
  • Increased in REM sleep
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16
Q

Metencephalon

A

Pons and cerebellum
+ Upper part of 4th ventricle

Part of Hindbrain (Rhombencephalon)

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17
Q

Myelencephalon

A

Medulla
+ Lower part of 4th ventricle

Part of Hindbrain (Rhombencephalon)

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18
Q

Diencephalon

A

Thalamus + Third ventricle

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19
Q

Mesencephalon

A

Midbrain + aqueduct

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20
Q

Nucleus accumbens

A

Site of GABA synthesis
- Glutamate converted to GABA by glutamate decarboxylase

*Decreased synthesis in anxiety, Huntington’s

GABA receptor types:

  • GABA(A)= Cl- influx in brain (ion channel)
  • GABA(B)= K+ efflux, decreased Ca+2 influx inhibit adenylyl cyclase (G-protein)
  • GABA(C)= Cl- influx in retina

*Decreased GABA(A) in long term EtOH/benzo use–> withdrawal seizures

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21
Q

Cross BBB

A

Glucose and AA by carrier-mediated transport (slow)

Non-polar/lipid-soluble cross rapidly

Specialized areas with fenetrated capillaries:

  • Area postrema (vomiting post-chemo)
  • OVLT (osmotic sensing
  • Neurosecretory products (neurohypophysis–> ADH)
  • Hypothalamic inputs/outputs
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22
Q

Hypothalamus areas

A

Lateral: regulates hunger

  • Inhibited by leptin
  • Destruction–> anorexia

Ventromedial: regulates satiety

  • Stimulated by leptin
  • Destruction (craniopharyngioma)–> hyerphagia

Anterior: cooling, parasympathetic

Posterior: Heating, sympathetic

Suprachiasmatic nucleus: circadian rhythm

**Posterior pituitary (neurohypophysis) recieves axonal projections from supraoptic nuclei (ADH) and paraventricular nuclei (oxytocin)

    • Anterior pituitary (adenohypophysis) recieves stimulation from hypothalamus:
  • DA–> inhibits Prolactin
  • GHRH–> GH release
  • LHRH–> LH release, FSH release
  • CRH—> ACTH release
  • TRH–> TSH release
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23
Q

Thalamus

A

VPL: Pain, temp, pressure, touch, vibration, proprioception

VPM: Face sensation and taste (Makeup on the face)

LGN: Vision

MGN: Hearing

VL: motor

Thalamus strok= post-stroke pain (burning/stabbing sensation)

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24
Q

Cerebellar peduncles

A

Input= climbing, mossy fibers

  • Inferior: ipsilateral proprioceptive info
  • Middle: Contralateral cortex

Output= Purkinje fibers
- Superior: Deep nuclei to contralateral cortex

  • Deep nuclei (lat–> med): Dentate, Emboliform, Globose, Fastigial (Don’t Eat Greasy Foods)
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25
Q

Mesolimbic pathway

A

Dopaminergic pathway
Midbrain VTA–> Limbic nucleus accumbens

  • Stimulation–> delusions, hallucinations, pleasure (Pathway to addiction)
  • D3, D4 receptors, inhibited by atypical antipsychotics
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26
Q

Mesocortical pathway

A

Dopaminergic pathway

Midbrain VTA–> limbic cortex (dorsolateral prefrontal)

  • Cortex= cognition; defects–> negative symptoms of psychosis
  • D3, D4 receptors, inhibited by atypical antipsychotics
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27
Q

Nigrostriatal pathway

A

Dopaminergic pathway

Substantia nigra–> basal ganglia (striatum)

*Movement pathway (“nigrostride”); damage–> Parkinson’s

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28
Q

Tubuloinfunibular pathway

A

Dopaminergic pathway

Arcuate nucleus (hypothalamus)–> anterior pituitary

  • Inhibit DA–> increased prolactin productions
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29
Q

Basal ganglia nuclei

A

Striatum:
- Putamen (motor) and caudate (cognitive)

Lentiform:
- Putamen and globus pallidus

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30
Q

Hemiballismus

A

Contralateral subthalamic nucleus
- Lacunar stroke

Sudden, wild flailing of 1 arm +/- ipsilateral leg

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31
Q

Kluver-Bucy syndrome

A

Lesion of amygdala, associated with HSV-1

Symptoms:

  • Hyperorality (taste, eat anything)
  • Hypersexuality
  • Disinhibited behavior
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32
Q

Cerebellar hemisphere lesion

A

Intention Tremor, limb ataxia, loss of balance

Damage–> ipsilateral deficits–> fall toward lesion

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33
Q

Cerebellar vermis lesion

A

Truncal ataxia, dysarthria

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34
Q

Paramedian pontine reticular formation lesion

A

Eyes look away from side of lesion

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35
Q

Frontal eye field lesion

A

Eyes look towards lesion

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36
Q

Conduction aphasia

A

Poor repetition with fluent speech, in tact comprehension
- Damage to arcuate fasciculus (connecting Wernicke’s to Broca’s)

Can’t repeat phrase: “No ifs, ands, or buts”

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37
Q

Therapeutic hyperventilation and cerebral perfusion

A

Cerebral perfusion regulated by PCO2 (except in severe hypoxia= PO2 < 60)

Hyperventilation–> decreased CO2–> decreased ICP in cases of acute cerebral edema (stroke, trauma)–> decreases cerebral perfusion

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38
Q

Lateral striate artery

A

Supplies striatum, internal capsule

Lesion–> contralateral hemiparesis, hemiplegia

  • *Posterior internal capsule stroke has pure motor/pure sensory deficits
    • Genu of internal capsule= dysarthria-clumsy hand syndrome
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39
Q

Anterior spinal artery (ASA)

A

Supplies:

  • Lateral corticospinal tract
  • Medial lemniscus
  • Caudal medulla (hypoglossal nerve)

** Lesion= Medial medullary syndrome
Stroke: commonly bilateral
- Contralateral hemiparesis, proprioception
- Ipsilateral hypoglossal dysfunction (tongue deviates to side of lesion)

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40
Q

PICA (posterior inferior cerebellar artery)

A

Supplies:
- Lateral medulla: vestibular nuclei, lateral spinothalamic tract, spinal trigeminal nucleus, nucleus ambiguus, sympathetic fibers, inferior cerebellar peduncle

Lesion= Lateral medullary (Wallenberg’s) syndrome

  • Dysphagia, Hoarsenss, decreased gag reflex
  • Vomiting, vertigo, nystagmus
  • Decreased pain and temperature sensation to limbs/face
  • ipsilateral Horner’s
  • Ataxia, dysmetria
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41
Q

AICA (anterior inferior cerebellar artery)

A

Supplies:

  • Lateral pons (cranial nerve nuclei)
  • Vestibular nuclei, facial nucleus
  • Spinal trigeminal
  • Cochlear nuclei
  • Sympathetic fibers
  • Middle and inferior cerebellar peduncles

Symptoms:

  • Paralysis of face
  • Decreased lacrimation, salivation, taste of anterior 2/3 of tongue, corneal reflex
  • Decreased pain, temp sensation on face
  • Ipsilateral decreased hearing, Horner’s syndrome
  • Vomiting, vertigo, nystagmus
  • Ataxia, dysmetria
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42
Q

PCA (posterior cerebral artery)

A

Supplies:
- occipital cortex, visual cortex

Symptoms:
- Contralateral hemianopia with macular sparing

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43
Q

Anterior communicating artery (AComm)

A

Saccular/berry aneurysm site–> impinge cranial nerves

- Visual field defects

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44
Q

Posterior communicating artery (Pcomm)

A

Berry aneurysm

- CNIII palsy (eye down and out, ptosis, pupil dilation

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45
Q

Charcot-Bouchard microaneurysm

A

Associated with chronic HTN (small vessels in basal ganglia, thalamus)
- Visible on CT

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46
Q

Epidural hematoma

A

Accumulation of blood between cavarium and dura

  • Creates high-pressure system within the skull
  • Usually results from trauma to side of head

Ex: Fracture of temporal bone–> transection of middle meningeal artery

Symptoms:

  • Lucid interval after trauma
  • Expansion–> transtentorial herniation, CNIII palsy

CT:

  • biconvex (lentiform), hyperdense blood collection
  • Does not cross suture lines, but can cross falx, tentorium
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47
Q

Subdural hematoma

A

Rupture of bridging veins

  • Slow onset (venous blood- less pressure)
  • Seen in elderly, alcoholics, blunt trauma, shaken baby (brain atrophy, shaking/whiplash)

CT:

  • Crescent-shaped hemorrhage crosses suture lines
  • midline shift
  • Cannot cross falx, tentorium
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48
Q

Subarachnoid hemorrhage

A

Rupture of aneurysm (berry) d/t Marfan’s, Ehlers-Danlos, ADPKD, or AVM

  • Rapid onset
  • Worst Headache of my Life (WHOML)

Bloody/yellow spinal tap

Risk of vasospasm due to blood breakdown products: avoid with nimodipine (Ca+2 channel blocker)

    • Spontaneous intracranial hemorrhage due to AVM, ruptured crerebral aneurysms, cocaine use
  • Berry aneurysms associated with coarctation of aorta (HTN in branches proximal to arch–> increased pressure on cerebral arteries)
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49
Q

Intraparenchymal (HTN) hemorrhage

A

Systemic hypertension, amyloid angiopathy, vasculitis, neoplasm

Occurs in bassal ganglia, internal capsule (Charcot-Bouchard aneurysm)

  • *Amyloid angiopathy= recurrent hemorrhagic stroke w/o HTN (milder onset)
  • Seen in cerebral hemispheres (vs basal ganglia)
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50
Q

Noncommunicating hydrocephalus

A

Structural blockage of CSF circulation in ventricular system (stenosis of aqueduct of sylvius)

Due to:

  • Type II Arnold-Chiari malformations (babies)
  • Hereditary aqueductal stenosis
  • Prenatal infections (toxoplasmosis)

Presentation:

  • Irritable, poor feeding
  • Periventricular pyramid tracts stretched—> UMN damage
  • Hypertonic muscles, hyperreflexia
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51
Q

Dorsal column

A

Tract: medial lemniscus

Function: ascending pressure, vibration, fine touch, proprioception

Synapse 1: ipsilateral nucleus cuneatus (Upper body) or gracilis (lower body)

Synapse 2: decusses in medulla –> contralateral medial lemniscus–> VPL (thalamus)

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52
Q

Spinothalamic tract

A

Function:

  • Lateral= pain, temperature
  • Anterior= crude touch, pressure

Synapse 1: ipsilateral gray matter (spinal cord)

Synapse 2: decussates at AWC–> ascends contralaterally–> VPL (thalamus)

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53
Q

Poliomyelitis, Werdnig-Hoffmann disease

A

LMN lesion: destruction of anterior horns
–> flaccid paralysis, weakness, atrophy, fasciculations, hyporeflexia, muscle atrophy

Poliomyelitis: fecal-oral transmitted Picorna virus (ssRNA+, non-enveloped)

  • Replicates in oropharnx, small intestine–> bloodstream, CNS
  • Diagnosis: CSF with increased WBCs with slight protein elevation (no glucose changes); recover virus from stool, throat

Werdnig-Hoffman: congenital degeneration of anterior horns of spinal cord

  • -> “Floppy baby” with hypotonia, tongue fasciculations
  • Autosomal recessive
  • Death by 7 months
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54
Q

ALS (amyotrophic lateral sclerosis)

A

UMN and LMN deficits
- No sensory, cognitive, oculomotor deficits

Defect in superoxide dismutase 1

Tx: Riluzole: decreases presynaptic Glutamate release–> increased survival

55
Q

Tabes dorsalis

A

Tertiary syphillis–> demyelination of dorsal columns, roots
–> lose sensation, proprioception, sensory ataxia

Conditions:

  • Charcot’s joints
  • Shooting pain
  • Argyll Robertson Pupils: small bilateral pupils constrict to accomodation, not light
  • Absent DTRs, positive Romberg (UMN and LMN signs)
56
Q

Syringomyelia

A

Syrinx (cyst in spinal cord) expands–> damage AWC (anterior white commisure) of spinothalamic tract

  • -> bilateral loss of pain and temp (C8-T1)= Cape-like loss of sensation
  • Seen in Arnold-Chiari I malformation
57
Q

Vitamin B12, Vitamin E deficiency

A

Subacute combined degeneration- demyelination of:

  • Dorsal columns
  • Lateral corticospinal tracts
  • Spinocerebellar tracts

Symptoms:

  • Ataxic gait
  • Paresthesias
  • Impaired position, vibration sense
58
Q

Friedreich’s Ataxia

A

Autosomal recessive trinucleotide repeat disorder (GAA on Chromosome 9)
–> mitochondrial function impaired

  1. Cerebellar dysfunction–> ataxia
    - staggering gait, frequent falling, nystagmus (saccades), dysarthria
  2. Degeneration of dorsal columns–> loss of position, vibration sensation
    - pes cavus, hammer toes
    - May see DM in 10%

Presents in childhood with kyphoscoliosis

Death due to hypertrophic cardiomyopathy:

  • Arrhthmias
  • CHF
  • Bulbar dysfunction (can’t protect airway)
59
Q

Brown-Sequard Syndrome

A

Lateral hemisection of spinal cord:

  • Ipsilateral UMN signs below lesion, LMN signs at lesion, loss of tactile sensation, discrimination below lesion, loss of all sensation at lesion
  • Contralateral pain and temp loss (2-3 segments below where AWC knocked out)

Lesion above T1: may see Horner’s syndrome (damage sympathetic ganglion)

60
Q

Cauda equina syndrome

A

Damage to S2-S4 nerve roots

  • Low back pain radiating to leg(s)
  • Loss of ankle jerk reflex with plantar weakness
  • Saddle anesthesia, loss of anocutaneous reflex (sphincter pinprick–> contraction)
61
Q

Conus medullaris Syndrome

A

Lesion at S2–>

  • Flaccid paralysis of bladder, rectum, impotence
  • S3-S5: saddle anesthesia
  • Mild weakness of leg muscles if it spares cord/ roots
62
Q

Moro reflex

A

“Hang on for life” reflex:

- Abduct/extend limbs when startled, then draw together

63
Q

Parinaud syndrome

A

Lesion of brainstem superior colliculi (damage to oculomotor, trochlear nerves, Edinger-Westphal nucleus):

  • Paralysis of conjugate vertical gaze
  • Absent pupillary light reflex, failure to converge
  • Wide-based gait
  • Caused by pinealoma
  • Inferior colliculi= auditory center
64
Q

Cranial nerve nuclei: location of emergence from brainstem

A

Midbrain: CN III, IV
Pons: CN V, VI, VII, VIII
Medulla: CN IX, X, XII
Spinal cord: CN XI

    • Medial nuclei= Motor (basal plate)
    • Lateral nuclei= Sensory (aLar plate)
65
Q

Vagus branches

A

Superior laryngeal nerve:

  • External branch= cricothyroid m (runs with superior thyroid artery and vein)
  • Internal branch: Sensory above vocal cords

Recurrent laryngeal:

  • All laryngeal muscles (-ary-) except cricothyroid
  • Sensory below vocal cords
66
Q

Nucleus solitarius

A

Visceral Sensory information (taste, baroreceptors, gut distention)

CN VII, IX, X

67
Q

Nucleus aMbiguus

A

Motor innervation of pharynx, larynx, upper esophagus

CN IX, X

68
Q

Dorsal motor nucleus

A

Parasympathetic (autonomic) innervation to heart, lungs, upper GI

CN X

69
Q

Cavernous sinus syndrome

A

Cavernous sinus= venous sinus around pituitary

  • Blood from eye/superficial cortex–> cavernous sinus–> internal jugular vein
  • Contains CN III, IV, V1, V2, VI and postganglionic sympathetic fibers

Mass effect, fistula, thrombosis:
- Decreased corneal, maxillary sensation with normal vision

70
Q

Hearing loss types

A

Conductive:

  • AbnL Rinne test (Bone > air)
  • Weber test localizes to affected ear (vibration>air conduction)
  • Ex: middle ossicle otosclerosis; rupture of tympanic membrane d/t loud sound

Sensorineural

  • normal Rinne test
  • Weber localizes to unaffected ear (normal ear picks up sound/vibration, other doesn’t)

Noise-induced:

  • Damage to stereocilliated cells in organ of corti (shearing forces against tectorial membrane
  • Loss of high-frequency hearing 1st

Acoustic reflex: dampen effects of prolonged noise by contracting tensor tympani muscle (via chorda tympani)–> decreased ossicle responsiveness

71
Q

Muscles of mastication

A

CN V
Open mouth: Masseter, Temporalis, Medial pterygoid

Close mouth: Lateral pterygoid (Lateral Lowers jaw)

72
Q

Accomodation

A

Focus on near objects–> ciliary muscle tightens–> zonular fibers relax–> lens becomes more convex
- Occurs with convergence, miosis

    • Presbyopia= sclerosis, decreased elastility of lens–> decreased ability to focus during accomodation
  • Myopes see improvement in distance vision as lens scleroses–> decreased elasticity, changes in lens curvature, decreased ciliary muscle strength
73
Q

Uveitis

A

Inflammation of uveal coat (iris, ciliary body, choroid)

  • Associated with inflammatory disorders (RA, sarcoid, TB)
  • HLA-B27 associated conditions
74
Q

Pupillary miosis

A

Parasympathetic constriction

1st neuron: Edinger-Westphal nucleus to ciliary ganglion (via CNIII)
2nd neuron: short ciliary nerves–> pupillary sphincter muscles

75
Q

Pupillary mydriasis

A

Sympathetic dilation

1st neuron: hypothalamus–> ciliospinal center of Budge (C8-T2)
2nd neuron: Exit T1–> superior cervical ganglion (along cervical sympathetic chain near lung apex)–> subclavian vessels
3rd neuron: plexus along internal carotid–> cavernous sinus–> orbit (long ciliary nerve)–> pupillary dilator muscles

76
Q

Pupillary light reflex

A

Light–> CNII–> pretectal nuclei–> midbrain bilateral Edinger Westphal nuclei–> bilateral contraction

Marcus Gunn pupil= afferent pupillary defect (optic nerve damage, retinal detachment)
- Decreased constriction when light shined in affected eye during “swinging flashlight test”

77
Q

CN III components

A

Motor= interior of nerve
- Vascular disease–> decreased O2, nutrients–> ptosis, down and out gaze (seen in Diabetes: glucose–> sorbitol)

Parasympathetic: outer part of nerve

  • Affected first by compression (PCA aneurysm, uncal herniation)
  • Diminished/absent pupillary light reflex (“blown out” pupil)
78
Q

Meyer’s loop

A

inferior retina: Carries superior visual field

  • Temporal lobe
  • Loops around inferior horn of lateral ventricle
  • more susceptible to damage
79
Q

Dorsal optic radiation

A

Superior retina: inferior visual field

  • Parietal lobe
  • Shortest path via internal capsule (retrolenticular limb)
  • Projects onto occipital cortex
80
Q

Internuclear ophthalmoplegia (INO)

A

MLF (medial longitudinal fasciculus)= tract communicating between CN VI (lateral rectus) and CN III (medial rectus) to coordinate horizontal gaze

Normal:
- R CN VI activates (abduct R eye)–> R nucleus of CN VI–> Left MLF–> L CN III activation (adduct L eye)

Lesion:

  • R abducts–> L MLF lesioned–> no L eye adduction
  • Right then develops nystagmus to compensate for Left= Left INO

** Seen in Multiple Sclerosis

81
Q

Alzheimer’s disease

A

Inheritance:

  1. Down’s syndrome: increased risk due to Amyloid precursor protein (APP) expression on Chrom 21
  2. Familial form: 10%:
    - Early onset: APP (chrom 21), presenilin-1 (chrom 14), presinilin-2 (chrom 1)
    - Late onset: ApoE4 (chrom 19)= protective

Pathophys:
1. Widespread cortical atrophy–> decreased Ach (deficiency of choline acetyltransferase on nucleus basalis of Meynert + hippocampal changes)

  1. Plaques form first–> Neurofibrillary tangles

Amyloid plaques:

  • Extracellular accumulation of A-beta (fragment of the amyloid precursor protein)
  • Abnormal processing of APP critical to pathophysiology of Alzheimer’s disease

Neurofibrillary tangles:

  • Intracellular, paired helical structures composed of hyperphosphorylated tau.
  • Correlate well with disease severity and neuronal death.
82
Q

Neural tube defect markers

A

Low serum folate
Elevated fetal, maternal serum alpha-fetoprotein (AFP)
Elevated amniotic AchEsterase

83
Q

Epinephrine

A

Alpha-agonist used for Glaucoma
MOA: Decrease aqueous humor synthesis via vasoconstriction

Tox: Mydriasis (do NOT use in closed-angle glaucoma)

84
Q

Brimonidine

A

Alpha-2 agonist for Glaucoma

MOA: decrease aqueous humor synthesis

Tox: blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritis

85
Q

Timolol, betaxolol, carteolol

A

Beta-blockers for glaucoma

MOA: decrease aqueous humor synthesis

86
Q

Acetazolamide

A

Diuretic used for Glaucoma

MOA: Carbonic anhydrase inhibitor–> decreased aqueous humor synthesis

87
Q

Pilocarpine, carbachol

A

Direct cholinomimetics for glaucoma

MOA: Increase outflow of aqueous humor via contraction of ciliary muscle, opening meshwork
** Use pilocarpine in emergencies (opens canal of Schlemm)

Tox: miosis, cyclospasm (contraction of ciliary muscle)

88
Q

Physostigmine, echothiophate

A

Indirect cholinomimetics for glaucoma

MOA: Increase outflow of aqueous humor via contraction of ciliary muscle, opening meshwork

Tox: miosis, cyclospasm (contraction of ciliary muscle)

89
Q

Latanoprost

A

Prostaglandin for glaucoma

MOA: increases outflow of aqueous humor

Tox: darkens iris (brown)

90
Q

Opioid analgesics

A

Morphine, fentanyl, codeine, heroine, methadone, meperidine, dextromethorphan, diphenoxylate

MOA:

  • Agonist at opioid receptors: Mu= morphine, delta= enkephalin, kappa= dynorphin
  • Modulates synaptic transmission:
  • Opens K+ channels–> hyperpolarization–> stop pain transmission
  • Closes Ca+2 channels
  • Inhibits cAMP formation
  • Decreased synpatic transmission
  • -> inhibit release of ACh, NE, 5-HT, glutamate, substance P

Use:

  • Pain
  • Cough suppression (dextromethorphan)
  • Diarrhea (loperamide, diphenoxylate), acute pulmonary edema
  • Maintenance: potent, long-acting opiate with good bioavailability (Methadone)

Tox:

  • Addiction
  • Respiratory depression, additive CNS depression with other drugs
  • Constipation, miosis (tolerance does NOT develop)

** Overdose: Naloxone, Naltrexone)

91
Q

Butorphanol, Nalbuphine, Pentazocine

A

Mixed agonist/antagonist

  • K and Mu agonist (without other opioid)
  • Antagonist of Mu in presence of other opioids

Uses:

  • Counteract AEs of opioids (respiratory depression, constipation)pain)
  • Central Kappa effect: dysphoria
  • Labor pain
92
Q

Tramadol

A

Dual action: Mu opioid receptor (weak), NE and serotonin reuptake inhibitor

Use: chronic pain

Tox: similar to opioids, decreased seizure threshold

93
Q

Phenytoin

A

Treats:

  • GTC (1st line**), Focal seizures
  • Status Epilepticus prophylaxis (1st line**)
  • Class Ib Antiarrhythmic

MOA:
- Na+ channel block in cortical neurons (can’t recover from depolarization)

AEs:

  • Purple glove
  • Gingival hyperplasia
  • Nystagmus, diplopia, ataxia, sedation
  • Hirsutism
  • Megaloblastic anemia
  • Teratogenic (fetal hyantoin syndrome)
  • SLE-like syndrome (slow alkylators)/ serum sickness
  • Generalized lymphadenopathy
  • Stevens-Johson
  • Osteopenia
  • Teratogenic: fetal hydantoin syndrome= microcephaly, dysmorphic craniofacial features, hypoplastic nails and distal phalanges, cardiac defects, IUGR, mental retardation
94
Q

Carbamazepine

A

Treats:

  • GTC (1st line), focal seizures (1st line)
  • Bipolar disorder
  • Trigeminal neuralgia

MOA:
- Na+ channel block in cortical neurons (can’t recover from depolarization)

AEs:

  • Reacts with everything
  • Autoinducer
  • Must perform HLA-typing
  • DON’T use in myoclonic, absense, aclonic seizures
  • SIADH
  • Stevens-Johnson
  • Diplopia, ataxia
  • Blood dyscrasias (agranulocytosis, aplastic anemia)
  • Teratogen= neural tube defects, craniofacial defects, fingernail hypoplasia, developmental delay, IUGR
95
Q

Lamotrigine

A

Treats:

  • ALL seizure types
  • GOOD Bipolar med

MOA:
- Na+ channel block

AEs:
- Toxic epidermal necrolysis!!

96
Q

Gabapentin

A

Treats:

  • GTC, focal seizures
  • pain

MOA:
- alpha-2 delta subunit of Ca+2

Tox:
- Sedation, ataxia

97
Q

Topiramate

A

Treats:

  • ALL seizure but absence type
  • Migraine
  • Weight loss

MOA:

  • Increase GABA
  • Decrease NMDA (Na+ channel block)
  • CA inhibitor
  • Ca+2 block in hippocampus

AEs:

  • Kidney stones
  • Weight loss
  • Sedation, mental dulling
98
Q

Phenobarbital

A

Treats:
- GTC, focal seizures in INFANTS

MOA:

  • Opens Cl- channel LONGER in GABA
  • In high enough dose–> binds GABA receptor directly–> opens channel w/o GABA

AEs:

  • Overdose- don’t use except in children
  • Sedation, tolerance, dependence
  • CyP-450 induction
99
Q

Benzodiazepines

A

Treats:

  • ALL seizure types
  • Status epilepticus (1st line for acute**)
  • EtOH withdrawal
  • Anxiety
  • Sleep (decreases REM sleep)
  • Night terrors, sleepwalking
  • General anesthetic (amnesia, muscle relaxation)

MOA:

  • Increases Cl- channel opening FREQUENCY in GABA
  • Long term: decreased GABA receptors

AEs:

  • Withdrawal seizures
  • Do not take with EtOH
  • Respiratory depression

** Treat overdose with Flumazenil

100
Q

Valproic acid

A

Treats:

  • ALL seizure types
  • 1st line for Tonic-Clonic**
  • Bipolar disorder
  • Migraines

MOA:

  • GABA increase
  • Block NMDA receptors (K+) in hippocampus
  • Na+ channel block in cortical neurons (can’t recover)

AEs:

  • Thrombocytopenia
  • Children: Pancreatitis, Hepatitis
  • Neural tube defects (due to inhibition of folate absorption)
  • Tremor, weight gain
101
Q

Ethosuximide

A

Treats:
- Absence seizures (1st line**)

MOA:
- T-type Ca+2 channels in Thalamus–> hyperpolarization

Tox:

  • GI distress, Fatigue, H/A, urticaria
  • Stevens-Johnson
102
Q

Tigabine

A

Treats:
- partial seizures

MOA:
- GABA increase (inhibits GABA reuptake)

103
Q

Vigabatrin

A

Treats:
- Partial seizures

MOA;
- Irreversibly inhibits GABA transaminase–> increased GABA

104
Q

Levitiracetam

A

Treats:

  • GTC
  • Focal epilepsy
  • Myoclonic epilepsy

MOA:
- SV2A

105
Q

Zolpidem, Zaleplon, Eszopiclone

A

MOA: Act via BZ1 subunit of GABA receptor

Use: Insomnia

Tox:

  • Ataxia, H/A, confusion
  • Modest day-after psychomotor depression, fewer amnestic effects
  • Lower dependence risk than benzos

**Reverse effects with flumazenil

106
Q

Principles of anesthetics

A

CNS drugs must be lipid soluble (cross BBB) or actively transported

  • Drugs with decreased solubility in blood= rapid induction, recovery
  • Increased solubility in blood= high AV concentration gradient, slow onset, slow recovery
  • Drugs with increased solubility in lipid= increased potency

Potency= 1/MAC
MAC= minimal alveolar concentration at which 50% of population anesthetized
- Varies with ambient temperature and AGE (NOT surgery type, duration of administration, sex, height, weight)

Arterial tension curve:

  • Depends on solubility of anaesthetic in blood
  • Less soluble in blood: steeper curve (partial pressure of substance in blood increases steeply)
107
Q

Inhaled anesthetics

A

Halothane, -fluranes, NO

MOA: unknown

Effects:

  • Decreased myocardial contractility–> decreased renal, hepatic blood flow
  • Decreased respiratory drive
  • Decreased pulmonary vascular resistance
  • Decreased mucocillary reflex
  • N/V
  • Increased Cerebral blood flow (increased ICP)

Tox:

  • Hepatotoxic (halothane)
  • Nephrotoxic (methoxyflurane)
  • Proconvulsant (enflurane)
  • Malignant hyperthermia (all but NO)–> reverse with dantrolene sodium
  • Expansion of trapped gas in body (NO–> the bends)
108
Q

Thiopental

A

IV anesthetic= Barbituate

  • High potency, high lipid solubility (rapid entry into brain)
  • **DECREASES CBF: used in stroke to decrease cerebral edema

Use: induction of anesthesia, short procedures
- Terminated by rapid redistribution into tissue (skeletal muscle)

109
Q

Midazolam

A

IV anesthetic= benzo

Use: endoscopy
- Used with gaseous anesthetics, narcotics

Tox: respiratory depression (post-op)

  • Decreased BP (tx overdose with flumazenil)
  • Amnesia
110
Q

Ketamines

A

IV anesthetic
Arylcyclohexylamines= PCP analogs
- Dissociative anesthetics
- Block NMDA receptors (via glutamate + glycine)

Tox:

  • CV stimulants
  • Disorientation, hallucinations, nightmares
  • Increase CBF
111
Q

Propafol

A

IV anesthetic
Use: sedation in ICU
- Rapid anesthesia induction
- Short procedures

    • decreased postoperative nausea than thiopental
  • Potentiates GABA(A)
112
Q

Local anesthetics

A 
Esters= procaine, cocaine, tetracaine
Amides= 2 I's in name

MOA: block Na+ channels by binding receptor on inner channel

  • Bind to activated Na+ channels (most effective in rapidly firing neurons
  • Tertiary amines penetrate membrane uncharged and bind ion channels in charged form

Principles:

  • Given with vasoconstrictors
  • Acidic tissue (infected)–> charges alkaline anesthetics–> can’t penetrate membrane–> need to administer more
  • Order of blockade: small myelinated > small unmyelinated (C-fibers) > large myelinated > large unmyelinated
  • Lose: 1. pain, 2. temp, 3. touch. 4. pressure

Use: minor surgical procedures, spinal anesthesia

Tox: CNS excitation

  • CV toxicity (bupivacaine)
  • HTN, hypotension
  • Arrhythmias (cocaine)
113
Q

Succinylcholine

A

Depolarizing NM blocking drug
MOA: Ach receptor agonist–> sustained depolarization, prevents muscle contraction
- Reverse blockade in 2 phases:
1. Prolonged depolarization (no antidote): block potentiated by AchE-I
2. Repolarized but blocked: Ach receptors available but desensitized
- Antidote= AchE-I (neostigmine)
“Train of 4 response”
- Slow metabolizers take longer to enter phase 2 (antidote won’t work until then)

Tox: hypercalcemia, hyperkalemia, malignant hyperthermia

114
Q

Tubocurarine, Atacurium, mivacurium, pancuronium, vecuronium, rocuronium

A

Nondepolarizing NM blocking drugs
MOA: Competitive antagonist of Ach receptors

Reversal: neostigmine, edrophonium, AchE-I

115
Q

Bromocriptine

A

Ergot dopamine agonist

116
Q

Pramipexole, Ropinerole, pergolide

A

Non-ergot dopamine agonist

- Used in treatment of Restless leg syndrome

117
Q

Amantadine

A

Increases dopamine release
- Also used as antiviral against rubella, Influenza A

Tox: ataxia

118
Q

Benzotropine

A

Antimuscarinic/anticholinergic drug used to improve tremor and rigidity associated with Parkinson’s
- Can also be used to treat EPS due to antipsychotic antagonism of DA receptors

119
Q

L-dopa

A

Increases dopamine in brain (can cross BBB)
- Converted by dopa decarboxylase to DA in CNS

Tox:

  • Long term use: dyskinesia after administeration, akinesia between doses
  • w/o Carbidopa: postural hypotension, N/V, Arrhythmias (increased peripheral catecholamine formation)
  • Anxiety, agitation, insomnia, confusion, hallucinations (too much DA)

** Vitamin B6 (pyridoxine)= cofactor for DOPA metabolism (therefore supplements can enhance degradation)

120
Q

Carbidopa

A

Peripheral dopa decarboxylase inhibitor

  • Prevents peripheral formation of dopamine
  • Increases CNS levels, limits peripheral side effects
121
Q

Selegiline

A

Selective MAO-B inhibitor: decreases central DA degradation

- MAO-B= metabolizes DA over NE/serotonin

122
Q

Entacapone, Tolcapone

A

COMT inihibtors: prevent L-dopa degradation

  • Entacapone= prevents peripheral breakdown
  • Tolcapone= prevents peripheral and central breakdown
123
Q

Memantine

A

NMDA receptor antagonist

  • Used in Alzheimer’s
  • Prevents excitatoxicity (mediated by Ca+2 influx)

Tox: dizziness, confusion, hallucinations

124
Q

Donepezil, galantamine, rivastigmine

A

AchE-Inhibitors used in Alzheimer’s

Tox: Nausea, dizziness, insomnia

125
Q

Huntington’s treatments

A

Tetrabenzine, Reserpine: block VMAT: limit DA packaging and release

Haloperidol: DA receptor antagonist

126
Q

Sumatriptan

A

Serotonin 1B/1D agonist

  • Inhibits trigeminal nerve activation
  • Prevents Vasoactive peptide release
  • Induces vasoconstriction

Use: acute migraine, cluster headache

Tox: coronary vasospasm (avoid in CAD, Prinzmetal angina), mild tingling

127
Q

Tetrodotoxan

A

Puffer fish venom

  • Blocks voltage-gate Na+ channels in nerve cell membranes
  • -> inhibits passive sodium transport
128
Q

Primidone

A

Antiepileptic drug

  • Metabolized to phenobarbital and phenylethylmalonamide
  • Used in treatment of essential tremor
129
Q

Alcohol and CNS

A

Thiamine deficiency:

  • Cerebellar atrophy–> Ataxia (weeks to months)= wide-based gait, truncal instability, intention tremor, “Parkinsonian tremor”
  • Loss of Purkinje cells in anterior lobes, cerebellar vermis
  • Wernicke-Korsakoff syndrome= confusion, ophthalmoplegia, ataxia; memory loss (antero- and retrograde), confabulation, personality changes
130
Q

Pontine hemorrhage

A

Pinpoint pupils
Loss of horizontal gaze
Quadriparesis
Decerebrate posturing (prostrate position, lesion below red nucleus)–> coma–> death

**Decorticate posturing (bent arms) due to lesion ABOVE red nucleus

131
Q

Thalamic hemorrhage

A

Contralateral sensory loss, aphasia, temporary homonymous hemianopia (unilateral abducens palsy, pupil asymmetry, nonreactive downward gaze)

132
Q

Peripheral vertigo

A

More common type

  • Inner ear etiology (semicircular canal debris, vestibular nerve infection, Meniere’s disease)
  • Positional testing-> delayed horizontal nystagmus
133
Q

Central vertigo

A

Brainstem/cerebellar lesion (vestibular nuclei stroke or posterior fossa tumor)

  • Directional change of nystagmus
  • Skew deviation, diplopia, dysmetira
  • Positional testing–> immediate nystagmus in any direction, may change directions

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